Periodontal Disease and Diabetes Mellitus

Transcription

{i}
C
Under the aegis of
EPHORB MEDLINE INTERNATIONAL Pvt. Ltd. ®
Registered Office – 12/44, Vasundhara, Ghaziabad, Delhi
NCR, India 201012
Website: http://www.idjsr.com
Email:[email protected]
Publication, Subscription, Printing, Distribution and Advertisement
handle by Innovative Publication:
NNOVATIVE PUBLICATION
H - 2 / 94, Bengali Colony, Mahavir Enclave, Part - 1,
New Delhi - 110045, India
Ph.: 91-11-25052216, Telefax: 011-25051061
Mo: +91-8826373757, 8527826746, 8826859373
Website:
www.innovativepublication.comEmail: editor@innovativepublic
ation.com, [email protected]
I
Dr. Ankur Rustagi, MDS (OMFS) (AIIMS) - India.
Dr. Pankaj Dhingra, BDS, DDS - USA
Dr. Anil Chandra, BDS, MDS (KGMU) - India
Dr. Zeeshan Sheikh, BDS, Dip Dental Hygiene, M.Sc (Dental
Materials), PhD - Canada
Dr. Ameet Vaman Revankar, BDS, MDS (Ortho) - India
Dr. Jitendra Sharan, BDS, MDS (Ortho), PhD (Ortho) (AIIMS) India
Dr. Pravesh Bizenia, BDS, MDS (Prostho) (AIIMS) - India
Dr. Sumeet Grover, BDS, MDS (Ortho) - Russia
Subscription Information: A subscription to International Dental
Journal of Student’s Researchcomprises four issues per year. Prices
include postage. Annual Subscription rate for Institutional is INR
5000/- and Individual INR 3000/- and International Institutional Price
US$ 200 and Individual US$ 125 including all postal exp. Free online
access with print subscription.
The amount shall be remitted as Cheque/DD/online transfer in favour
of “INNOVATIVE PUBLICATION” Kotak Mahindra Bank, Branch:
Harpool Singh Market, Main Dwarka Janakpuri Road, New Delhi –
110045, Account No: 7911500308, IFSC Code: KKBK0000177,
MICR Code: 110485008
Dr. Mahesh Sadhnani, BDS, MPH, DMD - USA
Founders
Dr. Kumar Anshul – Manipal College of Dental Sciences, India
Dr. Harsh Rajvanshi - I.T.S Dental College, India
Dr. Ayesha Zaka - Margalla College of Dentistry, Pakistan
Dr. Joharia Azhar Saadat, BDS, MSc (Oral Path) (London), Mphill
(NUST) – Pakistan
Indexed In
Index Copernicus
Genamics Journal Seek
Ulrichsweb Global Serial Dictionary
Directory of Open Access Journals (DOAJ)
DRJI (Directory of Research Journals Indexing)
IIFS (International Impact Factor Services)
ResearchGate.net
GIGA (German Institute of Global and Area Studies)
The Hong Kong Polytechnic University
Scientific Indexing Services
Dr. Kamran Habib Awan, BDS, Ph.D (Oral Medicine) - UK
Editorial Board
Dr. Kumar Anshul - Editor In Chief
Dr. Harsh Rajvanshi - Executive Editor
Dr. Ayesha Zaka - Executive Editor
Communications and Associate Editor
Dr. Paridhi Kalia, University of Louisville School of Dentistry, USA
Cover Art By
Dr. Ebadullah Shafi, Design and Graphics Incharge- RAK College of
Dental Sciences, UAE
Reviewers Panel
Dr. Gregori Kurtzman, DDS, Fellow in the AGD, AAIP, ACD, ICOI,
PFA, ADI. Mastership - AGD and ICOI. Diplomat- ICOI, ADIA –
USA
Dr. Saurabh Lall, BDS, MDS (Perio), Fellow PFA - India
Dr. Rajeev Chitguppi, BDS, MDS (Perio) - India
Dr. Thomas Thong Nguyen, DMD, AEGD, MSc Dental SciencesCanada
Dr. Ashith B. Acharya, BDS, GDFO, Forensic Odontologist - India
Dr. Mohamed-Nur Abdallah, BDS, M.Sc Dental Sciences - Canada
Dr Swati Pradeep Patel, BDS, MDS (Perio), PhD (Perio) - India
Dr. Emmanuel J. N. L. Silva, M.Sc (Endo), PhD (Endo) - Brazil
Dr. Jaime Díaz, DDS, M.Sc - Chile
Dr. Malay Kumar, BDS, MDS (Oral Path) - India
Dr. Fahim Ahmed Vora , MDS (Prostho), M Clin Dent (Prostho),
MFDS, RCPSG - UK
Dr Haby Mathew Somson, BDS. MDS (Prostho), Dip. in Laser
(Geneva) - India
Dr. Suresh Shenvi, BDS, MDS (Endo) - India
Dr. Satpreet Singh, BDS, MPH (USA) - India
Dr. Ramesh Kumaresan, BDS, MDS (OMFS) - Malaysia
Dr. Ala' Ersheidat, BSc, BDS, JB (Perio) – Kingdom of Jordan
Dr. Meena Jain, BDS, MDS (PHD), PhD (Dent. Sci.) India
Dr. Zohaib Khurshid, BDS, MRes in Biomaterials - UK
Dr. Shivani Kohli, BDS (MAHE), MDS (Prostho) - Malaysia
Dr. Naresh Sharma, BDS, MDS (Pedo), MADA (USA) - India
Dr. Christopher Majdi, MSHCA, CHBC, CBA - USA
Dr. Mohammed Jasim Al-juboori, BDS, M.Sc (Implant Specialist),
Fellow ICOI - Iraq
Dr. Stefan Theodor Serban, DMD, MPH- Netherlands
Dr. Qian Wang, DMD, Ph.D (China), Post-Doctoral Fellow- USA
Dr. Juan Carlos Munévar, MSc (Oral Biology) - Colombia
Dr. Shivlal Vishnoi, BDS, MDA (Perio) - India
Dr. Manu Dhillon, BDS, MDS (OMDR) - India
Dr. Shaveta Kaushal, MDS, MIPS (Prostho) - India
Dr. Narayan H Gandedkar, MDS (Ortho), FCFO - Taiwan
Dr. Ujjwal Pyakurel, BDS, MDS (Ortho) - Nepal
Dr. Ricardo Machado, Masters in Endo, PhD (Endo) - Brazil
Dr. Muhammad Sohail Zafar, BDS, PhD (UK), MSc (UK), F.I.C.D
(USA), F.A.D.I (USA) – Kingdom of Saudi Arabia
Dr. Mohamed El-Massry, MBBCh, MSc (Gen Surgery), BDS, PhD
(Oral, Plastic and Maxillofacial Surgery) - Egypt
International Dental Journal of Student’s Research, January – March 2015:3(2)
ii
VOLUME III ISSUE II
SPECIAL EDITION ON PERIODONTOLOGY
INDEX
S.No.
1.
2.
3.
TITLE
Title Page
A Foreword
GUEST EDITORIALS – Dr. Zeeshan Sheikh & Dr. Zohaib Khurshid
Page No.
4.
EDITORIAL – FOUNDERS
42
5.
ORIGINAL RESEARCH
In-vitro properties of calcium phosphate cement as a bone grafting material
43-45
40
41
6.
Dr. Ashar Jamelle, Professor Robert Hill, Dr. David Gillam
SHORT COMMUNICATION
Natural and synthetic hydrogels for periodontal tissue regeneration
46-48
7.
Dr. Marco Laurenti
CLINICAL CASE REPORT
Bone fenestration: A case report of management of a lower anterior buccal bone fenestration
49-51
8.
Dr. Murai Khalifa
CLINICAL DIAGNOSIS & GUIDELINES
A Histological and Clinical Evaluation of Shallow and Deep Probing Depths
52-55
9.
Siavash Hassanpour, Shlomi Tamam , Timur Shigapov
Prevention of mandibular nerve injury associated with dental implant placement: preoperative and
intraoperative recommendations
56-57
10.
Thomas T. Nguyen
Periodontal Disease and Diabetes Mellitus: Case Report
58-65
11.
H Marie Keeling, Tamara L. Wright
SYSTEMATIC REVIEW
Sinus lift grafting materials and immediate implant placement: A systematic review
66-71
12.
Dr. Kashif Hafeez, Dr. Aiyesha Wahaj, Dr. Muhammad Sohail Zafar , Dr. Sana Shahab
SYSTEMATIC REVIEW
Laboratorial and clinical impacts of tobacco on periodontal health: A systematic review
72-78
13.
Fahad Sikander Khan, Aisha Aziz , Dr. Sana Shahab, ,Dr. Muhammad Sohail Zafar
SHORT COMMUNICATION
A review of the use of laser in periodontal therapy
79-82
14.
Dr. Amir Manzoor Shah , Dr. Khurram Khan , Dr.Fahd Ahmed , Dr.Nida Amir
ORIGINAL RESEARCH
Prevalence of bleeding gums while tooth brushing among betel nut chewers vs non betel nut chewers in
school going children
83-87
15.
Dr. Syed Misbahdduin, Dr. Mansoor Ul Aziz, Dr. Asma Fazal, Dr. Tayyaba Khairuddin, Dr. Safia Khairuddin
SHORT COMMUNICATION
Short communication: Stem Cells for Periodontal Tissue Regeneration
88-92
16.
Dr. Mohamed-Nur Abdallah, Dr. Mai S. Ali
Periodontal Disease in Immunodeficient Patients: Clinical Guidelines for Diagnosis and Management.
93-104
17.
Morvarid Oviesi, Oriyah Barzilay, Ahmed A. Hanafi
Autogenous Connective Tissue Graft for the Treatment of Localized Gingival Recession: A Case Report
105-108
Dr Zohaib Akram, Dr Haroon Rashid, Dr FahimVohra
International Dental Journal Of Student’s Research, April-June 2015;3(2)
{40}
Dr. Nader Hamdan
BDS, MSc
Resident - Division of Periodontics
Department of Diagnostic and Surgical Sciences
College of Dentistry, Faculty of Health Sciences
University of Manitoba, Canada
Email: [email protected]
It is very hard to find somebody who does not agree that periodontology and its related sciences were the focus of
dental research in the last few decades thanks to its unique and special mix of biology, basic sciences, medicine, and
surgery. Interest in periodontology as a science and periodontics as a clinical practice was heightened even more
after the proven and suggested links between periodontal disease and a host of relatively common systemic
conditions, such as cardiovascular diseases, diabetes, arthritis, pneumonia, Alzheimer’s disease and gestation
outcome complications among others. Therefore, it was not surprising to dedicate this issue of the International
Dental Journal of Students' Research (IDJSR) to periodontology in order to shed more light on what do university
academics and their trainees contribute to this interesting and quickly progressing field.
This periodontology issue, which is the first special edition of IDJSR, includes studies originating from reputable
university research centers in the east and the west (Malaysia, Pakistan, Ireland, UK, USA, and Canada) offering
different perspectives and providing different levels of evidence ranging from case reports to systematic reviews in
addition to reports of original research and short communications. The material presented covers appealing topics
and addresses important questions of clinical relevance adding value to this issue through offering knowledge that
could be directly translated into clinical practice.
Since it was first established, IDJSR took big strides towards achieving its goal as the students’ committed researchdissemination hub and their exclusive vehicle to present scientific work and share intellectual output in the most
pertinent topics. This special edition on periodontology is just another example of that commitment and will mark an
important step forward for the IDJSR.
I hope you enjoy this issue as much as I enjoyed going over its versatile material. I would like to extend special
thanks to the authors who participated. My thanks also go to the guest editor Dr. Zeeshan Sheikh who devoted this
edition of the IDJSR to periodontology and honored me with the kind invitation to provide the “foreword section” as
my humble contribution!
Best Wishes!
International Dental Journal of Student’s Research, April - June 2015;3(2):40
{41}
GUEST EDITORIAL
Dr. Zeeshan Sheikh – Guest Editor
Matrix Dynamics Group. Faculty of Dentistry,
University of Toronto.
150 College Street, Room 222.Toronto, ON, Canada. M5S 3E2
Website: http://matrixdynamics.ca
E-Mail: [email protected]
Dear Colleagues,
It is an honor for me to be the guest editor for the periodontology special edition issue by the IDJSR. The primary
purpose of this special edition is to present the research and clinical case reports in the field of periodontology in
order to stimulate a critical analysis and a discussion on the future of the periodontal practice and research. The
initiatives being taken by this journal paves the way for dental students/clinicians/researchers from all over the
world to contribute and share their research. I can only see this journal go from strength to strength and I wish the
whole team of IDJSR the very best and look forward to being associated with them in the future.
We know from the current data from USA alone that about 46% of the population has some form of periodontitis.
This when coupled with an increase in life-expectancy leading to an aging population, means that the importance of
managing and treating periodontal disease is more important than ever. There is a need to develop more effective
strategies for periodontal therapy to achieve optimal outcomes with high levels of clinical success. Most of the
activities within the field of periodontology are largely focused on the development of implant placement
techniques, implant-related materials and state-of-the-art implant systems. As dentists, we treat patients by
acknowledging the importance of prevention by maintenance of oral hygiene, early diagnosis and intervention for
appropriate management of periodontal health. The same approach must be adopted for implant patients and a risk
assessment should be performed. Presence of different medical conditions, susceptibility to periodontal disease and
use of certain drugs can limit the success of implants. Implant loss, mucositis, marginal bone loss and periimplantitis are the more common types of complications reported in implant therapy. With the increasing number of
implants being placed currently, it can be expected that the frequency with which we encounter peri-implant lesions
will increase as well. There are constant advances being made in periodontal regenerative therapy,
immunoregulation, vaccination and community based approach to prevention. The knowledge and technology that is
available today makes it an exciting time in the field of periodontology. It is imperative that we decide wisely how
these professionals aids are going to be of benefit to our patients.
Dr Zohaib Khurshid – Co Guest Editor
B.D.S, MRes in Biomaterials (Student)
Cert. in Aesthetic Dentistry (Kings College London)
Cert. in Laser Dentistry (BACD, UK)
Senior Lecturer
Department of Dental Materials and Oral Biology
Altamash Institute of Dental Medicine
Karachi, Pakistan
Consultant Dental Advisor
Paramount Book Publisher, Pakistan
It is extremely difficult to ignore the research done on periodontal tissue in relation to its physiology and pathology,
diagnosis, epidemiology and prevention and therapy of periodontal disease. In present scenario where almost half of
the population is effected by some level of periodontal problem it is difficult to its importance. Therefore special
volume of this journal emphasises on publishing the original contributions of high merit from different part of
world.
International Dental Journal of Student’s Research, April - June 2015;3(2):41
{42}
EDITORIAL
Dr. Kumar Anshul
Dr. Harsh Rajvanshi
Dr. Ayesha Zaka
Founder & Editor In Chief
Manipal College of Dental
Sciences, India
Founder & Executive Editor
I.T.S Centre for Dental Studies
& Research, India
Founder &Executive Editor
Margalla College of Dentistry
Pakistan
“My family is like a sanctuary to me.I turn to them for support and strength. I take comfort in knowing no matter
which path I choose, my family stands behind me.”
Anonymous
Family is our support system. We rely on our family for everything – they are our pillars of strength. Same way for
the tooth – the periodontal structures are its family. No matter how much stress the tooth bears, family backs it up.
The care of these periodontal structures is necessary, for without it; the tooth cannot stand alone.
This is the era of Periodontology and as promised, the editorial board of IDJSR brings to you the dessert from the
Editorial Kitchen – The Special Issue on Periodontology. This delicacy is topped with creamy articles with
ingenious stuffing. With modernization, focus is being shifting to more prophylactic and conservative approaches
&Periodontics deals with the very same concept.
In this issue, we have two great researchers – Dr. Zeeshan Sheikh as the Guest Editor and Dr. Zohaib
Khurshidas the Co-Guest Editor who have kindly worked with us on this issue. We have articles from around the
world - Malaysia, Pakistan, Saudi, Canada, Egypt, Ireland, UK, USA with the stalwarts sharing their
experiences with us.
Readers, authors and peers – We shall be coming up with another regular issue hot off the press in the month of
August, 2015. The call for papers is open!
At IDJSR, we have always strived to bring something fresh and new to the field of Dental Literature. We hope that
this issue helps both the clinicians and researchers at large.
Happy Reading!
International Dental Journal of Student’s Research, April – June 2015;3(2):42
{43}
ORIGINAL RESEARCH
In-vitro properties of calcium phosphate cement as a
bone grafting material
Dr. Ashar Jamelle1,
Prof. Robert Hill2,
Dr. David Gillam3,
1
Masters clinical Periodontology, Queen Mary
University London, UK and Department of
Periodontology, Fatima Jinnah Dental Hospital,
Karachi, Pakistan
2
Professor of Physical Sciences in Relation to
Dentistry Institute of Dentistry Dental Physical
Sciences Unit
3
Clinical Senior Lecturer in Periodontology
(Specialist in Periodontology) Queen Mary
University London, UK
Corresponding author:
Dr. Ashar Jamelle
Access this Article Online
www.idjsr.com
Use the QR Code scanner to
access this article online in our
database
Article Code: IDJSR SE 0160
Quick Response Code
Abstract
In 1980’s researchers discovered CPCs (calcium
phosphate crystals) which are a bioactive and
biodegradable bone grafting material. Phases form
after mixing in different compositions with different
end products which are mainly two types; Brushite,
and a Apatite. Bioactive glass can undergo
dissolution in physiological solutions and form a
hydroxycarbonated apatite like phase (this includes
Octacalcium or Flouroapatite). Novel material can be
made by mixing bioglass and Ca(H2PO4)2 and have
cements set to form hydroxyapatite or brushite
produce HAP, brushite and fluorapatite forming
cements. The aims and objectives of this study were
to investigate the influence of storage media on the
Calcium Phosphate Cements combined with
bioactive glass, with respect to properties and phase
formed and strength of development. Would the
outcomes of storing in a media enriched in calcium
and phosphate (that more closely mimics the in vivo
conditions, Simulated body fluid) and Tris buffer
solution. To See histological and structural that do invivo implanted cements show the formation of more
hydroxyapatite and higher mineral contents. To
determine mechanical properties does it result in
higher compressive strength. Functionally does it aid
the conversion of Octacalcium phosphate to
Hydroxyapatite. Calcium phosphate was measured
0.98 gms and mixed with bioactive glass 1.02 gms
and placed in a 6 by 4 Cylinder, placed in aoven.
Cements were immersed into both TRIS buffer and
Simulated body fluid solution for 1hour, 1day, 7days
and 28 days .The compressive strength was
determined by a Instron machine. Characterization
of phases was seen by analysis through
FTIR(spectoscopy)
and
X-ray
diffraction
microtomography
(determine
quantitative
measurements of mineral concentration in hard
tissue). It was seen that the storage media does have a
influence in properties and phases formed.
Keywords: Calcium phosphate; Brushite; Apatite;
Bioactive glass; TRIS buffer; Simulated body fluid.
Introduction
One of the prerequisites of periodontal regeneration
is the formation of bone. Bone grafting is possible
because the bone tissue, unlike many other tissues,
has the ability to regenerate completely if there is
sufficient space to grow into. As bone grows, it will
generally replace the graft material completely, and
result in a totally integrated region of new bone. The
biological mechanisms providing a rationale for bone
grafting are the following osteoconduction,
osteoinduction, osteopromotion and osteogenesis.1
Osteoconduction phenomena occurred when the bone
graft material served as a scaffold for new bone
growth and therefore it was perpetuated by the native
bone. Osteoblast from the margin of the defect being
grafted utilized the bone graft material as a
framework upon which to spread and to synthesize
new bone.1 Bone grafting is a surgical procedure that
was performed to replace the missing bone with a
material from a patient's own body, an artificial,
synthetic, or a natural substitute. Bone grafting was
possible when the bone tissue had the ability to
regenerate completely if sufficient space was
International Dental Journal of Student’s Research, April-June 2015;3(2):43-45
{44}
provided into which the bone can grow. As natural
bone grows, it can generally replace the graft material
completely, and result in a fully integrated region of
new bone. Classification of the bone grafts based on
various material groups are2 Allograft-based bone
graft entails allograft bone, can be used alone or
incombination with other materials (e.g., Grafton®,
OrthoBlast®).
Factor-based bone graft are natural and recombinant
growth factors, which are used alone or in either in
merging with other materials, such as transforming
growth factor-beta (TGF-beta), Platelet-derived
growth factor (PDGF), fibroblast growth factors
(FGF), and bone morphogenetic protein (BMP). Cellbased bone grafts use cells to generate new tissue
alone or are added onto a support matrix, for
example, haemapoetic stem cells. Ceramic-based
bone graft substitutes which include material likes
calcium phosphate, calcium sulphate, and Bioglass
used alone or in combination; for example,
OsteoGraf®, ProOsteon®, OsteoSet®. Polymerbased bone graft used degradable and nondegradable
polymers alone or in combination with other
materials, for example, open porosity polylactic acid
polymers Flexible hydrogel-hydroxyapatite (HA)
composite has a mineral to organic matrix ratio,
which approximates that of the human bone.
Artificial bone can be created from ceramics, like
calcium phosphates (e.g., HA and tricalcium
phosphate), bioglass, and calciumsulphate are
biologically active depending on the solubility in a
physiological environment 3Alloplastic grafts can be
manufactured from hydroxyapatite, and was a
naturally occurring mineral (a main mineral
component of bone), made from bioactive glass.
Hydroxyapatite was a synthetic bone graft, which
was commonly used now due to its properties e.g.,
osteoconduction, hardness, and acceptability by bone.
Calcium orthophosphates have been studied as bone
repair materials for the last 80 years. Calcium
phosphates are part of a group of bioactive synthetic
materials and the most frequently used are the
hydroxyapatite and the tricalcium phosphate
materials. They are commonly used due to their
osteoconductivity, crystallographic structures, and
chemical composition similar to the skeletal tissue.
They are therefore classified according to their
'resorbability' which was that extent of degradation in
vivo. Hydroxyapatite in turn hasbeen described as
“non resorbable” and tricalcium phosphate has been
described as “resorbable”4,5. Calcium phosphate
materials demonstrate a positive interaction with
living tissue that included also the differentiation of
the immature cells towards bone cells5,6. Calcium
Orthophosphate cements (CPC) have been reported
to form two major end products: a precipitated poorly
crystalline HA or CDHA and DCPD (also called
‘‘brushite’’) and apatite cements. The final setting
product of the cements was of the paramount
importance as this would determine the solubility
and, therefore, the in vivo bioresorbability. The main
difference between the two cement types was the
solubility of the end-product: brushite was 1–2 orders
of magnitude more soluble than apatite’s at a
physiological pH and therefore brushite CPCs
normally resorb faster than that of apatite. It has
numerous properties which include osteotransductive, e.g., after implantation calcium
orthophosphate cements may be replaced by new
bone tissue and was osteo-conductive. Calcium
phosphate [Ca(H2PO4)2] cements (CPC) have been
used for the treatment of non-weight bearing bone
fractures or defects.
Bioactive glass has also been used in dentistry as a
bone substitute and a number of therapeutic agents
may be incorporated into the glass structure, for
example fluoride, strontium, chlorine etc. Bioactive
glass (BG) has been reported to form
hydroxycarbonate apatite (HCA). These materials
also exhibit excellent Osseo-integration with bone
and therefore were originally developed for
applications in bone regeneration. Strontium has been
reported in vitro and in vivo to enhance the
replication of pre-osteoblastic cells and decreases the
activity and the number of osteoclasts. The intake of
these strontium containing drugs lead to a greater
deposition of calcium in bone and DNA and bone
collagen synthesis are enhanced7.
Novel materials may also be formulated by mixing a
bioglass composition with CPC in order to improve
the physical properties. The ideal outcome of the new
product was to utilize the bioactivity and
resorbability of a bioactive glass with the added
clinical advantages of in situ setting and extrudability
of CPCs. Strontium can be added to bioglass to some
samples in 25% ratio as that enhances bone
formation.
The aim of the present study was to investigate the
influence of a storage media (Tris buffer solution and
Simulated Body Fluid (SBF) on a modified CPC
combined with a Bioactive glass composition, with
respect to both its properties (e.g., compressive
strength) and the phase formed (e.g., conversion of
Octacalcium phosphate [OCP] to Hydroxyapatite
[HA]) and compressive strength
Materials and Methods
To investigate the influence of storage media on the
Calcium Phosphate Cements, with respect to
properties and phase formed andstrength of
development).What would be the outcomes of storing
in a media enriched in calcium and phosphate (that
more closely mimics the in vivo conditions, e.g.,
Simulated body fluid) Structural; Do in-vivo
implanted cements show the formation of more
{45}
hydroxyapatite and higher mineral contents.
Mechanical; does it result in a higher compressive
strength of the new material calcium phosphate and
bioactive glass.Functional; does it aid the conversion
of Octacalcium phosphate to Hydroxyapatite.
The CPC/Bioglass composition was formulated by
measuring 0.98 gm of calcium phosphate and mixing
with 1.02 gm. of bioactive glass. The cement paste
was mixed and packed into 6 by 4 cylindrical steel
moulds and placed in an incubator at 370c for 120
minutes. The cylinders were removed from the
moulds and immersed in 50 ml of either TRIS buffer
solution or SBF at 370c for 1hour, 24 hours, 7 days
and 28 days The testing of the compressive strength
(Mpa) of the samples (n=8) was by an Instron
universal testing machine type 5567 and
characterization of the different phases of the samples
was by FTIR spectrum and X-rayDiffraction in order
to determine the quantitative measurements of the
mineral concentration in hard tissue.
Fig 2: XRD of the 25% Sr cement after immersion in
SBF Very similar behaviour was observed as for the 0% Sr
glass. However the OCP peak at 4.7o two theta had now
completely disappeared after four weeks of immersion and
the diffraction lines for apatite were slightly sharper. This
indicated that the 25% Sr cement was converting from OCP
to hydroxyapatite more rapidly.
Results
Fig 1: X-Ray Diffraction(XRD) of the 0% Sr cement
after immersion in SBF : shows as a function of time had
a XRD pattern that matched that of hydroxyapatite but in
addition it also had a sharp diffraction peak at 4.7 degrees
two theta which corresponded to the water layer in
octacalcium phosphate (Ca8(PO4)6 H2.5H2O (OCP) which
was thought to be a precursor to hydroxyapatite(HA)
formation in the biomineralisation of tooth and bone 8 .The
characteristic diffraction lines for apatite increased for
longer immersion times and the diffraction line at 4.7
degree two theta characteristic of OCP decreased with
immersion time.
Tris The phase development and phases present in the
25%Sr cement immersed in Tris buffer were similar to the
phases observed on immersion in SBF.
Tris: The phase development and phases present in the
25%Sr cement immersed in Tris buffer were similar to the
phases observed on immersion in SBF.
{46}
Fig 5: Shows the compressive strength for the cements
after immersion in SBF. The cements exhibit an
increasing compressive strength on immersion in SBF from
1 hour to 24 hours but then a marked decrease from 24
hours to 168 hours. This contrasted markedly with the
behaviour found on immersion in Tris buffer. The
reduction in the compressive strength has been associated
with the conversion of OCP to HA for conventional;
calcium phosphate cements.
The 4.7o two theta line of OCP was elucidating and
the results would suggest that immersion in Tris
buffer compared to immersion in SBF favoured the
conversion of OCP to hydroxyapatite. It was also
observed that the presence of calcium in SBF does
not accelerate the conversion process as expected and
in fact the conversion was slower in SBF compared
to Tris buffer. In the compressive strength data
cements exhibited an increasing compressive strength
on immersion in SBF from 1 hour to 24 hours but
then a marked decrease from 24 hours to 168 hours.
This contrasted markedly with the behaviour
observed on immersion in Tris buffer. The reduction
in the compressive strength has been associated with
the conversion of OCP to HA for conventional
calcium phosphate cements.
Table 1: Presence of OCP as a function of time
Discussion
There are limited data with regard to the novel
materials used in the present study although a recent
study by Sadiasaet al.9 in which the investigators
used injectable bone substitutes modified by placing
bioactive glass powders (synthesized via a ultrasonic
energy-assisted hydrothermal method) to the calcium
phosphate-based bone cement in order to improve its
biocompatibility. The present study did not use this
particular methodology (e.g., using the ultrasonic
energy assisted hydrothermal method) and therefore
it would be interesting to speculate on the differences
between the methods. For example in the Sadiasaet
al. 8 study the injectable bone substitutes were
initially composed of a powder component
(tetracalcium phosphate, dicalcium phosphate
dihydrate and calcium sulfate dehydrate) and a liquid
component (citric acid, chitosan and hydroxylpropyl-methyl-cellulose) to which was added various
concentrations of bioactive glass: 0%, 10%, 20% and
30%. By way of comparison in the present study the
liquid and powder ratio was different and the
bioactive glass content was with strontium 0% and
Strontium 25%. Furthermore in the Sadiasaet al.
9
study the setting time and compressive strength of
the injectable bone substitutes was evaluated and it
was reported that the bone substitute improved (in
terms of compressive strength) with the increased
bioactive glass content. Another difference between
the two studies was that the surface morphologies of
the material was not evaluated by scanning electron
microscope (SEM) before and after placing the
samples into simulated body fluid in the present
study.
There was however agreement between the two
studies with regard to the observation that there was
an increase in the apatite formation as shown by xray diffraction. The in vitro biocompatibility of the
injectable bone substitutes would therefore appear to
improve with the placement of bioactive glass as the
proliferation/adhesion behaviour of cells on the
material increased as reported by Sadiasaet al9.
Another element to the Sadiasaet al9study was that
human gene markers were expressed by real timepolymerase chain reaction and the samples were
reported to promote cell viability which appeared to
demonstrate an improved biocompatible as the
concentration of bioactive glass was increased. This
aspect was not explored in the present study. In
addition the In vivo biocompatibility of the various
samples containing 0% and 30% bioactive glass was
also evaluated using a Micro-CT and histological
staining after 3 months of implantation in male
rabbits' femurs. An interesting observation from the
that there was no inflammatory reaction and
significant bone .Another study of interest by Yu et
al10 also evaluated a novel injectable bioactive
cement in order to determine its composition,
microstructure,
setting
time,
injectability,
compressive strength and to observe the behaviour of
the material in simulated body fluid an aspect which
was similar to the present study. The in vitro cellular
{47}
responses of the osteoblasts and the in vivo tissue
responses following the implantation of calcium
phosphate cement and bioglass in the femoral
condyle defects of rabbits was also investigated by
Yu et al.10 As mentioned previously the present study
did not undertake any similar procedures in an animal
model to determine whether the product would be
suitable in terms of biocompatible which in retrospect
would have been an important component to the
investigation. In the Yu et al. study CPC-BG was
observed to have a retarded setting time and also an
improved injectability and mechanical properties than
CPC alone. It was also observed that a new Cadeficient apatite layer was deposited on the
composite surface after it was placed in SBF for 7
days. It was also observed that the CPC-BG samples
demonstrated a significantly improved degradability
and bioactivity compared to CPC in the simulated
body fluid (SBF). The improvement in cell
attachment, proliferation and differentiation on CPCBG were superior to cells observed on CPC.
Macroscopic evaluation, histological evaluation, and
micro-computed tomography (micro-CT) analysis
observations also demonstrated that CPC-BG
enhanced the efficiency of new bone formation in
comparison with CPC alone. No histological
evaluation or proliferation studies were undertaken in
the present study. The Yu et al.10study concluded that
a novel.HydroSet represented the next generation in
bone substitute technology and was reported to be an
excellent bone substitute solution for a number of
clinical applications and surgical specialties.
HydroSet was a self-setting calcium phosphate
cement and contained apatite which converted to
hydroxyapatite (the principal mineral component of
bone).
The crystalline structure and porosity of hydroSet
indicated that it was an effective osteoconductive and
osteointegrative material, with good biocompatibility
An Ovine Implant study in Britain was undertaken by
Hill et al.11 on bioactive glass (with three kinds of
glasses) plus Calcium phosphate and Hydroset. The
research group implanted the material into femur
sites both right and left sides distal and proximal. The
implantation was placed in one animal for six weeks
and in six animals for twelve weeks. Scattered SEMs
demonstrated that for the 6 weeks ovine implanted
there was relatively little resorbtion of the cement for
all cements including Hydroset. No thermal
emissions (isothermic) were observed during the
hardening phase at 6 weeks and three months.
Analysis was done using XMT, Histology, Peripheral
quantitative computed tomography (pQCTBack). It
was
observed
that
there
was
excellent
osseointegration with bioglass cements and that
HydroSet was more radio opaque due to higher
density at 6 weeks. New bone growth surrounded all
thecements and interdigitation of cements with the
host bone The novel cements were observed to set invivo and ‘wash out’ of the cement was not witnessed
and excellent osseointegration of all cement
compositions was evident. New bone formation
surrounding implanted cement high level of
resorption and remodeling at twelve weeks
octacalcium phosphate & hydroxyapatite forming
cements brushite Cements was observed.
Conclusion
The results from the present study demonstrated that
the media influenced how compressive strength
changes and storage in SBF resulted in an increase in
the compressive strength initially compared to a
reduction in Tris buffer. The presence of strontium
inhibited the formation of brushite probably because
the Sr2+ cation cannot replace Ca2+ ions in the
Brushite crystal lattice. It would therefore appear
according to the results obtained that storing the
combined CPC/Bioglass composition in Tris buffer
solution and Simulated Body Fluid had an influence
on both the compressive strength and the phase
formed over the media used to store the cements
influenced the phases formed and in particular the
conversion.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Klokkevold, P. 2002. Surface enhancement to optimize
the success of dental implants. Interview by Arun K.
Garg. Dent Implantol Update, 13, 17-23
Laurencin, C., Khan, Y. & EL-AMIN, S. F. 2006.
Bone graft substitutes. Expert Rev Med Devices, 3, 4957.
Prasanna JS, Karunakar P, Rajashree D, Solomon RV.
2013 .Bone regeneration in a periodontally challenged
hopeless tooth. J NTR Univ Health Sci;2:296-301
Legeros, R. Z. 1988. Calcium phosphate materials in
restorative dentistry: a review. Adv Dent Res, 2, 16480.
Hench, L. L. 1998. Bioceramics. Journal of the
American Ceramic Society, 81, 1705-1728.
T. V. Thamaraiselvi and S. Rajeswari.2004.Biological
Evaluation of Bioceramic Materials - A Review.Trends
Biomater.Artif. Organs, Vol 18 (1), pp 9-17 .
Dahl, S. G., Allain, P., Marie, P. J., Mauras, Y.,
Boivin, G., Ammann, P., Tsouderos, Y., Delmas, P. D.
&Christiansen, C. 2001. Incorporation and distribution
of strontium in bone. Bone, 28, 446-53.
Wang, X., Chen, L., Xiang, H. & YE, J. 2007.
Influence of anti-washout agents on the rheological
properties and injectability of a calcium phosphate
cement. Journal of Biomedical Materials Research
Part B: Applied Biomaterials, 81B, 410-418
Sadiasa, A., Sarkar, S. K., Franco, R. A., Min, Y. K. &
LEE, B. T. 2014. Bioactive glass incorporation in
calcium phosphate cement-based injectable bone
substitute for improved in vitro biocompatibility and in
vivo bone regeneration. J BiomaterAppl, 28, 739-56.
YU, L., LI, Y., Zhao, K., Tang, Y., Cheng, Z., Chen,
J., Zang, Y., WU, J., Kong, L., Liu, S., Lei, W. & WU,
{48}
Z. 2013. A novel injectable calcium phosphate cementbioactive glass composite for bone regeneration. PLoS
One, 8, e62570
11.
Karpukhina D.N., Kent &Hill (2013 submitted) highly
bioactive glass reacts to form in vitro setting calcium
phosphate bone cement.
__________________________________________________
{46}
SHORT COMMUNICATION
Natural and synthetic hydrogels for periodontal tissue
regeneration
Dr. Marco Laurenti1
Dr. Mohamed-Nur Abdallah2
1
MSc, PhD, Postdoctoral Fellow,
BDS, MSc, PhD,
Faculty of Dentistry, McGill University, Montreal,
Quebec, Canada
2
Corresponding Author
Dr. Marco Laurenti
www.idjsr.com
database
Quick Response Code
Over the past few decades, there has been a great
interest in periodontal regeneration therapy to restore
the tissues destroyed by periodontal diseases, which
are probably one of the most common bacterial
infections in humans and the leading cause of tooth
loss in adults. Periodontal diseases involve a set of
inflammatory processes that are progressively
destroying the tooth-supporting tissues (gingiva,
periodontal ligament (PDL), alveolar bone and root
cementum). Untreated periodontitis may cause
irreversible destruction to these tissues leading to
increased tooth mobility and subsequent tooth
loss[1].
Currently, there is still no ideal therapeutic method to
cure periodontitis or to optimally regenerate
periodontal tissues in a predictable manner.
Conventional
mechanical
or
anti-infective
periodontal therapies eliminate the inflammatory
processes, and hinders or halts the diseases resulting
generally in tissue repair without any notable signs of
regeneration. Therefore, various regenerative
approaches have been proposed and evaluated to
restore the lost tooth-supporting tissues. These
approaches included a wide range of surgical
procedures and the use of various bone grafts,
occlusal barrier membranes, purified protein
mixtures, growth factors. Some of these approaches
have achieved some success in regenerating the
damaged periodontal tissues in certain ideal clinical
cases; however, the outcomes are still very variable
and unpredictable. Even with bone grafts, which are
considered the current gold-standard material for
bone regeneration, have reported failure rates up to
30% in maxillofacial and craniofacial surgeries, in
addition to their drawbacks such as limited
availability and donor-site morbidity. It is evident
that a considerable research activity is required to
improve the current periodontal therapies and to
develop novel treatments to reach the ultimate goal of
periodontal therapy, which is the predictable
reconstruction of the lost periodontal tissues.
Periodontal tissue possess the capacity to regenerate
itself and substantial efforts in the tissue engineering
field have been done to understand this ability in
order to overcome the current limitations of
therapeutic and regenerative procedures [3]. Tissue
engineering is a multidisciplinary field that aims to
guide body regeneration by specifically controlling
the biological environment or developing biological
substitutes to restore tissue functions. The damage to
any tissue or organ results in the destruction and loss
of extracellular matrix (ECM) with the absence of
functional cells. For this reason, it is of paramount
importance to restore the structure, properties, and
functions of the native natural tissue. The general
approach to restore the initial tissue condition is to
use a three-dimensional (3D) scaffold which has the
function to temporary supports the cell growth and
new tissue development. The 3D scaffold may be
designed as purely structural support providing with
biological moieties incorporated into the scaffold to
guide cell and tissue growth. Regeneration of
dental/craniofacial tissues may be successfully
achieved from the inimitable blend of human cells
seeded biomaterial scaffolds with/without growth
factors [4]. The combination of stem-cells,
biomaterials, and physio-biochemical factors is the
basis and major contribution of tissue engineering to
regenerative medicine. In this approach, the
biomaterial is critical to the regeneration of tissue
since it serves as a three dimensional artificial ECM
or scaffold to provide structural organization and
support for the proliferation and differentiation of
cells to create a neo-tissue. It is the interaction of the
cells’ with the artificial ECM that is pivotal in recreating and maintaining the functional and 3D
International Dental Journal of Student’s Research, April - June 2015;3(2):46-48
{47}
structural integrity of the tissue [4a, 4c]. These
scaffolds should be biocompatible facilitating cell
attachment and proliferation, and biodegradable so
that they do not require any surgical procedure for
removal[5]. Hydrogels are highly hydrated polymeric
biomaterials composed of hydrophilic polymeric
network, either of synthetic or natural origin, and
used as 3D scaffolds for periodontal tissue
engineering
applications[6].
Hydrogels
are
biodegradable, can be tailored to confer mechanical
and structural properties similar to many ECM
tissues, processed under mild conditions required to
encapsulate biological moieties, and delivered in a
minimally invasive manner[7].
Natural biomaterials have been extensively used in
the development of matrix-based regenerative
therapies that aim to accelerate clinical application
due
to
their
excellent
biocompatibility,
biodegradability, affinity for biomolecules and
wound healing activity [8]. Materials such as
collagen, hyaluronic acid, alginate and chitosan
scaffolds have been used in periodontal regenerative
research for more than two decades. The natural
origin of these materials allows the design and
engineering of biomaterial systems that function at
the molecular level, often minimizing chronic
inflammation. They can also be easily chemically and
physically modified to form desired structures. The
use of natural polymers in the form of hydrogels
allows for the incorporation of biological agents by
promoting cross-linking when the growth factor is
dispersed in the polymer solution. Because natural
polymers are often soluble in water, the creation of
hydrogels may occur under mild fabrication
conditions that are relatively harmless to the
bioactivity of the growth factors. Normally, these
hydrogels are degraded by enzymes and/or acid
hydrolysis at a rate depending on the degree of
crosslinking or the molecular weight [8].
Collagen is one of the most used biomaterials due to
its excellent biocompatibility, weak antigenicity,
biodegradability, and safety. Collagen hydrogel fits
well with injectable cell delivery and highly porous
cross-linked scaffolds provide good mechanical
stability. For these reasons, collagen hydrogels have
been used as support for in vitro growth of many
types of tissues and to deliver different kinds of
growth factors. Following the clinical use of collagen
carriers delivering bone morphogenetic proteins for
tibial shaft fractures [9], spine fusions and long-bone
nonunions [10], collagen is currently being evaluated
for widespread clinical periodontal regeneration. For
example, there are commercially available collagen
composite scaffolds such as Formagraft™ and
OssiMend™ for periodontal regeneration currently
used in animal studiesand clinical trials [11].
Chitosan is biodegradable natural polymer and it has
been used as a cell vehicle material due to its ability
to be molded into various geometries (e.g. porous
structures). In addition, chitosan has minimal foreign
body reaction and high affinity for in vivo
macromolecules [12]. However, chitosan is not
strongly supportive of tissue regeneration as
demonstrated by its effect on the width of keratinized
gingiva in dogs [13]. The addition of hydroxyapatite
to chitosan hydrogels produced a 3D scaffold in
which the pore sizes and interconnectivity were
preserved, resulting in a suitable 3D environment to
support cellular structure, proliferation and
mineralization [14].
Synthetic polymers have been widely used for
scaffolding applications because of their ability to
provide controllable and reproducible structural
properties,
biocompatibility,
and
tailored
biodegradation rates [15]. Scaffolds made of
synthetic polymers can be produced by a variety of
fabrication techniques, and they can be manufactured
into preformed sizes and shapes according to clinical
requirements. There are several synthetic polymers
approved by the US Food and Drug Administration
such as poly(glycolic acid) (PGA), poly(L-lactic
acid) (PLA), their copolymers poly(lactic-co-glycolic
acid) (PLGA), and poly(caprolactone) (PCL). Solid
scaffolds are typically porous matrices fabricated by
techniques such as solvent casting, gas foaming,
particulate leaching, and electrospinning [5, 15].
Other degradable polymers have also been explored
and tested for periodontal tissue regeneration
including poly(ethylene glycol) (PEG) [16],
polylactide and polyglycolide [17]. Amorphous
poly(D,L-Lactic acid) (PDLLA) used in combination
with bioactive glasses ensure the creation of a
macroporous structure within the bioceramic
materials showing promising properties for
periodontal tissue regeneration [5]. Synthetic
polymers can be also used in combination with
natural biomaterials. For example, the rapid
degradation of fibrin, a biopolymer critical to
hemostasis and wound healing, can be decelerated by
modification with (PEG) [18].
Recently, nanocomposites based on polymers and
nanosilica nanoparticles have been applied in
periodontal tissue engineering. Silica nanoparticles
are obtained by the sol–gel method and they can be
incorporated into a polymeric matrix resulting in a
nanocomposites with unique properties such as high
mechanical resistance, chemical stability, and heat
resistance [19]. Tubular nanocomposite scaffolds of
poly(ethyl methacrylate-co-hydroxyethyl acrylate)
[P(EMA-co-HEA)] were synthesized with different
concentrations of silica nanoparticles by fibertemplating method in order to mimic the structure
and functions of natural dentin [20]. These tubular
structures were found to induce the precipitation of
{48}
hydroxyapatite on their surface, and they can
facilitate odontoblastic cell growth with the
integration of host mineralized tissue. Hybrid
P(EMA-co-HEA)/SiO2nanocomposite
matrix
incubated in simulated body fluid for 14 days showed
the best cellular distribution and neo-dentin like
pattern. These constructs also showed enhanced
mechanical properties to withstand functional stresses
[20]. All these results indicate that the nanohybrid
matrix scaffolds could be promising potential sources
for dentin repair and regeneration.
Summary and Challenges
Periodontal regeneration remains a highly
challenging task, since the existing therapeutic and
regenerative approaches have not achieved a
complete or predictable regeneration of the lost
periodontal tissues in humans. The purpose of
research into periodontal regeneration is to establish a
new approach that overcomes the limitations of the
current therapeutic and regeneration procedures. The
synergistic approach of nanomedicine and tissue
engineering is a promising field and has lead, so far,
to a remarkable progress in the field of periodontal
tissue regeneration. Several approaches utilizing
collagen, chitosan, or nano-composites as hydrogels
or rigid scaffolds have been found to promote and
guide periodontal tissue regeneration. However, these
studies are still limited to in vitro and in vivo studies
which highlights the need of future investigation in
this promising field.
Acknowledgment
The authors would like to acknowledge the Network
of Oral and Bone Health Research, and the Faculty of
Dentistry of McGill University for their financial
support.
References
1.
2.
3.
4.
5.
6.
Yuan, Y. Zhu, Y. Y. Zhang, X. L. Li, Y. Zhang, K. D.
Yao, Eur. Polym. J. 2006, 42, 2013-2022.
7.
J. L. Drury, D. J. Mooney, Biomaterials 2003, 24,
4337-4351.
8.
J. F. Mano, G. A. Silva, H. S. Azevedo, P. B.
Malafaya, R. A. Sousa, S. S. Silva, L. F. Boesel, J. M.
Oliveira, T. C. Santos, A. P. Marques, N. M. Neves, R.
L. Reis, J. R. Soc. Interface 2007, 4, 999-1030.
9.
R. Cancedda, P. Giannoni, M. Mastrogiacomo,
Biomaterials 2007, 28, 4240-4250.
10.
A. P. White, A. R. Vaccaro, J. A. Hall, P. G. Whang,
B. C. Friel, M. D. McKee, Int. Orthop. 2007, 31, 735741.
11.
aF. Feng, K. Akiyama, Y. Liu, T. Yamaza, T. M.
Wang, J. H. Chen, B. B. Wang, G. T. Huang, S. Wang,
S. Shi, Oral. Dis. 2010, 16, 20-28; bT. G. Kim, U. M.
Wikesjo, K. S. Cho, J. K. Chai, S. D. Pippig, M.
Siedler, C. K. Kim, J. Clin. Periodontol. 2009, 36, 589597.
12.
I. Y. Kim, S. J. Seo, H. S. Moon, M. K. Yoo, I. Y.
Park, B. C. Kim, C. S. Cho, Biotechnol. Adv. 2008, 26,
1-21.
13.
G. Lotfi, M. A. Shokrgozar, R. Mofid, F. M. Abbas, F.
Ghanavati, A. A. Bagheban, R. P. Shariati, J.
Periodontol. 2011, 82, 1367-1375.
14.
aA. C. Akman, R. S. Tigli, M. Gumusderelioglu, R. M.
Nohutcu, J. Biomed. Mater. Res. A 2010, 92, 953-962;
bY. Zhang, B. Shi, C. Li, Y. Wang, Y. Chen, W.
Zhang, T. Luo, X. Cheng, J. Control Release 2009,
136, 172-178; cF. Liao, Y. Chen, Z. Li, Y. Wang, B.
Shi, Z. Gong, X. Cheng, J. Mater. Sci. Mater. Med.
2010, 21, 489-496.
15.
P. Gunatillake, R. Mayadunne, R. Adhikari,
Biotechnol. Annu. Rev. 2006, 12, 301-347.
16.
P. Valderrama, R. E. Jung, D. S. Thoma, A. A. Jones,
D. L. Cochran, J. Periodontol. 2010, 81, 737-747.
17.
G. Serino, W. Rao, G. Iezzi, A. Piattelli, Clin. Oral.
Implan. Res. 2008, 19, 26-31.
18.
J. M. Galler, A. C. Cavender, U. Koeklue, L. J. Suggs,
G. Schmalz, R. N. D'Souza, Regen. Med. 2011, 6, 191200.
19.
aD. S. Achilias, D. N. Bikiaris, V. Karavelidis, G. P.
Karayannidis, Eur. Polym. J. 2008, 44, 3096-3107;
bM.Sadej-Bajerlain, H. Gojzewski, E. Andrzejewska,
Polymer 2011, 52, 1495-1503; cS.Barus, M. Zanetti,
M. Lazzari, L. Costa, Polymer 2009, 50, 2595-2600.
20.
A. V. Lluch, A. C. Fernandez, G. G. Ferrer, M. M.
Pradas, J. Biomed. Mater. Res. B 2009, 90b, 182-194.
__________________________________________________
B. L. Pihlstrom, B. S. Michalowicz, N. W. Johnson,
Lancet 2005, 366, 1809-1820.
H. F. Rios, Z. Lin, B. Oh, C. H. Park, W. V.
Giannobile, J. Periodontol. 2011, 82, 1223-1237.
F. M. Chen, Y. Jin, Tissue Eng. Part. B-Re 2010, 16,
219-255.
aV. Rosa, A. Della Bona, B. N. Cavalcanti, J. E. Nor,
Dent. Mater. 2012, 28, 341-348; bS. F. Yang, K. F.
Leong, Z. H. Du, C. K. Chua, Tissue Eng. 2001, 7,
679-689; cS. F. Yang, K. F. Leong, Z. H. Du, C. K.
Chua, Tissue Eng. 2002, 8, 1-11.
K. Rezwan, Q. Z. Chen, J. J. Blaker, A. R. Boccaccini,
Biomaterials 2006, 27, 3413-3431.
aC. R. Nuttelman, S. M. Henry, K. S. Anseth,
Biomaterials 2002, 23, 3617-3626; bB. Duan, X. Y.
{49}
Bone fenestration: A case report of management of a
lower anterior buccal bone fenestration
Dr. Murai Khalifa1
Yuliya Mulyar2
1
BDS, DDS, GPR, McGill University,
Family Dental Clinic, Strathmore,
Alberta, Canada
2
BA Psychology, DDS candidate
Schulich School of Medicine & Dentistry, Western
University, London, Ontario, Canada.
Corresponding Author:
Dr. Murai Khalifa
Email:[email protected]
www.idjsr.com
database
Article Code: IDJSR 0162
Quick Response Code
Abstract
The term fenestration refers to a circumscribed defect
that creates a "window" through the bone over the
prominent root. This lesion will be seen when the
alveolar bone is exposed by a flap surgery, its
associated with localized periodontal destruction.This
case reports a 62year-oldmale patient who presented
with persistent tooth pain at the lower right 2ed
incisor, despite repeated root canal treatments by a
general practitioner. When the patient visited our
clinic, a CT examination was performed and apical
fenestration was diagnosed. The tooth was not
restorable due to a fracture in the apical third from a
previous root canal therapy. Suggested treatment plan
was to extract the tooth, perform bone grafting and a
future implant.
revealed by a flap operation or on a skull preparation
the coronal portion of the root is often not covered by
bone"dehiscence" or there is a fenestration. Isolated
areas in which the root is denuded of bone and the
root surface is covered only by periosteum and
overlying gingiva are termed fenestrations. In these
areas, the marginal bone is intact [1,2]. Such defects
occur on approximately 20% of the teeth; they occur
more often on the facial bone than on the lingual
bone, they are more common on anterior teeth than
on posterior teeth, and they are frequently bilateral.
Microscopic evidence of lacunar resorption may be
present at the margins. The causes of these defects
are not clear. However, predisposing factors include
prominent root contours, malposition and labial
protrusion of the root in combination with a thin bony
plate[3].
Incidence
The incidence of apical fenestration is between 7.5%
and 20%, and is higher in the maxillary than in the
mandibular teeth. It has also been reported that the
incidences higher in the anterior than in the posterior
teeth. The most commonly observed regions are the
canine root and the mesio-buccal root of the
maxillary first molar. Although the cause of apical
fenestration is still unclear, it has been suggested that
anatomical factors such as age-related changes and
the positional relationship between the tooth and the
alveolar bone might be involved. Moreover, occlusal
dysfunction should also be considered.[4]
Management
Fenestration and dehiscence defects have been
managed with barrier membranes or simply with flap
closure. Also, bone grafts has been used in this case.
The only controlled comparison studies between
membrane treatment and periosteal flap coverage of
exposed implant surfaces in humans demonstrated
Keywords:Bone fenestration; Tooth;Graft.
that the membrane treatment was far superior with
regard to bone fill.11Another controlled study in
Introduction
humans has shown better results in the membrane
groups; Infour outof six sites (67%) treated with a
In a healthy periodontium the facial margin of the
membrane resulted in 95% to 100% elimination of
alveolar crest lies approximately 2 mm apical to the
the dehiscence and total coverage of the threads. In
gingival margin, which courses near to the cement
the control sites, only 2 of 6 sites (33%) showed
enamel junction. The facial aspect of the alveolar
moderate-to-complete bone fill.43All other clinical
bone covering the root is usually very thin. As
studies which are in the form of case reports,
{50}
demonstrates coverage of an implant dehiscence
using a barrier membrane. Admittedly, without a
biopsy, it cannot be determined whether the tissue
covering the implant is bone or firm connective
tissue.[5,6]
A one-year multicenter study evaluating 55
Brånemark implants (i.e., machined-surface, external
hex) with bone dehiscence in 45 patients, treated by
ePTFE membrane alone, demonstrated an average
bone fill of 82%.12. The average initial defect height
was 4.7 mm. The 1-year follow-up of these implants
demonstrated a favorable response to loading. Of the
55 implants, a total of 6 failed, corresponding to a
cumulative survival rate of 84.7% in the maxilla and
95.0% in the mandible, which is similar to previously
published results for this implant design. A clinical
report on the use of TR membranes demonstrated the
biologic potential to fill a large protected space in
four patients. 24Bone dehiscence at implant sites
ranged from 5 to 12 mm (mean:8.2 mm). They were
covered with a TR membrane alone (no graft).
Re-entry after 7 to 8 months of submerged healing
found complete bone coverage over all the implants.
Radiographic evaluation demonstrated that the
implants were functioning with normal crestal bone
support after 1 year.
No clinical comparisons are available in the literature
evaluating the placement of bone grafts with or
without barrier membranes on implant dehiscence
defects. Most evidence supports the use of graft
materials in conjunction with membrane treatment,
particularly the use of FDBA in conjunction with
GBR. In a study with 40 patients, 110 implants were
placed in conjunction with barrier membranes and
FDBA; a success rate of 96.8% was achieved with
complete bone fill (defined as >90% fill of
dehiscence)[7].This study reported a membrane
exposure rate of 29%, but noted little adverse effect
on the bone regeneration.
Figure 1. Preoperative diagnostic CT scan
Figure 2. Post extraction Periapical radiograph
It was decided and explained to the patient that the
best approach was to extract tooth 4.2 followed by a
bone graft and an implant 6 months later. The patient
consented to the proposed treatment and subsequently
full mouth impressions were taken to develop study
casts. Upon extraction, the bone fenestration was
noticed with loss of the buccal alveolar bone wall.
Fig3
Case report
A 62 years male patient presented to our clinic with
persistent pain related to the lower 2ed right incisor
tooth. Patient wanted the tooth extracted and implant
placed. Patient medical history was normal. Upon
oral examination, tooth 4.2 was positive to percussion
with possible horizontal fracture. Mobility class II
was noticed and upon radiographic examination, well
circumscribed radiolucent lesion surrounding the
apex of tooth 4.2 was notices, which turned to be a
periapical granuloma after a biopsy.Fig 1,2
Figure 3. Intraoral view showing the alveolar bone
loss and fenestration
Curettage of the lesion was completed and was sent
for biopsy. Next step was to graft the socket using 2
{51}
types of bone. We used a mix of allograft material
which is composed of 50% mineralized cortical and
50% mineralized cancellous size 0.25 mm with the
4bone bch composed of 60 % hydroxyapatite and
40% beta-Tricalcium Phosphate that was covered
with a resorbable membrane. Fig4
Figure 4:Facial view showing bone graft covered
by the membrane
References
1.
Color atlas of Dental Medicine Periodontology By
Herbert F. Wolf, Edith M. Rateitschak-Pluss
2.
Caranza's Clinical periodontology , By Michael G.
Newman, Henry Takei, Perry R. Klokkevold, Fermin
A. Carranza
3.
Elliot JR, Bowers GM: Alveolar dehiscence and
fenestration. Periodontics1:245, 1963.
4.
Bulletin of Tokyo Dental College, 53(1): 23-26
5.
Jensen OT, Greer RO, Jr, Johnson L, et al: Vertical
guided bone-graft augmentation in a new canine
mandibular model. Int J Oral MaxillofacImplants
10:335–344, 1995.
6.
Klokkevold PR, Han TJ, Camargo PM: Aesthetic
management of extractions for implant site
development: delayed versus staged implant
placement. Pract Periodontics Aesthet Dent 11:603–
610, quiz 612,1999.
7.
Klokkevold PR, Han TJ, Camargo PM: Aesthetic
management
ofextractions
for
implant
site
development: delayed versus staged implant
placement. Pract Periodontics Aesthet Dent 11:603–
610, quiz 612,1999.
__________________________________________________
The flap then was closed using silk sutures size 3.0.
An antibiotic course was started and analgesics were
prescribed to patient and he was scheduled for
follow-ups.Fig5
Figure5: Periapical radiograph6 weeks follow up.
The patient reported that pain and discomfort
disappeared. Site healing was optimal and patient will
be ready for an implant in a four months period.
Conclusion
The etiology of bone fenestration is still unclear. In
most cases, early diagnosis and treatment can lead to
successful management and do not require extensive
treatment. In this case, we were able to preserve the
socket for a future implant and give patient more
options to restore the missing tooth.
{52}
A Histological and Clinical Evaluation of Shallow and
Deep Probing Depths
Siavash Hassanpour1,
Shlomi Tamam2,
Timur Shigapov3,
1
H.BSc., M.Sc. DDS, Matrix Dynamics Group,
Faculty of Dentistry, University of Toronto, Canada
2
H.BSc., M.Sc. DDS, East Village Dental Center,
Oshawa, Canada.
3
H.BSc, DDS, De Man and Hoediono Dentistry,
Kitchener, Canada
Siavash Hassanpour
www.idjsr.com
database
Quick Response Code
New and improved diagnostic aides are constantly
being developed and deployed to improve our ability
to correctly identify, diagnose and treat a variety of
medical conditions. Despite several attempts at
developing a new gold standard tool for the diagnosis
of periodontal disease [1], dental professionals still
largely, although not exclusively, rely on the
periodontal probe and periodontal probing depth
(PD) for the identification and classification of
periodontal diseases. PD is commonly used to
evaluate the presence or absence of periodontal
disease, and PD values are relied on for the
determination of periodontal disease severity[2,3]. To
these authors’ knowledge, no clinical study has
conclusively defined the healthy PD. Generally
speaking, in the absence of gingival recession or
enlargement, shallow PDs of 1-3mm are considered
to be indicative of a healthy or normal periodontal
sulcus. Sites with PD values of 4-6mm are considered
moderately deep and indicative of early stages of
periodontal disease. Ultimately, sites with PD values
greater than 7mm are considered as deep sites,
typically caused by advanced periodontal disease. As
such, clinicians view sites with progressively larger
PDs with increasing concern. The aim of this short
commentary is to use evidence from histological and
clinical studies to discuss the merits of considering a
shallow probing depth as healthy and to highlight
changes induced by periodontal disease that lead to
deepening periodontal pockets.
PD is defined as the distance from the gingival
margin to the deepest part of the probable crevice.
Historically, the terms PD and pocket depth were
used interchangeably. In 1971, Listgarten noted that
PD measurements only offer an estimation of the true
pocket depth, as the probe tip routinely goes beyond
the sulcus and into the attachment apparatus of the
tooth [4]. He further suggested that the only way to
measure the depth of the anatomical sulcus, or
pocket, is through histological means. One of the first
studies to examine the physiological attachment
around healthy human teeth was carried out in 1961
by Gargiulo et al. In this study, Gargiulo defined the
dentogingival complex as the physiological and
functional
supporting
tissue
of
teeth[5].
Measurements were made along 325 surfaces of
presumably healthy teeth in human cadaver jaws.
They concluded that the dentogingival junction is
composed of the junctional epithelium (formerly the
epithelial attachment) and the connective tissue
fibrous attachment. In the study, Gargulio measured
the depth of the true gingival sulcus, the length of the
junctional epithelium and the length of connective
tissue attachment throughout various phases of
passive eruption. The study found the average sulcus
depth to be 0.69mm (range 0.61mm - 1.71mm). The
average length of the junctional epithelium was
0.97mm (range 0.71mm – 1.35mm), while the
average length of the connective tissue attachment
was 1.07mm (range 1.03mm – 1.07mm) [5](Figure
1). As such, assuming a periodontal probe could
precisely measure the depth of a healthy sulcus, we
would expect to get measurements ranging from
0.61-1.71mm. However, the anatomic sulcus or
pocket depth rarely corresponds to the clinical PD
measurement. The periodontal probe routinely goes
beyond the sulcus and penetrates the coronal part of
the junctional epithelium [6]. Even in periodontal
health and in absence of inflammation, the
periodontal probe penetrates the junctional
epithelium by 0.5mm, stopping 0.4mm coronal to the
termination of the junctional epithelium [6]. This
increases the expected PD in healthy tissues to 1.112.21mm (1.11mm = 0.61mm +0.5mm; 2.21mm =
1.71mm + 0.5mm). Also, seeing that probing depth
{53}
measurements are accurate to within 1mm 90% of the
time [7], we can expect healthy probing depths to
range between 0.11mm-3.21mm (0.11mm = 1.11mm
- 1mm ; 3.21 mm = 2.21mm + 1mm) or simply up to
3mm(Figure 2A).
To understand why PD values increase with
periodontal disease progression, one has to examine
the pathophysiology of gingivitis and periodontitis.
Gingivitis is defined by the presence of gingival
inflammation without the loss of periodontal
attachment [8]. Histologically, gingivitis is
characterized by an increase in blood flow, an influx
of inflammatory cells and breakdown of perivascular
connective tissue (Figure 2B)[9]. All together, these
changes lead to clinical features consisting of
edematous, erythematous and friable gingival tissues
that typically extend coronal to the cement enamel
junction (CEJ) and readily bleed upon probing. Even
without periodontal attachment loss, clinical PD
values are increased in gingivitis when compared to
clinically healthy sites. The increased PD during
gingivitis is explained partly by the gingival
enlargement and partly by increased penetration of
the periodontal probe in inflamed tissues. Studies
have shown that the tip of a periodontal probe
penetrates the full length of the junctional epithelium,
stopping 0.1mm to the apical termination of the
junctional epithelium in an inflamed site[6],
compared to 0.4mm in healthy periodontium as
discussed above. Together, these two factors explain
why increased PD values are often associated with
gingivitis in the absence of concurrent loss of
periodontal attachment or loss of alveolar bone.
Unlike gingivitis, periodontitis is characterized by the
pathological loss of collagen fibers, apical migration
of the junctional epithelium, loss of alveolar bone and
periodontal attachment (Figure 2C). Histologic
studies of the progression of periodontitis have
shown that early periodontal lesions are initially
localized to the gingival sulcus and later progress to
the periodontium proper, the periodontal ligament,
cementum and alveolar bone. Histological studies in
more advanced periodontal disease have shown that
during probing, the probe tip penetrates the full
length of the junctional epithelium and extends deep
into the connective tissue attachment[6,10], resulting
in progressively increased probing depth proportional
to the degree of attachment loss. For this reason, deep
PDs are seen in tissues undergoing periodontal
breakdown due to the concurrent apical migration of
the junctional epithelium, the inflamed nature of the
connective tissues and the loss of alveolar bone.
Clinical studies routinely classify pockets into three
groups: 1-3mm, 4-6mm and 7mm and greater [1113].The reason for this common classification system
is twofold. Firstly, this classification system stratifies
diseased sites and helps determine the aggressiveness
of treatment including the need for surgical
periodontal therapy [14]. Secondly, the shallow,
moderate and deep stratification system allows
clinicians to determine the expected outcome of
treatment. Clinicians are often less concerned with
shallow pockets, as shallow pockets are more
amendable to routine oral hygiene at home and are
easier to maintain under professional care. Shallow
pockets are more likely to be adequately cleansed by
manual tooth brushing, which penetrate 0.9mm
below the gingival margin [15]. Likewise, selfadministered oral hygiene routines can remove
interproximal plaque up to 2.5mm subgingivally [16].
Also, when receiving professional prophylaxis and
scaling and root planning (SRP), Brayer et al. found
that even inexperienced practitioners can adequately
cleanse shallow pockets[17]. These shallow pockets
are compatible with good health and function for
many years [18]. While SRP is less efficient at
removing the etiological agents that cause disease
progression in deeper sites, it can effectively remove
plaque and calculus up to 3.73mm subgingivally.
Deeper pockets (> 5mm), however, are rarely free of
plaque and calculus following SRP [19].
Longitudinal studies comparing surgical and nonsurgical therapy have validated the need for surgical
therapy when faced with deep(>7mm) PDs [13,20].
For pockets greater than or equal to 7mm, surgical
periodontal intervention resulted in significantly
greater reduction in probing depth than SRP alone.
This can be attributed to increased access, direct
visualization and correction of unfavorable osseous
architecture during periodontal surgery. In 1982,
Lindhe described the concept as the critical probing
depth (CPD) [21]. CPD is defined as the threshold
PD where gain of clinical attachment can be expected
following treatment. Lindhe found that the CPD for
SRP was 2.9mm, while the CPD of surgical therapy
(Modified Widmann Flap) was 4.2mm. Together,
these results indicate that shallow pockets < 3mm can
be adequately maintained without further loss of
attachment by scaling alone, while promoting the use
of surgical therapy in sites with deeper initial PDs.
Periodontal probing is not a flawless diagnostic
instrument and should not be used in isolation. A
high PD value alone does not imply active disease
nor disease progression[22]. Variations in PD can be
introduced by probing force, probe angulation, probe
thickness, probe type as well as tooth site and local
anatomy [3]. Further, intra- and inter-clinician
variability and reproducibility in PD have been
reported [7,23]. In addition, the depth of probe
penetration is directly proportional to the degree of
inflammation [24-26]. In fact, rather than simply
measuring PD, a better indicator of periodontal
disease severity is clinical attachment level (CAL).
CAL, which is calculated by summing PD and
recession, more accurately estimates loss of
periodontal attachment as a result of periodontal
{54}
disease [27]. Nonetheless, periodontal probing
provides clinicians with a useful estimate of the
location of the most coronal insertion of the intact
connective tissue fibers and thereby verifying the
presence or absence of periodontal disease.
Gingival enlargement in combination with increased
periodontal probe penetration result in increased PD in
tissues suffering from gingivitis. Typically, in tissues
affected by gingivitis, the tip of a periodontal probe
penetrates the full length of the junctional epithelium and
enters the connective tissue attachment, resulting in probing
depth of ≥4mm.
C) Periodontitis is characterized by the pathological loss of
collagen fibers, apical migration of the junctional
epithelium, loss of alveolar bone and periodontal
attachment. In advanced periodontal disease, the probe tip
penetrates the full length of the junctional epithelium and
extends deep into the connective tissue attachment; the
more severe the periodontal attachment loss, the greater the
corresponding probing depths. Inspiration for image comes
from the Color Atlas of Dental Medicine Periodontology,
3rd Edition, and was kindly illustrated by Ms. Gretchen
Kramer.
References
1.
Figure 1. The Dentongingival Complex
The attachment apparatus of a tooth is comprised of the
dentogingival complex and the periodontal ligament. The
dentogingival complex is composed of the junctional
epithelium and the connective tissue fibrous attachment.
The average sulcus depth is 0.69mm (range 0.61mm 1.71mm). The average length of the junctional epithelium
is 0.97mm (range 0.71mm – 1.35mm) and the average
length of the connective tissue attachment is 1.07mm
(range 1.03mm – 1.07mm). Inspiration for image comes
from the Color Atlas of Dental Medicine Periodontology,
3rd Edition, and was kindly illustrated by Ms. Gretchen
Kramer.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Figure 2. The Progression of Periodontal Disease
A) In periodontal health, the periodontal probe penetrates
the entire length of the anatomical sulcus and half way
through the junctional epithelium, resulting in probing
depths of 1-3mm.
B) Histologically, gingivitis is characterized by an increase
in blood flow, an influx of inflammatory cells and
breakdown of perivascular connective tissue resulting in
edematous, erythematous and friable gingival tissues.
13.
14.
15.
Wolf DL, Lamster IB. Contemporary concepts in the
diagnosis of periodontal disease. Dent Clin North Am
2011;55:47–61.
Listgarten MA. A perspective on periodontal
diagnosis. J Clin Periodontol 1986;13:175–81.
Listgarten MA. Periodontal probing: What does it
mean? J Clin Periodontol 1980;7:165–76.
Listgarten MA. Normal development, structure,
physiology and repair of gingival epithelium. Oral Sci
Rev 1972;1:3–67.
Gargiulo AW, Wentz FM. Dimensions and relations of
the dentogingival junction in humans. Journal of
Periodotology 1961;32:261–7.
Armitage GC, Svanberg GK, Loe H. Microscopic
evaluation of clinical measurements of connective
tissue attachment levels. J Clin Periodontol
1977;4:173–90.
Advances in measurements of periodontal bone and
attachment loss. 2000;17:56–72.
Theilade E, Wright WH, Jensen SB, Loe H.
Experimental gingivitis in man. J Periodontal Res
1966;1:1–13.
Page RC, Schroeder HE. Pathogenesis of inflammatory
periodontal disease. A summary of current work. Lab
Invest 1976;34:235–49.
JF S, FG B. Probing of pockets related to the
attachment level. J Periodontol 1976;47:281–6.
Hill RW, Ramfjord SP, Morrison EC, Appleberry EA,
Caffesse RG, Kerry GJ, et al. Four types of periodontal
treatment compared over two years. J Periodontol
1981;52:655–62.
Ramfjord SP, Morrison EC, Burgett FG, Nissle RR,
Shick RA, Zann GJ, et al. Oral hygiene and
maintenance of periodontal support. J Periodontol
1982;53:26–30.
Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP,
Dyer JK. Long-term evaluation of periodontal therapy:
I. Response to 4 therapeutic modalities. J Periodontol
1996;67:93–102.
Greenwell H, Stovsky DA, Bissada NF. Periodontics in
general practice: perspectives on nonsurgical therapy. J
Am Dent Assoc 1987;115:591–5.
Waerhaug J. Effect of Toothbrushing on Subgingival
Plaque Formation. J Periodontol 1981;52:30–4.
{55}
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
Waerhaug J. The interdental brush and its place in
operative and crown and bridge dentistry. Journal of
Oral Rehabilitation 1976;3:107–13.
Brayer WK, Mellonig JT, Dunlap RM, Marinak KW,
Carson RE. Scaling and root planing effectiveness: the
effect of root surface access and operator experience. J
Periodontol 1989;60:67–72.
Merchant AT, Oranbandid S, Jethwani M. Position
paper: epidemiology of periodontal diseases. J
Periodontol 2005;76:1406–19.
Stambaugh RV, Dragoo M, Smith DM, Carasali L. The
limits of subgingival scaling. The International Journal
of Periodontics & Restorative Dentistry 1981;1:30–41.
Becker W, Berg L, Becker BE. The long term
evaluation of periodontal treatment and maintenance in
95 patients. The International Journal of Periodontics
& Restorative Dentistry 1984;4:54–71.
Lindhe J, Socransky SS, Nyman S, Haffajee A,
Westfelt E. “Critical probing depths” in periodontal
therapy. J Clin Periodontol 1982;9:323–36.
Claffey N, Nylund K, Kiger R, Garrett S, Egelberg J.
Diagnostic predictability of scores of plaque, bleeding,
suppuration and probing depth for probing attachment
loss. 3 1/2 years of observation following initial
periodontal therapy. J Clin Periodontol 1990;17:108–
14.
Isidor F, Karring T, Attström R. Reproducibility of
pocket depth and attachment level measurements when
using a flexible splint. J Clin Periodontol 1984;11:662–
8.
Schroeder HE, Listgarten MA. Fine structure of the
developing epithelial attachment of human teeth.
Monogr Dev Biol 1971;2:1–134.
Spray JR, Garnick JJ, Doles LR, Klawitter JJ.
Microscopic demonstration of the position of
periodontal probes. J Periodontol 1978;49:148–52.
Caton J, Greenstein G. Depth of Periodontal Probe
Penetration Related to Clinical and Histologic Signs of
Gingival Inflammation*. Journal of Periodotology
1981.
Armitage GC. Position Paper: Diagnosis of Periodontal
Diseases. J Periodontol 2003;74:1237–47.
___________________________________________
{56}
CLINICAL DISCUSSION
Prevention of mandibular nerve injury associated with
dental implant placement: preoperative and
intraoperative recommendations
Thomas T. Nguyen
DMD, MSc, Resident in Periodontology,
University of Minnesota, School of Dentistry,
Minnesota, USA.
Dr. Thomas T. Nguyen
www.idjsr.com
database
Quick Response Code
Clinical Question
How can we minimize mandibular nerve injury
during dental implant placement?
One of the common complications after implant
placement is nerve injury. This complication usually
results in the altered sensation of the lower lip, chin,
mucosa, alveolar gingiva, teeth and/or tongue. The
mandibular nerve injury is the most frequent due to
the reabsorption of the alveolar ridge after its atrophy
due to lack of stimuli after extraction.
Pre-operative recommendations
 Informed consent for implant placement must be
given to the patient. The surgeon should
forewarn the patient regarding the possibility of
postoperative impaired sensation.
 A thorough clinical examination and treatment
planning must be performed.
 Radiographic examination to assess the location
of the inferior alveolar canal (IAC) of the
mandibular nerve and the mental foramen:
 The panoramic radiograph, preferably
digital, is useful as the primary image study
to assess the vertical distance from the crest
of the edentulous mandibular alveolar ridge
to the superior aspect of the IAC.
If the panoramic film shows inadequate
distance from the edentulous alveolar crest
to the IAC to place an implant, a computed
tomography (CT) scan is required.
CT scans have improved resolution and allow:
 Visualization of the IAC in 3 dimensions.1
 Coronal sections which are the most useful
to
assess
structural
bucco-lingual
relationships and assessment of the IAC’s
shape (round, teardrop, dumbbell) and
osseous cortication.2


Intra-operative recommendations
 Intra-operative radiographs during implant
preparation and after implant placement are
required in order to assess the position and
angulation of the implant.
 Surgical equipment with predetermined depth
stops as well as careful surgical technique is
necessary.
 During implant placement, cancellous bone may
be compressed against the contents of the IAC,
possibly causing mandibular nerve damage.
 If the post-operative radiograph indicates
encroachment on the IAC:
 The implant should be removed;
 Dexamethasone should be introduced into the
osteotomy site as follows3:
 Dexamethasone liquid 4 mg./ml. applied
topically for 1 minute and repeated once.
 Followed by a 7day day regimen of
dexamethasone orally as follows:
 Days one and two: 8mg. per day
 Days three and four: 6 mg. per day
 Days five and six: 4 mg. per day
 Day seven: 2 mg.
 An appropriate antibiotic must be
prescribed.
 Oral dexamethasone must be voided in
patients
with
preexisting
cardiac,
hypertensive and/or renal issues since such
high doses may lead to a hypertensive crisis.
 A shorter implant should be considered and no
bone grafting materials should be placed in order
to avoid migration into IAC.4
{57}
Conclusion
One of the serious complications of posterior
mandibular implant placement is nerve injury. Proper
understanding of the involved anatomy and the
surgical procedures, along with proper treatment
planning, will reduce the chances of such morbidity
to the patient. If nerve injury occurs, early and proper
management is the key to maximizing the chances of
recovery.
References
1.
Khan I, Halli R, Gadre P, et al. Correlation of
panoramic radiographs and spiral CT scan in the
preoperative assessment of intimacy of the inferior
alveolar canal to impacted mandibular third molars. J
Craniofacial Surg. 2011;22(2):566-570.
2.
Ueda M, Nakamori K, Shiratori K, et al. Clinical
significance of computed tomographic assessment and
anatomic features of the inferior alveolar canal as risk
factors for injury of the inferior alveolar nerve at third
molar surgery. J Oral Maxillofac Surg. 2012;70:514520.
3.
Misch CE, Resnik Randolph. Mandibular nerve
neurosensory impairment after dental implant surgery :
management and protocol. Implant Dentistry.
2010;19(5).
4.
Bagheri AC, Meyer RA. Management of mandibular
nerve injuries from dental implants. Atlas Oral
Maxillofac Surg Clin N Am. 2011;19:47-61.
__________________________________________________
{58}
Periodontal Disease and Diabetes Mellitus: Case Report
H Marie Keeling1
Tamara L. Wright2
and dental conditions along with her social habits was
taken.
1
Medical History
Dental Student at Dalhousie University, BA, MA,
Faculty of Dentistry, Dalhousie University, Halifax,
NS, Canada
2
BSc, MSc, DMD, Dip Perio, Department of Dental
Clinical Sciences, Faculty of Dentistry, Dalhousie
University, Halifax, NS, Canada
Heather Marie Keeling
www.idjsr.com
database
Quick Response Code
Introduction
The mechanisms linking oral and systemic health are
of utmost importance in patients with chronic
inflammatory disease. In this particular case, the
patient presented with chronic poorly diabetes
mellitus, which is known to have a negative impact
on periodontal health. Periodontal pathogens have
been found to illicit biomolecular responses that
result in poor glycemic control. Aside from diabetes
the patient was also being treated for cardiovascular
disease; hypertension and also for hyperlipidemia.
Patients with diabetes have a greater chance of
cardiovascular complications than those without
diabetes(1). Periodontitis and cardiovascular disease
are linked through several biomolecular pathways,
including the inflammatory response to bacteremia.
The patient also presented a 10 pack-year history of
smoking.
Patient History
The present case report is about a 65-year-old female
patient who was admitted to the Dalhousie University
Dental Clinic for an initial screening and treatment
planning. The patient had a chief complaint of, “My
teeth are getting loose and my private dentist’s fees
are too expensive, so I cannot afford my needed
dental treatments”. Detailed history of her medical
The patient’s medical history included type II
diabetes
mellitus
(DM),
hypertension,
hyperlipidemia, and gout. The patient was diagnosed
with DM 12 years prior, and her average blood
glucose was relatively well controlled (5-7mmol/L).
The prescribed medications for treatment of DM
were Metformin, 500mg 1x/day, and Gliclazide,
30mg 2x/day. Dental implications to consider are
taste disorder and morning scheduling of
appointments to decrease risk of stress induced
hypoglycemia. The patient was diagnosed with
hypertension and hyperlipidemia one year prior to
initial dental visit at the school. The patient’s blood
pressure was well controlled (120/80 mmHg) with
Sandoz-Condesartan 12.5mg, 1x/day. The patient’s
hyperlipidemia
was
well
controlled
with
Rosuvastatin, 40mg 1x/day.
The patient also reported a history of Gout. The last
episode was in February 2013 and she had two
episodes within the prior year. The patient believed
that specific foods and drinks brought on the
episodes.
Dental history
The patient stated that in the last 4 years her teeth had
become progressively looser. She also reported
sensitivity to hot and cold of the remaining maxillary
teeth.
Prior to being treated at the dental school, the patient
reported no flossing and brushing once per day with a
manual toothbrush. The last time she had seen a
dentist was 6 years prior.
Social habits
The patient does not currently smoke but reported
that she quit smoking over 20 years ago. She
confessed to smoking about a half pack of cigarettes
a day for 20 years. The patient does not consume
alcohol.
Clinical and radiographic findings
Extraoral findings were within normal limits.
Intraoral clinical and radiographic findings indicated
questionable prognosis for all of her teeth. A
panoramic radiograph and full mouth series of
intraoral radiographs (including vertical bitewings
and periapical) were taken at the screening
{59}
appointment (September 2013) (see Appendix
A).Gingival margins were red and edematous and
generalized heavy calculus and plaque accumulation
(PI=100%) were noted. The following teeth were
missing: 3-8, 3-6, 4-5 and 4-6. Full mouth probing
depths, recession, clinical attachment level, mobility,
and furcation involvement were recorded. The
deepest pockets were present at 4-3, 4-4, and 4-7.
More than half of her teeth showed generalized
advanced bone loss with CAL ranging from 8mm to
12mm plus mobility of grade 2 or 3.The 4 lower
incisors were splinted with a composite periodontal
splint. The maxillary teeth were especially sensitive
to cold, air, and water. (See Appendix B for
periodontal
charting).
There
was
sinus
pneumatization due to loss of the posterior maxillary
teeth (2-6) as well.
Diagnosis
Upon completion of the initial comprehensive
examination a diagnosis of generalized advanced
chronic periodontitis was made for her based on
Armitage classification (2). Modifying factors
included diabetes mellitus and a history of smoking.
Prognosis
Initial comprehensive examination determined the
prognosis of all maxillary teeth, 4-1, 3-1, 4-3 and 4-7
to be hopeless, according to McGuire’s classification
system(3), and teeth4-2 and 3-2 had questionable
prognosis as well.
Two major factors contributing to the patient’s
periodontal status could be due to her poor oral
hygiene and systemic medical condition besides
being a former smoker. The patient mentioned that
her diabetes was recently controlled, however, her
fasting blood glucose level was still greater than the
normal range (7.5mmol/L) on the morning of most of
her appointments.
Treatment Plan
Initial periodontal therapy; included full arch scaling
and root planing (SRP) with hand instruments and
ultrasonics under local anesthetic in 2 separate
appointments, following by a reevaluation after 6
weeks. At the time of the reevaluation (Appendix B),
periodontal and prosthodontics consultations were
done. Because of the hopeless prognosis of the
maxillary teeth, clearance was planned for the
maxillary arch followed by fabrication of a complete
upper denture. In the mandibular arch, teeth with
hopeless prognoses were extracted. The prognoses of
teeth 48, 44, 33, 34, 35 and 37 had improved from
questionable to poor, so it was decided to maintain
these teeth (Fall 2013). Since the patient’s oral
hygiene was still not acceptable (PI>25%) a second
round of scaling and root planning was completed
under local anesthesia with the hope of patient’s selfperformed oral hygiene (including brushing and
flossing) would improve. After each appointment oral
hygiene instructions were reviewed, following by
emphasizing the important association between her
periodontal status and her medical systemic condition
(4). Oral hygiene instruments that were suggested to
the patient were manual or electric tooth brushing,
and the use of floss, super floss, Sulcabrush, and
interproximal brush. Oral hygiene effectiveness was
recorded at each appointment. Unfortunately, the
BOP and plaque index measurements at all reevaluations and recall examinations were not ideal.
After eight weeks a the second reevaluation was done
(Winter 2014) (Appendix B) at which time better oral
hygiene status was noted with decreasing probing
pocket depths so we were able to proceed with the
prosthodontic treatment including fabrication of the
lower removable partial denture that was planned for
her at the initial reevaluation. The splint was also
removed from the lower incisors at the end of the
second round of SRP, so they could be extracted.
Oral hygiene was again stressed with the patient as
she was planned for a L-RPD; which itself may cause
plaque accumulation.
The patient’s diagnosis after the extraction of all
hopeless teeth was generalized moderate chronic
periodontitis. Due to inadequate width of keratinized
gingiva on the facial aspect of teeth 33, 34, 35 and44
(<2mm)(5), after the periodontal consultation by one
of the periodontics instructors two free gingival grafts
(FGG) were planned for her prior to the L-RPD
treatment. In the meantime, we proceed with the
CUD. Upon completion of the treatment in the
graduate periodontics clinic by a periodontics
resident (SD) (Appendix C for clinical photographs),
the L-RPD treatment started.
During the fabrication of the CUD, due to the curve
of Spee of the lower teeth and the mobility associated
with the 3-2 and 4-2, it was determined that these two
teeth should also be extracted prior to RPD
fabrication. Extractions were completed on April 16,
2014.
In Fall 2014 the patient was seen for a recall
examination including complete periodontal charting.
BOP and plaque index had again improved since the
last appointment. It was decided that the patient
should continue to be seen on 3-monthperiodontal
recalls and fabrication of the L-RPD could now
begin. Three-month recall was suggested because of
the patient’s periodontal status (moderate chronic
periodontitis) and the presence of modifying factors
(diabetes). Recall intervals that are 3months apart
will allow for removal of subgingival plaque
containing periodontal pathogens, close monitoring
of periodontal condition to prevent further attachment
loss, and to reinforce optimal oral hygiene(6). Also,
since the patient will be wearing a partial denture in
{60}
the near future it is especially important to ensure that
the patient is keeping up with oral hygiene, as partial
dentures are known to act as a plaque trap.
Discussion
Modifying factors
Diabetes mellitus
Poorly controlled diabetes is linked to a variety of
oral health complications. Patients with poorly
controlled diabetes have an increased risk of oral
infections, decreased salivary flow and impaired
wound healing (7). They also respond differently to
bacterial plaque due to increased levels of cytokines
in the gingival tissues. Also increased glucose
concentration in the crevicular fluid may change the
bacterial composition of the oral microbiota(8).
Periodontal disease can also have systemic effects.
Systemic response to periodontal disease results in an
increase in inflammatory mediators such as tumor
necrosis factor-alpha and interleukins (6). These
inflammatory mediators may result in increased
insulin resistance and therefore make it more difficult
for the patient to maintain glycemic control (1, 7, 9).
Some studies have indicated that periodontal therapy
may decrease HbA1c levels by approximately 0.4%
(7, 10).
Cardiovascular Disease: Hyperlipidemia
&Hypertension
Periodontitis and cardiovascular disease are linked
through their inflammatory effects. Both diseases
lead to chronic states of inflammation and have
effects on the vasculature if appropriate treatment is
not initiated. Stimulation of inflammatory
mechanisms by periodontal pathogens has been
shown to have negative effects on atherosclerotic
pathogenesis (1, 9).
Former smoker
The impacts of smoking on oral health are numerous.
Smoking results in an increased risk for periodontitis
due to impaired microcirculation, inhibition of
neutrophil function, and increased calculus
formation. Patients who smoke present with greater
bone loss than those that don’t and have decreased
response to periodontal therapy (11). The cessation of
smoking can decrease the progression of
periodontitis, however attachment loss will not be
regained (11).
In order to see the most optimal results following
initial therapy coronal and root surfaces need to be
completely debrided and free of calculus and plaque
deposits (12). When initial probing depths are greater
than 6mm, then surgical debridement is favoured and
greater clinical attachment gain can be achieved
along with a greater reduction in probing depths (12).
When pockets are greater than 6mm, instrumentation
of deeper root surfaces may not be achievable and,
therefore, flap surgery provides better access (12).
Unfortunately, in this patient’s case due topoor oral
hygiene and constant high PI (>25%) we did not
proceed with surgical debridement due to the need for
a low plaque score for optimal healing to occur (12).
Limitations of patient treatment in the
undergraduate clinic:
Unfortunately, due to the academic schedule it is
difficult for treatment in undergraduate clinics in
dental faculties to permit ideal timing in terms of
periodontal treatment. At Dalhousie, in the summer
only the third year students provide treatments in the
clinic. This may contribute to longer wait times for
patient treatment. In this case, more than half the
patient’s teeth had hopeless prognoses and were
ultimately be extracted. The patient’s oral health
condition was extremely poor and she also had a
large draining periodontal abscess distal to the 4-3.
Ideally, the patient should have been seen
immediately in the clinic after treatment planning
instead of having waited nearly 6 months for removal
of the hopeless teeth.
{61}
Appendix A
March 27, 2013
{62}
Appendix B
September 19, 2013
November 26, 2013
March 4, 2014
September 10, 2014
{63}
Appendix C
May 29, 2014
44 graft site
Pre-treatment donor site (palate)
33, 34, 35 graft site
Pre-treatment graft site (44)
44 graft in place
Pre-treatment graft site (33, 34, 35)
33, 34, 35 graft in place
{64}
June 5, 2014
44 graft site 1-week post op
33, 34, 35 graft site 1-week post op
33, 34, 35 graft site 6 weeks post op
Donor site (palate) 6 weeks post op
March 2015
Donor site (palate) 1-week post op
Delivery of L-RPD Lower Left Side View
July 17, 2014
44 graft site 6 weeks post op
Delivery of L-RPD Lower Right Side View
{65}
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Masayuki Shimoe TY, Yoshhiro Iwamoto, Nobuyuki
Shiomi, Hiroshi Maeda, Fusanori Nishimura and
Shogo Takashiba. Chronic Periodontitis with Multiple
Risk Factor Syndrome: A Case Report. Journal of the
International
Academy
of
Periodontology.
2011;13(2):40-7.
Armitage GC. Development of a classification system
for periodontal diseases and conditions. Ann
Periodontol. 1999 Dec;4(1):1-6. Review.
MK M. Prognosis versus actual outcome: a long-term
survey of 100 treated periodontal patients under
maintenance care. Journal of periodontology.
1991;62(1):51-8.
Weinstein P, Milgrom P, Melnick S, Beach B,
Spadafora A. How effective is oral hygiene
instruction? Results after 6 and 24 weeks. Journal of
public health dentistry. 1989 Winter;49(1):32-8.
PubMed PMID: 2911075.
Kim DM NR. Periodontal soft tissue non-root coverage
procedures: a systematic review from the AAP
Regeneration Workshop. Journal of periodontology.
2015;86(2):56-72.
Darcey J, M. A. (2011). "The rationale for the three
monthly periodontal recall interval: a risk based
approach." Br Dent J 211(8): 279-385.
Casanova L, Hughes FJ, Preshaw PM. Diabetes and
periodontal disease: a two-way relationship. British
dental journal. 2014 Oct;217(8):433-7.
Wang TF, Jen IA, Chou C, Lei YP. Effects of
periodontal therapy on metabolic control in patients
with type 2 diabetes mellitus and periodontal disease: a
meta-analysis. Medicine. 2014 Dec;93(28):e292.
Li C, Lv Z, Shi Z, Zhu Y, Wu Y, Li L, et al.
Periodontal therapy for the management of
cardiovascular disease in patients with chronic
periodontitis. The Cochrane database of systematic
reviews. 2014;8:CD009197.
Simpson TC, Needleman I, Wild SH, Moles DR, Mills
EJ. Treatment of periodontal disease for glycaemic
control in people with diabetes. The Cochrane database
of systematic reviews. 2010 (5):CD004714.
Sham A, Cheung L.K., Jin L.J., Corbet E.F. The
Effects of Tobacco Use on Oral Health. Hong Kong
Med J. 2003 August;9(4):271-277
Heitz-Mayfield LJ, Lang NP. Surgical and nonsurgical
periodontal therapy. Learned and unlearned concepts.
Periodontology 2000. 2013 Jun;62(1):218-31.
__________________________________________________
{66}
SYSTEMATIC REVIEW
Sinus lift grafting materials and immediate implant
placement: A systematic review
Dr. Kashif Hafeez1
Dr. Aiyesha Wahaj2
Dr. Muhammad Sohail Zafar3
Dr. Sana Shahab4
1
BDS, MFDS(RCSI), FFDS(RCSI), FFDS(RCSEd)
Postgraduate Dental Foundation Trainer, Oxford
Deanery; Broadshires Dental Practice, Carterton,
Oxon, OX18 1JA, UK
2
BDS, FCPS. Postgraduate Resident, Department of
Orthodontics, Dr. Ishrat-ul-Ebad KhanInstitute of
Oral Health Sciences, Dow University, Karachi,
Pakistan
3
BDS, MSc, PhD, FADI, FICD, Assistant Professor,
College of Dentistry, Taibah University, Madinah Al
Munawwarah, Saudi Arabia.
4
BDS, MSc. Department of Dental Materials Science,
Sir Syed College of Medical Sciences for Girls,
Karachi, Pakistan
Dr. Muhammad Sohail Zafar
E-mail: [email protected]
www.idjsr.com
database
Quick Response Code
Abstract
Sinus lift is one of the intricate methods of increasing
bone height in the posterior maxilla. Graft materials
are used to provide the height and hence increase the
implant support and success rate. Successful
osseointegration of dental implants required a stable
and sufficient amount of bone. There are different
types of bone grafting materials including autogenous
bone grafts, allografts and xeno grafts. Other newly
used materials such as platelet rich plasma is also
found to have optimal results. The current study was
aimed to assess the implications of dental implants
after immediate sinus augmentation and type of graft
materials which are suitable to support the sinus lift
procedures. A data search was performed based on
available electronic data bases (Cochrane data base,
Medline/PubMed) for articles published from19902013.Sinus lift is combined with various graft
materials to increase the bone height. The long term
survival of implant depends on surgical techniques,
bone volume, graft materials and Implant surface
features.
Keywords: Endosseous implant, Bone grafting
materials, Hydroxyapatite (HA).
Introduction
Surgical placement of dental implant is a demanding
technique particularly if alveolar bone height is
compromised in the posterior maxillary region.
Multiple surgical methods have continuously been
adopted to encounter these clinical problems
including reduced alveolar ridge height and density13
.The most common surgical procedure for obtaining
clinically adequate bone height before the placement
of endosseous implants in the maxilla is grafting of
the maxillary sinus floor. The sinus augmentation
technique was discovered about forty years ago. This
was achieved using the autogenous cancellous bone
material from the lateral iliac crest and repaired
though Caldwell-Luc yechnique. Later on, various
methods were discovered in the precision of the sinus
grafting techniques1-6. This was performed to make
the procedure more comprehensive yet clinically an
effective way to increase bone height.
A wide range of materials including allografts,
xenografts and alloplastic grafts have been used for
bone substitution to make implantation more
predictable and successful clinically5,7-9. Implant
success is found to have dictated by primary stability
factors such as implant diameter, shape, thread forms
and pitch values. Secondary stability factors included
the host environment where bone density plays a vital
role
in
their
placement
and
successful
osseointegration. For example, osseointegration can
be enhanced using osteogenic surface coated dental
implants10.
Radiographic techniques including cone beam
tomography is frequently used for anatomic
assessment of orodental tissues11-13. For example,
computed tomography is used to assess the core basal
value and density of alveolar bone in order to make
sinus augmentation valuable in long term. This
{67}
review discusses the significance of sinus lift
procedures with immediate dental implant placement
in combinations with different graft materials. Based
on previous clinical studies, clinical survival
predictability of graft materials and implant success
rate has been discussed.
Material and Methods
A data search was performed based on available
electronic data base(Cochrane, Medline and PubMed)
for studies published during 1990-2013. The search
strategy was based on search terms such as;
endosseous implant, bone grafting, sinus lift, and
implant survival. Inclusion criteria included the sinus
lift procedure with significant results using proper
implant techniques.
Table 1: Lekholm classification scheme for
evaluating bone and dental implant14
Type Criteria
I
Dense bone that delivers great cortical
anchorage; limited vascularity
II
Delivers better cortical anchorage for
primary stability and better vascularity
III
Soft bone texture
IV
Least successful soft bone texture
Exclusion criteria included syndromic patients,
interrupted treatment timings, bone graft failures with
no conclusive results, immunocompromised, postoperative infections, autoimmune diseases, history of
trauma or re-implant procedures, tumor and
systematic metabolic diseases. In order to evaluate
the quality of bone and dental implant placement,
Lekholm classification scheme14 was used (Table 1).
Results
Initial search recovered 3510 peer reviewer papers
(figure 1) and reduced to 1724 after filtering out
duplicate papers. After going through the titles,
abstracts and full texts of 279 papers we excluded
151 papers because of high risk of bias. Considering
the inclusion criteria carefully, only 40 papers were
included in the review.
Figure 1: Article screening criteria used in this study. PubMed/MEDLINE and Cochrane electronic databases
were searched for articles published from 2000 to 2013.
{68}
The key outcome of inclusive research studies including the type of graft augmentation has been summarized (table2).
Table 2: Reviewed studies with basic research outcome
Researcher
Graft type for augmentation
Cochrane1
Not specified
Lazzara et al2
Not mentioned
Khang et al3
Not specified
Wallace et al4
Del et al5
Stach et al6
Autogenous allograft/ direct
Autogenous composite/ non
autogenous
Not specified
Peleg et al15
Not specified
Winter et al16
Not specified
Peleg et al17
Lozada et al18
Hallman et al19
Engelke20
Not specified
Autogenous
Bovine HA and autogenous bone
Particulate alloplastic bone
(autogenous) and blood
Autogenous
Autologous calvarial bone, human
recombinant tissue factor, platelet
plasma & tetracycline.
Deproteinated bovine bone +
platelet rich plasma
Autogenous
Iliac corticocancellous bone
Autogenous & ePTFE membrane
Alloplastic
Autogenous
Autologous
Autogenous
Organic bovine bone with/without
autogenous bone.
Autogenous
Autogenous/allograft/Gore-Tex
membrane
Autogenous cancellous bone/HA
Autogenous
Autogenous bone/xenograft
mixture 2:1
Resorbable membrane, collagen
and inorganic bone mineral
McCarthy et al21
Philippart et al22
Rodriguez et al23
Stricker et al24
Bloomqvist et al25
Hurzeler et al26
Zinner et al27
Block et al28
Daelemans et al29
Block et al30
Wallace et al31
Karabuda et al32
Fugazzotto33
Kaptein et al34
Van et al35
Hatano et al36
Schwarz et al37
Valentine et al38
Emmerich et al39
Leonardis et al40
Khoury et al41
Lekholm et al14
Porous bone minerals
Various
Calcium sulphate
Autogenous
Inlay/onlay graft
Peleg et al42
Lovenzoni et al43
Autogenous
Autogenous
Main Outcome
Sand blasted/acid etched titanium implants promote
osseous contact than plasma sprayed.
Cumulative implant survival rate 99.8% at 10.5 months
loading in non-complicated implants. Clinically
investigation suggested that functional loading is possible
at 2 months.
Cumulative success rate for post loading three year 96.8%
(acid etched) and 84.8% (machined surface).
Survival rate of implant in augmented sinus ~92.6%.
Bone substitutes are successful for sinus augmentation.
Cumulative success rate (4 years) for machined implants
92.7% (dense bone) & 88.2% (poor bone)
Immediate implant insertion can be a likely choice for
patients with 1-2mm of vertical residual bone height.
In atrophic posterior maxilla, primary stability was
achieved with tapered implants.
Simultaneous implant placement favorable results.
Less dense bone required large diameter implants.
Acceptable short term results and less resorption.
Adequate bone height achieved.
Sufficient bone volume achieved.
High bone regeneration capacity.
Favorable results obtained.
Grafted bone showed good prognosis.
Total implant survival rates report favorable.
98.8% survival rate.
Good alternative
Good on functional stability.
Favorable results.
Significant volume of bone for augmentation
Vital bone formation in sinus graft when a membrane is
placed. Implant survival similar in both types
Overall survival rate 95.9%.
Favorable response 97.5%.
Cumulative success rate 82%.
Favorable response.
Favorable response.
The survival rate of implant placed under repaired
membrane correlates inversely with size of perforation;
less than 5mm showed good results.
Good osteoconductive properties.
Elevation with osteotome; short term clinical success.
Suitable material for sinus augmentation.
Best bone regeneration.
Implant placement (23%failure). Inlay/onlay technique;
60% less favorable results.
Favorable results.
Success rate of 92.7% for implants.
{69}
Pal et al44
Butz et al45
Guers et al46
Kahnberg et al47
Autogenous
Alloplastic
Autogenous
Autogenous
A number of researchers4,5,18-21,24-26 reported a high
success rate for using either autogenous bone grafts
or composite materials containing autogenous bone
(Table 2). Use of alloplastic grafts also produced
favorable results27,45. Zinner et al27 described
alloplastic grafts as a good alternative to autogenous
bone grafts. Regarding the applications of inorganic
biomaterials, bioactive materials based on calcium
and phosphates have been used either alone or in
combination with natural organic materials. Porous
bone minerals showed great osteoconductive
properties38. Leonardis et al40 has reported calcium
sulphate as a suitable material for sinus lift
applications.
Discussion
There are various techniques for sinus augmentation
such as lateral window, crestal approach, summers
osteotomy, bone aided augmentation. The most
popular technique for sinus lift is found to be lateral
window with autogenous corticocancellous grafts.
Autogenous bone grafts have always been considered
the most effective standardized grafting material due
toosteoinductiveand osteoconductive potential 1-6,15,16.
Various alternative materials havealso been used in
this
context,
however
compromising
the
osteoinductive potential. The property of biomaterials
in providing graft maturation and effective provision
to the endosseous implants is the most significant
element believed for the success of sinus graft
augmentation procedures17-24.
Implants placed in grafts composed of a combination
of autogenous bone and synthetic materials found to
have better survival rates than implants placed using
the autogenous graft only17-24. Such response is
probably due to its high resorption values. The
reviewed studies explained that a majority of
implants had textured surface followed by machined
surface. Textured surface implants have shown
significant results (p<0.05) contrast to machined
(p>0.05). No association was observed in context to
bone graft materials. This might refer to the adequate
results with rough surfaced implants in
immunological risk patients or those who have
insufficient bone this seems regardless in bone with
adequate height and density1-5.Direct implant
placement is usually a recommended protocol in such
cases25-31. Primary implant stability and graft is
related to adequate bone height. Delayed implant
placement is not recommended for badly destructed
alveolar ridge with no proper implant base.
Significant gain in bone height; mean 8.5mm,
Favorable success rate.
Good response.
Favorable results.
Implant surgical procedures are found to have a
profound effect on implant placement32-39.This
included significant results (p<0.05) using lateral
swing door technique, osteotome sinus elevation.
Clinically, these techniques provided a significant
amount of bone height for implant placement. A
recent study by Pal et al44 explained that the increase
in bone height found to be significantly greater with
lateral antrostomy than in indirect method by crestal
approach. This might be beneficial when more than
6mm bone height present and increase required up to
4mm. In case of advanced bone loss, a direct method
using lateral antrostomy is beneficial. Implant
survival comparison showed no significant
differences14,40-47.
Reviewed studies (Table 2) showed different types of
graft materials amongst which autogenous iliac crest
corticocancellous were the commonest one. A
combination of autogenous and xenograft have been
used because of better success predictability in
relation
to
less
bone
resorption
postoperatively36.Advanced graft materials such as
platelet rich plasma, xenograft mixture with
autogenous and deproteinated bovine have showed
promising results when used in conjuncture with
autogenous graft. These graft types provided
stabilized bone base for immediate implant
placement following sinus augmentation. These graft
materials also assessed for cross antibody reaction
and resorption, and later found to be insignificant in
this regard (p>0.05). A significant failures with
inlay/onlay graft (p<0.05) upon three year interval
has been reported14.Membranes (absorbable and nonabsorbable) found no significant effects (p<0.05) in
relation to osseointegration37. Although the mean
values showed good results with absorbable however
no statistically significant effects.
Short term data explicitly suggested that implant
placement after sinus augmentation is found to be a
stable procedure however; a large number of
longitudinal data is required.
Considering the complications of such procedures,
sinus perforation was found to be the most frequent
however not affecting the osseointegrationin case of
perforation 5mm or less. The repaired sinus with
graft and ePTFE membranes26 is also found to have
significant good prognosis in this regard, however
long term prognosis is required to be assessed. Sinus
infection can affect the osseointegration potentially.
None of the included studies reported the sinus
infection postoperatively following the sinus
augmentation. Natural silk based materials have been
reviewed recently for bone grafting and
{70}
regeneration48. From biomaterials prospective, there
is an intense need of new materials for these
applications. The limitations of clinical studies
included inadequate sample size, lack of integrated
systemized similar approaches and variability in data
collection. All accounts towards the specific need of
more rational case control and randomized clinical
trials. This approach can further encompass the
various human physiologically mediated conditions
required to be discussed. There is also found to have
constant need of long term follow up related to
implant stability.
Conclusion
8.
9.
10.
11.
12.
Predictability of sinus augmentation is substantially
based upon factors that need further understanding.
This
comprehensively
explained
statistically
significant results using rough surfaced implant
compared to the smooth surface. The most commonly
used graft material is autogenous corticocancellous
iliac crest. New graft materials (such as xenografts,
deprotonated bovine, platelet rich plasma) are being
used in combination with autogenous graft sand
providing promising basal support forimplant
insertion. Success rate improves remarkably with
immediate implant placement in a good quality basal
bone support. However, immediate implant
placement is not recommended if site is lacking a
good quality bone support.
13.
14.
15.
16.
17.
References
1.
2.
3.
4.
5.
6.
7.
Cochran D, Schenk R, Lussi A, Higginbottom F, Buser
D. Bone response to unloaded and loaded titanium
implants with a sandblasted and acid-etched surface: A
histometric study in the canine mandible. J Biomed
Mater Res. 1998; 40: 1-11.
Lazzara RJ, Porter SS, Testori T, Galante J, Zetterqvist
L. A prospective multicenter study evaluating loading
of osseotite implants two months after placement:
One‐Year results. J Esthetic Restorative Dent. 1998;
10: 280-9.
Khang W, Feldman S, Hawley C, Gunsolley J. A
multi-center study comparing dual acid-etched and
machined-surfaced implants in various bone qualities.
J Periodontol. 2001; 72: 1384-90.
Wallace SS, Froum SJ. Effect of maxillary sinus
augmentation on the survival of endosseous dental
implants. A systematic review. Ann periodontol. 2003;
8: 328-43.
Del Fabbro M, Testori T, Francetti L, Weinstein R.
Systematic review of survival rates for implants placed
in the grafted maxillary sinus. J Prosthet Dent. 2005;
94: 266.
Stach RM, Kohles SS. A meta-analysis examining the
clinical survivability of machined-surfaced and
osseotite implants in poor-quality bone. Implant Dent.
2003; 12: 87-96.
Blus C, Szmukler-Moncler S, Salama M, Salama H,
Garber D. Sinus bone grafting procedures using
18.
19.
20.
21.
22.
23.
ultrasonic bone surgery: 5-year experience. Int J
Periodontics Restorative Dent. 2008; 28: 221-9.
Wahaj A, Hafeez K, Zafar MS. Role of bone graft
materials for cleft lip and palate patients: A systematic
review. Saudi J Dent Res 2015;Epub Ahead of print;
doi:10.1016/j.sjdr.2015.02.001.
Semb G. Alveolar bone grafting. Front Oral Biol.
2012; 16: 124-36.
Javed F, Vohra F, Zafar S, Almas K. Significance of
osteogenic surface coatings on implants to enhance
osseointegration under osteoporotic-like conditions.
Implant Dent. 2014; 23: 679-86.
Zafar MS, Javed E. Extraoral radiography: An
alternative to intraoral radiography for endodontic
(root canal system) length determination. Eur Sci J.
2013; 9: 51-61.
Alrahabi M, Zafar MS. Evaluation of root canal
morphology of maxillary molars using cone beam
computed tomography. Pak J Med Sci. 2015; 31: 42630.
Zafar MS AM. Cone beam computed tomography for
exploring morphology of mandibular first molar.
British J Med Medical Res. 2015; 6: 514-21.
Lekholm U, Wannfors K, Isaksson S, Adielsson B.
Oral implants in combination with bone grafts. Int J
Oral & Maxillofac Surg. 1999; 28: 181-7.
Peleg M, Mazor Z, Chaushu G, Garg AK. Sinus floor
augmentation with simultaneous implant placement in
the severely atrophic maxilla. J Periodontol. 1998; 69:
1397-403.
Winter AA, Pollack AS, Odrich RB. Placement of
implants in the severely atrophic posterior maxilla
using localized management of the sinus floor: A
preliminary study. Int J Oral Maxillofac Implants.
2002; 17: 687-95.
Peleg M, Garg AK, Mazor Z. Predictability of
simultaneous implant placement in the severely
atrophic posterior maxilla: A 9-year longitudinal
experience study of 2132 implants placed into 731
human sinus grafts. Int J Oral Maxillofac Implants.
2006; 21: 94-102.
Lozada JL, Emanuelli S, James RA, Boskovic M,
Lindsted K. Root-form implants placed in subantral
grafted sites. J Calif Dent Assoc. 1993; 21: 31-5.
Hallman M, Hedin M, Sennerby L, Lundgren S. A
prospective 1-year clinical and radiographic study of
implants placed after maxillary sinus floor
augmentation with bovine hydroxyapatite and
autogenous bone. J oral and maxillofac surg. 2002; 60:
277-84.
Engelke W, Schwarzwaller W, Behnsen A, Jacobs HG.
Subantroscopic laterobasal sinus floor augmentation
(SALSA): An up-to-5-year clinical study. Int J Oral
Maxillofac Implants. 2003; 18: 135-43.
McCarthy C, Patel RR, Wragg PF, Brook IM. Sinus
augmentation bone grafts for the provision of dental
implants: Report of clinical outcome. Int J Oral
Philippart P, Brasseur M, Hoyaux D, Pochet R. Human
recombinant tissue factor, platelet-rich plasma, and
tetracycilne induce a high-quality human bone graft: A
5-year survey. Int J Oral Maxillofac Implants. 2003;
18: 411-6.
Rodriguez A, Anastassov GE, Lee H, Buchbinder D,
Wettan H. Maxillary sinus augmentation with
deproteinated bovine bone and platelet rich plasma
with simultaneous insertion of endosseous implants. J
Oral and Maxillofac Surg. 2003; 61: 157-63.
{71}
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
Stricker A, Voss PJ, Gutwald R, Schramm A,
Schmelzeisen R. Maxillary sinus floor augmention
with autogenous bone grafts to enable placement of
SLA‐surfaced implants: Preliminary results after 15–
40 months. Clin Oral Implants Res 2003; 14: 207-12.
Blomqvist JE, Alberius P, Isaksson S. Retrospective
analysis of one-stage maxillary sinus augmentation
with endosseous implants. Int J Oral Maxillofac
Implants 1996; 11: 512-21.
Hurzeler MB, Kirsch A, Ackermann KL, Quinones
CR. Reconstruction of the severely resorbed maxilla
with dental implants in the augmented maxillary sinus:
A 5-year clinical investigation. Int J Oral Maxillofac
Implants 1996; 11: 466-75.
Zinner ID, Small SA. Sinus-lift graft: Using the
maxillary sinuses to support implants. J Am Dent
Assoc. 1996; 127: 51-7.
Block MS, Kent JN. Sinus augmentation for dental
implants: The use of autogenous bone. J Oral
Maxillofac Surg 1997; 55: 1281-6.
Daelemans P, Hermans M, Godet F, Malevez C.
Autologous bone graft to augment the maxillary sinus
in conjunction with immediate endosseous implants: A
retrospective study up to 5 years. Int J Periodontics
Restorative Dent. 1997; 17: 27-39.
Block MS, Kent JN, Kallukaran FU, Thunthy K,
Weinberg R. Bone maintenance 5 to 10 years after
sinus grafting. J Oral Maxillofac Surg. 1998; 56: 70614.
Wallace SS, Froum SJ, Cho SC, Elian N, Monteiro D,
Kim BS, Tarnow DP. Sinus augmentation utilizing
anorganic bovine bone (bio-oss) with absorbable and
nonabsorbable membranes placed over the lateral
window: Histomorphometric and clinical analyses. Int
J Periodontics Restorative Dent. 2005; 25: 551-9.
Karabuda C, Arisan V, Hakan Ö. Effects of sinus
membrane perforations on the success of dental
implants placed in the augmented sinus. J Periodontol.
2006; 77: 1991-7.
Fugazzotto PA, Vlassis J. Long-term success of sinus
augmentation using various surgical approaches and
grafting materials. Int J Oral Maxillofac Implants.
1998; 13: 52-8.
Kaptein ML, de Putter C, de Lange GL, Blijdorp PA.
Survival of cylindrical implants in composite grafted
maxillary sinuses. Joral maxillofac surg. 1998; 56:
1376-80.
van den Bergh J, ten Bruggenkate CM, Krekeler G,
Tuinzing DB. Sinus floor elevation and grafting with
autogenous iliac crest bone. Clin Oral Implants Res.
1998; 9: 429-35.
Hatano N, Shimizu Y, Ooya K. A clinical long‐term
radiographic evaluation of graft height changes after
maxillary sinus floor augmentation with a 2: 1
autogenous bone/xenograft mixture and simultaneous
placement of dental implants. Clin Oral Implants Res.
2004; 15: 339-45.
Schwartz-Arad D, Herzberg R, Dolev E. The
prevalence of surgical complications of the sinus graft
procedure and their impact on implant survival. J
Periodontol. 2004; 75: 511-6.
Valentini P, Abensur D, Wenz B, Peetz M, Schenk R.
Sinus grafting with porous bone mineral (bio-oss) for
implant placement: A 5-year study on 15 patients. Int J
Periodontics Restorative Dent. 2000; 20: 245-53.
39.
Emmerich D, Att W, Stappert C. Sinus floor elevation
using osteotomes: A systematic review and metaanalysis. J Periodontol. 2005; 76: 1237-51.
40.
De Leonardis D, Pecora GE. Augmentation of the
maxillary sinus with calcium sulfate: One-year clinical
report from a prospective longitudinal study. Int J Oral
41.
Khoury F. Augmentation of the sinus floor with
mandibular bone block and simultaneous implantation:
A 6-year clinical investigation. Int J Oral Maxillofac
Implants. 1999; 14: 557-64.
42.
Peleg M, Mazor Z, Garg AK. Augmentation grafting
of the maxillary sinus and simultaneous implant
placement in patients with 3 to 5 mm of residual
alveolar bone height. Int J Oral Maxillofac Implants.
1999; 14: 549-56.
43.
Lorenzoni M, Pertl C, Wegscheider W, Keil C,
Penkner K, Polansky R, Bratschko RO. Retrospective
analysis of frialit-2 implants in the augmented sinus.
Int J Periodontics Restorative Dent. 2000; 20: 255-67.
44.
Pal U, Sharma NK, Singh R, Mahammad S, Mehrotra
D, Singh N, Mandhyan D. Direct vs. indirect sinus lift
procedure: A comparison. Nat j maxillofac surg. 2012;
3: 31-7.
45.
Butz SJ, Huys LW. Long-term success of sinus
augmentation using a synthetic alloplast: A 20 patients,
7 years clinical report. Implant Dent. 2005; 14: 36-42.
46.
Geurs NC, Wang IC, Shulman LB, Jeffcoat MK.
Retrospective radiographic analysis of sinus graft and
implant placement procedures from the academy of
osseointegration consensus conference on sinus grafts.
Int J Periodontics Restorative Dent. 2001; 21: 517-23.
47.
Kahnberg K, Nilsson P, Hirsch J, Ekestubbe A,
Gröndahl K. Sinus lifting procedure. Clin Oral
Implants Res. 2001; 12: 479-87.
48.
Zafar MS, Al-Samadani KH. Potential use of natural
silk for bio-dental applications. J Taibah Uni Med Sci.
2014; 9: 171-7.
__________________________________________________
{72}
SYSTEMATIC REVIEW
Laboratorial and clinical impacts of tobacco on
periodontal health: A systematic review
Fahad Sikander Khan1,
Aisha Aziz2,
Dr. Sana Shahab3,
Dr. Muhammad Sohail Zafar4
1
B.D.S, MSc, Dip (Public Health), Health officer,
Comfort Care, St. Albans, United Kingdom
2
B.D.S, Dip (Microbiology), General Dental
Practioner, Private Clinic, Karachi, Pakistan
3
BDS, MSc. Department of Dental Materials Science,
Sir Syed College of Medical Sciences for Girls,
Karachi, Pakistan
4
BDS, MSc, PhD, FADI, FICD. Assistant Professor,
College of Dentistry, Taibah University, Madinah Al
Munawwarah, Saudi Arabia.
Dr. Sana Shahab
E-mail: [email protected]
www.idjsr.com
database
Quick Response Code
Abstract
Use of tobacco has been documented a significant
risk factor for the progression of periodontal
conditions. The consumption of tobacco is related to
intensified depth of periodontal pockets and ligament
detachment, alveolar bone loss and susceptible to
tooth loss. The main aggravating part in development
of periodontal disease is contributed by nicotine that
is pharmaceutically active component and a primary
constituent of tobacco. It have been documented that
negative impact on periodontal tissues is due to
hindrance in connective tissue proliferation as a result
of affected gingival blood circulation and neutrophil,
cytokine production caused by nicotine. Thus,
abeyance of tobacco is most important part of
periodontal treatments as this renders positive
influence on the patients' oral and systemic
wellbeing. Tobacco cessation has been included as a
part of periodontal therapy and encouraged by dental
practitioners. Tobacco cessation counselling is
required to educate patient and for the best interest of
their oral health. The aim of this review is to report
the clinical and laboratory findings on periodontal
health. In additions risks involved in tobacco use and
possible professional intervention has been discussed.
Keywords: Tobacco, Periodontal Diseases,
Gingivitis.
Introduction
It has been known since late 1040's that tobacco
exhibits detrimental effects on periodontal tissues
health when association of ANUG (Acute
Necrotising Ulcerative Gingivitis) was noticed with
smoking1. A diverse range of periodontal diseases
have been investigated observing their relationship
with smoking. A substantial amount of scientific
literature is available on the basis of which this
review has been formulated. The basic aim and
objective of this review is to conduct effective review
for having clear idea of tobacco’s effect on
periodontal health from the perspective adopted in
clinical trial and error and to analyse the effect of
tobacco consumption on periodontitis and its types
(Chromic periodontitis, Aggressive periodontitis).
Cross-sectional studies prove that smokers exhibit
prevalence and severity of periodontal disease more
than twice as compared to individuals who do not
smoke. This is evidence that smoking exhibits a
major connection with periodontal diseases. More
cases of tooth loss are also reported in smokers with
periodontal disease as it aggravates the pathological
condition.
According to research conducted in 19972, observe
that negligence of oral hygiene among youth is
ironical because they tend to be more health
conscious, as the number of people visiting gyms and
health clubs has increased with the onset of the new
millennium. While awareness on diseases like obesity
has received widespread awareness, the issues in
relation to maintenance of oral health have not come
into limelight. Life threatening diseases like cancer
have been the chief concern of medics in relation to
tobacco addiction.
The knowledge on maintaining proper oral hygiene
among general people is very limited. From the onset
of childhood pupils are taught about brushing twice
{73}
and dental flossing to keep the menace of tooth decay
at bay. However, importance of food habit and
lifestyle in relation to oral health remains ignored.
Observing the adverse influence of smoking on
periodontal health, the aim of this review is to
highlight the unfavorable impact of smoking in
relation to periodontal conditions and focus on
cessation of smoking, highlighting its significance on
periodontal health and outcomes of diseased
periodontal tissues' treatment.
Literature review
Epidemiological literature provides various evidences
related to connection of smoking with detrimental
periodontal diseases when studies of about more than
two decades are reviewed3-5. The conclusions
provided by Asmaand Tomar6 based on statistics
from the NHANES III study, may be considered a
sturdy body of evidence of nicotine as a peril factor
for periodontal diseases. Authors proposed that in
USA almost fifty percent of patients suffering from
periodontal pathologies were smokers. It was also
noted that susceptibility of periodontal disorder was
directly related to rate of smoking intensity of an
individual and prevalent smokers were more than 3
times susceptible to periodontal diseases in
comparison to non-smokers.
Literature based in clinical studies clearly reveals that
smoking has deleterious effects on periodontal tissue;
it causes quick and greater loss of periodontal
attachment, gingival recession, pocket formation and
bone loss in diseased condition7. Clinical study
conducted by Mullally et al. in 2004 reviled that odds
ratio between periodontal disease was as high as 14.1
for patients who smoked, exhibiting that smoking
acts as the strong predator of progressive
periodontitis, causing early loss of periodontal
attachments and progression of other signs and
symptoms.8
Connection between smoking and periodontal disease
is known very clearly and proved by epidemiological
studies but the true mechanism by which smoking
causes deleterious effects on progression of
periodontal pathology are still unknown.
Methodology
To obtain the desire article following database will be
use like Pub Med, Medline, Lancet, Google scholar,
Cochrane library and from different organization who
are actively working on tobacco like TTAC (tobacco
technical assistance consortium America).
The following keywords will be used during
searching; effects, role, tobacco, smoking, oral,
mouth and periodontium or gingivitis. Articles
published between 2000 and 2012 and in English
language were included for review of literature.
English language was selected for articles so that
reviewer did not face any difficulty in understanding
of materials and thus kept himself away from any
potential language bias in translating materials from
one language to other.
Moreover with the aim that only studies relevant to
the topic were included in the systematic review, this
step was taken. This step of selection involved
assessments of the study topic, their abstracts and list
of references identified through search strategy. Full
length reports of all potentially relevant articles were
then accessed for eligibility assessment, which was
based on review inclusion criteria 9. Reference lists of
eligible studies were then again analysed for
obtaining further studies. Critical appraisal stage that
is the last stage in selecting studies was done and the
studies whose topic did not resemble with review,
those published before inclusion review years and
those which were not in English were excluded 10.
Even those studies in which participants’ age was not
clearly stated were excluded from review (as
exclusion criteria of study). All studies were
searched, analysed and selected by the researcher.
The study has been concluded based on three main
forms of studies, epidemiological, laboratorial and
studies based on perceptions of the common public
on dental health care. For the epidemiological
studies, the range of age varies from 18 and above.
This is because; the rate of tobacco consumption is
high among this particular age group. Since the
consumption of tobacco is more common among
males than the females, a gender based study has also
been included in the research. An effort has also been
made to find out cultural influences on tobacco
consumption and its impact on gum diseases like
periodontitis 11.
For the study, the primary research outcome is
formed based on the impact of tobacco intake on
dental diseases like periodontitis.
On the other hand secondary outcomes are measured
on laboratorial studies on the relationship of tobacco
consumption and periodontitis. The already existing
knowledge of dental healthcare professionals and
their recommended ways to cessation of smoking are
also measured. Awareness of general public on dental
health and impact of tobacco are also taken into
account to determine the research outcomes.
While conducting a research on any topic, it is very
important to evaluate the quality of the studies that
are selected to establish and attain the proposed
research outcomes12. This is done with the objective
to avoid any form of bias that may affect the research
findings and outcomes.
In case of the concerned research study, the articles
that are included are independently assessed by
utilizing a critical appraisal framework. By following
the framework, the researcher has been successfully
{74}
able to critically evaluate the qualitative and
quantitative methods. As per CASP or Critical
Appraisal Skills Programme, the framework consists
of several questions that are keenly analysed to meet
up factors like relevance of the study, the results,
validity, reliability and similar such 13. Through the
aid of the questions for study assessment, the
following segments of the entire study for instance,
study design, objective of the research, target
population sample, concerns related to research
ethics, data analysis and findings and many such.
Data Extraction and Analysis
For this research study, narrative synthesis of the
research outcomes has been done as the data that has
been extracted from each of the articles do not bring
about similar quantitative findings and analyses. The
data extracted from each of the study include, the
process of identification of each study, determining
the characteristics of the study and the ultimate
results of the study. While identifying the study, the
name of the researcher, title, publication year, origin
of the study and such are found. The characteristics
of the study on the other hand make sure that the aim
of the study, study design along with inclusion and
exclusion criteria.
The methods of data collection will be based on the
nature and design of the study and also the source and
kind of the collected data. Since, the data analysis of
the study has been conducted by using the narrative
approach; the study involves a process of detailed
documentation. The document reflects relationship
established between the understandings from all the
studies and the evidence of overall validity of the
studies made. As the study is not made in accordance
to the meta-analysis format, an effective approach
towards in detailed documentation and analysis of the
research outcomes from various studies related to the
topic has been adopted. The process of data analysis
has been purposely made transparent by observing
research ethics and values. Therefore, the entire study
has been presented in a narrative format providing all
possible details. This process has made way to
effectively understand the relationship between
tobacco consumption and development of gum
diseases or periodontitis.
Results
After analyzing literature, we concluded different
tables (1, 2 and 3) with author’s details, year of
reporting, title of study, study design, which
population targeted, country of study, their aims with
result outcomes.
Table 1: Epidemiological Studies
Population/
Country
Aim/Aims of
Age
of Study
Study
Author
Year of
Publication
D.F.
Kinane and
I.G.
Chestnutt14
Title of
Study
Study
Design
Smoking and
Periodontal
Disease
Cross
Sectional and
Longitudinal
Study on
Patients
1361 Case
(n= 873)
Target Age
Group 25-74
Erie
County,
New
York State
Strength of
Association
between
Tobacco and
Periodontal
Brian H.
Mullally15
The
Influence of
Tobacco
Smoking on
the Onset of
Periodontitis
in Young
Persons
Tobacco Use
and Its
Effects on
the
Periodontium
and
Periodontal
Therapy
Hospital
Case Study
17, 22 Case,
Target Age
Group 17-34
years.
Africa
Prevalence of
early onset or
aggressive
periodontitis
in young
adults.
Cross
sectional
12,329 Case,
Target Group
18 years and
above
USA
Reviewing
potential
biological
mechanisms
related to
effects of
tobacco on
periodontal
disease.
Vandana
K. Laxman
and
Sridhar
Annaji16
Results
The risk of severe tooth
and bone loss is more in
case of smokers. Ratios
vary from 3.25 to 7.28,
from light smokers to
heavy smokers.
Identification of
significant genetic
components in relation
to aggressive
periodontitis.
Tobacco smoking
significantly contributes
to the development of
periodontal disease.
{75}
NurcanBud
uneli17
Jose
LopezLopez et al
18
Effects of
Tobacco
Smoking on
Chronic
Periodontitis
and
Periodontal
Treatment
Tobacco
Smoking and
Radiographic
Periapical
Status
Cross
Sectional
Study
550 Case
Target Group
18 to 45
Turkey
Impact of
Tobacco
Smoking on
Chronic
Periodontitis
A positive association
between smoking and
various biochemical,
clinical signs of
periodontitis and
chances of periodontitis
among smokers.
Case Control
Study
79 Case,
Target Group
– 18 and
above
UK
Radiographic
investigating
the
relationship
between
tobacco
smoking and
periapical
status.
After taking into
account the age, gender,
total number of teeth,
endodontic status, root
filling quality and
diabetic level, tobacco
is strongly considered
to be associated to
periapical lesions.
Table 2: Laboratorial Studies
Country
Aims and Objective
of Study
of study
Author
Name and
Year of
Publication
Cristina
Cunha Villar
and Antonio
Fernando
Martorelli
de Lima 19
Title of Study
Smoking Influences on
the Thickness of
Marginal Gingival
Epithelium
Brazil
Evaluation of the
thickness of marginal
gingival oral
epithelium and
non0smokers who
have clinically healthy
gingivae.
FlonaM.Coll
ins20
Tobacco Cessation and
the Impact of Tobacco
Use on Oral Health
United
States
Types of tobacco and
its prevalence among
US population. Impact
of tobacco use on oral
health. Biochemical
and generic factors
associated to oral
health. Recommended
methods for tobacco
cessation.
GirishParma
r, et al 21
Effect of Chewing a
Mixture of Areca Nut
and Tobacco on
Periodontal Tissues and
Oral Hygiene Status
Prevalence of and Risk
Indicators for Chronic
Periodontitis in Males
from Campeche.
India
Clarifying the effects
of chewing areca nut
and tobacco on
periodontal tissue and
status of oral hygiene.
Determining
prevalence of
extension/severity of
chronic periodontitis
and determining the
various risk factors
among the policemen
of Campeche, using
electron probe.
MirnaMinay
a-Sanchez et
al22
Brazil
Results
Among all significant negative
consequences of tobacco on the
periodontium, influence of tobacco
on the various signs and symptoms
of gingival inflammation that are
induced by plaque accumulation
must be necessarily considered.
Smoking must be taken as a high
risk factor for the development of
chronic periodontal disease.
Interventions made by an able
dental team can help in quitting
tobacco intake. The dental experts
can effectively educate and
motivate patients who suffer from
the danger of tobacco on oral health.
Interventions recommended on a
routine patient care. Tobacco
cessation can best be carried out
under medical supervision and
restrictions.
Chewing areca nut and tobacco
plays a causative role in the
development of oral lesions,
degradation of periodontal status
and oral hygiene.
Many of the participants were found
to suffer from poor periodontal
disease. Over use of tobacco along
with aging causes presence of
gingivitis.
{76}
Author Names
and Year of
Publication
ZHS Lung,
MGD
Kelleher, R W
J Porter, J
Gonzalez and
R F H Lung. 23
Table 3: Studies based on Knowledge and Service Delivery
Design of
Target
Country
Aims and
Study
Population
of Study
Objectives
Title of the Study
Poor Patient
Awareness of the
Relationship
between Smoking
and Periodontal
Diseases.
Cross Sectional
Survey based
on wellstructured
interview
Smoker
patients
attending
dental clinic
London,
UK
Investigating
patient’s
knowledge of
the effects of
smoking on
periodontal
disease.
Yuval Vered
and Harold D
Sgan-Cohen.24
Self-perceived
and clinically
diagnosed dental
and periodontal
health status
among young
adult and their
implications for
epidemiological
surveys.
Cross Sectional
Survey based
on wellstructured
interview
21 year old
Israeli
Defense
Forces after
being
released
from
military
services.
Israel
Investigating
parity
between selfperceived
and clinically
diagnosed
dental and
periodontal
health status.
ShaileeFotedar
et al, et et al 25
Knowledge of
Attitude Towards
and Prevalence of
Tobacco Use
Among Dental
Students in
Himachal
Pradesh.
Cross Sectional
Survey based
on wellstructured
interview
Third year
Students of
Bachelor of
Dental
Surgery.
India
Assessing
prevalence of
tobacco and
its use along
with
knowledge of
cessation
counseling
among dental
students in
the state of
Himachal
Pradesh,
India.
Results
The patients
were found to be
less aware of the
relationship
between
smoking and
periodontal
diseases as only
6% of the total
were aware of
the fact.
The selfassessment of
individuals was
found to have
been low. The
low level
awareness will
directly impact
care-taking
behavior and
need for public
health action.
The prevalence
of tobacco use
among the
students is found
to be low.
Though, use of
skills to support
quitting of
smoking is
necessary.
having a variety of general consequences which can
change the reaction of the effected person, cigarette
smoking would also emerge to have substantial
Regarding the “influence of tobacco smoking on the
limited effects which may report for the early
onset of periodontitis in young person’s” written by
establishment of the disease development in, at risk
Brian H.Mullally8, in which he has tried to explain
young adults. Legal restrictions in the developed
his views on the extent of cigarette smoking can
countries like U.S or Europe has barred the tobacco
actually put forth on periodontal tissues were not
companies for their advertisements and sales and thus
completely agreed by other theorists like. According
these companies have targeted the developing
2
to Vandana K. Laxman and Sridhar Annaji , its
countries as their replacement. Thus, the developing
consequences are linked to the period and number of
nations are susceptible to face an increase in the
cigarettes consumed. The smoking habits of the
prevalence of harsh periodontal situation including
family members may also be significant both in view
acute periodontitis. To be able to follow the strategies
to behavioral influences and the probable results of
of avoidance, early recognition of the disease and
passive smoking 26 is of the opinion that the second
quick intrusion by the dental professionals should be
spot is in need of additional research. Moreover
able to aim and inform the young patients about the
Discussion
{77}
consequences of smoking on periodontal health. By
this mode dental department will also be playing a
major role in the general health and well-being of the
youth.
By the epidemiological study about the treatment of
the individuals addicted to cigarettes, the theorists
have suggested that non-surgical treatment will
generally be productive in requisites of penetrating
depth reduction and gingivitis. Thus the
consequences of smoking on the result of
periodontitis treatment may be concluded as Short
term effects in terms of less gingivitis resolution, less
probing depth reduction, less attachment gain among
the smokers.
It has been noticed and stated by López-López, J.,18
80 to 90% of the cases in long term effects are
treatment failures among the smokers. He has also
stated that 70-80% of the cases are not successful in
the implantation among the smokers. Thus smoking
does have a negative effect on the treatment
procedure of the periodontitis diseases. Keeping this
in mind, the patients suffering from periodontitis
diseases need to be advised and counselled about the
consequences of smoking.
Study on effects of tobacco use on periodontal health
and treatment has made evident that over the past 50
years, knowledge and concern about obnoxious
effects of tobacco smoking on periodontal health has
progressed significantly. Hence, in today’s world
there is little doubt on the fact that tobacco smokers
are at a high risk of getting affected by periodontitis.
They are also found to be slow responders to
periodontitis treatment.
Tobacco smoking in fact, is found to have wide
spread effects on oral health. The mechanisms of
tobacco smoking for increased level of susceptibility
to periodontitis and poorer response to remedial
treatments are some of the ill-effects on over all oral
health and recovery process. Another, significant
outcome of the tobacco smoking is that it acts as a
strong environmental factor. Smoking of tobacco
interacts with the body of host and bacterial growth
associated with the disease periodontitis 14. The
genetic built of the host and interaction with the
environmental factors like cigarette smoking makes
way to further exploration of the relationship between
tobacco smoking and related genetic factor of the
host.
The effects of tobacco smoking on formation of
chronic periodontitis have also been found to impair
the microcirculatory system and changes on the
vascular formation system. This in turn leads to
negatively influence the immune system and
inflammatory reactions on healthy periodontal
tissues. It is found that smokers have less number of
vessels and existence of highly inflamed gingival
tissues as compared to non-smokers. According to
researchers it has been found that smoking of tobacco
on long term basis makes a negative impact on the
process of vasculature of the periodontal tissues.
Also, high level exposure to long term smoking leads
to gingival hyperaemia. The gingival hyperaemia is
mainly caused due to increase in blood pressure
levels in comparison to small yet significant
sympathetic vasoconstriction on healthy gingival
tissues22.
Due to continued process of repeated attacks of
vasoconstriction and presence of impaired
revascularization caused due to cigarette smoking
may lead to low rate of immune response, delayed
healing process and ultimately increased risk of
periodontal disease 21.
It is quite evident from the study on tobacco smoking
and radiographic periapical status that that there is a
statistically significant association between radiographically diagnosed lesions and tobacco smoking.
In this particular study the oral health maintained by
the subject was quite satisfactory but due to tobacco
smoking, there had been consistent bone loss. Also,
among smokers it was found that functions of
polymorph nuclear leukocytes, T-cell lymphocytes,
antibodies, immunoglobulin’s A, G and M and
macrophages are highly suppressed18.
The swelling results due to the dental plaque
gathering can be modified by tobacco by-products,
such as cotinine, a by-product of nicotine that has a
marginal vasoconstriction action that decreases
gingival clinical symptoms of bleeding, redness, and
oedema. The morphometric investigation showed an
augment in the MET in clinically healthy gingival
samples in comparison to the swelled samples in the
case of both smoking and non-smoking patients. This
difference did not attain statistical implication. The
gingival swelling decreases the epithelial thickness
and can lead to clinical ulceration19.The findings thus
propose that among all the adverse effects of tobacco
on the periodontium, the effect of tobacco related to
the symptoms of gingival swelling caused by plaque
gathering should be taken into consideration. Even
though the accurate means of its power is still not
very clear, yet smoking should be considered to be
the main risk factor for chronic periodontal disease.
Conclusions
Smoking is a well-known causing and aggravating
factor for periodontal problems. Smokers exhibited
more than twice chances of having periodontitis.
Therefore, cessation of smoking plays a significant
role in the cure of periodontal diseases. Patients
should be educated and motivated by their dentists to
quit smoking. Dentists can have very effective and
influential position, as patients tend to visit them
more regularly in comparison to their physicians.
However, success in cessation of smoking may be
{78}
certainly influence by mutual coordination among
dentists and physicians.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
Pindborg, Jens Jorgen. Tobacco and gingivitis. Journal of
dental research 1947: 26(3): 261-264.
Laxman, Vandana K., and Sridhar Annaji. "Tobacco use
and its effects on the periodontium and periodontal
therapy." J Contemp Dent Pract 2008:9(7): 97-107.
Stoltenberg, J. L., Osborn, J. B., Pihlstrom, B. L.,
Herzberg, M. C., Aeppli, D. M., Wolff, L. F., & Fischer,
G. E. Association between cigarette smoking, bacterial
pathogens, and periodontal status. Journal of
periodontology, 1993: 64(12), 1225-1230.
Tonetti M. Cigarette smoking and periodontal diseases:
Etiology and management of disease. Ann Periodontol
2001; 3:88-101.
Krall EA, Dawson-Hughes B, Garvey Al, Garcia RI
(1997).Smoking, smoking cessation, and tooth loss.
Journal Dent Res 76:1653-1659.
Tomar, Scott L., and Samira Asma. "Smokingattributable periodontitis in the United States: findings
from NHANES III." Journal of periodontology 2000:
743-751.
Baljoon M, Natto S, Bergstorm J JClinPeriodontol
2005:32(7):789-97.
Mullally, B. H. The influence of tobacco smoking on the
onset of periodontitis in young persons. TobInduc Dis
2004: 2.1, 6.
Kervin, J. Methods for Business Research 1992: 3rd ed.
Torrington, D. management Face to Face. 1991 4th ed.
London: Prentice Hall
Kothari, C. R. Research methodology: methods and
techniques. New Age International.
Denscombe, M (2002) Ground Rules for Good Research,
Maidenhead, Open University Press 2004.
Silverman, D. Interpreting Qualitative Data, Methods for
Analysing Talk, Text and Interaction 1993. 4th ed.
Kinane, D. F., & Chestnutt, I. G. Smoking and
periodontal disease. Critical Reviews in Oral Biology &
Medicine, 2000:11:356-365.
Mullally, B. H. The influence of tobacco smoking on the
onset of periodontitis in young persons. TobInduc Dis,
2004: 2: 6.
Laxman, V. K., & Annaji, S. Tobacco use and its effects
on the periodontium and periodontal therapy. J Contemp
Dent Pract 2008: 9(7): 97-107.
Buduneli, N. Effects of Tobacco Smoking on Chronic
Periodontitis and Periodontal Treatment.
López-López, J., Jané-Salas, E., Martín-González, J.,
Castellanos-Cosano, L., Llamas-Carreras, J. M., VelascoOrtega, E., & Segura-Egea, J. J. Tobacco smoking and
radiographic periapical status: a retrospective case-control
study. Journal of endodontics 2012: 38(5): 584-588.
Villar, C. C., & Lima, A. F. M. D. Smoking influences on
the thickness of marginal gingival epithelium. Pesquisa
Odontológica Brasileira, 2003: 17(1): 41-45.
Collins, F. M. Tobacco Cessation and the Impact of
Tobacco Use on Oral Health. RDH. Oklahoma: Penwell
Dental Group 2010.
Parmar, G., Sangwan, P., Vashi, P., Kulkarni, P., &
Kumar, S. Effect of chewing a mixture of areca nut and
tobacco on periodontal tissues and oral hygiene status.
Journal of oral science 2008: 50(1): 57-62.
Minaya-Sánchez, M., Medina-Solís, C. E., Maupomé, G.,
Vallejos-Sánchez, A. A., Casanova-Rosado, J. F., &
Marquez-Corona, M. D. L. Prevalence of and risk
indicators for chronic periodontitis in males from
Campeche, Mexico. Revista de SaludPública 2007: 9(3):
388-398.
23. Lung, Z. H. S., Kelleher, M. G. D., Porter, R. W. J.,
Gonzalez, J., & Lung, R. F. H. Poor patient awareness of
the relationship between smoking and periodontal
diseases. British dental journal 2005: 199(11): 731-737.
24. Vered, Y., & Sgan-Cohen, H. D. Self–perceived and
clinically diagnosed dental and periodontal health status
among young adults and their implications for
epidemiological surveys. BMC Oral Health 2003: 3(1): 3.
25. Fotedar, S., Sogi, G. M., Fotedar, V., Bhushan, B., Singh,
B., Dahiya, P., & Thakur, A. S. Knowledge of, Attitude
Towards, and Prevalence of Tobacco Use Among Dental
Students in Himachal Pradesh State, India. Oral health
and dental management 2013: 12(2): 73-79.
26. Preshaw PM, HeasmanL, Stacey F, Steen N, McCracken
GI,Heasman PA J ClinPeriodontaol, 2005;32(8):869-79.
__________________________________________________
{79}
SHORT COMMUNICATION
A review of the use of laser in periodontal therapy
Dr. Amir Manzoor Shah1,
Dr. Khurram Khan2,
Dr. Fahd Ahmed3,
Dr. Nida Amir4
1,
BDS, MSc, M-Dent Perio Resident, 2BDS, MSc,
BDS, MSc, Faculty of Dentistry, Division of Oral
Health and Society, McGill University, Montreal
Quebec, Canada.
1
Division of Periodontics, Dental Diagnostics and
Surgical Sciences, Faculty of Dentistry
University of Manitoba, Winnipeg Manitoba, Canada
4
BDS, MSc, MSc-Peads-Dent Resident, Department
of Pediatric Dentistry, Nobel Biocare Oral Health
Centre, University of British Columbia, Vancouver
BC, Canada.
3
Dr. Amir Manzoor Shah
E-Mail: [email protected]
www.idjsr.com
database
Quick Response Code
Abstract
The use of lasers has significantly developed in
modern dentistry, however the clinical value and
awareness on the benefits of their use is limited.
Lasers have made their way in dental treatment since
1994. They have been granted Food and Drug
Administration (FDA) approval, however the
American Dental Association (ADA) is still
researching on the outcomes of laser therapy1. This
article reviews the use of laser therapy in the initial
non-surgical phase of periodontal therapy.
field of dentistry with applications in various aspects
of clinical practice.
The field of restorative dentistry has utilized lasers,
for the removal of tooth decay, and this is where laser
therapy evolved from in dentistry. Lasers have been
used for the removal of the carious lesion and
preparation of the tooth for a restoration. Many
restorative materials incorporate laser in their
setting/curing system. Lasers help in controlling the
spread of pathological and non-pathological lesions
as well as acquiring tissue for biopsies. Lastly, tooth
whitening has become a quick and easy procedure for
patients and practitioners with the use of laser
technology. More recently, mechanical debridement
of subgingival root surfaces and periodontal pockets
are being treated with lasers as an adjunct or
substitute4.
Laser therapy has greatly advanced in recent years,
especially in restorative dentistry, however general
dentists are not aware of the many benefits they can
receive with the help of this developing therapeutic
tool in periodontology.
How Lasers Work
There are various types of lasers in the market and
each device emits energy at a specific wavelength.
For example, diode (gallium: arsenide) lasers emit
wavelengths ranging from 635-950 nm. Carbon
dioxide (CO2) lasers emit wavelengths at 10 600 nm4.
Secondly, radiation is delivered in different forms.
The radiations can be continuous, pulsed or running
pulse waveforms. The photon emitted through the
collimator for a unidirectional, monochromatic light
being emitted in coherence. Thirdly, the laser beam is
infrared and invisible; therefore light is incorporated
into the device to act as an aiming beam. Upon
exposure, the targeted tissue will absorb, reflect or
scatter the laser beam5. Two variables control this
affect; these are the wavelength and the properties of
the target tissue. Biologic tissues primarily absorb the
beam, while scattering only occurs in deep tissue
penetration5, 6.
Applications of lasers in dental procedures:
Introduction
The term “LASER” stands for “light amplification by
stimulating emission of radiation”2. Lasers were
introduced in the field of medicine approximately 50
years ago3. This technology trickled its way to the
Restorative Dentistry: Erbium-doped yttrium
aluminum garnet (Er: YAG) Lasers are useful in the
detection/removal of caries
with maximal
preservation of healthy mineralized enamel and the
cavity preparation for placement of filling materials.
Lasers have also been beneficial in the curing of
{80}
filling materials such
composite resins7,8.
asphotopolymerizationin
Oral and Maxillofacial Surgery (OMFS): Lasers in
OMFS are generally used for excisional/ incisional,
biopsy, ablation and hemostasis. Lasers are used for
biopsy in removing tissue for examination/inspection
of potential neoplastic tissue. Ablation is a process in
which superficial tissue is removed and unnecessary
tissue removal could be avoided9.Hemostasis is the
control of bleeding at the site if surgery.
Endodontics: Laser fibers and endodontic tips carry
out the following procedures: diagnosis, pulpotomy,
cleaning and obturation of the root canal system,
retreatment and apical surgeries. The laser Doppler
flowmetry is an advancement in endodontics as it
analyzes the blood flow in the canal system. This
evaluation was considered as one of the most
accurate methods in testing pulp vitality10.
Periodontal Disease: Periodontitis is a polymicrobial
infection caused by multiple types of bacteria,
harmfully interacting with the body’s immune
system. There are various types of bacteria that
accumulate in plaque (biofilm), which is found lining
the gums of the oral cavity. Inadequate oral hygiene
causes migration of these bacteria along the root
surface to form a hardened calcified substance known
as calculus (tartar). In response to this invasion of
bacteria, gum tissues become inflamed and ulcerated.
Further neglection may cause periodontal tissue
damage with regression of bone around the tooth,
ultimately leading to tooth loss11.
Lasers in periodontal therapy: Arresting the
disease process is the primary goal of periodontal
treatment12. Initial therapy is the first step to reestablish a healthy oral cavity. This is the process of
cleaning and disinfecting the affected root surfaces.
Once infection and inflammation in the oral cavity
are under control, secondary goals are outlined to
help in regeneration of healthy periodontal
attachment to the tooth surface, which may include
surgical treatment12, 13.
Treatment techniques for initial therapy: Phase 1
of periodontal therapy includes mechanical
debridement of the biofilm, which requires removal
of bacteria and calculus from the root surfaces of
affected teeth. This process is known as “scaling and
root planing” or “root debridement”14. Hand
instruments and/or ultrasonic (high frequency)
instruments are traditionally used to carry out the
procedure and require a high level of skill and tactile
sensitivity. An alternative option is non-surgical
therapy but this technique is sensitive and also time
consuming.
An invasive procedure carried out in the first phase of
periodontal therapy known as curettage, where the
lining of an inflamed pocket was removed from the
tooth or tissue has recently seen advancements in
research. Current literature suggests if bacteria are
affectively removed, tissue repair can occur without
the need for surgical intervention12, 14.
Treatment with lasers: An adjunct for non-surgical
debridement of bacteria from root surfaces can now
be conducted with the use of lasers. Neodymium:
Yttrium-Aluminium-Garnet (Nd: YAG) laser is one
example used in the treatment of periodontitis
providing the ability to carry out sub gingival
curettage, removal of sub gingival plaque and
calculus from infected root surfaces15.
Periodontal tissues have varying water and mineral
content, pigment and tissue density, which allows
them to absorb beams from Nd: YAGand diode
lasers16. On the other hand, CO2 lasers are better
suited for soft tissue procedures because its energy
beam is absorbed mostly by water. Hydroxyapatite is
better suited for other types of lasers17.
Other factors that affect absorption of energy beam
into the target include power, pulse duration, duration
of exposure, angle of energy delivery and waveform
(pulsed or continuous).
When choosing the type of laser, a specific goal
should be made in order to achieve the desired
results. This is because, energy absorption will cause
the target to warm up, coagulate, vaporize or melt
and recrystallize as seen in hard tissues.
Periodontal Disease and Lasers techniques: The
American Academy of Periodontology (AAP) has
suggested that using lasers during scaling and root
planing (SRP) may provide improvements in
procedures by decreasing bleeding, swelling and
discomfort during surgery.
Laser Assisted New Attachment Procedure (LANAP)
is a relatively new treatment option that helps remove
plaque and calculus, while limiting bacterial infection
to help fight periodontitis by regenerating rather than
resecting tissues. LANAP helps to remove infectioncausing bacteria in a safe and painless procedure that
promotes epithelial and periodontal fiber attachments
in the affected area18. Other uses of this technique
include removal of caries and preparation of teeth for
restorations or crowns.
Caution must be taken when using laser therapy
because of varying power levels and wavelengths.
Incorrect wavelength and/or power levels can result
in damage during periodontal treatment causing more
harm than good.
Benefits of Laser Treatment
{81}
Modern techniques using lasers can control the
spread of harmful bacteria and limit tooth loss
compared to standard periodontal treatment options.
Some benefits of laser treatment for gum disease
include: elimination of cutting and bleeding, soreness
and discomfort of the gums. Isolation of deep
periodontal pockets. Reduction in tooth loss.
Regeneration of bone and ligament tissues. Lastly,
increased chances of success with a solution in case
of setbacks that may occur19.
As compared to a dental hand piece, lasers are
advantageous in certain conditions causing less pain,
anxiety and discomfort for the patient. In addition,
soft tissue damage is minimized and the need for
anesthesia may be avoided in less invasive
procedures.
benefit of a less invasive treatment option coupled
with shorter treatment duration and discomfort for the
patient are attractive features of laser therapy but
studies have yet to prove its effectiveness. 10-15% of
the population that suffer from periodontal disease is
treated with long-term daily oral hygiene instructions.
Professional monitoring and evaluation with regular
periodontal maintenance every 3 months is the
desired level of care with no short cuts in the
foreseeable future.
References
1.
2.
Conclusion
With all the benefits of laser therapy outlined in this
review, we point out the lack of studies supporting its
use alone. There is no evidence in the literature to
suggest it may control adult chronic periodontitis
without conventional SRP and surgical treatment.
The advantage of laser therapy in conjunction with
traditional therapy are of benefit, yet current
challenges include increased operating costs for the
dentists and patients coupled with technique
sensitivity for operators.
The main advantages of laser therapy over
conventional
methods
are
reduced
tissue
inflammation and bleeding. Sterilization of the
affected area leading to a reduction in post-treatment
discomfort with higher patient satisfaction. With this
in mind, are lasers considered more advantageous
than traditional therapy? Current literature is
inconclusive.
In order to come up with a final conclusion,
evidence-based science provides strict research
protocols and parameters to make fair comparisons
between various treatments. Studies should have an
adequate sample size, be randomized with controls
and have specific treatment goals and criteria. To
show effectiveness and long-term results, an
appropriate time-line should be set.
In a systematic review of the literature on the use of
lasers in periodontal therapy, only 8 of 300 studies
met the criteria above. Researchers in only 5 out of 8
studies assessed the tissue attachment after treatment,
a gold standard in assessing periodontal treatment
outcome. The results of the review could not point to
any advantages of Nd:YAG lasers over conventional
periodontal therapy in the treatment of initial
periodontitis.
Initial non-surgical therapy of periodontitis remains
the treatment of choice with growing interest in lasers
as an adjunct treatment option for gum disease. The
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
ADA.org, ‘Statement on Lasers in Dentistry’ 2009.
http://www.ada.org/en/about-the-ada/ada-positionspolicies-and-statements/statement-on-lasers-in-dentistry
N.p.2015 .
Gould, R. Gordon (1959). "The LASER, Light
Amplification by Stimulated Emission of Radiation". In
Franken, P.A. and Sands, R.H. (Eds.). The Ann Arbor
Conference on Optical Pumping, the University of
Michigan, 15 June through 18 June 1959. p. 128.
Maiman TH. Stimulated optical radiation in ruby. Nature.
1960;187:493-4.
Matthews, D. C. (2009). Seeing the Light--the truth about
soft tissue lasers and nonsurgical periodontal therapy.
Journal (Canadian Dental Association), 76, a30-a30.
Cobb CM. Lasers in periodontics: a review of the
literature. J Periodontol. 2006;77(4):545-64.
Dederich DN, Bushick RD; ADA Council on Scientific
Affairs and Division of Science; Journal of the American
Dental Association. Lasers in dentistry: separating
science from hype. J Am Dent Assoc. 2004;135(2):20412. Erratum: J Am Dent Assoc. 2004;135(6):726-7.
PM Freitas, RS Navarro, JA Barros, C de Paula Eduardo
The use of Er:YAG laser for cavity preparation: an SEM
evaluation Microsc Res Tech, 70 (9) (2007), pp. 803–808.
U Keller, R Hibst Effects of Er:YAG laser in caries
treatment: a clinical pilot study Lasers Surg Med, 20
(1997), p. 32.
Bornstein, M. M., Winzap-Kälin, C., Cochran, D. L.,
&Buser, D. (2005). The CO2 laser for excisional biopsies
of oral lesions: a case series study. The International
journal of periodontics & restorative dentistry, 25(3),
221-229.
Y Kimura, P Wilder-Smith, K Matsumoto Lasers in
endodontics: a review IntEndod J, 33 (2000), pp. 173–
185.
Pihlstrom, B. L., Michalowicz, B. S., & Johnson, N. W.
(2005). Periodontal diseases. The Lancet, 366(9499),
1809-1820.
PERIODONTICS, S. O. (2001). Guidelines for
periodontal therapy. J Periodontol.
Nyman, S., Lindhe, J., Karring, T., &Rylander, H. (1982).
New attachment following surgical treatment of human
periodontal
disease. Journal
of
clinical
periodontology, 9(4), 290-296.
Van Dyke, T. E. (2008). The management of
inflammation in periodontal disease. Journal of
periodontology, 79(8S), 1601-1608.
Cobb, C. M. (2006). Lasers in periodontics: a review of
the literature. Journal of periodontology, 77(4), 545-564.
Folwaczny, M; Aggstaller, H; Mehl, A; Hickel, R:
Removal of bacterial endotoxin from root surface with
Er: YAG laser. Am J Dent 16(1):3–5, 2003.
Crespi, R., Barone, A., Covani, U., Ciaglia, R. N.,
&Romanos, G. E. (2002). Effects of CO2 laser treatment
{82}
on fibroblast attachment to root surfaces. A scanning
electron
microscopy
analysis. Journal
of
periodontology, 73(11), 1308-1312.
18. Yukna, R. A., Carr, R. L., & Evans, G. H. (2007).
Histologic evaluation of an Nd: YAG laser-assisted new
attachment procedure in humans. The International
journal of periodontics & restorative dentistry, 27(6),
577.
19. White, J. M., Goodis, H. E., & Rose, C. L. (1991). Use of
the pulsed Nd: YAG laser for intraoral soft tissue
surgery. Lasers in surgery and medicine, 11(5), 455-461.
__________________________________________________
{83}
ORIGINAL RESEARCH
Prevalence of bleeding gums while tooth brushing
among betel nut chewers vs non betel nut chewers in
school going children
Dr. Syed Misbahdduin1,
Dr. MansoorUl Aziz2,
Dr. Asma Fazal3,
Dr. Tayyaba Khairuddin4,
Dr. Safia Khairuddin5
University College Cork, Cork, Ireland
Associate Professor at Altamash Institute of Dental
Sciences
3
Our Lady’s Children Hospital Crumlin, Dublin,
Ireland
4
Registrar Psychiatrist at St. Joseph Intelectual
Disability, St. Itas Mental Health Services, Donabate,
Portrane, Dublin, Ireland
5
Department of Proteomics and HIV Research Lab,
Post-doc University of Southern California, USA
1
2
Dr. Syed Misbahuddin
www.idjsr.com
database
Quick Response Code
Abstract
Betel nut (BN) also referred to as Chalia/Supari has
been used for thousands of years. BN chewing is an
important and popular cultural habitin India,
Bangladesh and Pakistan (the subcontinent).It is
being used regularly on individual and family basis.
The use of BN is prevailing in the rural and urban
areas of Pakistan. In several studies, an association
between BN chewing and oral health problems like
bleeding gums, sore gums have been identified.
These lesions are reported in children and
adolescents. This is of great concern not only because
of the high cost involved in their management but the
morbidity and mortality associated with it. Low cost,
easy availability, advertising, role modelling, social
acceptance and perception of BN as harmless,
contribute to its use. The aim of this cross-sectional
study in Central District of Karachi (CDK) was to
assess the prevalence of oral soft tissue lesions and to
investigate the associations which may exist between
oral conditions and BN chewing among the young
school going children. Three hundred and sixty
students from 17 different schools participated in the
study. The mean age was 13.86 ±1.2 years with the
age range of 12 to 16 years. Out of these 360
students, 175 were females and 185 were males. The
results showed a high prevalence of bleeding gums
while tooth brushing among BN chewers (BNC)
compared to non-chewers (NBNC) (19% and 3%
respectively). The high prevalence of BN chewing
(59% of the low socio-economic young population
studied) should be addressed at local and government
level through support for effective preventive
programs and health promotion campaigns.
Promotion of oral health and eradication of BN
chewing are important goals for the prevention of
oral cancer among this population.
Introduction
The chewing of betel nut (BN) is an old practice in
South-East Asia, especially in the Indian
subcontinent1. This tradition is inherited by
generation after generation and has become a popular
cultural activity among people of Pakistan, India, Sri
Lanka, and Bangladesh2. BN is a fruit of areca tree
that widely grows in tropical Pacific, Asia and east
Africa3. It is a small feathery plant that grows to the
height of 1.5 m. The most common method of using
BN is to chop it into very small pieces with the help
of an especial instrument known in local language Urdu as “sarota”. Slurry of slaked lime and catechu
boiled in water is applied on a betel leaf and the
chopped pieces of BN are rolled in it to be kept in
mouth4,5.
BN contains the alkaloid arecoline in addition to
nitrosamines, which is carcinogenic.Various studies
have been conducted to determine the relation of BN
and other alternative chewing material to oral and
other associated cancers6,7. It has been proved that
BN, Gutka and Paan cause oral cancers8,9and alone in
India, out of 700,000 cancers diagnosed each year
{84}
300,000 cases are related to tobacco smoking and BN
chewing10,11.
Although, the use of BN and Gutka is associated with
certain oral conditions; the prevalence and effect on
oral health of school going children of 12-16 years of
age is not clearly known in local context. This study
was conducted to identify the prevalence of oral
lesions and to investigate association which may exist
between the oral conditions and BN/Gutka chewing
among the school going children.
Objectives of the study
To identify oral lesions present in school going
children and to compare the prevalence of oral
lesions among those who chew betel nut versus nonchewers.
Methodology
A cross sectional study was conducted in City
District, Karachi. A research questionnaire was
prepared, and sent along with the parental consent
and student assent forms to the Clinical Research
Ethics Committee of the Cork Teaching Hospital,
University College Cork for ethical approval, which
approved it. Ethical approval was also granted from
Baqai Dental College, Karachi for this study. The
questionnaire was scrutinized by the subject
specialists and was coded for statistical purposes. The
research questionnaire consisted of chewing habits,
clinical interview and findings of the clinical
examination.
The sample comprised of 360 students from 17
different schools in CD, Karachi. The age range of
sample population was 12 - 16 years. The authors
was trained and calibrated for the examination of oral
health and identification of oral lesions at Cork
University School and Dental Hospital. In Karachi,
the author hired qualified dental assistants and trained
and calibrated them. The subjects had their oral
examination done on the specified date by the author
and the trained dental staff.
Individuals were examined in the natural day light on
a chair in a separate room to maintain privacy. A
hand torch was also used in some cases, where natural
daylight was insufficient. A sterile CPITN probe was
used to observe bleeding on gentle probing. When
required the teeth were dried using cotton wool rolls.
Universal precautions were followed. Personal
protective clothing and equipment was worn by all
the examiners and recorders in attendance. Latex free
examination gloves were used for the examination of
each child and were changed before examining the
next child. A facemask was worn and changed at
frequent intervals. A disposable paper sheet was used
under each set of instruments and disposed after each
examination. The CPITN probes and mirrors were
placed in a container used solely for the transport of
“contaminated”
instruments.
All
re-usable
instruments were washed and autoclaved at the end
of each session. All contaminated waste, which
included gloves, facemasks, cotton wool rolls, tissues
and wipes, were disposed into ‘hazardous waste’
yellow bags in accordance with infection control best
practice. Two plastic boxes for instruments were used,
of which; one box was for transporting sterile
instruments only while the other box was for
contaminated instruments. All children were given
protective eye covers to wear. These were cleaned
with disinfectant wipes between examinations. The
torches were wiped with a disinfectant between
examinations.
Each child was asked to sit on the chair. Face masks
and tinted protective eyewear were used for all the
children. First, a visual examination was done to check
for dental caries. Teeth were examined wet, and a
CPITN probe was used to remove food debris as well
as to confirm dental cavitations. Soft tissues and oral
cavity were then examined for any abnormalities.
Statistical Analyses
SPSS Version 18® was used for statistical analysis.
The following information was obtained and
analysed:
 The number of children examined by gender and
age.
 The mean age in years of children that
participated in the study.
 Habit of BN chewing and its association with
gender.
 Frequency of tooth brushing habit.
 Distribution of subjects by gender and tooth
brushing habit
 Association of gender with the frequency of
bleeding gums while brushing teeth
Results
The distribution of males and females by the status of
betel nut chewing:
As illustrated in the table below, 61.61% of males
and 38.39% of females chewed betel nut (Table 1.1).
Table 1.1 BN chewing and gender distribution
Betel nut
Males% (n)
Females% (n)
chewing
Yes
61.61 (130)
38.39 (81)
No
36.91 (55)
63.08 (94)
The value of chi square is 21.32, df =1 and p= 0.000.
There was a significant difference in the habit of
betel nut chewing among males and females. Almost
{85}
twice the numbers of males (61.61%) chewed betel
nut as compared to females (38.39%).
Never
Twice a day More
60
50
40
30
20
10
0
53.71%
38.37% 37.83%
29.16%
12 years
13 years
14 years
15 years
16 years
Male
37
39
49
34
26
Female
32
44
40
34
25
Figure 1.1 Gender and age of the subject
Tooth brushing habit: Frequency of tooth brushing
was ascertained from question 1 of the oral hygiene
and chewing habits questionnaire (Appendix VI).
It was noted that 15.85% subjects never brushed their
teeth whereas45.83% brushed once a day, 33.61%
twice a day and 4.71% more than that (Graph 1.2).
16.75%
Males

BN chewing %
53.69%
42.65%
40.28%
15.85%
4.71%

Females
The association of tooth brushing with betel
nut chewing: When the tooth brushing habit of
both the groups was compared, it was noted that
among BNC, 11.86% never brushed their teeth,
40.28% brushed once a day, 42.65% twice a day
and 5.21% brushed more than twice a day. In
comparison, among NonBNC, 21.47% never
brushed their teeth, 53.69% brushed once a day,
20.80% twice a day and 4.04% brushed more
than that (Graph 1.4).
33.61%
Twice a
day
2.28%
Figure 1.3: The distribution of subjects by gender
and tooth brushing habit
45.83%
Once a
day
14.85%
7.05%
Brushing frequency
Never
Once a day
21.47%
20.80%
11.86%
5.21%
4.04%
More
Figure 1.2: Frequency of tooth brushing
Tooth brushing habit among males and
females: The results showed that 16.75% males
never brushed their teeth, 38.37% brushed once a
day, 37.83% twice a day and 7.05% more than
twice a day. Among females, 14.85% never
brushed their teeth, 53.71% brushed once a day,
29.16% twice a day and 2.28% more than that
(Graph 1.3).
Never
Once a
day
Twice a
day
More
Figure 1.4: Association of tooth brushing with
BNC
Chi square value is 21.29, df= 1 and p= 0.001.
There was a significant difference in the frequency of
tooth brushing among BNC and NonBNC. Eighty
eight point one four percent of BNC were brushing
teeth as compared to 78.53% of NonBNC.
{86}

The association of gender with the frequency
of bleeding gums while brushing teeth: It was
noted that 67.02% of males and 81.14% of
females never had bleeding gums while brushing
their teeth. Eighteen point three nine percent of
males and 14.86% of females occasionally had
bleeding, while 14.59% of males and 4% of
females frequently had bleeding from their gums
while brushing teeth (Graph 1.5)
Frequency of bleeding gums
Male
67.02%
Female
81.14%
14.59%
18.39% 14.86%
Never
Occasional
4%
Frequently
Figure 1.5: Association of gender with the
frequency of bleeding gums while brushing teeth
The value of chi square is 13.78, df= 2 and p=0.001.
There was a significant difference in complaints of
bleeding gums while brushing teeth between the
genders with females having gums that bleed less
often.

The association of betel nut chewing with the
frequency of bleeding gums while brushing
teeth: Among BNC, 18.95% occasionally had
bleeding gums and 10.44% frequently had
bleeding from gums while brushing their teeth.
However, among NonBNC; 13.43% occasionally
had and 8.05% frequently had bleeding from
gums while brushing their teeth (Table 1.2).
Table 1.2: The association of bleeding gums
while brushing teeth and betel nut chewing
Frequency
of BNC
Non BNC
bleeding gums while % (n)
% (n)
brushing teeth
Never
70.61
78.52
(149)
(117)
Occasionally
18.95 (40) 13.43 (20)
Frequently
10.44 (22) 8.05 (12)
Total
100 (211) 100 (149)
The value of chi square is 2.865, df= 2 and p= 0.239.
There was no significant difference in gum bleeding
while brushing teeth between BNC and NonBNC.

The association of bleeding gums without
brushing teeth with betel nut chewing: It was
noted that 5.69% BNChad bleeding gums
without brushing teeth. On the other hand, 0.68%
NonBNC had bleeding gums without brushing
theirteeth (Table 1.3).
Table 1.3 The association of bleeding gums
without brushing teeth and betel nut chewing
Bleeding
gums BNC
NonBNC
without brushing
% (n)
% (n)
teeth
Yes
5.69 (12)
0.68 (1)
No
94.31 (199) 99.32 (148)
Total
100 (211)
100 (149)
The value of chi square is 6.313, df= 1 and p= 0.012.
There was a significant difference among both the
groups with more BNC having bleeding gums
without brushing teeth as compared to NonBNC.
Discussion
In our study, we found out that twice a number of
males were indulged in Betel nut chewing as
compared to females. Females had the highest
percentage of brushing teeth but males predominated
in brushing teeth twice a day. It was also noticed that
tooth brushing was more common among BNC as
compared to Non BNC. In contrast to males, bleeding
gums was less common in females.
It is seen that mostly periodontal diseases progress
un-noticed. People commonly recognize it at an
advance stage. It is therefore important to make
dental health education mandatory for control and
maintenance of periodontal health.
Early recognition of periodontal conditions is not so
common because people do not understand the
connection between gum bleeding and gum disease.
According to Brady, 73% of patients with periodontal
disease did not know that they had it12. Almas et al
reported 42% of Saudis with bleeding gums13.
Khawamura and Eva Motto found that 3 quarters of
Japanese employees had bleeding gums14.
Gingivitis with bleeding gums is the first symptom of
periodontal disease. This symptom of disease is selfdetected and is the most reliable indicator of the
condition15. In order to prevent progression of
periodontal disease, the public needs dental health
education to connect gingival bleeding with gum
disease16. The aspect of dental health education
therefore has a key role in the awareness of
periodontal disease among different groups of
society.
{87}
Self-Reporting
Research conducted in Dundee dental hospital and
school revealed astonishing results about the
knowledge and understanding of periodontal disease
among the people who took part in the study. People
were unable to recognize that they have periodontal
disease while having gingival bleeding17. Although
people were aware of bleeding gums at times, there
were other times when it went unnoticed A.D. Gilbert
& N.M. Muttall. Radiographs were not used in order
to validate the self-reporting instrument and also to
avoid unnecessary radiation. The CPITN method
was normally used to determine periodontal
treatment needs and was considered more appropriate
to make patient realize that they have gum disease.
Conclusion
11.
12.
13.
14.
15.
16.
The results of this study indicate dental and oral care
education must be included in a national program that
promotes preventive oral care in schools as well in
other oral health educational programs aimed at the
general public. This recommendation is based on the
finding that children were aware of the importance of
dental care but need proper education and guidance.
17.
Summers RM, Williams SA, Curzon ME. The use of
tobacco and betel quid ('pan') among Bangladeshi
women in West Yorkshire. Community Dent
Health. 1994;11(1):12-6.
Brady WF. Periodontal disease awareness. The Journal
of the American Dental Association. 1984;109(5):70610.
Taani DQ. Periodontal awareness and knowledge, and
pattern of dental attendance among adults in Jordan.
International dental journal. 2002;52(2):94-8.
Okada M, Kawamura M, Kaihara Y, Matsuzaki Y,
Kuwahara S, Ishidori H, et al. Influence of parents’
oral health behaviour on oral health status of their
school children: an exploratory study employing a
causal modelling technique. International Journal of
Paediatric Dentistry. 2002;12(2):101-8.
Walsh MM. Effects of school‐based dental health
education on knowledge, attitudes and behavior of
adolescents in San Francisco. Community dentistry
and oral epidemiology. 1985;13(3):143-7.
Murtomaa H, Meurman J, Rytömaa I, Turtola L.
Periodontal status in university students. Journal of
clinical periodontology. 1987;14(8):462-5
Gilbert A, Nuttall N. periodontology: Self-reporting of
periodontal health status. British dental journal.
1999;186(5):241-4.
___________________________________________
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Rooney DF. Betel nut chewing in south East
Asia.http://rooneyarchive.net/lectures/lec_betel_chewi
ng_in_south-east_asia.htm
Gupta PC, Ray CS. Epidemiology of betel quid usage.
Ann Acad Med Singapore, 2004;33(suupl):31s-36s
en.wikipedia.org/wiki/Areca
Patel K. Helping members of the South Asian
community
quit
smokeless
tobacco.
http://www.nice.org.uk/newsroom/features/HelpingMe
mbersOfTheSouthAsianCommunityQuitSmokelessTob
acco.jsp
Nair U, Bartsch H, Nair J. Alert for an epidemic of oral
cancer due to use of the betel quid substitutes gutkha
and pan masala: a review of agents and causative
mechanisms. Mutagenesis. 2004;19(4):251-62.
Yang YH, Lien YC, Ho PS, Chen CH, Chang
JS, Cheng TC, Shieh TY. The effects of chewing
areca/betel quid with and without cigarette smoking on
oral submucous fibrosis and oral mucosal lesions. Oral
Dis. 2005;11 (2): 88-94.
Trivedy CR, Craig G, Warnakulasuriya S. The oral
health consequences of chewing areca nut. Addict
Biol. 2002;7(1):115-25.
Thomas and MacLennan (1992). "Slaked lime and
betel nut cancer in Papua New Guinea". The Lancet
Oncology 340 (8819): 577–578.
Shwu-Fei LC, Chiu-Lan C, Liang-Yi H, Pi-Chen H,
Jung-H C, Chang-Ming S, Chin-Wen C, and TsungYun L. Role of oxidative DNA damage in
hydroxychavicol-induced genotoxicity. Mutagenesis
vol.11 no.5 pp.519-523, 1996
SangeetaDarvekar
Charitable
Trust
[email protected]
{88}
SHORT COMMUNICATION
Short communication: Stem Cells for Periodontal Tissue
Regeneration
Dr. Mohamed-Nur Abdallah1,
Dr. Mai S. Ali2
1
Faculty of Dentistry, McGill University, Montreal,
Quebec, Canada.
2
Department of Restorative Dentistry and
Endodontics King Hussein Medical Center, Amman,
Jordan.
Dr. Mohamed-Nur Abdallah
www.idjsr.com
database
Quick Response Code
Introduction
Periodontal disease is an inflammatory condition that
causes pathological alterations in the periodontium,
potentially leading to tooth loss [1]. In the world,
35% of adults in the population suffer from moderate
periodontal disease, while up to 15 % were affected
by a more severe form at some stage of their life [2,
3].The periodontium has always proved to be one of
the structures with inherent regenerative capacities. It
gives rise to osteoblasts, periodontal ligament (PDL)
fibroblasts, and cementoblasts[4]. However, the
periodontium – which includes the periodontal
ligament, root cementum, alveolar bone and gingiva has a limited ability to regenerate once damaged [4].
For decades, periodontists have sought to repair the
damage from periodontitis and to achieve
regeneration through a variety of non-surgical
procedures and surgical procedures that include root
surface conditioning, bone graft placement, guided
tissue regeneration and the application of growth
factors [5-7]. However, current procedures allow the
periodontal tissue to be repaired rather than
regenerated with some approaches showing some
limited unpredictable regenerative outcome [8-12].
Recent advances in tissue engineering and stem cell
biology have paved the way to develop novel
approaches in the regenerative periodontal therapy or
to supplement existing treatment modalities for
periodontal disease.
Cell-based Tissue Engineering
In order to achieve a successful periodontal
regeneration, healing events must occur in an ordered
and programmed order, starting with the migration of
appropriate progenitor cells into the wound site and
attach to the denuded root surface [13]. These
progenitor cells have the ability to proliferate and
mature into the different component of the functional
periodontium. The success of these progenitor cells is
also dependant on the availability of the appropriate
growth factors and contact with the extracellular
matrix [14, 15]. This allows the formation of a
functional epithelial seal with an insertion of a new
connective tissue fibers into the root in conjunction
with a new acellular cementum covering the root
surface and the reestablishment of a proper alveolar
bone height that can ensure a healthy regenerated
periodontium [16, 17]. Current tissue engineering
trends have utilized the principles of periodontal
healing and cell biology in developing cellular-based
techniques for periodontal regeneration.
In the context of periodontal therapy, cell-based
tissue engineering involved incorporation of
progenitor cells in a prefabricated three-dimensional
biomaterial that is implanted into the defect site. This
approach overcomes some of the limitations of
conventional procedures and allows direct application
of progenitor cells and growth factors in the defect
area [18]. The success of the cell-based approach
requires the following essential factors [19]: (1)
appropriate progenitors cells that proliferate and
mature to tissue-forming phenotypes, including
fibroblasts, osteoblasts, and cement oblasts; (2)
appropriate signals to control cellular differentiation
and tissue formation; (3) a three dimensional scaffold
to support the cells and facilitate the previous
processes; and (4) good blood supply and promotion
of new vascular networks. Consequently, the most
critical factors in tissue engineering is the choice of
optimal stem cell population that give rise to the
progenitor cells and the selection of an appropriate
biomaterial that can serve as a scaffold that both
support these cells and possess adequate mechanical
properties.
{89}
Stem cells
By definition, a stem cell is a clonogenic, relatively
undifferentiated cell that is capable of self-renewal
and multi-lineage differentiation depending on
intrinsic signals modulated by extrinsic factors in the
stem cell niche[20, 21]. Stem cells (SCs) are
classified according to their origin and their
differentiation potential[16, 22]. They can be broadly
classified into three categories: (1) embryonic stem
cells (ESCs); (2) induced pluripotent stem cells
(iPSCs); (3) adult or postnatal SCs. ESCs are
totipotent or pluripotent cell, which means that they
possess the capacity to proliferate extensively and
differentiate into almost all possible cell types.
However, using embryos to obtain human embryonic
stem cells has raised many ethical concerns and
limited their usage. These concerns pushed
researchers to investigate the possibility of
genetically reprogramming somatic cells back to the
pluripotent phase, which lead to the generation of
iPSCs[23, 24]. They are comparable to the ESCs in
their function, morphology, gene expression and wide
differentiation capacity[23, 24]. Efforts were also
made to obtain iPSCs from gingival and periodontal
fibroblasts[25-27]. In general, the behaviour of iPSCs
can be unpredictable because the genetic
manipulations may alter their development and
growth characteristics, thus, limiting their in tissue
engineering[16]. Moreover, both the ESCs and the
iPSCs convey tumorigenic properties that raise
serious safety concerns that further limit their use in
regenerative therapies.
Somatic adult or postnatal stem cells can be derived
from the majority of fetal and adult tissues that
continually replenish themselves (e.g. dermis,
peripheral blood) [20, 28, 29]. They are multipotent
and can differentiate into limited number of cell
lineages such as endothelial, perivascular, neural,
bone or muscle cells [30]. It is thought that they
function in long-term tissue maintenance and
replacing cells that are either lost or injured [31].
Despite their limited life span, SCs have extensive
self-renewal capacity [32]. Even though adult SCs
exhibit more restricted capabilities compares to
ESCs, they are immunocompatible and are not
associated with any ethical concerns (Han). Their
most common sources are the bone marrow
(hematopoietic stem cells) and bone marrow stromal
cells (mesenchymal stromal stem cells) [33-35].
Hematopoietic stem cells were the first cells to be
used in regenerative therapies, mainly in the
treatment
of
blood
malignancies
and
immunodeficiency syndromes, but they lack the
ability to give rise to supporting connective tissues
[36]. On the contrary, mesenchymal stem cells
(MSCs) have been used to treat a range of
musculoskeletal abnormalities and are capable of
differentiate to connective tissue cells [36].
Consequently, MSCs serve as potential candidates for
periodontal regeneration.
Human mesenchymal stem cells in
periodontal regeneration
Human mesenchymal stems cells (hMSCs) are the
most commonly used stem used in periodontal
regeneration due to their extensive expansion rate,
immunocompatibility
(some
may
exhibit
immunosuppressive properties), and extensive
availability without any ethical restraints[37]. hMSCs
used for periodontal regeneration can be obtained
from both extraoral and intraoral tissues. Extraoral
sources include bone marrow and adipose tissues.
Past in vivo studies showed that implanted bone
marrow-derived MSCs can induce the regeneration of
cementum and alveolar bone up to 20% in
experimental Class III defects [38], and can
differentiate into cementoblasts, alveolar bone
osteoblasts and PDL fibroblasts [38-41]. Small
human clinical trials demonstrated that mixing bone
marrow-derived MSCs with platelet-rich plasma
(PRP) result in reduction in intrabony defect depth
and resolution of bleeding, while mixing these cells
with atelocollagen reduced the probing depth by
4mm [41]. Another potential extraoral source is
adipose tissue. In vivo studies in rats demonstrated
that adipose-derived stromal cells mixed with PRP
promoted periodontal regeneration [42]. Future
clinical studies are required to assess the candidacy of
adipose-derived MSCs for periodontal regeneration,
since they are more abundant, more easily accessible
to lipoaspirates with lower morbidity compared to the
more invasive procedures to obtain the bone marrowderived MSCs.
Dental-tissue derived MSCs can be obtained
intraorally from dental tissues (e.g. dentin or PDL or
pulp) either from permanent or deciduous teeth [4345]. They can be simply obtained using a chair side
procedure or immediately after tooth extraction [43].
However, these cells have a more restricted cellular
potency in comparison to bone marrow-derived
MSCs, as bone tissues are known to undergo more
remodelling than dental tissues [16]. There has a been
a particular interest in assessing the regenerative
capacity of mesenchymal stems derived from PDL
(PDLSCs), since being first isolated in
2004[46].They showed an increased proliferative
potential of cell populations that can differentiate into
either cementoblasts, osteoblasts, fibroblasts and
even adipocytes[47]. PDLSCs can exert different
benefits on multiple levels including tissue
regeneration,
neovascularization
and
immunomodulation, by which PDLSCs can inhibit
{90}
the immune response without an induction of an
inflammatory response, thus enabling the use of
allogenic
PDL
sources
for
periodontal
regeneration[48, 49]. Animal studies showed that
implanted PDLSCs in periodontal defects resulted in
the new formation of cementum and alveolar bone,
and new attachment apparatus[50-55]. Furthermore,
a study conducted on mini-pegs demonstrated the
formation of PDL- like tissue mimicking the
orientation of the fibre bundles similar to Sharpey’s
fibers within four weeks[51]. The results from human
clinical studies using PDLSCs are encouraging yet
still very limited and variable [56-58].Recent studies
even showed that MSCs can be derived from normal
and inflamed gingival tissues which might be a more
abundant potential source compared to PDL[59, 60].
More future studies are required to assess the benefits
and safety of using MSCs from dental origin and
important challenges need to be addressed before
applying such treatment protocols to standard clinical
practice[56].
3.
Final remarks
10.
The future applications of stem cells and tissue
engineering in periodontal therapy are one of the
most promising techniques capable of meeting a
variety of patients’ needs. However, many challenges
need to be tackled before reaching a clear consensus
regarding stem cells utilization. Biologically, it is
essential to fully understand the key cellular events
that occur during periodontal development,
knowledge of the specific cell types, the inductive
factors, the cellular and molecular processes involved
in formation of the periodontium, and the mechanism
in which stem cells promote differentiation.
Technical challenges such as the appropriate delivery
system and the most suitable scaffold matrix should
be addressed by advancing the techniques used in
handling stem cells. Concerning the clinical
challenges, it is very important to understand the
immune response after the delivery of the stem cells
and the safety considerations related to the use stem
cells. In addition, the cost effectiveness and the
patient benefits should be considered. More high
quality clinical research is essential to ensure that
such novel approaches supported by robust data and
are effective in meeting the patients’ needs.
4.
5.
6.
7.
8.
9.
11.
12.
13.
14.
15.
16.
17.
18.
References
19.
1.
2.
Pihlstrom, B.L., B.S. Michalowicz, and N.W. Johnson,
Periodontal diseases. Lancet, 2005. 366(9499): p.
1809-1820.
Albandar, J.M., Epidemiology and risk factors of
periodontal diseases. Dental clinics of North America,
2005. 49(3): p. 517-32, v-vi.
20.
Burt, B., et al., Position paper: epidemiology of
periodontal diseases. Journal of periodontology, 2005.
76(8): p. 1406-19.
Polimeni, G., A.V. Xiropaidis, and U.M. Wikesjo,
Biology and principles of periodontal wound
healing/regeneration. Periodontol 2000, 2006. 41: p.
30-47.
Keestra, J.A., et al., Non-surgical periodontal therapy
with systemic antibiotics in patients with untreated
chronic periodontitis: a systematic review and metaanalysis. J Periodontal Res, 2015. 50(3): p. 294-314.
Darby, I.B. and K.H. Morris, A systematic review of
the use of growth factors in human periodontal
regeneration. J Periodontol, 2013. 84(4): p. 465-76.
Chen, F.M. and Y. Jin, Periodontal tissue engineering
and regeneration: current approaches and expanding
opportunities. Tissue Eng Part B Rev, 2010. 16(2): p.
219-55.
Xiao, Y., et al., Expression of extracellular matrix
macromolecules around demineralized freeze-dried
bone allografts. Journal of Periodontology, 1996.
67(11): p. 1233-1244.
Venezia, E., et al., The use of enamel matrix derivative
in the treatment of periodontal defects: A literature
review and meta-analysis. Critical Reviews in Oral
Biology & Medicine, 2004. 15(6): p. 382-402.
Stavropoulos, A., et al., Deproteinized bovine bone
(Bio-Oss((R))) and bioactive glass (Biogran((R)))
arrest bone formation when used as an adjunct to
guided tissue regeneration (GTR) - An experimental
study in the rat.Journal of Clinical Periodontology,
2003. 30(7): p. 636-643.
Ripamonti, U. and A.H. Reddi, Tissue engineering,
morphogenesis, and regeneration of the periodontal
tissues by bone morphogenetic proteins. Critical
Reviews in Oral Biology & Medicine, 1997. 8(2): p.
154-163.
Sander, L. and T. Karring, HEALING OF
PERIODONTAL
LESIONS
IN
MONKEYS
FOLLOWING
THE
GUIDED
TISSUE
REGENERATION
PROCEDURE
A
HISTOLOGICAL STUDY. Journal of Clinical
Periodontology, 1995. 22(4): p. 332-337.
Bartold, P.M., et al., Tissue engineering: a new
paradigm for periodontal regeneration based on
molecular and cell biology. Periodontology 2000,
2000. 24: p. 253-269.
Aukhil, I., Biology of wound healing. Periodontology
2000, 2000. 22: p. 44-50.
Ivanovski, S., et al., Stem cells in the periodontal
ligament. Oral Diseases, 2006. 12(4): p. 358-363.
Han, J., et al., Stem cells, tissue engineering and
periodontal regeneration. Australian Dental Journal,
2014. 59: p. 117-130.
Pejcic, A., et al., STEM CELLS FOR
PERIODONTAL REGENERATION. Balkan Journal
of Medical Genetics, 2013. 16(1): p. 7-11.
Michalowicz, B.S., et al., Evidence of a substantial
genetic basis for risk of adult periodontitis. Journal of
Periodontology, 2000. 71(11): p. 1699-1707.
Hughes, F.J., M. Ghuman, and A. Talal, Periodontal
regeneration: a challenge for the tissue engineer?
Proceedings of the Institution of Mechanical Engineers
Part H-Journal of Engineering in Medicine, 2010.
224(H12): p. 1345-1358.
Smith, A., A glossary for stem-cell biology. Nature,
2006. 441(7097): p. 1060-1060.
{91}
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
Morrison, S.J., N.M. Shah, and D.J. Anderson,
Regulatory mechanisms in stem cell biology. Cell,
1997. 88(3): p. 287-98.
Lin, N.H., S. Gronthos, and P.M. Bartold, Stem cells
and periodontal regeneration. Australian Dental
Journal, 2008. 53(2): p. 108-121.
Takahashi, K., et al., Induction of pluripotent stem
cells from adult human fibroblasts by defined factors.
Cell, 2007. 131(5): p. 861-872.
Takahashi, K. and S. Yamanaka, Induction of
pluripotent stem cells from mouse embryonic and adult
fibroblast cultures by defined factors. Cell, 2006.
126(4): p. 663-76.
Egusa, H., et al., Gingival fibroblasts as a promising
source of induced pluripotent stem cells. PLoS One,
2010. 5(9): p. e12743.
Wada, N., et al., Induced pluripotent stem cell lines
derived from human gingival fibroblasts and
periodontal ligament fibroblasts. J Periodontal Res,
2011. 46(4): p. 438-47.
Nomura, Y., et al., Human periodontal ligament
fibroblasts are the optimal cell source for induced
pluripotent stem cells. Histochem Cell Biol, 2012.
137(6): p. 719-32.
Young, H.E., et al., Human reserve pluripotent
mesenchymal stem cells are present in the connective
tissues of skeletal muscle and dermis derived from
fetal, adult, and geriatric donors. Anatomical Record,
2001. 264(1): p. 51-62.
Smith, C. and B. Storms, Hematopoietic stem cells.
Clinical Orthopaedics and Related Research,
2000(379): p. S91-S97.
Pittenger, M.F., et al., Multilineage potential of adult
human mesenchymal stem cells. Science, 1999.
284(5411): p. 143-7.
Blau, H.M., T.R. Brazelton, and J.M. Weimann, The
evolving concept of a stem cell: Entity or function?
Cell, 2001. 105(7): p. 829-841.
Lin, N.H., S. Gronthos, and P.M. Bartold, Stem cells
and future periodontal regeneration. Periodontol 2000,
2009. 51: p. 239-51.
Till, J.E. and E.A. McCulloch, DIRECT
MEASUREMENT OF RADIATION SENSITIVITY
OF NORMAL MOUSE BONE MARROW CELLS.
Radiation Research, 1961. 14(2): p. 213-&.
Dominici, M., et al., Minimal criteria for defining
multipotent mesenchymal stromal cells. The
International Society for Cellular Therapy position
statement. Cytotherapy, 2006. 8(4): p. 315-317.
Horwitz, E.M., et al., Clarification of the nomenclature
for MSC: The international society for cellular therapy
position statement. Cytotherapy, 2005. 7(5): p. 393395.
Korbling, M. and Z. Estrov, Adult stem cells for tissue
repair - A new therapeutic concept? New England
Journal of Medicine, 2003. 349(6): p. 570-582.
Gronthos, S., et al., Telomerase accelerates
osteogenesis of bone marrow stromal stem cells by
upregulation of CBFA1, osterix, and osteocalcin.
Journal of Bone and Mineral Research, 2003. 18(4): p.
716-722.
Kawaguchi, H., et al., Enhancement of periodontal
tissue regeneration by transplantation of bone marrow
mesenchymal stem cells. J Periodontol, 2004. 75(9): p.
1281-7.
Hasegawa, N., et al., Behavior of transplanted bone
marrow-derived mesenchymal stem cells in periodontal
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
defects. Journal of Periodontology, 2006. 77(6): p.
1003-1007.
Li, H., et al., Application of autologous cryopreserved
bone marrow mesenchymal stem cells for periodontal
regeneration in dogs. Cells Tissues Organs, 2009.
190(2): p. 94-101.
Yamada, Y., et al., A novel approach to periodontal
tissue regeneration with mesenchymal stem cells and
platelet-rich plasma using tissue engineering
technology: A clinical case report. Int J Periodontics
Restorative Dent, 2006. 26(4): p. 363-9.
Tobita, M., et al., Periodontal tissue regeneration with
adipose-derived stem cells. Tissue Eng Part A, 2008.
14(6): p. 945-53.
La Noce, M., et al., Dental pulp stem cells: State of the
art and suggestions for a true translation of research
into therapy. Journal of Dentistry, 2014. 42(7): p. 761768.
Gronthos, S., et al., Postnatal human dental pulp stem
cells (DPSCs) in vitro and in vivo. Proceedings of the
National Academy of Sciences of the United States of
America, 2000. 97(25): p. 13625-13630.
Miura, M., et al., SHED: Stem cells from human
exfoliated deciduous teeth. Proceedings of the National
Academy of Sciences of the United States of America,
2003. 100(10): p. 5807-5812.
Seo, B.M., et al., Investigation of multipotent postnatal
stem cells from human periodontal ligament. Lancet,
2004. 364(9429): p. 149-55.
Shi, S., et al., The efficacy of mesenchymal stem cells
to regenerate and repair dental structures. Orthod
Craniofac Res, 2005. 8(3): p. 191-9.
Ding, G., et al., Allogeneic periodontal ligament stem
cell therapy for periodontitis in swine. Stem Cells,
2010. 28(10): p. 1829-38.
Koch, P.L., N. Tuross, and M.L. Fogel, The effects of
sample treatment and diagenesis on the isotopic
integrity of carbonate in biogenic hydroxylapatite.
Journal of Archaeological Science, 1997. 24(5): p.
417-429.
Isaka, J., et al., Participation of periodontal ligament
cells with regeneration of alveolar bone. J Periodontol,
2001. 72(3): p. 314-23.
Lang, H., et al., Formation of differentiated tissues in
vivo by periodontal cell populations cultured in vitro. J
Dent Res, 1995. 74(5): p. 1219-25.
Lang, H., N. Schuler, and R. Nolden, Attachment
formation following replantation of cultured cells into
periodontal defects - a study in minipigs. Journal of
Dental Research, 1998. 77(2): p. 393-405.
Liu, Y., et al., Periodontal ligament stem cell-mediated
treatment for periodontitis in miniature swine. Stem
Cells, 2008. 26(4): p. 1065-73.
Kim, S.H., et al., Alveolar bone regeneration by
transplantation of periodontal ligament stem cells and
bone marrow stem cells in a canine peri-implant defect
model: a pilot study. J Periodontol, 2009. 80(11): p.
1815-23.
Park, J.Y., S.H. Jeon, and P.H. Choung, Efficacy of
periodontal stem cell transplantation in the treatment of
advanced periodontitis. Cell Transplant, 2011. 20(2): p.
271-85.
Trofin, E.A., P. Monsarrat, and P. Kemoun, Cell
therapy of periodontium: from animal to human?
Frontiers in Physiology, 2013. 4: p. 11.
Feng, F., et al., Utility of PDL progenitors for in vivo
tissue regeneration: a report of 3 cases. Oral Dis, 2010.
16(1): p. 20-8.
{92}
58.
Gault, P., et al., Tissue-engineered ligament: implant
constructs for tooth replacement. J Clin Periodontol,
2010. 37(8): p. 750-8.
59.
Ge, S., et al., Isolation and characterization of
mesenchymal stem cell-like cells from healthy and
inflamed gingival tissue: potential use for clinical
therapy. Regen Med, 2012. 7(6): p. 819-32.
60.
Yang, H., et al., Comparison of mesenchymal stem
cells derived from gingival tissue and periodontal
ligament in different incubation conditions.
Biomaterials, 2013. 34(29): p. 7033-47.
__________________________________________________
{93}
Periodontal Disease in Immunodeficient Patients:
Clinical Guidelines for Diagnosis and Management
Introduction
Morvarid Oveisi1,
Oriyah Barzilay2,
Ahmed A. Hanafi3
1,2,3
Group of Matrix Dynamics, Faculty of Dentistry,
University of Toronto.
3
Periodontology Department, Faculty of Oral and
Dental Medicine, Cairo University
Morvarid Oveisi
www.idjsr.com
database
Quick Response Code
Abstract
Primary immunodeficiency diseases are rare
hereditary conditions that usually occur at a young
age; however, secondary immunodeficiency is
acquired due to disease, drug treatment and is
increasing in frequency among the population.
Although periodontal diseases related to these
conditions are secondary to other life threatening
manifestations, they are very common and easily
detectable by the patient, patient guardians and
periodontists. Periodontists have a major role in both
helping to detect undiagnosed diseases, as well as
improving the oral care of diagnosed patients, thus a
thorough knowledge of these conditions, causes,
local and systemic involvement, diagnostic tools and
proper management is very important. This article
summarizes selected primary and secondary
immunodeficiency conditions such as neutropenia,
leukocyte adhesion deficiency (LAD) and ChediakHegashi syndrome, and places schematic, diagnostic,
and management steps that may help periodontists
manage unexplained severe periodontal diseases
related to immunodeficiency.
Immunodeficiency diseases are defects in the
immune system in which the host defense mechanism
cannot function properly. Primary immunodeficiency
is inherited and therefore is caused by a gene defect.
However, secondary immunodeficiency conditions
are acquired and usually happen due a defect of
lymphocyte function as a result of the usage of drugs,
irradiation or invasion of pathogens such as HIV
virus and measles.[1]
There are many types of diseases caused by primary
immunodeficiency , which is a result of a defect in Tcell or B-cell function, antibody deficiency, or loss of
phagocyte function and/or number[2] ,which for the
latter these can be included as any deficiency in the
adhesion process of neutrophil [3], NADPH oxidase
or chemotaxis.[4]
The epidemiology of the diseases differ based on
race, gender, ethnic factors and geographic region[4].
It has been estimated that one in 1200 people are
affected by primary Immunodeficiency. Due to
cancer therapies, usage of immunosuppressant’s and
other biological therapies, the occurrence of
secondary immunodeficiency is growing. Organ
damage is preventable if there is minimal delay in
the diagnosis of immunodeficiency[5].
Periodontal disease is an inflammatory state of the
gingiva which affects the supporting structure of the
teeth.[6, 7]. Periodontal disease is caused by plaque
accumulation , and poor dental hygiene[8] leading to
inflammation of surrounding tissue[4].It has been
observed that individuals suffering from any types of
immunodeficiency diseases may manifest some oral,
dental and facial problems[4]which include
periodontal diseases, oral lesions and developmental
abnormalities. These can be a sign of immunity
defect. Therefore, it is crucial for physicians and
dentist to be able to recognize these systematic
disorders by the oral manifestation, carry out an
accurate diagnosis and perform the corresponding
treatment[9].
Neutropenia
Neutropenia is defined by a low absolute neutrophil
count (ANC) in the blood lasting more than 6
months, which can cause recurrent infections to a
patient [10] with varying severity from stomatitis
{94}
and gingivitis, to more severe pneumonia and sepsis.
[11] Different forms of neutropenia such as cyclic
neutropenia, chronic benign neutropenia and severe
congenital neutropenia (Kostmann syndrome) can all
cause periodontal disease.[10, 12]
Chronic benign neutropenia
Chronic neutropenia is defined by a non-cyclic low
count of neutrophils in the blood without a known
underlying systemic disease lasting less than 6
months. It is the most common form of neutropenia
in infants and children and is usually not inherited.
80-98% of patients tested positive for the antineutrophil antibody [13]. Its manifestation is less
severe than Kostmann syndrome, includes high
incidence of otitis media, upper respiratory
infections, lymphadenopathy and pneumonia but may
develop into life threatening infections and
sepsis.[10]
Oral Manifestations includes severe
gingival
inflammation,
edematous
and
hyperplastic
papilla,[14] may progress into periodontitis
[15]leading to severe horizontal bone loss and teeth
mobility [16]
Diagnosis is achieved by a persistent ANC 0.5x109/l
with a normal total white blood cell count due to
elevated numbers of lymphocytes and monocytes
[17] and confirmed by anti-neutrophil antibody.
Kostmann Syndrome
Severe congenital neutropenia (Kostmann Syndrome)
is a rare hereditary syndrome characterized by a very
low ANC (less than 0.2x109/l) [18] due to maturation
arrest during myelopoiesis process [4]and increased
apoptosis of myeloid progenitor cells in bone
marrow.[19]
Initial symptoms can be summarized as recurrent
bacterial infections of the skin, mucosa leading to
cellulitis, perirectal abscess, stomatitis, meningitis,
pneumonia, and sepsis [20] . Long term symptoms
are periodontitis, splenomegaly and hepatomegaly,
osteoporosis and myelodysplastic syndrome/acute
myeloid leukaemia (MDS/AML) [19].
Oral findings are usually more severe than other
forms of neutropenia, with recurrent painful
ulceration, [21] diffuse gingival inflammation,
alveolar bone loss, teeth mobility and loss of both
dentition [22]
Persistent ANC less than 0.5x109/l is a significant
laboratory finding and diagnosis is confirmed with
bone marrow aspiration showing an arrest of
neutrophil
hematopoiesis
at
the
promyelocyte/myelocyte stage.[10]
Cyclic neutropenia
Cyclic Neutropenia is characterized by the repetitive
occurrence of neutropenia at average of 21 day
period and last for approximately 3-6 days[23].The
mutation is passed along in an autosomal dominant
manner. It has been observed that this disease is
associated with the mutation in ELA2 gene mapped
to chromosome 19p13.3 which encodes neutrophil
elastase. Mutations in this gene lead to a shortened
neutrophil life[24] .
It is characterized by fever, mouth ulcers,
lymphadenopathy, multiple abscess formation,
exhaustion and susceptibility of infection which can
be lethal [25-29]. Reduction in the number of
polymorph nuclear leukocytes (PMNs) can be
associated with rapid and destructive periodontal
disease including aphthous-like lesions[10].
The initial oral characterization of patient includes
repetitive ulceration showing little evidence of an
inflammatory halo[30], severe gingival inflammation
and recession[14, 25],which extended from the
gingiva into the alveolar mucosa[25].Recurrent
gingival bleeding along with fever was noted as a
sign of this disease [25, 31],pocket depths exceeded
the 6- to 8-mm range[25] with various levels of tooth
mobility [31].
Diagnosis requires serial measurements of the ANC
(<1,500) daily or at least three times per week for
four to six weeks[32].
It has been demonstrated that Granulocyte ColonyStimulating Factor(GCSF) can be an efficient
treatment for neutropenia[33], as it can lead to a 10
fold increase in ANC and result in a higher life
expectancy[34].
Dental management is necessary for these patients to
control infections.





Regular dental appointments to check for the
accumulation of bacterial plaque.
Use of chlorhexidine gluconate mouth wash and
a light polishing and scaling in some part of the
teeth [25, 31].
Prophylactic antimicrobials.
Invasive dentistry should be avoided in
neutropenic episodes.
Oral surgeries to be performed only under
specific antibacterial (after microbiological
testing) and corticosteroid coverage [21]
LAD
LAD is a rare, autosomal recessive, primary
immunodeficiency syndrome; characterized by
impaired phagocytic functions[35]. LAD is classified
{95}
according to causative gene mutation into 3 types:
LAD I, LAD II and LAD III [36-38].
LAD I is caused by mutation in gene ITGB2 which
encodes for CD11/CD18 [39, 40] and ultimately
decreases the expression of three integrins on
leukocyte surfaces CD11a,CD11b and CD11c and
preventing the adhesion of neutrophils to endothelial
cells)[41]. Characterized delayed separation of
umbilical cord, major bacterial infections with no pus
formation [35] and impaired wound healing [40], the
severity of clinical features are directly related to
degree of CD18 deficiency and can be divided into
severe (less than 1% CD18 expression) and moderate
( 2.5% to 10% CD18 expression) [42, 43].
Morbidity rate of severe LAD I is high before the age
of 5 [44].
In LAD II, different gene mutations cause defects in
the specific Golgi GDP-fucose transporter [45, 46]
which reduce CD15s (Sialyl-Lewis X) on the
leukocyte surface, thus affecting the rolling phase of
neutrophil adhesion [35]. This is characterized by
mental retardation and less severe infections in
adolescence [41] . Less common LAD III, was only
reported in 4 patients suffering from bacterial
infections [38] and severe bleeding tendency[47], is
believed to be caused by general defect in integrin
activation [38].
Periodontal involvement starts as gingivitis at a
young age, just after primary teeth eruption. Deep
pocket formation and extensive bone loss [48, 49]
progress until partial or total premature loss of both
primary and permanent teeth [35]. Several case
reports showed oral ulceration and delayed wound
healing in more than 80% of patients.[35]
Primarily, blood test of patients with LAD shows
leukocytosis (20,000 to 80,000 cells/ml)[40,
50].Rebuck skin window or Boyden Chamber shows
decreased neutrophil migration and is confirmed
using flow cytometry which shows CD18 deficiency
in LAD I and sialy-Lewis x ligand deficiency in LAD
II [51]. Additional histological analysis of gingival
biopsy showed abundance of leukocytes in blood
vessels and no leukocyte in tissue [52].
{96}
Figure 1: Schematic laboratory tests for diagnosis of listed diseases. LAD, Leukocyte adhesion Deficiency.
DHR, Dihydrorhodamine. HIES, Hyper immunoglobulin E syndrome. CVID, Common Variable
Immunodeficiency.
Bone marrow transplant is the treatment of choice for
young LAD patients [53, 54].However if not
possible, several maneuvers to adjust host response
can be achieved such as white blood cell transfusion,
antibiotics, interferon and allogenic stem cell
transplant [55]. Periodontal treatment usually ends
with tooth loss [10] however maintaining the teeth is
advocated with the goal of improving patients’
physiologic and psychological health by
 Periodic oral prophylaxis [56]
 Prophylactic Antimicrobial
 Fluoride application and diet counseling
 Extraction should be avoided (due to delayed
wound healing)
Chediak-Hegashi Syndrome
Chediakhigashi is a rare condition which is inherited
in an autosomal manner. This disease is usually fatal
and appears with the irregularly enormous lysosomal
granules in the leukocytes [57, 58]. This disorder is
characterized by numerous repetitive bacterial
infections, oculocutaneous albinism, susceptibility to
bruising, and mucosal bleeding as well as peripheral
neuropathy. In addition, patients may show
neurologic dysfunction and movement disorders[3].
Furthermore, the accelerated phase of CHS named
Hemophagocyticlymphohistiocytosis (HLH) can be
recognized
by
cytopenia,
fever,
bleeding,
lymphadenopathy and hepatosplenomegaly [59-61].
This disorder is connected to the fusion of
cytoplasmic granules which can take place in the
myelopoieses and can lead to the death of myeloid
precursors in the marrow and cause neutropenia. Also
neutrophils can have a problem in phagocytosis,
chemotaxis and killing bacteria[62].
Intraoral examination showed a full mouth plaque
score of 85% [63], gingival bleeding and teeth
mobility [3, 58] , high frequency of periodontal
pockets and bone loss at an early age [10, 64, 65],
probing showed more than 30% of the sites 5-8mm
deep with concomitant recession defects [66]
Blood testing and examination of giant granules
within neutrophils, lymphocytes and natural killer
cells using nitrobluetetrazolium dye [10] are essential
for diagnosis. Bone marrow aspiration and
examination of giant eosinophilic or azurophilic
cytoplasmic inclusion bodies within the myeloid
lineage cells show a positive reaction to peroxidase
staining
People with Chediak-Higashi disorder can be
recognized at a young age, and bone marrow
transplantation can be a positive treatment which can
lower the risk of periodontal disease.[3]
It has been noted that continuous periodontal
treatments with regular follow up can help patients
avoid further infection and reduce gingival
inflammation [67]. In addition,Kornmanet et al
described the importance of periodontal therapy in
preventing progressive periodontitis [68].
Long-term
antibiotic
treatment
such
as
amoxicillin[69] is administered to patients with
progressive periodontal disease along with
metronidazole [70]to help reduce the periodontal
probing depth and promote attachment in patients
with the milder form of the disease. [67].However,
full mouth extraction is inevitable in patients with
severe progressive periodontal disease refractory to
treatment .[71]
Chronic granulomatous Disease
Chronic granulomatous disease(CGD) is a very rare
immune
deficiency
syndrome
perpetuated
genetically. CGD can be characterized by the
mutation of nicotinamide adenine dinucleotide
phosphate (NADPH) oxidase component, leading to
the failure of neutrophils and macrophages in killing
invading pathogens by impairing the respiratory
burst.
CYBB is a gene responsible for encoding the
gp91phox subunit and is reported as the most
common site of mutation. Liver abscesses, skin
infections, pneumonia, osteomyelitis, as well as
cervical or inguinal lymphadenitis can be seen in
young patients[72, 73]. Furthermore, infection and
sterile hyper inflammation is also present in CGD
patient[74].
Management of CDG is based on control of
infections. Broad spectrum antibacterial (as
cotrimoxazole)[75],
antifungal
prophylaxis
(asitraconazole)[76]. Interferon-ƴ has been shown to
improve oxidase activity in neutrophils and
monocytes of some patients[77], and to reduce
infection rates. Bone marrow transplantation is
effective and a more predictable treatment [78].
Some case reports show oral difficulties including
oral ulcers[79-84] such as multiple buccal mucosal
ulcers in direct contact with dental plaque [81],
severe gingivitis, periodontitis [79-81], enamel
hypoplasia
[84], oral candidiasis
[85]
,
granulomatous mucositis in the upper lip[86] and the
soft palate [87], geographic tongue[84] and
generalized prepubertal periodontitis,[88] loss of
attachment and recession of gingival was noted[88]
{97}
Variations of oral findings in CGD patients [72, 89,
90], and Neutrophil dysfunction[10, 91] are probably
due to immunosuppressive therapy specially steroids
[92].
Patients with CGD can be diagnosed through
flowcytometery, dihydrorhodamine 123 (DHR)
assay[93] and the nitrobluetetrazolium Test [94]
Treatment:
 Regular dental care and frequent follow-up.
 Antibacterial mouth washes.
 Antibiotics such as clavulanic acid and
amoxicillin is needed for any dental work and
surgery related to bacteremia[95]
 Antimycotic prophylaxis[95]
Hyper Immunoglobulin E Syndrome
HEIS or Jobs syndrome is a rare multisystemic
disease causing host immune defects as well as nonimmunological manifestations [96]. It presents itself
in two forms, the more common autosomal dominant
(AD-HEIS) and the less common autosomal
recessive (AR-HEIS) [97], both characterized by high
level of immunoglobulin E levels in blood, chronic
eczema, recurrent skin and lung infections [98] and
decreased bone density [99]. Although the etiology of
disease is not clear, several studies concluded that
immune defects may be due to defective neutrophil
chemotaxis, humoral and cellular immune response
impairment including T-cell cytokine signal
disruption.
Recent gene analysis showed that most AD-HIES
have a mutation in gene STAT3 which causes poor
maturation and activation of T17 helper cells,
however AR-HIES (different clinical picture with no
dental abnormalities) may be attributed to different
gene mutation, TYK2 gene (Tyrosine Kinase 2), or
the DOCK8 gene (Dedicator of Cytokinesis 8)[100].
Oral findings of AD-HIES is very characteristic to
retention of primary teeth or ―
Double-row‖ dentition
which is found in most reported cases (due to
persistence of Her twig epithelial root sheath on root
surface, thus preventing root resorption causing
delayed shedding) , severe candidiasis and oral
infections, poor oral hygiene and high plaque index,
gingivitis but rare progression to periodontitis, except
for 2 patients [79, 101] ( . This data contradicts most
immunodeficiency syndromes, which are more likely
to cause severe periodontal destruction.)
There is no one laboratory test that confirms HIES,
rather a scoring system (fig. 1)-based on all clinical
and laboratory tests is used to confirm HIES,
therefore diagnosis of HIES is usually difficult.
Recently some reported laboratory tests were added
to NIH-HIES score, that helps better detect HIES, as
very low Th17 CD4 cell count, and the genetic
analysis.[102]The presence of retained primary teeth
and unerupted permanent teeth resembles other
syndromes like Cleidocranial syndrome, Gardner’s
Syndrome, and Down syndrome. A differential
diagnosis with these syndromes is noted and
confirmed by clinical and laboratory tests. [103]
Treatment is based on prophylactic antimicrobials,
intravenous immunoglobulin, and bone marrow
transplant shows some success but not a full recovery
[104], dental management is focused on
 Periodic follow up and oral hygiene
assessment.
 Extraction of primary teeth at correct time of
shedding to prevent permanent teeth
impaction and enhance oral hygiene.
 Antifungal and antibacterial for oral
infections
 Orthodontic correction if needed.
Prognosis of gingival healing after extraction is fairly
good with no complications and in most patients
periodontal health of permanent teeth can be
maintained.
{98}
Table 1: Grimbacher et al[105] Scoring System for HIES
0
1
Highest serum immunoglobulin E
<200
200-500
Skin abscesses
None
Pneumonia (episodes)
None
Parenchymal lung anomalie
Absent
Retained primary teeth
None
Clinical and Laboratory Findings
1
2
3
8
10
501-1000
1001-2000
>2000
1-2
3-4
>4
1
2
2
4
5
6
3
>3
Bronchiectasis
Pneumatocele
3
o
15-20
7
>3
o
Scoliosis
<10
Fractures with minor trauma
None
Highest eosinophil count (cells/_L)
<700
Characteristic face
Absent
Midline anomaly
Absent
Eczema
Absent
Mild
Moderate
Sever
Upper respiratory infections/year
1-2
3
4-6
>6
Candidiasis
None
Oral
Finger Nails
Systemic
Fatal infection
Absent
Present
Hyperextensibility
Absent
Present
Lymphoma
Absent
Present
High palate
Absent
Present
>20o
1-2
>2
700-800
>800
Mild
Present
Present
Present
<15 points: patient not affected; 15 to 39 points: possible diagnosis; 40 to 59 points: probable diagnosis; >60 points definitive diagnosis
{99}
Common Variable Immunodeficiency
Common variable immunodeficiency (CVID) is a
common heterogeneous primary immune deficiency.
Patients with CVID have a deficiency in humoral
immunity leading to a defective antibody response,
causing repetitive infections of the gastrointestinal
and upper respiratory tracts, and susceptibility to
some cancers such as lymphoma and autoimmune
diseases. Hypogammaglobulinemia has also seen in
these patients.
Although normal B-cell numbers have been
identified in lymphoid tissue and peripheral blood of
patients, it has been noted that B-cells of these
individuals have difficulty in differentiating into
immunoglobulin-secreting plasma cells. Furthermore,
it should be mentioned that the deficiency in
monocyte and macrophage function has also been
recognized. In addition, in some CVID patients, Tcell malfunction has been identified with decreased
CD4 lymphocytes and T-cell receptors, loss of
antigen-specific and quick death of T-cells.[4]
Individual suffering from CVID have been diagnosed
by having a low level of IgG and IgA[106].
Mutations in a group of genes asTNFRSF13B
gene[107] involved in B-cells result in having a
defected immunity in CVID[108]
Clinical examinations show dental problems such as
gingivitis and lichenoid lesions with Wickham
striae,[109] necrotizing ulcerative periodontitis
(NUP) [109, 110] , severe periodontitis and gingival
pain along with bleeding and tooth mobility was
demonstrated in a case report.[110]
In order to treat CVID, the primary method used is to
replace the antibody by an intravenous or
subcutaneous means. This occurs in doses of 400600mg of antibody per kilogram of the patient’s
weight per month.[111]
Dental management as reported in some case reports
include
 Regular oral prophylaxis with crown polishing
[109]
 Chlorhexidinedigluconate rinse is recommended
twice a day.
 Antibiotic
therapy[109,
110]
such
as
Amoxycillin and clavulanic acid[109]
Acquired immunodeficiency syndrome
HIV advancement can be detect by monitoring the
HIV viral load and T helper cells(CD4+)
count,however,it should be noted that there are some
common oral manifestations associated with HIV
positive patients. Therefore, it can be a useful
indicator for screening the immune condition of
potential HIV positive individuals and can be easily
recognized and detected by clinicians.[113-116]
It has been estimated that 70-90% of individual
suffering from HIV manifest oral lesions during their
phase of the disease [117-119]. Individuals with oral
manifestations have less CD4+ than ones without,
and it has been observed that there is a correlation
between oral candidiasis and a decrease in the CD4+
count(less than 200 cells/mm3).[120]
Some of the important oral manifestation and Lesions
present in HIV positive patients are
 Oral candidiasis (most common oral lesion)
[113, 121-123] which are divided in to three
groups;pseudomembranous
candidiasis,
erythematous
candidiasis
and
angular
cheilitis[114]
 Oral hairy leukoplakia [114].
 ulcerative disease such as herpes simplex virus,
Aphthous ulcerations[114, 124], Neutropenic
ulceration [124]
 linear gingival erythema[120, 124]
 oral warts-human papilloma virus[124]
 Necrotizing
Ulcerative
gingivitis
and
Periodontitis(NUG/NUP)[124, 125]
The follow up appointments are needed for dental
care such as scaling and root planning. A 10%
povidone-iodine lavage or 0 .12% chlorhexidine
gluconate can be used for the elimination of dental
plaque and necrotic soft tissue.Utilizing antibiotics
such as clindamycin, metronidazole 500g and
amoxicillin can be helpful for the treatment. It is
crucial to establish proper nutrition in order to reduce
potential issues in the oral cavity that can be
produced by poor nutrition, as well as manage the
patient’s pain.[124]
Leukemia
Leukemia is a type of a cancer caused by an
uncontrolled differentiation and proliferation of blood
cell precursors resulting in the production of
immature cells.Clinically, leukemia is classified into
two types: chronic and acute, with the acute phase
possibly being fatal. In addition, according to
histogenicity, leukemia is divided in to lymphocytic
or myelocytic depending on the origin of the
cells[126-128].
Acute myeloid leukemia(AML) is more common in
adults and acute lymphoid leukemia (ALL) is mostly
seen in children[128-130]. Acute myeloblastic
leukemia (AML) is characterized by symptoms of
Acquired immunodeficiency syndrome(AIDS) is a
disease caused by a human immunodeficiency virus.
In this condition HIV targets and attacks T helper
cells(CD4) resulting in immune response suppression
, the disability of the body’s response to the invading
pathogen, predisposes the patient to neurological
problems, opportunistic infections ,malignancies and
oral manifestation [112].
{100}
pancytopenia including
fatigue, weaknesses,
infection,
gingival
bleeding,
ecchymoses,
menorrhagia, and epistaxis [131, 132]. The direct
penetration of leukemic cells in lymph nodes, spleen,
central nervous system and gingival has been
reported [126, 129, 133-135].
Oral complication can be observed in all types of
leukemia[136]. Individuals having leukemia are
suffering from extreme enlargement of the gingiva
along with bleeding[127, 135-139], bulbous
enlargement in the interdental papillae [126, 127] a
pale blue gum with glazed texture ,and loss of
stippling is one the symptoms of leukemia[126, 127],
generalized horizontal bone loss was reported[127]
however in some cases bone loss is not
recognized[126] Ulceration and petechiae was noted
as a frequent sign[135]. In patient with acute
monocytic leukemia and acute myelomonocytic
leukemia, gingival infiltration of leukemic cells are
commonly seen[140].
Diagnosis by complete blood count peripheral blood
smear, shows the presence of blast cells and reveals
the type and quantity of white blood cells[126], and
flow cytometry of peripheral blood are used for
leukemia diagnosis[126, 127], biopsy such as bone
marrow aspiration also can be used to confirm
diagnosis and type of leukemia[126, 127, 135]
Regular oral prophylaxis is needed. Antibacterials
can be used in conjugation with scaling and sub
gingival debridement to lower the risk of dental
infection during the chemotherapy. Tooth extraction
of hopeless teeth can eliminate the infection.[141]
Managing periodontal disease of immunodeficient
patients is essential for improvement of their physical
and psychological health, thus knowledge of these
conditions, diagnostic methods and management
options is crucial for every dentist. Diagnosis of these
diseases is challenging, however some clues may
guide the clinician towards a definitive diagnosis, so
it is important that precise steps of history taking
(medical, familial and dental), clinical examination
(extra and intra oral) and laboratory investigations are
followed to achieve a successful diagnosis.
References
2.
3.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
Conclusion
1.
4.
16.
17.
18.
19.
20.
Janeway, C.A., et al., Immunobiology: the immune
system in health and disease. Vol. 2. 2001: Churchill
Livingstone.
Notarangelo, L., et al., Primary immunodeficiency
diseases: an update. Journal of Allergy and Clinical
Immunology, 2004. 114(3): p. 677-687.
Sollecito, T.P., et al., Systemic conditions associated
with periodontitis in childhood and adolescence. A
21.
22.
review of diagnostic possibilities. Medicina oral,
patologia oral y cirugia bucal, 2004. 10(2): p. 142-150.
Szczawinska-Poplonyk, A., et al., Oral manifestations
of primary immune deficiencies in children. Oral
Surgery, Oral Medicine, Oral Pathology, Oral
Radiology, and Endodontology, 2009. 108(3): p. e9e20.
Bright, P.D., et al., Laboratory clues to
immunodeficiency; missed chances for early
diagnosis? Journal of clinical pathology. 68(1): p. 1-5.
Ellison, S.A., Oral bacteria and periodontal disease.
Journal of dental research, 1970. 49(2): p. 197-202.
Genco, R.J., R.T. Evans, and S.A. Ellison, Dental
research in microbiology with emphasis on periodontal
disease. The Journal of the American Dental
Association, 1969. 78(5): p. 1016-1036.
Ram, V.S., et al., Bonebiomarkers in Periodontal
Disease: A Review Article.
Garcia, R.I., M.M. Henshaw, and E.A. Krall,
Relationship between periodontal disease and systemic
health. Periodontology 2000, 2001. 25(1): p. 21-36.
Deas, D.E., S.A. Mackey, and H.T. McDonnell,
Systemic disease and periodontitis: manifestations of
neutrophil dysfunction. Periodontology 2000, 2003.
32(1): p. 82-104.
Bernini, J.C., Diagnosis and management of chronic
neutropenia during childhood. Pediatric Clinics of
North America, 1996. 43(3): p. 773-792.
Watanabeb, K., Prepubertal periodontitis: a review of
diagnostic criteria, pathogenesis, and differential
diagnosis. Journal of periodontal research, 1990. 25(1):
p. 31-48.
Bux J1, M.-E.C., Autoimmune neutropenia. Semin
Hematal., 1992 Jan. 29(1): p. 45-53.
Deasy, M.J., et al., Familial benign chronic
neutropenia associated with periodontal disease: a case
report. Journal of periodontology, 1980. 51(4): p. 206210.
Zaromb, A., et al., Periodontitis as a manifestation of
chronic benign neutropenia. Journal of periodontology,
2006. 77(11): p. 1921-1926.
Reichart, P.A. and H. Dornow, Gingivo-periodontal
manifestations in chronic benign neutropenia. Journal
of clinical periodontology, 1978. 5(1): p. 74-80.
Cutting, H.O. and J.E. Lang, Familial benign chronic
neutropenia. Annals of internal medicine, 1964.
61(5_Part_1): p. 876-887.
Aprikyan, A.A.G., et al., Cellular and molecular
abnormalities in severe congenital neutropenia
predisposing to leukemia. Experimental hematology,
2003. 31(5): p. 372-381.
Carlsson, G.r., et al., Kostmann syndrome or infantile
genetic agranulocytosis, part one: celebrating 50 years
of clinical and basic research on severe congenital
neutropenia. Acta Paediatrica, 2006. 95(12): p. 15261532.
Hakki, S.S., et al., Periodontal status in two siblings
with severe congenital neutropenia: diagnosis and
mutational analysis of the cases. Journal of
periodontology, 2005. 76(5): p. 837-844.
Tirali, R.E. and S.B.Ç. Zeynep Yalçınkaya-Erdemci,
Oral findings and clinical implications of patients with
congenital neutropenia: a literature review. The
Turkish journal of pediatrics. 55: p. 241-245.
Defraia, E. and A. Marinelli, Oral manifestations of
congenital neutropenia or Kostmann syndrome. Journal
of Clinical Pediatric Dentistry, 2002. 26(1): p. 99-102.
{101}
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
Dale, D.C. and W. Hammond, Cyclic neutropenia: a
clinical review. Blood reviews, 1988. 2(3): p. 178-185.
Dale, D.C., et al., Mutations in the gene encoding
neutrophil elastase in congenital and cyclic
neutropenia. Blood, 2000. 96(7): p. 2317-2322.
Prichard, J.F., et al., Prepubertal periodontitis affecting
the deciduous and permanent dentition in a patient with
cyclic neutropenia: a case report and discussion.
Journal of periodontology, 1984. 55(2): p. 114-122.
Spencer, P. and J.E. Fleming, Cyclic neutropenia: a
literature review and report of case. ASDC journal of
dentistry for children, 1985. 52(2): p. 108.
Andrews, R.G., et al., Chronic benign neutropenia of
childhood with associated oral manifestations. Oral
Surgery, Oral Medicine, Oral Pathology, 1965. 20(6):
p. 719-725.
Barrett, A.P., Neutropenic ulceration: a distinctive
clinical entity. Journal of periodontology, 1987. 58(1):
p. 51-55.
Gates, G.F., Chronic neutropenia presenting with oral
lesions. Oral Surgery, Oral Medicine, Oral Pathology,
1969. 27(4): p. 563-567.
Scully, C., E. MacFadyen, and A. Campbell, Oral
manifestation in cyclic neutropenia. British Journal of
Oral Surgery, 1982. 20(2): p. 96-101.
Yamahk, N., et al., Periodical gingival bleeding as a
presenting symptom of periodontitis due to underlying
cyclic neutropenia. Case report. Australian dental
journal, 1993. 38(4): p. 272-276.
Dale,
D.C.,
ELANE-Related
neutropenia.
GeneReviews [Internet]. Seattle (WA): University of
Washington, Seattle, 2002.
Hammond Iv, W.P., et al., Treatment of cyclic
neutropenia with granulocyte colony-stimulating
factor. New England Journal of Medicine, 1989.
320(20): p. 1306-1311.
Bux, J., et al., Influence of granulocyte antibodies on
granulocyte function. Vox sanguinis, 1993. 64(4): p.
220-225.
Nagendran, J., et al., Leukocyte adhesion deficiency: a
case report and review. Journal of Dentistry for
Children. 79(2): p. 105-110.
Etzioni, A., Adhesion molecules in host defense.
Clinical and diagnostic laboratory immunology, 1994.
1(1): p. 1.
Yakubenia, S. and M.K. Wild, Leukocyte adhesion
deficiency II. FEBS Journal, 2006. 273(19): p. 43904398.
Etzioni, A. and R. Alon, Leukocyte adhesion
deficiency III: a group of integrin activation defects in
hematopoietic lineage cells. Current opinion in allergy
and clinical immunology, 2004. 4(6): p. 485-490.
Schmidt, S., M. Moser, and M. Sperandio, The
molecular basis of leukocyte recruitment and its
deficiencies. Molecular immunology. 55(1): p. 49-58.
Anderson, D.C. and T.A. Springer, Leukocyte
adhesion deficiency: an inherited defect in the Mac-1,
LFA-1, and p150, 95 glycoproteins. Annual review of
medicine, 1987. 38(1): p. 175-194.
Dababneh, R., et al., Periodontal manifestation of
leukocyte adhesion deficiency type I. Journal of
Fischer, A., et al., Leukocyte adhesion deficiency:
molecular basis and functional consequences.
Immunodefic Rev, 1988. 1(1): p. 39-54.
Lakshman, R. and A. Finn, Neutrophil disorders and
their management. Journal of clinical pathology, 2001.
54(1): p. 7-19.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
Movahedi, M., et al., Clinical and laboratory findings
in Iranian patients with leukocyte adhesion deficiency
(study of 15 cases). Journal of clinical immunology,
2007. 27(3): p. 302-307.
Lühn, K., et al., The gene defective in leukocyte
adhesion deficiency II encodes a putative GDP-fucose
transporter. Nature genetics, 2001. 28(1): p. 69-72.
Lübke, T., et al., Complementation cloning identifies
CDG-IIc, a new type of congenital disorders of
glycosylation, as a GDP-fucose transporter deficiency.
Nature genetics, 2001. 28(1): p. 73-76.
McDowall, A., et al., A novel form of integrin
dysfunction involving β1, β2, and β3 integrins. Journal
of clinical investigation, 2003. 111(1): p. 51.
Dennison, D.K. and T.E. Dyke, The acute
inflammatory response and the role of phagocytic cells
in periodontal health and disease. Periodontology
2000, 1997. 14(1): p. 54-78.
Meyle, J., Leukocyte adhesion deficiency and
prepubertal periodontitis. Periodontology 2000, 1994.
6(1): p. 26-36.
Todd 3rd, R.F. and D.R. Freyer, The CD11/CD18
leukocyte
glycoprotein
deficiency.
Hematology/oncology clinics of North America, 1988.
2(1): p. 13-31.
Meyle, J. and J.R. Gonzales, Influences of systemic
diseases on periodontitis in children and adolescents.
Periodontology 2000, 2001. 26(1): p. 92-112.
Bowen, T.J., et al., Severe recurrent bacterial
infections associated with defective adherence and
chemotaxis in two patients with neutrophils deficient
in a cell-associated glycoprotein. The Journal of
pediatrics, 1982. 101(6): p. 932-940.
Haddadin, I., et al., Bone marrow transplantation for
leukocyte adhesion deficiency-I: Case report. Saudi
Journal of Kidney Diseases and Transplantation, 2006.
17(4): p. 564.
Hattori, H., et al., Successful human leukocyte antigen
one antigen-mismatched related bone marrow
transplantation in a 6-year-old boy with leukocyte
adhesion deficiency syndrome. Pediatrics international,
2001. 43(3): p. 306-309.
Engel, M.E., et al., Matched unrelated bone marrow
transplantation with reduced-intensity conditioning for
leukocyte adhesion deficiency. Bone marrow
transplantation, 2006. 37(7): p. 717-718.
Majorana, A., et al., Leukocyte adhesion deficiency in
a child with severe oral involvement. Oral Surgery,
Oral Medicine, Oral Pathology, Oral Radiology, and
Endodontology, 1999. 87(6): p. 691-694.
Wara-Aswapati, N., et al., Periodontitis in the child
and adolescent. ASDC journal of dentistry for children,
1999. 66: p. 167-174.
Delcourt-Debruyne, E.M.C., H.R.A. Boutigny, and
H.F. Hildebrand, Features of severe periodontal
disease in a teenager with Chediak-Higashi syndrome.
Journal of periodontology, 2000. 71(5): p. 816-824.
Nargund, A.R., et al., Accelerated Phase of Chediak
Higashi Syndrome Mimicking Lymphoma—A Case
Report. Journal of pediatric hematology/oncology.
32(6): p. e223-e226.
Gajendra, S., et al., Accelerated phase at initial
presentation in chediak-higashi syndrome: is it really
uncommon? Pediatric hematology and oncology.
31(4): p. 382-385.
Imran, T., et al., Chediak-Higashi syndrome presenting
in accelerated phase. J Coll Physicians Surg Pak.
22(8): p. 539-41.
{102}
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
Sánchez-Guiu, I., et al., Chediak–Higashi syndrome:
description of two novel homozygous missense
mutations causing divergent clinical phenotype.
European journal of haematology. 92(1): p. 49-58.
O'Leary, T.J., R.B. Drake, and J.E. Naylor, The plaque
control record. Journal of periodontology, 1972. 43(1):
p. 38-38.
Hart, T.C. and J.C. Atkinson, Mendelian forms of
periodontitis. Periodontology 2000, 2007. 45(1): p. 95112.
Hanna, S. and A. Etzioni, Leukocyte adhesion
deficiencies. Annals of the New York Academy of
Sciences. 1250(1): p. 50-55.
HR, M., Tooth mobility: a review of clinical aspects
and research findings. Journal of periodontology, 1967.
38(6): p. Suppl: 686.
Bailleul-Forestier, I., et al., Generalized periodontitis
associated with Chediak-Higashi syndrome. Journal of
Kornman, K.S., et al., The influence of supragingival
plaque control on clinical and microbial outcomes
following the use of antibiotics for the treatment of
periodontitis. Journal of periodontology, 1994. 65(9):
p. 848-854.
Winkel, E.G., et al., Clinical and microbiological
effects of initial periodontal therapy in conjunction
with amoxicillin and clavulanic acid in patients with
adult periodontitis. Journal of clinical periodontology,
1999. 26(7): p. 461-468.
Socransky, S.S., et al., Ecological considerations in the
treatment of Actinobacillus actinomycetemcomitans
and Porphyromonas gingivalis periodontal infections.
Periodontology 2000, 1999. 20(1): p. 341-362.
Shibutani, T., et al., Long-term follow-up of
periodontitis in a patient with Chediak-Higashi
syndrome. A case report. Journal of periodontology,
2000. 71(6): p. 1024-1028.
Winkelstein, J.A., et al., Chronic granulomatous
disease: report on a national registry of 368 patients.
Medicine, 2000. 79(3): p. 155-169.
Stasia, M.J. and X.J. Li. Genetics and
immunopathology of chronic granulomatous disease.
in Seminars in immunopathology. 2008: Springer.
Giannopoulou, C., K.-H. Krause, and M. F. The
NADPH oxidase NOX2 plays a role in periodontal
pathologies. in Seminars in immunopathology. 2008:
Springer.
Smith, J. and A. Finn, Antimicrobial prophylaxis.
Archives of disease in childhood, 1999. 80(4): p. 388392.
Mouy, R., et al., Long-term itraconazole prophylaxis
against Aspergillus infections in thirty-two patients
with chronic granulomatous disease. The Journal of
pediatrics, 1994. 125(6): p. 998-1003.
Ezekowitz, R.A.B., et al., Partial correction of the
phagocyte defect in patients with X-linked chronic
granulomatous disease by subcutaneous interferon
gamma. New England Journal of Medicine, 1988.
319(3): p. 146-151.
Calvino, M.C., et al., Bone marrow transplantation in
chronic granulomatous disease. European journal of
pediatrics, 1996. 155(10): p. 877-879.
Charon, J.A., S.E. Mergenhagen, and J.I. Gallin,
Gingivitis and oral ulceration in patients with
neutrophil dysfunction. Journal of Oral Pathology &
Medicine, 1985. 14(2): p. 150-155.
Cohen, M.S., P.A. Leong, and D.M. Simpson,
Phagocytic Cells in Periodontal Defense: Periodontal
81.
82.
83.
84.
85.
86.
87.
88.
89.
90.
91.
92.
93.
94.
95.
96.
97.
Status of Patients with Chronic Granulomatous Disease
of Childhood*. Journal of periodontology, 1985.
56(10): p. 611-617.
Wolf, J.E. and L.K. Ebel, Chronic granulomatous
disease: report of case and review of the literature. The
Journal of the American Dental Association, 1978.
96(2): p. 292-295.
Landing, B.H. and H.S. Shirkey, A syndrome of
recurrent infection and infiltration of viscera by
pigmented lipid histiocytes. Pediatrics, 1957. 20(3): p.
431-438.
De Ravin, S.S., et al., Chronic granulomatous disease
as a risk factor for autoimmune disease. Journal of
Allergy and Clinical Immunology, 2008. 122(6): p.
1097-1103.
Scully, C., Orofacial manifestations of chronic
granulomatous disease of childhood. Oral Surgery,
Oral Medicine, Oral Pathology, 1981. 51(2): p. 148151.
Movahedi, M., et al., Gastrointestinal manifestations of
patients with chronic granulomatous disease. Iranian
Journal of Allergy, Asthma and Immunology, 2004.
3(2): p. 83-88.
Dusi, S., et al., Chronic granulomatous disease in an
adult female with granulomatous cheilitis. Acta
haematologica, 1990. 84(1): p. 49-56.
Miller, R., C.M. Myer, and S. Gray, Otolaryngologic
manifestations of chronic granulomatous disease.
American journal of otolaryngology, 1988. 9(2): p. 7982.
Buduneli, N., et al., Prepubertal periodontitis
associated with chronic granulomatous disease. Journal
of clinical periodontology, 2001. 28(6): p. 589-593.
Hasui, T.H.E., Chronic granulomatous disease in
Japan: incidence and natural history. Pediatrics
international, 1999. 41(5): p. 589-593.
Ahlin, A., et al., Prevalence, genetics and clinical
presentation of chronic granulomatous disease in
Sweden. Acta Paediatrica, 1995. 84(12): p. 1386-1394.
Beertsen, W., et al., Impaired phagosomal maturation
in neutrophils leads to periodontitis in lysosomalassociated membrane protein-2 knockout mice. The
journal of immunology, 2008. 180(1): p. 475-482.
Kinane, D.F. and P. Mark Bartold, Clinical relevance
of the host responses of periodontitis. Periodontology
2000, 2007. 43(1): p. 278-293.
Jirapongsananuruk, O., et al., Diagnostic paradigm for
evaluation of male patients with chronic
granulomatous disease, based on the dihydrorhodamine
123 assay. Journal of Allergy and Clinical
Immunology, 2003. 111(2): p. 374-379.
Baehner, R.L. and D.G. Nathan, Quantitative nitroblue
tetrazolium test in chronic granulomatous disease. New
England Journal of Medicine, 1968. 278(18): p. 971976.
Heyworth, P.G., A.R. Cross, and J.T. Curnutte,
Chronic granulomatous disease. Current opinion in
immunology, 2003. 15(5): p. 578-584.
Grimbacher, B., et al., Hyper-IgE syndrome with
recurrent
infections--an
autosomal
dominant
multisystem disorder. New England Journal of
Medicine, 1999. 340(9): p. 692-702.
Renner, E.D., et al., Autosomal recessive
hyperimmunoglobulin E syndrome: a distinct disease
entity. The Journal of pediatrics, 2004. 144(1): p. 9399.
{103}
98.
99.
100.
101.
102.
103.
104.
105.
106.
107.
108.
109.
110.
111.
112.
113.
114.
115.
Grimbacher, B., B.H. Belohradsky, and S.M. Holland,
Immunoglobulin E in primary immunodeficiency
diseases. Allergy, 2002. 57(11): p. 995-1007.
Borges, W.G., et al., The face of Job. The Journal of
pediatrics, 1998. 133(2): p. 303-305.
Engelhardt, K.R., et al., Large deletions and point
mutations involving the dedicator of cytokinesis 8
(DOCK8) in the autosomal-recessive form of hyperIgE syndrome. Journal of Allergy and Clinical
Immunology, 2009. 124(6): p. 1289-1302. e4.
Tsang, P., et al., Severe periodontitis in a 5-year-old
girl with hyperimmunoglobulin E syndrome. Pediatric
dentistry, 2005. 27(1): p. 68-73.
Woellner, C., et al., Mutations in STAT3 and
diagnostic guidelines for hyper-IgE syndrome. Journal
of Allergy and Clinical Immunology. 125(2): p. 424432. e8.
AC O'Connell, A.C., et al., Delayed eruption of
permanent teeth in hyperimmunoglobulinemia E
recurrent infection syndrome. Oral Surgery, Oral
Medicine, Oral Pathology, Oral Radiology, and
Endodontology, 2000. 89(2): p. 177-185.
Grimbacher, B., S.M. Holland, and J.M. Puck, HyperIgE syndromes. Immunological reviews, 2005. 203(1):
p. 244-250.
Grimbacher, B., et al., Genetic linkage of hyper-IgE
syndrome to chromosome 4. The American Journal of
Human Genetics, 1999. 65(3): p. 735-744.
Cunningham-Rundles, C., How I treat common
variable immune deficiency. Blood.
Salzer, U., et al., Mutations in TNFRSF13B encoding
TACI are associated with common variable
immunodeficiency in humans. Nature genetics, 2005.
37(8): p. 820-828.
Salzer, U., S. Unger, and K. Warnatz, Common
variable immunodeficiency (CVID): exploring the
multiple dimensions of a heterogeneous disease.
Annals of the New York Academy of Sciences.
1250(1): p. 41-49.
Batista, E.L., et al., Necrotizing ulcerative periodontitis
associated with severe congenital immunodeficiency in
aprepubescent subject: clinical findings and response
to intravenous immunoglobulin treatment. Journal of
clinical periodontology, 1999. 26(8): p. 499-504.
Dalla Torre, D., et al., Necrotizing Periodontitis as a
possible manifestation of common variable
immunodeficiency. International journal of oral and
maxillofacial surgery. 41(12): p. 1546-1549.
Vukas, E., et al., Common variable immunodeficiency
case report. Journal of Health Sciences. 3(2): p. 170172.
Adurogbangba, M.I., et al., Oro-facial lesions and CD4
counts associated with HIV/AIDS in an adult
population in Oyo State, Nigeria. Oral diseases, 2004.
10(6): p. 319-326.
Patton, L.L., Sensitivity, specificity, and positive
predictive value of oral opportunistic infections in
adults with HIV/AIDS as markers of immune
suppression and viral burden. Oral Surgery, Oral
Medicine, Oral Pathology, Oral Radiology, and
Endodontology, 2000. 90(2): p. 182-188.
Pakfetrat, A., et al., Oral Manifestations of Human
Immunodeficiency Virus-Infected Patients. Iranian
journal of otorhinolaryngology. 27(78): p. 43.
Glick, M., et al., Oral manifestations associated with
HIV-related disease as markers for immune
suppression and AIDS. Oral Surgery, Oral Medicine,
Oral Pathology, 1994. 77(4): p. 344-349.
116.
117.
118.
119.
120.
121.
122.
123.
124.
125.
126.
127.
128.
129.
130.
131.
132.
133.
134.
135.
Margiotta, V., et al., HIV infection: oral lesions, CD4+
cell count and viral load in an ltalian study population.
Journal of Oral Pathology & Medicine, 1999. 28(4): p.
173-177.
Patton, L.L., et al., Oral manifestations of HIV in a
southeast USA population. Oral diseases, 1998. 4(3):
p. 164-169.
Patton, L.L., et al., Changing prevalence of oral
manifestations of human immuno-deficiency virus in
the era of protease inhibitor therapy. Oral Surgery,
Oral Medicine, Oral Pathology, Oral Radiology, and
Endodontology, 2000. 89(3): p. 299-304.
Arendorf, T.M., et al., Oral manifestations of HIV
infection in 600 South African patients. Journal of Oral
Pathology & Medicine, 1998. 27(4): p. 176-179.
Bodhade, A.S., S.M. Ganvir, and V.K. Hazarey, Oral
manifestations of HIV infection and their correlation
with CD4 count. Journal of oral science. 53(2): p. 203211.
Moniaci, D., et al., Epidemiology, clinical features and
prognostic value of HIV-1 related oral lesions. Journal
of Oral Pathology & Medicine, 1990. 19(10): p. 477481.
Nittayananta, W. and S. Chungpanich, Oral lesions in a
group of Thai people with AIDS. Oral diseases, 1997.
3(S1): p. S41-S45.
Laskaris, G., M. Hadjivassiliou, and J. Stratigos, Oral
signs and symptoms in 160 Greek HIV-infected
patients. Journal of Oral Pathology & Medicine, 1992.
21(3): p. 120-123.
Reznik, D.A., Oral manifestations of HIV disease.
Topics in HIV medicine: a publication of the
International AIDS Society, USA, 2004. 13(5): p. 143148.
Patton, L.L., Oral lesions associated with human
immunodeficiency virus disease. Dental clinics of
North America. 57(4): p. 673-698.
Demirer, S., et al., Gingival hyperplasia as an early
diagnostic oral manifestation in acute monocytic
leukemia: a case report. European journal of dentistry,
2007. 1(2): p. 111.
Lim, H.-C. and C.-S. Kim, Oral signs of acute
leukemia for early detection. Journal of periodontal &
implant science. 44(6): p. 293-299.
Bennett, J.M., et al., Proposed revised criteria for the
classification of acute myeloid leukemia: a report of
the French-American-British Cooperative Group.
Annals of internal medicine, 1985. 103(4): p. 620-625.
Williams, W.J., et al., Haematology. 1983, New York:
McGraw-Hill.
Little, J.W., Dental management of the medically
compromised patient. 1997: Mosby.
Orbak, R. and Z. Orbak, Oral condition of patients
with leukemia and lymphoma. The Journal of Nihon
University School of Dentistry, 1997. 39(2): p. 67-70.
Barrett, A.P., Gingival Lesions in Leukemia: A
Classification*. Journal of periodontology, 1984.
55(10): p. 585-588.
Fatahzadeh, M. and A.M. Krakow, Manifestation of
acute monocytic leukemia in the oral cavity: a case
report. Special Care in Dentistry, 2008. 28(5): p. 190194.
Reenesh, M., S. Munishwar, and S.K. Rath,
Generalised leukaemic gingival enlargement: a case
report. Journal of oral & maxillofacial research. 3(3).
Wu, J., J.E. Fantasia, and R. Kaplan, Oral
manifestations of acute myelomonocytic leukemia: a
case report and review of the classification of
{104}
136.
137.
138.
139.
140.
leukemias. Journal of periodontology, 2002. 73(6): p.
664-668.
Bergmann, O.J., H.P. Philipsen, and J. Ellegaard,
Isolated gingival relapse in acute myeloid leukaemia.
European journal of haematology, 1988. 40(5): p. 473476.
Anil, S., et al., Gingival enlargement as a diagnostic
indicator in leukaemia. Case report. Australian dental
journal, 1996. 41(4): p. 235-237.
Hou, G.-L. and C.-C. Tsai, Primary gingival
enlargement as a diagnostic indicator in acute
myelomonocytic leukemia: a case report. Journal of
Long, R.G., L. Hlousek, and J.L. Doyle, Oral
manifestations of systemic diseases. The Mount Sinai
journal of medicine, New York, 1997. 65(5-6): p. 309315.
Felix, D.E. and J. Lukens, Oral symptoms as a chief
sign of acute monoblastic leukemia: report of case.
141.
Journal of the American Dental Association (1939),
1986. 113(6): p. 899-900.
Stoopler, E.T., D.T. Vogl, and E.A. Stadtmauer,
Medical management update: multiple myeloma. Oral
Surgery, Oral Medicine, Oral Pathology, Oral
Radiology, and Endodontology, 2007. 103(5): p. 599609.
{105}
Autogenous Connective Tissue Graft for the Treatment
of Localized Gingival Recession: A Case Report
Dr Zohaib Akram1,
Dr Haroon Rashid2,
Dr Fahim Vohra3
1
BDS, Department of Restorative Dentistry,
University of Malaya, Kuala Lumpur, Malaysia.
2
MDSc, BDS, Faculty, Department of Prosthodontics,
College Of Dentistry, Ziauddin University, Karachi
Pakistan;
3
MRDRCS, M Clin Dent, MFDS, BDS, Department
of Prosthetic Dental Science (SDS), College of
Dentistry, King Saud University, Riyadh, Saudi
Arabia
Dr. Fahim Vohra
www.idjsr.com
database
Quick Response Code
Introduction
Gingival recession is defined as the apical migration
of the gingival margin in relation to the cementoenamel junction causing root exposure. The negative
effects of exposed roots may lead to dentine
hypersensitivity, root caries, and poor esthetics(1).
One of the reasons of mucogingival surgery is to gain
root coverage with procedures that warrant sound
predictability and good esthetics.
There are several periodontal plastic surgery
proceduresto cover exposed root surfaces which
include pedicle grafts (2), free gingival grafts (3),
connective tissue grafts (4, 5), membrane barrier
guided tissue regeneration technique (6), and
acellular dermal matrix allografts (7, 8). However,
the predictability of such surgical procedures may be
associated with different conditions. Out of number
of procedures, subepithelial connective tissue graft
can be considered as the ‘gold standard’ technique for
treating teeth with gingival recessions (9). A number
of systematic reviews (9-11)have validated the use of
connective tissue graft (CTG) as the most suitable
procedure for Millers Class I and II gingival
recession lesions. Besides improving clinical
attachment, probing depths, thickness of keratinized
mucosa and root coverage, these procedures offer
better uniformity of color between the surgical
grafted area and adjacent tissues
Therefore, this manuscript presents a case report
detailing the successful use of autogenous CTG in the
management of a Class II gingival recession lesion.
Case Report
Clinical case presentation
A 28-year-old male with no medical problems was
referred to the Department of Periodontology with
complain of an un-aesthetic mandibular incisor tooth
(tooth #41) with sensitivity to hot and cold stimulus
from approximately 12 months. Clinical evaluation
revealed gingival recession on the labial surface
extending 2 mm apical to the cemento-enamel
junction (CEJ) and narrow zone of attached gingiva
measuring approximately 1 mm (Fig 1). There was
no loss of interdental papillary height on the distal
aspect of the incisor and mild loss of papilla on the
mesial aspect. Plaque control and oral hygiene was
good with no apparent staining on the teeth. There
was no evidence of interdental bone loss (i.e. the
distance between the crestal bone and CEJ was not
greater than 2 mm). The case was diagnosed to be
sensitivity associated with Class II Miller recession.
The goal of the treatment was to restore harmonious
appearance of the gingiva by covering the root
surface to the height similar to the adjacent tooth and
to increase the zone of attached gingiva.
Figure 1: Intraoral image showing gingival
recession on the labial surface extending 2 mm
apical to the CEJ and a narrow zone of attached
gingiva.
{106}
Autogenous Connective Tissue Graft
(ACTG)
Following local anesthesia with 2% lidocaine,
epinephrine 1:100,000, the exposed root surface was
thoroughly planed and scaled first with ultrasonic
instrument and then manually with the use of hand
instruments to remove plaque, accretions and root
surface irregularities. The exposed root surface was
then conditioned with a saturated solution of
tetracycline-HCL for 2 minutes (100mg tetracyclineHCL/1 ml of sterile distilled water). A sulcular
incision was made at both sides through the bottom
of the crevice allowing dissection of the papillae
adjacent to the site of recession defect until the
proximal line angles of the adjacent teeth. Afterwards
two vertical releasing incisions were placed both
mesial and distal involving adjacent teeth, distant
from the main defect. A full thickness flap providing
a broader surgical bed was elevated in an apical
direction exposing the alveolar plate of bone until the
mucogingival junction (MGJ). The periosteum was
released and blunt dissection into the vestibular lining
mucosa was performed to eliminate tension to help
re-position the flap coronal at the level of CEJ. The
interdental papilla of the adjacent teeth were not
involved (Fig 2).
The donor site for the sub-epithelial connective tissue
graft was the palate in the bicuspid region of the same
subject (Fig 3). Donor palatal tissue was harvested in
the following way: a horizontal incision was placed
in the palate 2 to 3 mm from the free gingival margin,
and two parallel internal vertical incisions, one
superficial and one deep, were made and connected
mesially and distally. The underlying connective
tissue was released at its base and removed (Fig 4).
The wound was closed with simple interrupted 3-0
silk sutures. The donor site on the palate healed by
primary intention after two week of suture removal.
The graft was shaped to fit the recipient site and
secured to the wound bed (Fig 5) with a continuous
sling suture using 5-0 vicryl material to the papilla on
either side of the graft. Silk sutures were removed
after 15 days; visible portions of the vicryl suture
were removed after 3 weeks.
Figure 2: Full thickness flap elevated exposing the
alveolar plate of bone. The interdental papilla of
the adjacent teeth were not involved.
Figure 3: Subepithelial connective tissue graft
harvested from the palate of the same subject.
Figure 4: Resected palatal subepithelial connective
tissue graft
Figure 5: Graft secured to the papilla on either
side using continuous sling suture 5-0 vicryl.
{107}
Postsurgical Care
Patient was instructed to avoid trauma and to
discontinue tooth brushing at the surgical site during
the first 15 days. Patient was instructed to use 0.12%
chlorhexidinedigluconate solution rinse for 60
seconds twice daily for 2 weeks. After 15 days, a
modified brushing technique was advised in order to
minimize apically directed trauma to the soft tissue
around the surgical site. Throughout the treatment,
recall visits for prophylaxis treatment were arranged
at 1, 3, 5, 8, 12, 16 and 32 weeks.
Healing was uneventful. At 2nd week, the gingiva at
the surgical site was still edematous (Fig 6). Only
erythema could be observed along the border of
attached gingiva which improved at 8th week of
follow-up. At 9 months postoperatively, the amount
of attached gingiva was approximately 3 mm, and the
gingiva was firmly attached. Probing depth at the mid
buccal site was less than 1 mm and the free gingival
margin was located less than 1 mm apically to the
apical border of the CEJ (Fig 7).
Figure 6: 2nd week postoperative. Gingiva is still
edematous and erythema could be observed along
the border of the attached gingiva.
Figure 7: At 2 months postoperatively the
periodontal tissue is less edematous and
improvement in erythema is clinically evident.
Figure 8: At 9 months the probing depth at mid
buccal site was 1 mm and free gingival margin
was located 1 mm apical to CEJ.
Discussion
This case report evaluated the treatment of localized
gingival recession by using palatal connective tissue
graft for the treatment of Class II Miller recession.
The present clinical result is encouraging and
indicates significant coverage of the exposed root
with the palatal connective tissue graft that has
provided restoration of clinical attachment. Overall
surgical procedure was aimed to reduce any risks
involved with no harmful events in the healing
process along with patient comfort. The connective
tissue graft for the restoration of root defect was
harvested from the palate of the same subject.
Horizontal incisions were placed in the palatal tissue
with two parallel vertical incisions along each side of
the horizontal incision to remove adequate tissue
from the underlying connective tissue. The incisions
were placed to ensure primary intention healing and
comfort for the patient.
Multiple factors can effect the degree of root
coverage including, biocompatibility of root surface,
sufficient vascularization of the surgical bed, surgical
manipulation, tissue width and ideal plaque control
(12). Meticulous root planing on the exposed root
surface was performed with the use of hand
instruments to remove plaque and accretions and
further increasing the surface biocompatibility.
Special care was taken to prepare recipient surgical
bed. Sutures were performed without stretching the
graft tissue, preventing the displacement of graft
without tension, thereby avoiding impaired
vascularization. The grafts were also compressed to
promote the tensile strength and stability of the
wound.
Coronally advanced flaps (CAF) with or without
enamel matrix derivatives have been recommended
as an alternative to CTG in the management of Class
I & II recession lesions. Nemcovsky et al, (13)
compared the clinical outcome of CAF and CTG in
the management of recession defects, concluding that
CTG was superior to CAF in the percentage of
coverage and increase in width of keratinized tissue.
{108}
In addition, soft tissue allografts have been used as an
alternate to autogenous CTG to provide root coverage
without the need of a second surgical site intra-orally
(14).However CTG additional increases the gingival
tissue thickness and width of keratinized tissue, two
critical features, which warrant the use of connective
tissue graft over allografts (15).
Conclusion
This surgical technique aided complete root coverage
as well as improved the thickness of attached gingiva.
The interpretations made in the present case report
indicate that connective tissue graft can be a
successful treatment option in achieving soft tissue
root coverage and gain of clinical attachment in
Miller’s class II root defects.
systematic review. Annals of Periodontology 2003; 8:
303-320.
12.
Burkhardt R, Lang NP. Coverage of localized gingival
recessions: comparison of micro‐and macrosurgical
techniques. Journal of clinical periodontology 2005;
32: 287-293.
13.
Nemcovsky CE, Artzi Z, Tal H, Kozlovsky A, Moses
O.A multicenter comparative study of two root
coverage procedures: coronally advanced flap with
addition of enamel matrix proteins and subpedicle
connective tissue graft. J Periodontol 2004;75:600-7.
14.
Saadoun AP. Root coverage with Emdogain/Alloderm:
a new way to treat gingival recessions. Eur J Esthet
Dent 2008 ;3:46.
15.
Silva, R.C.D., et al., Root coverage using the coronally
positioned flap with or without a subepithelial
connective tissue graft. J Periodontol 2004;75:413-19.
__________________________________________________
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Bouchard P, Malet J, Borghetti A. Decision‐making in
aesthetics: root coverage revisited. Periodontology
2000 2001; 27: 97-120.
Harris RJ, Harris AW. The coronally positioned
pedicle graft with inlaid margins: a predictable method
of obtaining root coverage of shallow defects. The
International journal of periodontics & restorative
dentistry 1994; 14: 228-241.
Miller Jr PD. Root coverage with the free gingival
graft: factors associated with incomplete coverage.
Journal of Periodontology 1987; 58: 674-681.
Langer B, Langer L. Subepithelial connective tissue
graft technique for root coverage. Journal of
periodontology 1985; 56: 715-720.
Bruno JF. Connective tissue graft technique assuring
wide root coverage. The International journal of
periodontics & restorative dentistry 1994; 14: 126-137.
Müller H-P, Stahl M, Eger T. Root coverage
employing an envelope technique or guided tissue
regeneration with a bioabsorbable membrane. Journal
of periodontology 1999; 70: 743-751.
Tal H, Moses O, Zohar R, Meir H, Nemcovsky C. Root
coverage of advanced gingival recession: A
comparative study between acellular dermal matrix
allograft and subepithelial connective tissue grafts.
Journal of periodontology 2002; 73: 1405-1411.
Harris RJ. Root Coverage With a Connective Tissue
With Partial Thickness Double Pedicle Graft and an
Acellular Dermal Matrix Graft: A Clinical and
Histological Evaluation of a Case Report*. Journal of
periodontology 1998; 69: 1305-1311.
Chambrone L, Chambrone D, Pustiglioni FE,
Chambrone LA, Lima LA. Can subepithelial
connective tissue grafts be considered the gold
standard procedure in the treatment of Miller Class I
and II recession-type defects? Journal of dentistry
2008; 36: 659-671.
Roccuzzo M, Bunino M, Needleman I, Sanz M.
Periodontal plastic surgery for treatment of localized
gingival recessions: a systematic review. Journal of
Clinical Periodontology 2002; 29: 178-194.
Oates TW, Robinson M, Gunsolley JC. Surgical
therapies for the treatment of gingival recession. A

Periodontal Disease and Diabetes Mellitus

Transcription

Similar documents

education

Periodontal Treatment - University of Adelaide

Informational Flyer - Osteogenics Biomedical

Managed Care of North America, Inc. (MCNA Dental Plans) offers a

Penny-Power-7-IMPLANT-SEM

HELP DENTAID TO END ORAL PAIN

CSOP Bldg1 Suite 107 broch - 1123

The Roots of Periodontology - New Mexico Dental Hygienists

Children in Need of Dental Treatment Program

to this!