SENSITIVE TEETH*

Transcription

SENSITIVE TEETH*

3rd quarter 2014 • volume 15 no. 3 • ISSN 1018-1466
OHASA
JOURNAL
O f f i c i a l m o u t h p i e c e o f t h e O r a l H y g i e n i s t s ’ A s s o c i a t i o n o f So u t h A f r i c a
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Dr. Mark Hughes
Dentist, London
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Reference:
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Scientific Work Cited: 1. Addy M. Int Dent J. 2002;52(suppl 5):367-375.
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CONTENTS
EDITORIAL
ADVERTORIAL
2 Increasing the bottom line
16Oral-B symposium and product launch
N Swart
CLINICAL REVIEW
3 From the president’s desk
S Lamprecht
Guest editorial
4 Nutrition and Oral Health: Our Role as
Oral Hygienists
Glynnis Vergotine
CLINICAL REVIEW
6The association between periodontitis
and pre‑term birth and/or low birth
weight: a literature review
CS Sitholimela, LS Shangase
ADVERTORIAL
10Hain Lifescience SA Saving the world
one mouth at a time
21 Infective endocarditis and antibiotic
prophylaxis an update for South
African dental practitioners
Pieter van der Bijl jr, Pieter van der Bijl
Ethics
24Periodontal treatment and allegations
of neglect
Prof. Sue Naidoo
ohasa news
26Guidelines for authors
Continuous professional
development
27CPD questionnaire
Material Report
11 Guidelines for the selection of tooth
whitening products amongst those
available on the market
RA Basson, SR Grobler, TJ vW Kotze,
Y Osman
Editorial committee
Managing Editor Natasha Swart, Tel: (012) 319 2687, Cell: 082 414 1142, E-mail: [email protected], [email protected] | Co-Editors Renè du Bruyn, E-mail: rene.dubruyn@‌up.‌ac.‌za;
Marie Ferreira, E-mail: [email protected]; Stella Lamprecht, E-mail: [email protected]; Candida Kruger, E-mail: [email protected]
OHASA Office
PO Box 830, Newlands, 0049 | Fax: 086 696 7313 | E-mail: [email protected] | Website: http://www.ohasa.co.za
Publisher
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ISSN 1018-1466 © 2014 All rights reserved in text: OHASA. © 2014 All rights reserved in design: Kashan Advertising. OHASA Journal is published four times
a year on behalf of (OHASA), the Oral Hygienists’ Association of South Africa.
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Opinions and statements of whatever nature are published under the authority of the submitting author, and the inclusion or exclusion of any medicine
or procedure; do not necessarily reflect the view of the editor, The Oral Hygienists’ Association of South Africa or Kashan Advertising. While every
effort is made to ensure accurate reproduction, the authors, advisors, publishers and their employees or agents shall not be responsible, or in any way
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The publication of advertisements in this magazine does not imply an endorsement by the publisher or its editorial office/board and does not guarantee
any claims made for products by their manufacturers.
3 rd quarter 2014 • volume 15 no. 3
PAGE 1
EDITORIAL
Increasing the
bottom line
In business it all comes down to the bottom line
and how we can make more with what we have.
In reality, we usually have only one hour with each
patient to complete all of the “routine” procedures,
and the thought of adding one more thing can be
maddening. How many of you are pressed by your
dentist for just a little more production? There are
goals to be met and overhead to be covered, and
this can become stressful for the entire staff.
In many offices there is a production bonus for
exceeding set goals, and this benefits both the
staff and dentist. We can increase the production
and income of the oral hygiene department and
practice without much added work. It all comes
down to working smarter, but not necessarily harder.
A good leading question for patients is asking
them what they would change about their smiles if
they had the chance. The majority of patients I talk
to say they would like a whiter smile, and many are
unaware that it is possible and relatively inexpensive.
It can be quick and easy to spark interest and
generate extra income during conversations with
patients. As clinicians, we should be performing
intra-oral and extra-oral exams with each patient.
Next time, take an extra 30 seconds to show
them the tooth shade guide for an initial shade to
enter into the chart. Curious patients will question
why you are taking a shade. Explain how teeth can
change and darken over time with age, diet, and
other factors, and that you are keeping track of
changes for future reference. This will get patients
thinking about their shade and smile.
When you show patients the shade guide and
where their teeth are now, many want to know
how to get a whiter shade. As you move on with
the appointment, the foundation has been set to
discuss whitening options, whether it is take-home
bleach trays, in-office whitening, or something more
involved such as veneers or crowns.
The cost to take impressions and make bleach
trays is minimal; however, the potential for income
is great for many reasons. Patients are happy to
have the desired whitening effect, and the result is
that many will talk to friends and hopefully generate
referrals to the practice. In addition, they will purchase
whitening gel during future visits to touch up their
glowing smiles. Those 30 seconds of added effort
PAGE 2
during their oral hygiene visit have the potential to
generate easy profits for years to come.
The majority of medical aid companies do not
cover an in-office fluoride treatment for adults. In
my experience, if the benefits of fluoride treatment
are explained to patients who have hypersensitivity
or a high caries rate, they often choose to receive
in-office fluoride and understand that it is a small
added expense for a good potential benefit. Paying
a small amount for a fluoride varnish treatment to
decrease sensitivity makes the expense worth it
for most patients. We never know what a patient
values or may be willing to pay unless we offer it.
We have all discussed the increased caries rate
with people and looked for options to decrease
the risk. What percentage of South Africans chews
gum or mints throughout the day? How about
recommending xylitol mints or gum?
Studies have shown that xylitol can decrease
the caries rate, and xylitol products are available in
mints, gum, toothpaste, rinses, and nasal sprays. It
is safe for all ages and for diabetics, as it is a sugar
substitute that does not significantly raise glucose
levels. Do not forget to warn people of the potential
side effects if these products are consumed in large
quantities. Most people do not experience side
effects if they consume less than 5 mg per day.
While there are many brands available over the
counter, keep xylitol in the practice as well. We are
a society of convenience, and having a few in the
practice does not take up much space and allows
for a quick and easy profit.
From my experience as a hygienist, the biggest
added time is needed when we have a child or
teenager in the chair in need of sealants. After you
or the dentist has diagnosed the need for sealants,
placing the sealants during the same visit as the
prophylaxis is an added convenience for the parent
or guardian. The additional five to 10 minutes to
place fissure sealants has the potential to boost the
daily production greatly. The extra time provides the
opportunity to generate an additional few hundred rand
for the practice, and potentially for the oral hygienist
if it is a production-based pay rate or bonus system.
I used to recommend a power toothbrush as part
of my home-care instructions for the majority of my
patients, and I am sure many of you do too. Often
Natasha Swart
Managing editor
a patient will ask for a brand recommendation and
keeping two or three brands on hand and charged
allows people to hold and feel the action the power
toothbrushes offer. We have all explained the benefits
of power toothbrushes versus manual brushes, and
by allowing patients to hold and touch, they are
able to see and feel the difference.
How many times have we put off buying something
or forgotten to pick up something, even if it was
recommended by a health-care professional? By
keeping the brushes in the practice and having
a professional recommend them, many patients
will conveniently purchase on site. As consumers,
we like to have choices in products without being
overwhelmed by the options. Having choices on
a few different models at different prices allows
patients to purchase brushes within their budgets.
This makes it a win-win for the patient and practice,
adding easy production for the practice.
Now your patients have beautiful white teeth and
are using power toothbrushes, but how is the caries
rate? We all have those patients who have one or two
new cavities every six months, and they just cannot
figure out why. We discuss the options to reduce
the caries rate, ranging from fluoride treatments to
xylitol and chlorhexidine. Does your practice have
these products on hand for patients to purchase,
or do you give them a note with everything they
should buy? Having a small supply in the practice is
convenient for patients, freeing them from having
to drive to pick up your recommended items, and
increasing the likelihood of patient compliance. ●
OHASA JOURNAL
EDITORIAL
From the
president’s desk
Stella Lamprecht
OHASA president
Dear OHASA Members and Colleagues
The third quarter is on our doorstep and the start
of spring. New beginnings! With the new publishers
delivering a very professional looking Journal and
a new interactive website we can only present a
more professional image.
Some obstacles are opportunities. If you seek
a way past them, you will eventually find success.
Others are impenetrable. They are too big, broad,
high or deep. No matter how much effort you make,
you will be wasting your time. How are any of us
supposed to know the differences between these
two types of difficulties? There is only one way we
can find out – we try for a while and see how far we
get. One such challenge is Independent practice –
we can now have a shot at it. Which leads to Ethics.
Ethics should be infused into all oral hygienists’
professional life and not only the lives of those who
are practising independently. The public will be the
greater beneficiary of the focus on ethics and the
profession too will benefit from a reputational aspect.
The question is how to promote the culture of
ethics among practising professionals. Professor
Su Naidoo has, over the years, been writing the
ethical articles in the Journal. The profession is
defined among other things by the commitment
of its members to standards of behaviour that are
founded in ethics and best practice. These standards
go beyond the general law of the land, in terms of
which members of trades as opposed to professionals
are held accountable. So as dental professionals
we must continue to be held accountable to higher
values than the average businessman or politician.
In striving for those higher values, what happens
to practitioners that are faced with choices or
decisions that need to be benchmarked against
the rules of the professional conduct of the medical
and dental profession?
Oral hygienists throughout the world are
specialised professionals who place the interests
of their patients above their own, and strive to obtain
the best treatment for them. They have to combine
a continuous update on dental developments with a
service to their patients, and maintain a reasonable
standard of living – between these elements there
is often tension.
The rules of professional conduct, the demands
of a practice and the need to earn a living – this
is where an independent practitioner may need
assistance in navigating the pressures. It will be
possible to turn to the ethics committee of the HPCSA
but in today’s fast-paced life, practitioners need an
open, immediate and confidential channel that can
provide real-time responses to ethical dilemmas. This
is where the knowledge share on the new website
will come in handy, with the experienced older
practitioner providing guidance on a confidential
basis. We can even have a database of questions
and answers that is updated and accessible.
The database would serve a dual purpose by
providing immediate information and serving as a
resource to monitor trends and practice requirements.
Ethics, like morals, are intangible and cannot
be taught. The impact of immoral and unethical
actions in the profession is real and far reaching
for the practitioner, the patient and the profession
as a whole.
The promotion of a culture of ethics requires the
commitment of every oral hygienist for it to remain
a proficient profession.
God Bless
Stella ●
OHASA’s VISION OHASA is a dedicated, dynamic, professional association representing hygienists as invaluable members of the health profession team.
OHASA’s MISSION OHASA aims to promote quality oral health care by representing, protecting and advancing the profession in partnership with stakeholders.
OHASA National Executive Committee
President Stella Lamprecht Vice-President Karen Paulse Secretariat Natasha Swart Treasurer Marie Ferreira Additional Member Maggie Naidoo SADA Liaison Petro Steyn; Susan Burger
ohasa branch chairpersons and representatives
Gauteng Branch Representative Natasha Swart, Cell: 082 414 1142, E-mail: [email protected], [email protected]
Chairperson Stella Lamprecht, Cell: 082 890 6949, E-mail: [email protected]
Eastern Cape Branch Representative Marie Ferreira, Cell: 082 897 6252, E-mail: [email protected], [email protected]
Chairperson Mart-Marié Potgieter, Cell: 083 661 9382 a/h, E-mail: [email protected]
Kwazulu-Natal Branch Representative Maggie Naidoo, Cell: 083 777 9420, E-mail: [email protected]
Chairperson Suzette Pirow, Cell: 082 568 0173, E-mail: [email protected]
Western CaPe Branch Representative Karen Paulse, Cell: 083 357 8759, E-mail: [email protected]
Chairperson Gail Smith, Cell: 083 422 7020, E-mail: [email protected]
PAGE 3
GUEST EDITORIAL
NUTRITION AND ORAL HEALTH:
OUR ROLE AS ORAL HYGIENISTS
Glynnis Vergotine: Dip OH, BA, B Ed (Hons), M Ed (Diss)
Lecturer at the University of the Witwatersrand, Johannesburg
As South Africans, food is central to our identity. At
mealtimes our families meet around the table, during
holidays and special occasions we gather over a braai
or the potjie which reflects the remarkable diversity
of our country. However, there are pressing concerns
linked to nutrition for our nation, with the rising
incidence of food insecurity and non-communicable
diseases (such as obesity, diabetes and coronary
heart disease). Food insecurity findings in South
Africa show that the nutrient density of the diet
consumed by children is insufficient to meet daily
nutrient requirements1. Similarly, there is low food
variety and household dietary diversity especially in
poorer communities, with one child in four under the
age of six years (translating to approximately 1.5 million
children) stunted due to chronic malnutrition. Oral
disease is classified as a non-communicable disease
(NCD) by the World Health Organization (WHO),
and adopting the common risk factor approach for
NCDs through interventions with individuals and
communities will assist in preventing a number of
diseases2. At-risk people can be accessed through
private and public health clinics, social development
centres and other government services. As the rate
of systemic health problems such as malnutrition,
diabetes, obesity, and cardiac disease continues
to increase, the need for oral hygienists to provide
dietary guidance is also growing.
• Enjoy a variety of foods
• Be active
• Make starchy foods the basis of most
meals
• Eat plenty of vegetables and fruit
every day
• Eat dry beans, peas, lentils, and soy
regularly
• Chicken, fish, milk, meat, or eggs can
be eaten daily
• Eat fats sparingly
• Drink lots of clean, safe water
• If you drink alcohol, drink sensibly
• Use salt sparingly
• Eat and drink food and drinks that
contain sugar sparingly and not
between meals
PAGE 4
So, when we think about the role of the Oral
Hygienist in understanding the nutritional status
and nutrition education of South Africans there
are a number of questions which come to mind.
What messages are being given to our patients
and communities about nutrition? To what extent
are Oral Hygienists addressing nutrition as part of
their daily work? And, what type of interaction do we
have with our colleagues in associated professions
about the important link between oral health and
general health.
In South Africa, dental caries is regarded as a
condition of high prevalence and burden as it is the
most common condition affecting children. Sixty
percent of 6 year olds, in their primary dentition,
have decay, and 55% untreated decay, therefore
91% goes untreated. Only 18% of 12 year olds have
healthy gums and only 2% of 44 year olds have
healthy gums3. Outside of demineralisation and
caries formation, many patients and health care
providers do not realise the strong association
that exists between nutrition and oral health. Oral
hygienists are well positioned to educate both
patients and medical colleagues about this link.
Oral hygienists have to be informed on the most
current research in dentistry and oral hygiene, as
well as allied fields. This will enable us to provide
our patients with meaningful nutrition information,
as well as prevent and rectify misconceptions
about nutrition to improve both health literacy and
patient compliance with dietary recommendations.
This can be achieved through regular continued
professional development courses and gaining
access to evidence-based resources. Some resources
which can be accessed by oral health professionals
include the South African Food-based Dietary
Guidelines for people aged >6 years, which takes
into consideration both over-nutrition and undernutrition4. The guidelines related to oral health are
highlighted to the left. Further details of South African
food guidelines can be seen in policy documents
and articles on nutrition in South Africa.
Other commonly used educational resources for
delivering general nutrition advice and promoting
healthy eating are the 2010 Dietary Guidelines
Glynnis Vergotine
for Americans, the Choose MyPlate, published by
the United States Department of Agriculture and
US Department of Health and Human Services5,6
and the Eatwell Plate used by the Food Standards
Agency in the UK7. These resources explain the
basic guidelines for a healthy diet and take into
consideration the correct balance of food intake.
Understanding the importance of added sugars
in our diets and the effects on oral and general
health is vital. Sugars are undoubtedly the most
important dietary factor in the development of
dental caries. The term ‘added sugars’ refers
to monosaccharides and disaccharides. Sugar
consumption must address the quantity, frequency,
and timing of sugar consumption, with sugar intake
<40 g/day in areas in which water is not fluoridated
and <55 g/day in fluoridated areas. This equates to
about 6–10% of energy intake4. Messages such as
‘consume foods with fewer added sugars, and limit
it to four times daily’ have to be consistently used
by all health professionals. Teaching our patients to
check food product labelling is important in getting
them to realise the amount of added sugar and that
sugars have various names.
Some other significant measures for oral
hygienists to follow will include the following: taking
a thorough medical and dental history can provide
the necessary information to discuss patients’ oral
health needs, as well as their nutritional requirements;
routinely providing healthy eating advice to the
public to promote good oral and general health;
OHASA JOURNAL
GUEST EDITORIAL
and offering nutritional screening/counselling as
it pertains to oral health prevention and disease
management. Going beyond this will require
a referral to a dietician, nutritionist, or medical
provider. Developing relationships between oral
health professionals and dieticians can be helpful
in obtaining nutritional and dietary information or
requesting guidance regarding patients. Important
links would be with the Association for Dietetics in
South Africa and the Nutrition Society of South Africa.
Collaborating with other health professionals is key
to maintaining optimal, comprehensive oral care for
all patients. With the introduction of the Bachelors
degree in Oral Hygiene, training institutions are in
the best position to highlight the vital link between
nutrition and oral health. This will ensure that when
educating patients, communities and other health
care providers, there will be a deliberate attempt
to improve the health of our nation.
It is therefore our role as Oral hygienists to be
knowledgeable about our country’s nutritional needs
and to provide evidence-based nutrition and dietary
information to patients in clinical and/or community
oral settings as it relates to oral health.
4. Steyn, NP, Myburgh, NG, & Nel, JH. (2003). Evidence
to support a food-based dietary guideline on sugar
consumption in South Africa. Bulletin of the World Health
Organization, 81(8), 599–608.
5.United States Department of Agriculture; United States
Department of Health and Human Services. Dietary
Guidelines for Americans. 2010. Available at:
health.gov/dietaryguidelines/dga2010/
DietaryGuidelines2010.pdf.
6.United States Department of Agriculture. Choose
MyPlate. Available at: choosemyplate.gov.
7.www.food.gov.uk/healthiereating/eatwellplate/
Acknowledgement: Mrs Magdeline Brits-Alcock
– Registered Dietician ●
References
1. Bulletin of the World Health Organization 2011;
89:891–899. doi: 10.2471/BLT.11.089243
2.http://blogs.sun.ac.za/fsi/food-security-challenges-insouth-africa/
3. Strategic Plan for the Prevention and Control of
Non‑Communicable Diseases 2013-17
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CLINICAL Review
The association between
periodontitis and
pre‑term birth and/or
low birth weight:
a literature review
CS Sitholimela, LS Shangase
Infections have been strongly associated with adverse
pregnancy outcomes like pre-term and/or low birth
weight (PTLBW). There is substantial evidence on
the direct association of genito-urinary infections
and the incidence of PTLBW. Numerous cases of
adverse pregnancy outcomes without maternal
genito-urinary infection but nevertheless high
levels of the tumour necrosis factor alpha (TNF-α)
and prostaglandin E2 (PGE) in the amniotic fluid,
have been recorded. These findings alluded to the
presence of infection elsewhere in the body. This
paper reviews the literature on the association
between the infective condition of periodontitis
and PTLBW.
Key words: Adverse pregnancy outcomes, pre-term
birth, low birth weight, periodontitis
Introduction
Numerous studies have been conducted to evaluate
the relationship between periodontitis, pregnancy
and adverse pregnancy outcomes such as pre-term
birth, low birth weight and the combination of
the two. The increase in research activity on this
subject has been triggered by adverse pregnancy
outcomes presenting a major public health problem
worldwide,1 despite improvements in prenatal,
antenatal, postnatal and maternal care including
public awareness.2,3 Pre-term birth and/or low
birth weight contribute significantly to the health
care, economic and social burden imposed on the
government, communities and families involved.2,4
According to the global action report on pre-term
birth, there are approximately 15 million pre-term
births annually.5 Global statistics published by the
World Health Organisation (WHO) indicate that over
60% of pre-term births occur in Africa and South
Asia. Some regions within sub-Saharan Africa record
pre-term birth rates as high as over 15%.7,6
Whilst results from most studies have suggested
that this association may exist, such findings have
not been consistent. This is partly as result of the
heterogeneity in the methodology of the studies
PAGE 6
conducted. The variations range from the diversity
of populations, sample sizes, case definitions of
periodontitis and pregnancy outcomes.
Periodontitis is a chronic infectious disease,
and when present is characterised by periods of
exacerbation and remission. It is predominantly
associated with gram negative organisms within the
subgingival plaque biofilm,7 and can be modified
by the host immuno-inflammatory response,
environmental, genetic and systemic factors.
The tissue destruction seen in periodontitis is
mainly related to the inflammatory process which,
in an attempt to combat infection, results in tissue
damage.8 The inflammatory mediators secreted in
response to endotoxin/lipopolysaccharides (LPS)
include pro inflammatory cytokines e.g. IL-1ß and
TNF-α that bind to specific receptors on target cells;
prostaglandins (PGE), which cause vasodilatation
and matrix-metallo-proteases (MMPs), which are
able to degrade collagen, gelatine and elastin.4,9
These inflammatory mediators are secreted locally
within the periodontium and can be detected in
the crevicular fluid and systemically following
exposure to LPS.
Without intervention the diseased periodontium
can serve as a reservoir for gram negative
anaerobes, their virulence factor (LPS) and the
associated inflammatory mediators which are
able to enter the systemic circulation4 resulting in
constant activation of the systemic host response.
Hence periodontitis is associated with increased
levels of c-reactive protein (CRP), an acute phase
protein produced by hepatocytes in response
to the circulating pro-inflammatory cytokines
including TNF-α and IL-1,8 which is a diagnostic
marker for clinical infections. Given the large
epithelial surface that could be ulcerated in the
periodontal pocket, periodontitis can be regarded as
a constant pathogenic and inflammatory challenge
at a systemic level.
Pre-term birth, as defined by the WHO, refers
to all live births before 37 weeks of completed
gestation. Pre-term birth can be further classified
according to gestational period or age: extremely
pre-term (<28 weeks), very pre-term (≥28 but <32
weeks), moderate pre-term (≥32 but <37 weeks);
as determined by the last menstrual day and by
ultrasound.7 Low birth weight has been defined
as less than 2,500 g and is believed to reflect the
health status of the immediate community into
which the infant is born.10 A very low birth weight
refers to a weight below 1,500 g.11 In developing
countries, low birth weight is usually caused by
intrauterine growth restriction, whereas in developed
countries it is more often as a result of pre-term
birth.1 Paradoxically, there are cases where infants
born at > 37 weeks present with low birth weight,
whilst in some cases premature infants may have
a weight ≥ 2,500 g.12
Infections during pregnancy have been strongly
associated with pre-term birth and/or low birth weight
(PTLBW). Maternal genito-urinary tract infections
have been most frequently associated with such
outcomes.4 However, there have been a number
of cases with these adverse outcomes, displaying
high levels of TNF-α and PGE in the amniotic fluid,
but in the absence of maternal genito-urinary tract
infections. Such observations are suggestive of
an infection arising from elsewhere in the body.9
An estimated 80 % of all births at less than 30
weeks of gestation are due to infections which
precede the pregnancy complications leading to
pre-term birth.13 Recognition of risk factors facilitates
the identification of those at risk of adverse
pregnancy outcomes,1 and may thus inform policies
on the prevention of PTLBW. This paper therefore
seeks to review the literature on the association
between periodontitis and PTLBW, highlighting the
possible mechanisms of the association and the
significance of oral health care in the prevention
of these unfavourable outcomes of pregnancy.
Evidence-based association between
pregnancy and periodontitis
Periodontal infections have been associated with
a number of systemic diseases including adverse
OHASA JOURNAL
CLINICAL Review
pregnancy outcomes like pre-term birth, low
birth weight and the combination of the two. The
relationship between periodontitis and pregnancy
is proposed to be bi-directional with one having an
effect on the other.14
Effect of pregnancy on periodontitis
Pregnant women are said to be more susceptible
to the development of periodontitis as a result of
hormonal changes. The levels of ovarian hormones,
namely, oestrogen and progesterone increase during
pregnancy. These hormones increase, starting from
the second month of the pregnancy and continue to
rise until the eighth month, after which their levels
begin to decline. This rise and fall pattern of the
hormones coincides with the onset and peak of
the gingival inflammation observed in pregnancy.
When, after the eighth month, the levels of these
hormones drop rapidly, a simultaneous reduction
in the gingival inflammation may be observed. The
timing and occurrence of these gingival changes in
step with the fluctuations in hormone levels give
credibility to the notion that hormonal changes
cause the gingival inflammation.15 An increase
in oestrogen and progesterone levels increases
the risk of gingival inflammation. A number of
mechanisms have been proposed for the effect of
hormonal changes on gingival tissues: the known
effects of these hormones is to increase capillary
dilatation and permeability which would account
for the gingival inflammation.15
Whilst this may explain only the inflammatory
changes, unattended gingivitis may progress to
periodontitis.
Type and amount of subgingival flora present
during pregnancy
Kornman and Loesche and a study by Li et al showed
a significant increase in the ratio of anaerobic to
aerobic bacteria, particularly from the thirteenth
to the sixteenth weeks of pregnancy16,17 which
remained high till the third trimester. The subgingival
concentrations of Bacteroides intermedius (now
Prevotellaintermedia) increased significantly, up
to five-fold at the peak of gingival bleeding.16
Oestrogen and progesterone stimulate bacterial
growth causing a shift in bacterial flora,18 and
specifically substitute for menadione as an essential
growth factor for B. intermedius with a resultant
increased growth activity.16
Jensen et al observed an increase in the gingival
crevicular fluid flow and in gingival score indices
amongst pregnant women compared with nonpregnant controls. This difference was ascribed
to alterations in the composition of the subgingival
plaque, influenced by sex hormones.19
Immunosuppression
The role of oestrogen and progesterone among
other hormones is to suppress the mother’s immune
system to prevent the rejection of the foetus. Whilst
the underlying mechanisms of immunosuppression
are not clear, a number of plausible suggestions
have been put forth. These include an altered T cell
response and an impaired lymphocyte proliferation,20
blockage of K+ channels21 and depression of cellmediated immunity.22
Impaired collagen repair
Pregnancy, through alterations in hormonal levels,
alters the rate and pattern of collagen production
in the gingivae with a resultant reduction in the
body’s ability to repair and maintain the gingival
tissues. This compromised collagen repair may
also be effected through folate deficiency caused
by oestrogen and progesterone.18
Effect of periodontitis on pregnancy
outcomes
Periodontitis is claimed to be strongly associated with
PTLBW, as it has been diagnosed more frequently
among mothers with pre-term and/or low birth
weight infants when compared with mothers who
delivered full-term infants with normal birth weight.23
Mechanisms proposed and described to account
for this association include the following:
Common risk factors
Specific bacteria within the dental plaque are etiologic
for periodontitis. Whilst these bacteria may initiate
the disease process, they alone are not sufficient to
effect, to propagate and to sustain periodontitis. A
susceptible host is necessary for disease to occur.
Host susceptibility is influenced by certain factors,
which may be environmental, genetic or systemic.
These may include tobacco and alcohol use, stress,
immunosuppression and diabetes, to name a few;
and are referred to as risk factors. A risk factor by
definition is that which increases the chances of an
individual to contract a disease, or makes one more
likely to have a disease. Periodontitis shares some
of these risk factors with PTLBW24 e.g. tobacco and
alcohol abuse, genetic factors, and stress. Therefore
given this analogy, the possibility of a mother with
periodontitis giving birth pre-term, or giving birth
to an infant with low birth weight is quite high but
is mostly likely a coincidence.
Bacteraemia and inflammation
Periodontitis is a common clinical finding amongst
many pregnant women and is believed to provide
an oral route of infectious burden to the foetal
placental unit. 1 The concept is not new that
periodontal pathogens, their shed virulence factors
and/or inflammatory cytokines from the periodontal
pocket may gain access into the bloodstream and
disseminate through the body. Miller reported
this idea in 1891 when he published the theory
of focal infection, but it became dormant due to
lack of scientific evidence.25 Collins et al in the
early 1990s rehashed the case and hypothesised
that periodontitis could be a reservoir for bacteria
that can access the systemic circulation and
trans- locate into the foetal-placental unit where
it may induce complications in the pregnancy.26
This bacteraemia can be elicited by processes as
simple as chewing or tooth brushing. Translocated
bacteria reaching a distant site with a susceptible
environment trigger an inflammatory response
with resultant complications. PAGE 7
CLINICAL Review
This concept is supported by animal and clinical
studies. Collins et al conducted a number of animal
studies to test the hypothesis that periodontitis as
an oral infection represents a significant source
of infection and inflammation which would cause
bacteraemia and pregnancy complications. The
result of these studies in hamsters showed that
P.gingivalis can reduce the foetal weight by over
15–16%, with an increase in PGE2 and TNF-α.
Through these studies they also showed reduction
of 22.5% in the foetal mean weight of hamsters that
received plaque promoting diet and the exogenous
P.gingivalis orally. These results suggest that low
level oral infections can possibly produce adverse
pregnancy outcomes.26
Forty percent of all pregnancies are associated
with a certain degree of foetal IgM antibody
response to a pathogen of maternal oral origin.
Results from clinical studies on foetal cord blood
from spontaneous pre-term births support this
concept, having shown a significant increase of
in-utero IgM antibody response which was specific
to numerous periodontal pathogens including
P.gingivalis. This antibody response induced an
inflammatory response at the foetal-placental
unit with resultant pre-term birth.27,28,29 A similar
immuno-inflammatory response may ensue in the
foetal circulation if the pathogens, their virulent
components or inflammatory cytokine cross the
placenta.2
Periodontitis is associated with increased serum
levels of C-reactive protein (CRP), an acute phase
protein produced by hepatocytes in response to
the circulating pro-inflammatory cytokines including
TNF-α and IL-1 that enter the circulation from the
damaged periodontium.8 The CRP is an important
diagnostic marker for clinical infections.
A few possible mechanisms through which an
inflammatory response can effect PTLBW have
been proposed:2
• Whilst inflammatory cytokines are produced to
combat the infection, they may cause tissue
destruction. The normal exchange of nutrients
between the foetus and the mother is dependent
on the structural integrity of the placenta. Damage
to the placental tissue would therefore contribute
to impaired foetal growth with resultant LBW.
PAGE 8
•The normal blood flow between the foetus and
the mother may be disrupted as a result of the
structural damage of the placenta. This disruption
affects the maternal blood pressure, thus leading
to pre-eclampsia which may necessitate planned
pre-term delivery.
• Whilst pro-inflammatory cytokines are necessary
for normal parturition to occur, premature increase
in production of these cytokines, as occurs in
an inflammatory response due to infection, may
contribute to pre-term rupture of the membranes
and contraction of the uterus with resultant preterm delivery or miscarriage depending on the
severity of the response.
•In the foetus, local inflammatory response may
cause structural damage of tissue and organ
systems. The foetus may or may not survive
the perinatal period, and if it does, it may have
deficiencies that may negatively impact on the
quality of life, depending on the extent of the
tissue damage.
Whilst these mechanisms may sound plausible,
further in-depth investigations are necessary for
their confirmation.
Lin et al in their study on mice found that
P.gingivalis restricted foetal growth and even resulted
in foetal death in some. Their proposed mechanism
was a shift in the TH1/TH2 ratio which led to TH1
cytokine dominance with adverse outcomes as a
result of increased production of pro-inflammatory
cytokines. In another study, toll like receptors, in
particular TLR4 was shown to mediate an inflammatory
response to specific pathogens in murines, which
led to restricted foetal growth and foetal resorption.
These receptors were over-expressed on trophoblast
surfaces in mice that experienced these adverse
outcomes.31,32
Mice that were deficient in TLR4 were protected
against pre-term birth induced by bacterial influences
and by LPS.
Apoptosis
Besides the inflammatory response concept,
P. gingivalis can, through haematogenous spread,
also invade trophoblasts in the placenta and
cause apoptosis and cell cycle arrest, which may
synergistically contribute to PTLBW.33
Effect of periodontal therapy on
pregnancy outcomes
The systemic impact of periodontal inflammation
has been hypothesised as a plausible mechanism.
It is on this basis that studies to assess the effect
of periodontal therapy on levels of the biomarkers
for inflammation and pregnancy outcomes have
been conducted.
Interventional studies assessing the impact of
periodontal therapy on pregnancy outcomes have
yielded contradictory results. The hypothesis for
these studies is that if periodontitis has an effect
on the pregnancy outcomes, its treatment amongst
pregnant women should therefore reduce the
incidence of PTLBW. A number of studies have
indeed reported a reduction in the incidence of
PTLBW in women on whom periodontal therapy
had been undertaken.34,35,36,37
Jeffcoat et al in their pilot study on women
between gestational weeks 21 and 25, concluded
that scaling and root planing in pregnant women
with periodontitis may result in the reduction of
pre-term births.35 These results were similar to
those reported in an earlier study by Lopez on
pregnant women in the same gestational period.36
Offenbacher et al reported a significant reduction
in pre-term births following periodontal therapy.34
Whilst Mitchell-Lewis et al also reported similar
findings, these were not significant in their study.37
This could be linked to the age of the subjects, who
were in their teens. Low maternal age is a known
risk factor for adverse pregnancy outcomes.
A number of studies reported a reduction in the
levels of the biomarkers in either the GCF or serum
following periodontal therapy.34,38,39,40,41
Taylor et al and Michalowicz et al in their studies
reported no reduction in PTLBW and no significant
differences in the levels of biomarkers evaluated
following periodontal therapy.42,43,44 The findings
of this study, conducted in 2006, could have been
influenced by the fact that the control group had
regular examination recalls. Though there was no
active treatment carried out in this group, their
awareness of the recalls could have influenced
their oral hygiene practices.
In the light of these conflicting results, the
evidence in the literature is therefore inconclusive
on the effect of periodontal therapy on pregnancy
OHASA JOURNAL
CLINICAL Review
outcomes. More interventional studies are needed
to validate the association between periodontitis
and adverse pregnancy outcomes.
Randomised trials and progressive cohort
studies
The evidence from randomised trials, case-control
and cohort studies that assessed the association
between periodontitis and pregnancy outcomes
including systematic reviews is conflicting.45,46,47,48,49,50
Most of the studies, however, reported a positive
association. In a systematic review, Xiong et al
reported that out of 22 cohort and case control studies
reviewed, 17 found a positive association between
periodontitis and adverse pregnancy outcomes and
the remaining five found no association.45 Four out
of the 17 positive studies reported periodontitis as
an independent risk factor for PTLBW.36,50,51,52 In
contradiction, two recent studies have reported no
association between periodontitis and PTLBW.44,53
The challenge mostly encountered in systematic
reviews was the heterogeneity of the studies
conducted, which sometimes made meta-analytical
studies impossible. The differences ranged from
population sample and case definitions, to the quality
of the methodology; and where the variations were
great the intensity of the association was small.
Heterogeneity in methodology also reduced the
pool of the studies reviewed.
Conclusion
Overall, the majority of studies have shown that
maternal periodontitis is associated with PTLBW,
and this association may even be independent
of other risk factors. This association has further
been supported by studies on interventional
studies. The association however, does not imply
causality and should be interpreted with caution.
Notwithstanding the fact that findings contrary to
this association have been reported, more studies
with better methodologies and inclusive of other
adverse pregnancy outcomes like stillbirths, late
miscarriages etc. should be conducted.
Given the impact of PTLBW on the mother, the live
births that survive, families and communities; the
authors recommend that oral health care should be
incorporated into existing maternal and child health
care programmes in the private and public sectors.
Bearing in mind that the results from intervention
studies are inconclusive, focus should be placed
on prevention of the onset of disease. ●
11.Lawn JE, Kerber K, Enweronu-Laaryea C, Cousens S.
3.6 Million neonatal deaths-What is progressing and what
is not? Semi-nPerinatol. 2010; 34: 395–407.
12.Collins JG, Windley HW, Arnold RR, Offenbacher S.
Effects of a Porphyromonasgingivalis infection on
inflammatory mediator response and pregnancy
outcome in Hamsters. Infect. Immun.1994; 62 (10):
4356–61.
13.Inaba H, Kuboniwa M, Sugita H, Lamont RJ, Amano
A. Identification of signalling pathways mediating cell
cycle arrest and apoptosis induced by Porphyromonas
gingivalis in human trophoblasts. ASM Infection and
Immunity 2012; 80(8): 2847–57.
14.Offenbacher S. Periodontal diseases: pathogenesis. Ann
Periodontol 1996; 1(1): 821–78.
15. Garcia RI, Henshaw MM, Krall EA. Relationship between
periodontal disease and systemic health. Periodontol
2000 2001; 25: 21–36.
16. Kornmam KS, Loesche WJ. The subgingival flora during
pregnancy. J Periodontal Res 1980; 15: 111–22.
17. Zachariasen RD. The effect of elevated ovarian
hormones on periodontal health: oral contraceptives and
pregnancy. Women Health 1993; 20(2): 21–30
18.Mccormick MC. The contribution of low birth weight to
infant mortality and child morbidity. N Engl J Med 1985;
312: 82–90.
19.Matthiesen l, Berg G, Ernerudh J, Hakansson l.
Lymphocyte subsets and mitogen stimulation of blood
lymphocytes in normal pregnancy. Am J Reprod Immunol
1996; 35:70–9.
20.Ehring GR, Kershbaum HH, Eder C, Neben AL et al. a
non-genomic mechanism for progesterone-mediated
immunosuppression, inhibition of K+ channels, Ca2+
signalling and gene expression in T lymphocytes. J Exp
Med 1998; 188: 1593–1602.
21.O’neil TC. Plasma female sex-hormones levels and
gingivitis in pregnancy. Periodontol 1979; 50: 279–82.
22.Mesa F, Pozo E, Blanc V, Puertas, Bravo M et al.
Periodontal bacterial profiles and placental inflammatory
infiltrate in pregnancy related to birth outcomes. J
Periodontal 2012 Nov 3 (Epub ahead of print.)
23.Agueda A, Ramon JM, Manau C, Guerrero A, Echeverria
JJ. Periodontal disease as a risk factor for adverse
pregnancy outcomes: a prospective cohort study. J Clin
Periodontal. 2008; 35(1):16–22.
24.Miller WD. The human mouth as a focus of infection.
Dental Cosmos 1891; 33: 689–713.
25.Collins JG, Smith MA, Arnold RR, Offenbacher S. Effects
of Escherichia coli and Porphyromonas gingivalis
lipopolysaccharide on pregnancy outcome in the golden
hamster. Infect Immun 1994; 62(10):4652–55.
26.Madianos PN, Lieff S, Murtha AP, Boggess KA et al. Maternal
periodontitis and prematurity. Part ii: maternal infection
and fetal exposure. Ann Periodontol 2001; 6: 175–82.
27. Boggess KA, Moss K, Madianos P, Murtha AP et al. Fetal
immune response to oral pathogens and risk of pre-term
birth. Am J Obstet Gynecol 2005; 193: 1121–6.
28.Moutsopoulos NM, Madianos PN. Low-grade inflammation
in chronic infectious diseases: paradigm of periodontal
infections. Ann N Y Acad Sci 2006; 1088: 251–64.
29.Lin D, Smith MA, Elter J, Champagne C et al.
Porphyromonas gingivalis infection during pregnancy
increases maternal tumor necrosis factor alpha,
suppresses maternal interleukin-10, and enhances fetal
growth restriction and resorption in mice. Infect Immun
2003: 5156–62.
30.Liu H, Redline RW, Han YW. Fusobacterium Nucleatum
induces fetal death in mice via stimulation of
Tlr4‑mediated placental inflammatory response.
J Immunol 2007; 179(4): 2501–8.
References
1. Baskaradoss JK, Geevarghese A, Al Dosari AA. Causes of
adverse pregnancy outcomes and the role of maternal
periodontal status – a review of the literature. Open Den
J. 2012; 6: 79–84.
2. Bobetsis YA, Barros SP, Offenbacher S. Exploring the
relationship between periodontal disease and pregnancy
complications. JADA 2006; 137(10): 7–13.
3.UsluToygar H, Seydaoglu G, Kurklu S, Guzeldemir E,
Arpak N. Periodontal health and adverse pregnancy
outcome in 3,576 Turkish women. J Periodontal 2007;
78(11): 2081–94.
4.Offenbacher S, Katz V, Fertik G, Collins J, Boyd D et al.
Periodontal infection as a possible risk factor for pre-term
low birth weight. J Periodontal 1996; 67: 1103–13.
5. Blencowe H, Cousens S, Oestergaard M, Chou D, Moller
AB et al. National, regional and worldwide estimates of
pre-term birth. The Lancet 2012; 9: 379.
6. WHO. Born too soon: The Global action report on Preterm Birth, 2012.
7.Lin D, Smith MA, Elter J, Champagne C, Downey CL et
al. Porphyromonasgingivalis infection in pregnant mice
is associated with placental dissemination, an increase
in placental Th1/Th2 cytokine ratio, and foetal growth
restriction. infectimmun. 2003; 71(9): 5163–8.
8.Renuka DR, Vijaykumar N, Raghavendra R, Nalini E,
Yuvaraja M. a review of A-reactive protein: a diagnostic
indicator in periodontal medicine. J Pharm Bioallied Sci.
2012; 4: 422–6.
9. World Health Organization: WklyEpidem Rec. 1984; 59:
205–12
10.Van der Merwe K, Hoffman R, Black V, Chersich M,
Coovadia A et al. Birth outcomes in South African
women receiving highly active antiretroviral therapy:
a retrospective observational study. Journal of the
international AIDS Society 2011; 14:42.
PAGE 9
ADVERTORIAL
Hain Lifescience SA
Saving the world one mouth at a time
Hain Lifescience SA held its first dental study group
on 26 July 2014 at its offices in Corporate Park,
Midrand. The speakers, company and of course
the refreshments were excellent. Dr PJ Lofstedt, a
dentist from Johannesburg, gave a very informative
talk about the importance of perio-pathogenic
organisms and the role of molecular testing in the
treatment plan for periodontitis. Dr J Fourie is a
specialist in oral medicine and periodontics and
her presentation shed some light on the nature of
periodontal infections. An oral hygienist, Christine
de Sousa explained oral hygiene in layman’s terms
and also displayed her new products from ‘Rollys’.
The study group clearly showed that there is a
need to discuss ongoing developments in the dental
diagnostic field and to educate patients on the risks
associated with periodontitis. A demonstration
of Hain Lifescience’s new periodontal tests, the
MicroIdent 11 and IL-1, was performed. These tests
improved the approach to the treatment plan and
also the final outcome of patients’ oral hygiene.
The feedback from the users in the study group,
on that day, confirmed this.
The day was a great success and dental
professionals should be on the lookout for more
Hain Lifescience study groups because this was
definitely the first of many to come. ●
For more queries or demonstrations please contact
Hain Lifescience at [email protected]
NOMADS
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OHASA JOURNAL
MATERIAL REPORT
Guidelines for the
selection of tooth
whitening products
amongst those available on the market
SADJ April 2013, Vol. 68 no. 3 p. 122–129
RA Basson, SR Grobler*, TJ vW Kotze, Y Osman
* Oral and Dental Research Institute, Faculty of Dentistry, University of the Western Cape, Tygerberg. E-mail: [email protected]
Summary
Background: Several tooth whiteners are available
on the market, and the ideal choice should be
determined by efficacy and optimal clinical results.
Objectives: The purpose of this study was to
compare the reported clinical success rates of
different tooth whitening products.
Search strategy: The relevant literature (1998–2011)
was studied, using as sources the databases: Google
Scholar, Science Direct, Medline and Pubmed.
Selection criteria: The material was clearly identified,
the manufacturers’ instructions were respected and
the sample size stated.
Results and conclusions: This descriptive report
on 49 papers focuses on the total colour change,
measured with a calibrated shade guide and
also numerically (colourimeter, chromameter or
spectrophotometer), the relapse of the colour
change and tooth sensitivity. In general, the
dentist supervised at-home bleaching and the
in-office treatment gave approximately the same
initial percentage improvement of tooth whitening.
However, the relapse after a four week or longer
period was significantly higher for the in-office
treatment. The treatment of choice should be a
dentist supervised at-home bleaching product
which generally contains ~10% carbamide peroxide
applied over about 14 days for about eight hours
per night. Tooth sensitivity should not be a general
problem although some subjects might choose
to discontinue treatment as a result of sensitivity.
BACKGROUND
Dentists and oral hygienist in clinical practice are
faced with a large number of tooth whiteners available
and advertised on the market. Furthermore, they
are bombarded with results based on laboratory
studies and to a lesser extent on clinical studies.1-4
How then does the oral health professional select a
tooth whitener which will be effective and provide
optimal clinical results? Important also is the extent
of colour relapse over time.
Peroxide is the chemical most frequently used
as a tooth whitening agent with two types being
generally employed i.e. hydrogen peroxide (H2O2) or
carbamide peroxide (CH6N2O3). Due to the instability of
hydrogen peroxide it is mostly added to the whitener
just before the application process, while carbamide
peroxide is the more stable oxidising agent and can
be included in the whitener itself. Thus, the hydrogen
peroxide can be applied directly on the tooth surface
as such or is produced from carbamide peroxide
which dissociates into hydrogen peroxide and urea
upon contact with water.5,6 Urea further breaks down
into ammonia and carbon dioxide.
It has been reported7 that a 10% carbamide
peroxide solution can produce only about 3–3.35%
hydrogen peroxide. Hydrogen peroxide is a very
strong oxidising agent. When it decomposes it
forms free radicals which are responsible for the
strong bleaching effect on organic and inorganic
chemicals in and on enamel and dentine.2 However,
more of the stronger per-hydroxyl radical is formed
in alkaline mediums with a resulting higher bleaching
effect on teeth.6
To the public, the most important aspects
of tooth whiteners are the effectiveness of the
whitener, how long-lasting the effect is, the cost
of the treatment and the duration of the required
treatment. Therefore, if money is not an issue, the
in-office treatment would basically be the treatment
of choice, since the resultant whitening effect can
be observed just after the chair session.
Tooth-bleaching or tooth-whitening is mainly
performed according to four different protocols:
1) dentist/oral hygienist-supervised at-home
bleaching, 2) in-office bleaching, 3) over-thecounter whitening products for self-application
and 4) combination therapy (in-office followed
by at-home treatment). In general, the most
effective would be the first two, as the peroxide
concentrations and application time of over-thecounter products are simply too low. In contrast,
the peroxide concentrations (~35%) of the in-office
bleaching whiteners are high (Table 1)8-36 and applied
for short bursts of time (~30 minutes) which might
be repeated in the same session (or occasionally
over more sessions) to show the effect before
the patient goes home. Alternatively, the dentist/
oral hygienist‑supervised at-home bleaching
process normally makes use of lower peroxide
concentrations (~10% carbamide peroxide) and
patient self-application at home, mostly over-night
and over several days, for a good result. PAGE 11
MATERIAL REPORT
% HP
Category
Application
Tooth Sensitivity
% Colour
improvement
% Colour relapse
after 4 weeks+
1
Browning 20088
Opalescence PF (plus nitrate and fluoride)
10%
-
At-home
2 weeks/x6 hrs per night
45%
88%
14%
2
Browning 20088
Opalescence formulation (F)
10%
-
At-home
2 weeks/x6 hrs per night
62%
83%
0%
3
Matis, 19989
Opalescence Tooth Whitening Gel
10%
-
At-home
2 weeks /8 hrs per night
Mild
73%
41%
4
Matis, 200010
Opalescence F
15%
-
At-home
-
69%
18%
15%
-
At-home
Mild
67%
24%
-
7.5%
At-home
2 weeks /1 hr twice a day
Mild
67%
13%
Product
Study #
Reference
% CP
Table 1: Shade guide measurements
11
5
Matis, 2007
Opalescence PF
6
Mokhlis, 200012
Day White
7
Mokhlis, 200012
Opalescence Tooth Whitening Gel PF
20%
-
At-home
2 weeks /1 hr x2 daily
-
67%
11%
8
Zekonis, 200313
Opalescence Tooth Whitening Gel
10%
-
At-home
Mild
67%
46%
9
Matis, 200010
Dental Whitening Agent
10%
-
At-home
2 weeks/8 hrs per night
-
64%
55%
10
Matis, 200711
Nite White
16%
-
At-home
Mild
63%
55%
11
Deliperi, 200414
Opalescence Xtra Boost plus Opalescence
PF
10%
38%
In-office &
At-home
3 days (30 min in‑office/
60 min at home
None
56%
-
12
Gurgan, 200915
Oplasecence Xtra Boost
-
38%
In-office
x2/15 min
-
54%
-
13
Matis, 200716
Brite Smile
-
15%
In-office
3x20 min
-
54%
68%
14
Gurgan, 200915
Laser-White 1-Laser Smile
-
37%
In-office
x3/8 min
Mild
54%
-
15
17
Gurgan, 2005
By White-Biowhite
16
Deliperi, 200414
Opalescence Xtra plus Opalescence PF
17
Gurgan, 200915
Remewhite-Remecure
18
Giniger, 200517
ACP containing bleaching gel
19
Browning, 200418
Experimental Product E
Nupro Gold bleaching gel
20 Swift, 199919
21
17
Giniger, 2005
22 Kihn, 200020
-
38%
In-office
x2/20 min
-
53%
-
10%
35%
In-office &
At-home
3 days (30 min in-office/
60 min at home)
None
53%
-
-
35%
In-office
x3/20 min
-
53%
-
16%
-
At-home
2 weeks/3 hrs per day
Mild
51%
-
10%
-
At-home
Mild
50%
0%
10%
-
At-home
-
50%
0%
Nite White Excel 3 Regular
16%
-
At-home
2 weeks/3 hrs per day
-
48%
-
Nupro Gold bleaching gel
10%
-
At-home
2 weeks/at least 4 hrs
per night
-
48%
-
10%
-
At-home
1 week/8 hrs per night
Mild
47%
-
23
Heyman, 199821
Colgate Platinum Professional Overnight
Whitening System
24
Matis, 200716
PolaOffice
-
35%
In-office
x3/12 min
-
47%
69%
One-hour Smile
-
35%
In-office
x3/15 min
-
44%
54%
32%
25 Matis, 200716
22
26 Cibrika, 1999
StarBrite
35%
-
In-office
x2/3x10 min
Mild
44%
27
Matis, 200716
Opalescence
10%
-
At-home
-
44%
-
28
Matis, 200716
Niveous
-
25%
In-office
3x15 min
-
43%
72%
29 Matis, 200716
ArcBrite
-
30%
In-office
3x20 min
-
41%
53%
Zoom!
-
25%
In-office
3x20 min
-
39%
50%
Accelerated
-
40% and
30%
In-office
5x3 min
-
39%
81%
Opalescence Treswhite
-
9%
At-home
10 days /1 hr daily
Mild
38%
-
30 Matis, 2007
16
31
Matis, 200716
32
Li, 200523
24
33
Auschill, 2005
Opalescence PF
10%
-
At-home
1 week/8 hrs per night
-
38%
-
34
Auschill, 200524
Opalescence Xtra Boost
-
38%
In-office
3x15 min
-
38%
-
35
Auschill, 200524
Whitestrips
-
5.3%
At-home
2 weeks/30 min 2x daily
-
38%
-
25
0%
36
Zantner, 2006
Odol-med3 gel
37
de la Pena, 200626
Opalescence Ultradent
38
de la Pena, 200626
39
40
Calatayud, 2009
41
Kugel, 200028
-
-
At-home
None
33%
10%
-
At-home
4 weeks/3 hrs daily
Mild
31%
-
FKD (Kin Lab)
-
3.5%
At-home
4 weeks/3 hrs daily
Mild
31%
-
Calatayud, 200927
Vivastyle Paint on Plus
-
6%
At-home
10 days/10 min 1x daily
-
30%
-
27
Vivastyle Paint on Plus
-
6%
In-office
2 sessions 1 week apart/
5x10 min
-
29%
-
Crest Whitestrips
-
5.3%
At-home
-
28%
-
PAGE 12
OHASA JOURNAL
% HP
Category
Application
Tooth Sensitivity
% Colour
improvement
% Colour relapse
after 4 weeks+
42 Zantner, 200625
Colgate Simply White
-
5.9
At-home
None
28%
3%
43 Abu Alenain,
Opalescence Treswhite
-
9%
At-home
1 week/60 min per day
Mild
28%
-
illumine
-
15%
In-office
x3/20 min
-
25%
18%
Product
Study #
Reference
% CP
MATERIAL REPORT
200929
44 Matis, 200716
22
45 Cibirka, 1999
Nite White Excel
46 Hannig, 200730
Whitestrips
47 Hannig, 200730
48 Abu Alenain,
10%
-
At-home
-
25%
-
-
6%
At-home
2 weeks/2x daily for 30 min
Mild
24%
-
Vivadent Vivastyle
10%
-
At-home
2 weeks/1x daily for 60 min
Mild
24%
-
White-Smile
10%
-
At-home
1 week/2 hrs daily
Mild
21%
-
200929
49 Al Shethri, 200331
Star Brite
-
35%
In-office
2 treatments 1 week apart/
x3 daily for 10 min
Mild
21%
-
50 Bernardon, 201032
Whiteness HP maxx FGM
-
35%
In-office
2 sessions, 3 applications
per session, 15 day interval
-
21%
-
Al Shethri, 200331
-
38%
In-office
x3 daily for 10 min
Mild
20%
-
-
35%
In-office
2 sessions/3 applications of
15 min/15 day interval
-
19%
-
Whiteness Perfect FGM
10%
-
At-home
-
19%
0%
54 Leonard, 200133
Nightguard vital bleaching
10%
-
At-home
Mild
19%
0%
55 Meireless, 200834
Whiteness Perfect
10%
-
At-home
3 weeks/x2 hrs daily
-
14%
9%
34
Whiteness Perfect
51
56 Meireless, 2008
57 dos Santos, 200835 Opalescence PF
16%
-
At-home
-
13%
2%
10%
-
At-home
36%
13%
-
0%
(Control)
-
At-home
1 week/2 hrs daily
-
10%
-
58 Braun, 200636
Voco CP solution
59 Abu, 200929
CleverWhite over- the-counter
-
6%
At-home
1 week/30 min per day
Mild
8%
-
60 Braun,200636
Voco CP solution
10%
-
At-home
1 week/2 hrs daily
-
8%
-
Braun, 200636
Voco CP solution
17%
-
At-home
1 week/2 hrs daily
-
7%
-
61
OBEJECTIVES
The objective of this study was firstly to evaluate
and compare the clinical success rates of different
commercially available tooth whitening products as
reported in selected clinical trials in which the application
was effected according to the instructions of the
manufacturer. Secondly, to thereby enable clinicians
to make an informed decision regarding the choice
of the products which are most clinically effective.
SEARCH STRATEGY
This was accomplished by means of a comprehensive
study of the literature which had reported on relevant
clinical trials between 1998 and 2011, using the
databases: Google Scholar, Science Direct, Medline
and Pubmed respectively, with any combination of the
keywords: tooth whitening, tooth bleaching, clinical
studies, at-home, and in-office. The search was
performed only on published, peer-reviewed articles.
CRITERIA FOR SELECTION OF STUDIES
The papers included were clinical studies in which:
• the whiteners had been applied according to the
manufacturers’ instructions. (The performance
of the product could then be fairly evaluated in
the circumstances under which it was expected
to be applied in practice);
• the brand name of the tooth whitener was clearly
specified;
• the sample size had been recorded.
Reporting the degree of relapse was not a
criterion for inclusion, nor was assessment of
tooth sensitivity, although, in the small number
of cases where it was measured, the latter data
were recorded on a word ordinal scale and in
some cases as a percentage. Figure 1: Representation of colour solid for L*a*b*
colour space from Minolate.
PAGE 13
MATERIAL REPORT
ASSESSING COLOUR CHANGES
Basically, there are two different ways to measure
the effect of tooth whiteners, namely, by means of
matching with a calibrated shade guide or numerically
(colourimeter, chromameter or spectrophotometer).
Some papers provided the shade guide assessments
and some, numerical values, while a few provided both.
These varied methods of reporting complicated the
summary of the research results. Evaluations using
a shade guide are subjective, while the numerical
measurements are objective, providing more reliable
and accurate results.1,2 Most important are the
improved accuracy and the quantification of colours by
measurement in a three dimensional colour space, of
which the L*a*b* (also known as the CIELAB3) is presently
the most popular for the measurement of tooth colour
(Figure 1). In this space L* indicates lightness/darkness
(white/black), a* varies from green (negative side)
to red (positive side), while the b* value varies from
blue (negative side) to yellow (positive side).4 (The
asterisk is used to differentiate the CIELAB system
from previous colour space descriptions.) As with the
shade guide, colour change measurements with the
spectrophotometer can be given in one value, namely
the ∆E*ab (Minolta), where ∆E*ab = [(∆L*)2 + (∆a*)2 +
(∆b*)2]1/2 and ∆L*, ∆a* and ∆b* provide the changes
which occurred in these components.
MATERIALS AND METHODS
Based on the above selection criteria a total of ~49
full-length published articles were included. Most of
these articles reported on two or more studies on
different products and some 45 products had been
tested. All data were recorded in Excel® tables. The
variables for which data were sought are as follows:
Product name; percentage carbamide peroxide (CP)
and hydrogen peroxide (HP); Category (in-office
or at-home bleaching); Application method; Tooth
sensitivity; Percentage colour improvement; Total
colour change obtained immediately after the
treatment process; Percentage colour relapse
after 4 weeks; and ∆E*ab after treatment. Where
the percentage colour improvement or relapse
was not given, it was calculated from the results.
These results were summarised in two tables (1 and
2). Table 1 reflects data according to shade guide
measurements and Table 2 those according to
numerical values (spectrophotometer, chromameter
and colourimeter).
Each study included a number of trials from
which the specific authors had calculated an
average for their sample for colour changes. To
gain an impression of the average efficacy in tooth
whitening achieved by the products under test, the
reported averages were added and an average
of the averages derived. These data were used
to compare the general efficacy of in-office and
at-home treatments.
RESULTS
Table 1 provides a summary of the results reported
(or calculated) in the selected clinical studies
assessing the efficacy of tooth bleaching through
shade guide assessments.8-36 The data were sorted
from the highest to lowest percentage perceived
colour improvement just after bleaching according
to column 9 and the studies were numbered
(column 1). The percentage colour relapse after
a four week or longer period had been assessed
and was recorded in column 10. In a few studies
where both the shade guide and ∆E*ab values
were given in a study, the average percentage
improvement of the two was calculated and
noted (Table 1).
Table 22,4,9-13,15,16,25,31,32,34,37-45 includes the same
columns as for Table 1, except Column 9 now shows
the ∆E*ab values (total colour change) which indicate
the colour improvement as measured numerically
and column 10 the percentage relapse as calculated
from the ∆E*ab values. This table was also sorted
according to highest to lowest ∆E*ab values (column
9) immediately after treatment.
% HP
Category
Application
Tooth Sensitivity
% Colour
improvement
% Colour relapse
after 4 weeks+
1
Zekonis, 200313
Opalescence Tooth Whitening gel
10%
-
At-home
Mild
12.32
46
2
Matis , 200010
Opalescence F
15%
-
At-home
-
11.03
-
Product
Study #
Reference
% CP
Table 2: Shade guide measurements
11
3
Matis, 2007
Opalescence PF
15%
-
At-home
Mild
9.57
57
4
Tsuburu, 200537
Polanight
10%
-
At-home
Mild
9.23
-
5
Mokhlis, 200012
Day White
-
7.50%
At-home
2 weeks/1 hour twice a day
Mild
9.2
-
6
Matis, 200010
Opalescence Dental Whitening Agent
10%
-
At-home
-
8.79
-
7
Matis, 19989
Opalescence Whitening Gel
10%
-
At-home
Mild
8.6
41
8
Bernardon, 201032
Whiteness Perfect FGM
10%
-
At-home
-
8.4
0
9
Zantner, 200625
Colgate Simply White
-
5.90%
At-home
2 weeks/x2 daily for 15 min
None
8.38
3
Chlorite
chlorite
At-home
2 weeks/x2 daily for 10 min
None
8.22
0
-
25%
In-office
3x15 min
-
8.1
72
25
10
Zantner, 2006
Odol-med3 Gel
11
Matis, 200716
Niveous
12
Matis, 200716
Nite White
16%
-
At-home
Mild
8.04
55
13
Matis, 200716
Brite Smile
-
15%
In-office
3x20 min
-
7.9
68
Opalescence
10%
-
At-home
Mild
7.78
-
Opalescence Tooth Whitening Gel PF
20%
-
At-home
2 weeks/1 hr x 2 daily
-
7.6
-
37
14
Tsuburu, 2005
15
Mokhlis, 200012
PAGE 14
OHASA JOURNAL
% HP
Category
Application
Tooth Sensitivity
% Colour
improvement
% Colour relapse
after 4 weeks+
Matis, 200716
ArcBrite
-
30%
In-office
3x20 min
-
6.8
53
17
Bernardon, 201032
-
35%
In-office
2 sessions/3 applications of
15 min/15 day interval
-
6.64
-
18
Matis, 200716
Accelerated
-
40% and
30%
In-office
5x3 min
-
6.6
82
19
Bizhang, 20094
Illumine Home
10%
-
At-home
-
6.57
24
Zoom!
-
25%
In-office
x3/20 min
-
6.4
50
-
35%
In-office
2 sessions, 3 applications
per session, 15 day interval
-
6.17
-
22 Matis, 200716
PolaOffice
-
35%
In-office
x3/12 min
-
5.9
69
23
Ishikawa-Nagal,
20042
Opalescence PF
10%
-
At-home
2 weeks/4 hrs daily
Mild
5.84
-
24
Bizhang, 20094
Illumine Office
Product
Reference
16
Study #
% CP
MATERIAL REPORT
16
20 Matis, 2007
21
Bernardon, 201032
25 Gurgan, 200915
5
26 Gurgan, 20091
15%
-
In-office
45 min/x3 over 3 weeks
-
5.77
20
Laser-White 1--Laser Smile
-
37%
In-office
x3/8 min
Mild
5.69
-
Oplasecence Xtra Boost
-
38%
In-office
x2/15 min
-
5.54
-
27
Matis, 200716
Illumine
-
15%
In-office
x3/20 min
-
5.5
36
28
Gurgan, 200915
By White-Biowhite
-
38%
In-office
x2/20 min
-
5.43
-
16
29 Matis, 2007
One-hour Smile
-
35%
In-office
x3/15 min
-
5.4
54
30 Zekonis, 200313
StarBrite
35%
-
In-office
x2/3x10 min
Mild
5.32
32
31
Grobler, 201038
Nite White ACP
10%
-
At-home
Low
5.29
27
32
Grobler, 201139
Nite White ACP
10%
-
At-home
Low
5.29
31
15
33
Gurgan, 2009
Remewhite-Remecure
-
35%
In-office
x3/20 min
-
5.28
-
34
Benbachir, 200840
Vivastyle Paint On Plus
-
6%
In-office
3 days over 2 weeks/10 min
x5 times per session
-
5.25
-
35
Grobler, 201139
Opalescence PF
10%
-
At-home
Low
5.2
18
36
Ishikawa-Nagal,
20042
Nite White Excel
10%
-
At-home
2 weeks/4 hrs daily
Mild
5.03
-
37
Luo, 200741
Crest White Strips
-
6%
At-home
2 weeks/30 min x2 daily
-
4.95
--
16%
-
At-home
-
4.6
2
-
6.50%
At-home
-
4.55
-
10%
-
At-home
-
4.3
9
-
6%
At-home
-
3.58
16
34
38
Meireless, 2008
Whiteness Perfect
39
Gerlach, 200242
Crest Professional Whitestrips
40
Meireless, 200834
Whiteness Perfect
41
Bizhang, 20094
Whitestrips
43
42
Salem, 2010
Yotuel Special
43
Grobler, 201044
Opalescence PF
44
Karpinia, 200245
45
42
46
-
35%
In-office
20 min x 3 (1 session)
Mild
3.56
53
10%
-
At-home
Low
3.25
8
Professional crest Whitestrips
-
6.50%
At-home
Mild
3.15
-
Gerlach, 2002
Nite White Excel 2-tray system
10%
-
At-home
2 weeks/x2 hr daily
-
2.55
-
Al Shethri, 200331
-
38%
In-office
x3 daily for 10 min
Mild
2.45
-
47
Al Shethri, 200331
Star Brite
-
35%
In-office
x3 daily for 10 min
Mild
2.31
-
48
Karpinia, 200245
Nite White Excel2
49
Luo, 200741
Colgate Great regular Flavour
10%
-
At-home
2 weeks/2 hrs daily
Mild
1.94
-
-
0%
(Control)
At-home
2 weeks/x1 min x 2 daily
-
1.27
-
To page 18 3 rd quarter 2014 • volume 15 no. 3
PAGE 15
ADVERTORIAL
Oral-B symposium
and product launch
An Oral-B symposium and product launch was held
in Cape Town on 24June 2014.
The event was attended by 74 external participants
(3 Dental Deans of Universities, 3 Heads of Periodontal
Departments at Universities, 5 Private Practicing
Periodontist, 14 Heads and Lecturers of Oral Hygiene
departments from Universities, 14 Private Dental
Specialists, and the balance were top influencers,
recommenders and sellers of our existing range
of dental products from private practices, mostly
Practicing Oral Hygienists).
The event commenced with a Luxury Bus tour
of areas of the Winelands of the Western Cape,
with a stop to purchase wines at a farm stall,
then on to Asara Wine Farm for a guided wine
tour, wine and chocolate tasting, a three-course
lunch at the restaurant overlooking a lake and
the beautiful blue mountains of the Western Cape
Winelands, and entertainment by Saxophonist
Debbie Parkinson. The bus departed after lunch
for the modern upmarket 15 on Orange Hotel in
Gardens Cape Town, where KOL’s then registered
for the Symposium and were escorted through to
the Judges Lounge for canapés and drinks. An
hour later the symposium began with the Opening
PAGE 16
Speaker Lorna Carneiro, President of the IADR for
Africa, giving an overview of the dental landscape in
Africa. Next up was Mr Francois Facomprez, followed
by Mr Guy Goffin and Mr Adam Boulding, together
revealing the science, research and development
behind Stabilised Stannous technology of the Oral-B
Pro-Expert Paste.
For the product reveal, Pro Expert samples of
paste and manual brushes, patient leaflets, product
overviews and books of Clinical Trials were magically
brought to the tables under cover of darkness in
glass boxes with blue LED lights.
Some of the KOLs tried the product after the
product reveal and gave us interviews and feedback
on the survey forms.
Product samples were also delivered to the
rooms of the delegates.
Dinner was served and delegates were entertained
during dinner by Sterling EQ, a classy trio of ladies
who played the violin and other instruments. The
evening wrapped up at around 10:00 pm after a
dessert buffet and coffees.
Delegates were so excited to have the new
product and are looking forward to recommending
it to their patients! ●
OHASA JOURNAL
ADVERTORIAL
PAGE 17
MATERIAL REPORT
Table 3: Descriptive statistics of colour improvement (shade guide assessment)
immediately after ‘At-home’ and ‘In-office’ treatment.
Table 5: Descriptive statistics of colour improvement (∆E*ab-scale) immediately
after treatment for ‘At-home’ and ‘in-office’ treatment.
Category
Values
Category
At-home
In-office
At-home
In-office
Number of studies
40
19
Values
Number of studies
29
20
Number of studies indicating % colour improvement
19
9
Number of studies indicating colour improvement
13
11
Average of average of % colour improvements
39.3%
38.8%
Average of average ∆E*ab after treatments
6 .36
5.60
Std Dev of % colour improvement
22.4%
12.7%
Std Dev of ∆E*ab after treatment
2.80
1.48
Min % colour improvement
6.9%
19.1%
Min ∆E*ab after treatment
1.27
2.31
Max % colour improvement
88.1%
54.4%
Max ∆E*ab after treatment
12.32
8.1
Table 4: Descriptive statistics of colour relapse (shade guide assessment) after
four weeks for ‘At-home’ and ‘In-office’ treatment.
Table 6: Descriptive statistics of colour relapse (∆E*ab-scale) after 4 weeks for
‘At-home’ and ‘in-office’ treatment.
Category
Values
Category
At-home
In-office
Number of studies
40
19
Number of studies indicating % colour relapse after
4 weeks
19
9
Average of average % colour relapses after 4 weeks
13.1%
55.2%
Std Dev of % colour relapse after 4 weeks
17.0%
20.2%
Min % colour relapse after 4 weeks
0.0%
18.0%
Max % colour relapse after 4 weeks
55.0%
81.0%
DISCUSSION
The values of shade guides cannot be directly
compared with those numerically measured. A
shade guide provides only a combination value
for the three colour components (e.g. L*, a* & b*).
The distances between ‘before’ and ‘after’ colour
measurements on each treated tooth differ when
estimated with shade guides or taken numerically
and these values could not be directly compared.
Hence these data are assembled separately in
two tables (Tables 1 and 2). As ∆E* is a difference
between two values the percentage change could
only be determined in the relapse phase when
there are indeed two such ∆E*values. In relapse
calculations where both methods had been used
to determine the changes (a few cases only), the
percentage relapses determined by shade guide
and by numerical methods were first separately
calculated and the average of the two then noted.
The percentage improvement (Table 2) could
not be calculated for studies where only ∆E*ab
values were given as ∆E*ab gives the difference
between the tooth colour at base-line and that
after treatment.
For the shade guide values, (Table 1), the top
ten achievers were at-home products and likewise
according to ∆E*ab (Table 2) the top ten achievers
were also at-home products. The highest values
PAGE 18
Values
Number of studies
Number of studies indicating % colour relapse
At-home
In-office
29
20
13
11
Average of average of % colour relapses
26.02%
53.60%
Std Dev of % colour relapses
18.98%
18.65%
Min % colour relapse
2.17%
20.45%
Max % colour relapse
57.37%
81.82%
reported (Tables 1 and 2) were with a 10% or 15%
carbamide peroxide treatment over a relatively
long treatment period (two weeks 6/8 hours per
night). In general, the treatment periods for top
achievers (Table 1 and 2) were all scheduled
over relatively long time-periods which, as seen
in Table 1, varied from two hours/day for two
weeks, to six hours/night for two weeks and to
eight hours/night for two weeks. For Table 2 the
first eight study achievers were for eight hours/
night for two weeks (with the exception of study
# 5 which was for one hour twice daily for two
weeks. The shortest treatment period (Table 1)
within the ten top achievers (studies # 6 and 7)
was one hour/twice-a-day for 14 days but this
was a trial using 7.5% HP (~25% CP) and 20% CP
in comparison with the more general treatment
which uses 10% carbamide peroxide. In Table 2
the shortest treatment period within the top ten
at-home achievers was twice a day for 15 min
(study # 9) but as for Table 1, this study relied
on a high peroxide concentration (5.9% HP). The
other treatment with a short application time
was with chlorite (study # 10). Therefore, it can
be deduced that to obtain the same success rate
as with 10% carbamide peroxide it seems that a
shorter treatment period might be indicated but
using a higher peroxide concentration.
In general, it can be seen that in-office treatments
(even with high peroxide concentrations) were
far less successful (Table 1 and 2) than at-home
treatments with ~10% carbamide peroxide. On the
ranking list, in-office applications came in well below
the highest achievers at study # 11 (Table 1) and
study # 11 (Table 2). Why then is the high peroxide
concentration treatment unexpectedly found to be
less successful? The reason may be found in the
length of the application period. In-office applications
(Table 1, studies # 11–17; Table 2, study # 11 and others)
were performed over a short period in comparison
with the dentist/oral hygienist supervised at-home
treatment procedures. The in-office treatment
periods were normally short bursts, for example
three x 15 minutes/session, three x 20 minutes/
session, etc. (Tables 1 and 2). However, there were
a few examples (Table 1, studies # 40 and 49–52)
where the in-office sessions were repeated over
days but only two of these studies (Table 1, studies
# 11 and 16) were further extended to an at-home
treatment. However, to allow subjects to personally
handle such a high peroxide concentration is very
risky and should not be recommended.
There are probably two main reasons for the short
application period of in-office treatments: the first
reason is financial, in that the longer the in-chair
session, the more expensive the treatment becomes;
OHASA JOURNAL
MATERIAL REPORT
the second is that high peroxide application has a
possible hazardous effect (related to the oxidising
strength) on the soft tissue of the oral cavity.
From Table 3 (shade guide) it can be deduced that
overall, both at-home (39.3%) and in-office (38.8%)
treatments showed more or less the same initial
colour improvement. However, a major difference
could be seen in the relapse after a four week or
longer period (at-home 13.1%; in-office 55.2%: Table
4). From the ∆E*ab (Table 5) numerical values, the
initial colour improvements for in-office and at-home
were also about the same (5.60 against 6.36).
When the relapse was calculated from ∆E*ab
values (Table 6), in-office treatment gave a value
of 53.6%, similar to that found with the shade
guide assessments (55.2%) (Table 4). However,
the at-home relapse was 26.02% (Table 6) which
is about double that when calculated from shade
guide measurements (13.1%) (Table 4).
Other findings reported on the combination of
dentally supervised at-home treatments: Leonard
et al.33 revealed that the whitening effected by 10%
carbamide peroxide (Nite White Classic; eight to
ten hours per day for 14 days) reported five tabs
lighter teeth, an effect which lasted over a 3.8 year
period. In two different articles46,47 reporting on
10% carbamide peroxide which was applied for
two hours per day for three weeks, no relapse was
reported after one year. No comparable results
were reported for any in-office treatment. Only
two studies reported results for a combination of
in-office and at-home treatments (studies # 11 and
16). Study # 11 showed a colour improvement of 56%
(Table 1) and study # 16 also showed a high colour
improvement of 53%. These results may indicate
that a combination of the in-office and at-home
treatments could produce the most positive results.
Unfortunately no assessment on any colour relapse
was reported in these two studies.
The most commonly tested product was
Opalescence PF, a material evaluated in 11 studies.
The average of the average colour improvements
as reflected on the shade guide scale, was 54%
compared with 36% for all the other products.
With regard to numerical measurements, the five
studies using that method of assessment recorded
6.9 (∆E*) for the average of the average colour
improvements for Opalescence PF and an average
of 5.95 (∆E*) for all the other products. These
values can be considered high spectrophotometer
readings, possibly highlighting the accuracy of
the technology in comparison with shade guide
measurements.
The mean relapse measured numerically after
four weeks was 27.8% for Opalescence (n=3) which
is considerably lower than the mean of 40.2%
recorded for all the other products (n=21). Not all
studies recorded relapse values (Opalescence 3
of 5; other products: 21 of 44) and these findings
should therefore be regarded only as an indication
of relapse potentials.
The next question which may be posed is which
of the in-office or dentist/oral hygienist supervised
at-home treatments would give the lowest tooth
sensitivity scores? Not all studies reported on this,
but the data recorded in Tables 1 and 2 reveals no
significant differences in tooth sensitivities between
the routines, and overall these effects were low
– with an exception of the two top achievers in
bleaching (Table 1), where a higher sensitivity was
in fact noted (62% and 45%). However, it should
also be observed that in some instances during
treatments, the sensitivity might be so high that
the individual prefers to terminate the application.
Some of the manufacturers (studies # 1 and 4) added
chemicals (potassium nitrate and fluoride) to their
bleaching products in an attempt to counteract
sensitivity. However, the clinical data (Table) indicates
uncertainty on the possible positive effects of those
materials, or on amorphous calcium phosphate and
no general conclusion could be reached.11,16,17,38,48,49
Furthermore, from the published results (Tables 1 and
2), it can also be concluded that in general, where
tooth sensitivity was noted during the whitening
process, it disappeared spontaneously after the
treatment period.
CONCLUSION
This analysis of the data shows that the dentist/
oral hygienist-supervised at-home-bleaching and
the in-office treatment gave nearly the same initial
tooth whitening improvement. However, the relapse
after a four week or longer period was found to
be much higher for the in-office treatment at a
relapse of ~55% on average, while the at-home
treatment showed a much lower relapse over
the same period of about 13% to 26%. Overall,
it can be concluded that the treatment of choice
should be a dentist/oral hygienist-supervised athome bleaching process using a product which in
general contains about 10% carbamide peroxide
applied over ~14 days and for ~8 hours per night
on average. Tooth sensitivity should not be seen
as a consistent problem although some subjects
might choose to discontinue treatment as a result
of experiencing the problem.
Acknowledgement: This study was financially
supported by the Dentistry Development Fund of
the South African Dental Association and by the
University of the Western Cape.
Disclaimer: The South African Dental Association
does not necessarily support the findings or
conclusions made in this article.
Declaration: No conflict of interest declared. ●
References
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GM, Lovadino JR. In vitro evaluation of the effectiveness
of bleaching agents activated by different light sources. J
Prosthodont 2009; 18(3):249–54.
2.Ishikawa-Nagai S, Terui T, Ishibashi K, Weber HP,
Ferguson M. Comparison of effectiveness of two 10%
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Dent 2004; 16:368–76.
3.Minolta, Precise colour communication, Minolta, Co., Ltd.,
Osaka, Japan, 1994; 9242-4830-92 IHCAJ.
4. Bizhang M, Chun YH, Damerau K, Singh P, Raab WH,
Zimmer S. Comparative clinical study of the effectiveness
of three different bleaching methods. Operative Dent
2009; 34–6:635–41.
5. Joiner A. The bleaching of teeth: A review of the
literature. J of Dent 2006; 34:412–9.
6. Frysh H, Bowles WH, Baker F, Rivera-Hidalgo F, Guillen
G. Effect of pH on hydrogen peroxide bleaching agents. J
Esthet Restor Dent 1995; 7:130–3.
7.American Dental Association. Council on Scientific Affairs.
http:// www.ada.org/1902.aspx).
8. Browning WD, Chan DC, Myers ML, Brackett WW,
Brackett MG, Pashley DH. Comparison of traditional
and low sensitivity whiteners. Operative Dent 2008;
33(4):379–85.
9.Matis BA, Cochran MA, Eckert G, Carlson TJ. The efficacy
and safety of a 10% carbamide peroxide bleaching gel.
1998; 29:555–63.
10.Matis BA, Mousa HN, Cochran MA, Eckert GJ.
Clinical evaluation of bleaching agents of different
concentrations. Quintessence Int 2000; 31:303–10.
PAGE 19
MATERIAL REPORT
11.Matis BA, Cochran MA, Eckert GJ, Matis JI. In vivo study of
two carbamide peroxide gels with different desensitizing
agents. Operative Dent 2007; 32(6):549–55.
12.Mokhlis GR, Matis BA, Cochran MA, Eckert GJ. A clinical
evaluation of carbamide peroxide and hydrogen peroxide
whitening agents during daytime use. J Am Dent Assoc
2000; 131: 1269–77.
13. Zekonis R, Matis BA, Cochran MA, Al Shetri SE, Eckert GJ,
Carlson TJ. Clinical evaluation of in-office and at-home
bleaching treatments. Operative Dent 2003; 28(2):114–21.
14.Deliperi S, Bardwell DN, Papathanasiou A. Clinical
evaluation of a combined in-office and take-home
bleaching system. J Am Dent Assoc 2004;135:628–34
15. Gurgan S, Cakir FY, Yazici E. Different light-activated
in-office bleaching systems: A clinical evaluation. Lasers
Med Sci 2009; DOI 10.1007/s10103-009-0688-x.
16.Matis BA, Cochran MA, Franco M, Al-Ammar W, Eckert
GJ, Stropes M. Eight in-office tooth whitening systems
evaluated in vivo: a pilot Operative Dent 2007;
32–4:322–7.
17. Giniger M, MacDonald J, Ziemba S, Felix H. The clinical
performance of professionally dispensed bleaching gel
with added amorphous calcium phosphate. J Am Dent
Assoc 2005; 136:383–92.
18. Browning WD, Chan DCN, Frazier KB, Callan RS, Blalock
JS. Safety and efficacy of a nightguard bleaching agent
containing sodium fluoride and potassium nitrate.
Quintessence Int 2004; 35:693–8.
19. Swift EJ, May KN, Wilder AD, Heymann HO, Bayne SC.
Two-year clinical evaluation of tooth whitening using
an at-home bleaching system. J of Esthet Dent 1999;
11(1):36–42.
20.Kihn PW, Barnes DM, Romberg E, Peterson K. A clinical
evaluation of 10 percent vs. 15 percent carbamide
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21. Heymann HO, Swift EJ Jr, Bayne SC, May KN Jr, Wilder
AD Jr, Mann GB, Peterson CA. Clinical evaluation of two
carbamide peroxide tooth-whitening agents. Compend
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22.Cibirka RM, Myers M, Downey MC, Nelson SK, Browning
WD, Hawkins IK, Dickinson GL. Clinical study of tooth
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J. Evaluation of clinical efficacy and safety of Treswhite
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techprogramforcd/A64584.htm.
24.Auschill TM, Hellwig E, Schmidale S, Sculean A, Arweiler
NB. Efficacy, side-effects and patients’ acceptance of
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Operative Dent 2005; 30(2):156–63.
25.Zantner C, Derdilopoulou F, Martus P, Kielbassa AM.
Randomized clinical trial on the efficacy of two overthe-counter whitening systems. Quintessence Int 2006;
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26.De la Pena VA, Cabrita B. Comparison of the clinical
efficacy and safety of carbamide peroxide and hydrogen
peroxide in at-home bleaching gels. Quintesssence Int.
2006; 37:551–6.
27. Kugel G, Kastali S. Tooth-whitening efficacy and safety:
A randomized and controlled clinical trial. Compendium /
Supplement No 29. 2000; 21:S16–S21.
28.Abu Alenain DA, Amin HE, Al-Zahrani NA, Harbi NA,
Al-qadi SF, Al-qarni AA. Bleaching efficiency and side
effects of three home bleaching systems. JKAU:Med Sci.
2009;16(3):43-58. DOi:10.4197/Med.16–4.
29.Hannig C, Lindner D, Attin T. Efficacy and tolerability of
two home bleaching systems having different peroxide
delivery. Clin Oral invest 2007; 11:321–9.
30.Bernardon JK, Sartori N, Ballarin A, Perdigao J, Lopes
G, Baratieri LN. Clinical performance of vital bleaching
techniques. Oper Dent 2010; Jan-Feb: 35(1):3–10.
31.Leonard RH, Bentley C, Eagle JC, Garland GE, Knight MC,
Phil- lips C. Nightguard vital bleaching: A long-term study
on efficacy, shade retention, side effects and patients’
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32.Meireless SS, Heckmann SS, Leida FL, dos Santos IS, Della
Bona A, Demarco FF. Efficacy and safety of 10% and 16%
carbamide peroxide tooth-whitening gels: A randomized
clinical trial. Operative Dentistry 2008; 33(6): 606–12.
33.Dos Santos Medeiros MC, de Lima KC. Effectiveness of
night-guard vital bleaching with 10% carbamide peroxide:
– A clinical study. J of the Can Dent Assoc 2008; 74:
163–163e.
34.Braun A, Jepsen S, Krause F. Spectrophotometric and
visual evaluation of vital tooth bleaching employing
different carbamide peroxide concentrations. Dental
Materials 2007; 23:165–9.
35.Tsuburu S, Yamaguchi R. Clinical evaluation of a
new bleaching product “Polanight” in a Japanese
population. Odontology 2005; 93:52–5.
36.Grobler SR, Majeed A, Hayward R, Rossouw RJ,
Moola MH, Kotze TJvW. A clinical study of the
effectiveness of two different 10% carbamide peroxide
bleaching products: A 6-month follow- up. Int J of
Dent. 2011 (online); Article ID 167525, 6 pages, doi
10.1155/2011/167525.
37. Benbachir N, Ardu S, Krejci I. Spectrophotometric
evaluation of the accuracy of a new in-office bleaching
technique. Quintessence Int 2008; 39:299–306.
38.Luo W, Westland S, Brunton P, Ellwood R, Pretty IA,
Mohan N. Comparison of the ability of different colour
indices to assess changes in tooth whiteness. J of Dent
2007; 35:109–16.
39.Gerlach RW, Zhou X. Comparative clinical efficacy of
two professional bleaching systems. Compendium/
Special issue 2002; 23(1A):35–41.
40.Salem Y & Osman Yi. The effect of in-office vital
bleaching and patients’ perception of the shade
change. SADJ 2011; 66(2):70–6.
41. Grobler SR, Hayward R, Wiese S, Moola MH, Kotze
TJvW. Spectrophotometric assessment of the
effectiveness of Opalescence PF 10%: A 14-month
clinical study. J of Dent 2010; 38:113–7.
42.Karpinia KA, Magnusson I, Sagel PA, Zhou X, Gerlach
RW. Vital bleaching with two at-home professional
systems. Amer J of Dent 2002; 15(Special issue):13A–
18A.
43.Meireless SS, Dos Santos IS, Della Bona A, Demarco
FF. A double blind randomized controlled clinical trial
of 10 percent versus 16 percent carbamide peroxide
tooth-bleaching agents. J Am Dent Assoc 2009; 140
(9):1109–17.
44.Meireless SS, Heckmann SS, Santos IS, Della Bona A,
Demarco FF. A double blind randomized clinical trial of
at-home tooth bleaching using two carbamide peroxide
concentrations: two year follow-up. J of Dent 2010;
38:956–63.
45.Tam LE. Clinical trial of three 10% carbamide peroxide
bleaching products. J Can Dent Assoc 1999; 65:201–5.
46.Chen HP, Chang CH, Liu JK, Chuang SF, Yang JY. Effect
of fluoride containing bleaching agents on enamel
surface properties. J Dent 2008; 36(7):18–25.
OHASA Logo Competition
winner announced
The winner of the OHASA Logo Competition run by the Professional and Public
Relations Committee is Emma Coulter from the Western Cape Branch. The Competition
was very tight with a variety of entries but in the end it was Emma’s that won. ●
PAGE 20
OHASA JOURNAL
CLINICAL Review
Infective endocarditis and
antibiotic prophylaxis
an update for South African dental
practitioners
Pieter van der Bijl jr, Pieter van der Bijl
Since the 1950s, the practice of prescribing antibiotics
for the prophylaxis of endocarditis prior to invasive
procedures has been widely accepted by the dental
profession. The rationale for this is to reduce or
eliminate the bacteraemia that may result from
such procedures. The paradigm of this model is the
prevention of bacterial endocarditis – a rare, but
life-threatening disease. In developed countries,
empiric guidelines for antibiotic prophylaxis for
endocarditis, based primarily on pathophysiology
and expert opinion, are put forward by committees
of the American Heart Association (AHA), European
Society of Cardiology (ESC) and British Society
for Antimicrobial Chemotherapy (BSAC). These
commonly-used guidelines, which are not in the
first instance based on clinical evidence, have
been periodically updated and we reviewed the
latest recommendations of the AHA and BSAC in
the SADJ in 2008.1 In that paper we referred to
the lack of scientific evidence for linking infective
endocarditis to dental procedures and the uncertainty
regarding the effectiveness of prophylaxis – both
these factors challenging the entire concept of
antibiotic prophylaxis in dentistry.1 Subsequent to
our review of 2008, important communications
have appeared in the literature. In 2008, an
updated version of the Cochrane review of 2004
on antibiotics for the prophylaxis of bacterial
endocarditis in dentistry was published, as well
as a guideline by the United Kingdom’s National
Institute for Health and Clinical Excellence (NICE).2,3
Furthermore, a survey was conducted among
dental practitioners in South Africa to determine
their knowledge of the guidelines of the AHA and
NICE.4 Although this survey had a low response
rate, it was clear that knowledge in the profession
of the use of infective endocarditis prophylaxis and
compliance with existing guidelines was generally
poor. In the current update we attempt to clarify
some of the prevailing confusion among South
African dental professionals regarding when and
for whom antibiotic prophylaxis is indicated.
GUIDELINES
The traditionally accepted guidelines of the BSAC
and the AHA as modified in 2006 and 2007
respectively, are recommended for use by South
African dental practitioners.5,6 Their advantages and
disadvantages, as well as the proposed antibiotic
regimens of both these sets of guidelines have been
discussed in some detail in our previous review.1 As
mentioned in that review, the main characteristics
of both guidelines are a simplification, in terms
of complexity and broadness, of the published
pre-2006 and pre-2007 guidelines, resulting
in a reduction in the indications for antibiotic
prophylaxis. Only a few categories of high-risk
patients, who require antibiotic prophylaxis prior to
dental procedures, are identified in the 2006 and
2007 guidelines. The dental procedures requiring
prophylaxis are those involving manipulation of
gingival tissue or the periapical region of teeth,
or perforation of the oral mucosa. Of significance
is that the updated Cochrane review of 2008 has
not provided conclusive evidence about whether
penicillin prophylaxis is effective against bacterial
endocarditis in people at risk who are about to
undergo an invasive dental procedure.2 Evidence
from that review is insufficient to support previously
published guidelines, such as those of the BSAC and
AHA. Additionally, it is of interest that the overall
incidence of infective endocarditis has remained
stable from 1950 to 2000, i.e. approximately
3.6–7.0 cases per 100 000 patient-years.7 This
incidence has remained unchanged over half a
century despite improvements in cardiac imaging
techniques, which may have enhanced the detection
of endocarditis.
In March 2008, the National Institute for Health
and Clinical Excellence (NICE) in the United Kingdom
published a controversial new guideline, which was
a radical departure in that it recommends complete
abolition of antibiotic prophylaxis for patients at
risk of infective endocarditis undergoing dental
and a wide range of other invasive procedures.3
The rationale of the NICE guidelines is the absence
of a consistent association between interventional
procedures, dental or otherwise, and the development
of endocarditis as well as the unproven effectiveness,
the potential mortality of anaphylaxis and increased
expense. NICE guidelines recommend that antibiotic
cover should be offered to patients only if the
procedure is at a site where there is already a
suspected infection. Furthermore, the NICE guidelines
do not recommend the use of chlorhexidine
mouthrinses prior to dental procedures. Although the
guidelines do recognise certain cardiac conditions
which present a high risk for developing infective
endocarditis, these are mainly listed to emphasise
the need for good oral hygiene and awareness of
infective endocarditis. Although the AHA and ESC
for Cardiology modified their guidelines more or
less simultaneously, both of these authoritative
bodies still recommended administering antibiotic
prophylaxis in certain high-risk groups.6,8 PAGE 21
CLINICAL Review
CONTROVERSIES
Theoretically, antibiotic prophylaxis in patients
with cardiac risk factors should decrease the
incidence of infective endocarditis; however, to
date this principle has not been underpinned
by sound scientific evidence. Several factors
contribute to this failure of what appears to be a
linear-logic approach. While it has been shown that
invasive procedures, e.g. dental extractions, cause
bacteraemias, other common daily activities, e.g.
toothbrusing, interdental flossing and mastication,
do so as well. The transient bacteraemias which
may be caused by surgical dental procedures are
several orders of magnitude higher than those
resulting from common daily activities.9 The latter,
however, may cumulatively be several million times
higher than those resulting from single invasive
procedures (so-called cumulative bacteraemia).9
Additionally, it has been shown that only a small
proportion, if any, of cases of infective endocarditis
were causally linked to dental procedures.10,11
Conflicting evidence has been reported regarding
the reduction or prevention of bacteraemias by
means of antibiotic prophylaxis.12
It is contentious whether antibiotic prophylaxis
is cost-effective for at-risk patients.12 Strains of
antibiotic-resistant organisms may emerge and
antibiotic-related side-effects do occur, but these
phenomena are both rare following high, singledose antibiotic administration on an infrequent
basis, such as during prophylaxis. While minor
unwanted effects may occur during prophylactic
antibiotic usage, no cases of anaphylaxis have
been reported to the AHA during the 50 years that
they have recommended using a penicillin for the
prophylaxis of infective endocarditis.13 The AHA
believes that it is safe to administer a single dose
of a broad-spectrum penicillin, e.g. amoxicillin or
ampicillin, to persons who do not have a history of
hypersensitivity to a penicillin, such as anaphylaxis,
urticaria or angioedema. While the NICE committee
quotes the potential of fatal anaphylaxis to penicillins
PAGE 22
as one of the reasons for their stance, reports of
oral amoxicillin causing this condition have never
been reported in the world literature.14
DISCUSSION
Publication of the NICE guidelines in the UK in 2008
has challenged the standard of care for prevention
of infective endocarditis. That these guidelines
have been accepted by many practitioners in the
UK is evidenced by a 78.6% reduction in antibiotic
prophylaxis.15 NICE is unique in recommending
no antibiotic prophylaxis for cardiac patients
undergoing dental or non-dental procedures,
except for manipulations at an infected site.14 While
most national or international guidelines from the
USA, Europe and Australia have pared down their
indications, they still recommend prophylaxis for
certain dental procedures in high-risk cardiac
patients (Table 1).14 Even though the NICE committee
correctly stated that, in the absence of prospective,
randomised trials, the clinical effectiveness of
antibiotic prophylaxis remains unproven, some
clinical and animal studies reviewed by the AHA and
BSAC have suggested that there are benefits.5,6,14 It
has been estimated that a randomised, placebocontrolled trial to demonstrate the effectiveness
of antibiotic prophylaxis for infective endocarditis
would require the participation of 60,000 individuals,
making such a study unlikely to transpire.16
THE SOUTH AFRICAN CONTEXT
A variety of arguments have been advanced that
the guidelines emanating from the USA and Europe
cannot be extrapolated to the local situation,
namely: (i) the high prevalence of rheumatic heart
disease predisposes to IE; (ii) HIV might predispose
to infective endocarditis; and (iii) the local microbiological profile of infective endocarditis differs.17
The theory of cumulative bacteraemia takes
rheumatic heart disease into account. However, there
is no evidence that it poses a significantly higher
risk for development of infective endocarditis than
other, accepted, risk factors or that the severity and
consequences of the disease are far worse than
those seen with other risk factors. Therefore, it should
not be seen as an exception. The evidence that
HIV predisposes to infective endocarditis is scant.
Although the data are scarce, the most common
pathogenic organisms in a South African setting are
oral streptococci, and the antibiotic choice should
therefore be no different to that of the international
guidelines.18 This is an issue unrelated to the
threshold/indications for prophylaxis.
The opinion of the authors, as evidenced in our
previous review, is that in the absence of any data
to the contrary, the guidelines as set forth by the
AHA, ESC and BSAC are appropriate and apply also
in the South African context. It is clear that the risk of
developing infective endocarditis following dental
TABLE 1: Cardiac conditions requiring antibiotic prophylaxis for high-risk dental procedures included in international
guidelines, but excluded by NICE
•Replacement valves or prosthetic material used for cardiac valve repair
• Previous episodes of infective endocarditis
•Congenital heart disease
•Unrepaired cyanotic congenital heart disease including palliative shunts and conduits
•Completely repaired using prosthetic material or device during the first 6 months after procedure
(surgical or percutaneous)
•Repaired with residual defect at the site or adjacent to the site of a prosthetic patch or device
•Cardiac transplantation with valvular regurgitation due to a structurally abnormal valve*
*Included in the AHA guideline, but excluded in the ESC guideline
OHASA JOURNAL
CLINICAL Review
procedures is low. There is little scientific evidence
that prophylactic administration of antibiotics prior to
dental procedures would lower the risk of developing
the disease and it should be kept in mind that the
above guidelines are not infallible. However, in the
absence of hard evidence on prophylactic efficacy and
being mindful of the potential legal consequences,
we recommend adherence to the AHA, ESC and
BSAC guidelines in high-risk cardiac patients (Table 1)
who are undergoing manipulation of dento-gingival
tissue, procedures involving the periapical region of
teeth and endodontics. Of further importance is that
dental treatment plans be drawn up and executed in
such a manner that patients are not unnecessarily
exposed to prophylactic antibiotics – this might
include concurrent execution of procedures. Where
that is not possible, the AHA and BSAC respectively
recommended intervals of at least 10 and 14 days.
Otherwise, amoxicillin may be alternated with
clindamycin and, in patients being treated with these
two antibiotics for other infections, azithromycin or
clarithromycin may be substituted.
Patients should be well-informed by their dental
practitioner, with the option of obtaining written
consent for the administration/omission of prophylaxis
being very reasonable. They should be advised to
report any adverse effects following prophylaxis to
their practitioner via a direct line of communication.
7. Karchmer AW. Infective endocarditis. In: Libby P,
Bonow RO, Mann DL, Zipes DP, eds. Braunwald’s Heart
Disease: A Textbook of Cardiovascular Medicine. 8th ed.
Philadelphia, PA: Saunders Elsevier, 2007:1713–38.
8. Habib G, Hoen B, Tornos P, et al. Guidelines on the
prevention, diagnosis, and treatment of infective
endocarditis (new version 2009): The Task Force on
the Prevention, Diagnosis, and Treatment of Infective
Endocarditis of the European Society of Cardiology (ESC).
Eur Heart J 2009; 30:2369–413.
9.Roberts GJ. Dentists are innocent! “Everyday”
bacteraemia is the real culprit: a review and assessment
of the evidence that dental surgical procedures are a
principal cause of bacterial endocarditis in children.
Pediatr Cardiol 1999; 20:317–25.
10.Van der Meer JT, Thompson J, Valkenburg HA, Michel
MF. Epidemiology of bacterial endocarditis in The
Netherlands. II. Antecedent procedures and use of
prophylaxis. Arch Intern Med 1992; 152:1869–73.
11. Strom BL, Abrutyn E, Berlin JA, et al. Dental and cardiac
risk factors for infective endocarditis. A population-based,
case-control study. Ann Intern Med 1998; 129:761-9.
12. Gopalakrishnan PP, Sanjay K. Shukla SK, Tak T. Infective
Endocarditis: Rationale for Revised Guidelines for Antibiotic
Prophylaxis. Clinical Medicine & Research 1999; 7:63–8.
13. Friedlander AH. Antibiotic prophylaxis for dentistry is not
associated with fatal anaphylaxis. Clinical Medicine &
Research 2010; 8:79.
14.Chambers JB, Shanson D, Hall R, Pepper J, Venn G,
McGurk M. Antibiotic prophylaxis: the rest of the world
and NICE. J R Soc Med 2011; 104:138–40.
15.Thornhill MH, Dayer MJ, Forde JM, et al. Impact of the
NICE guideline recommending cessation of antibiotic
prophylaxis for prevention of infective endocarditis:
before and after study. BMJ 2011; 342:92.
16. Parrish A, Maharaj B. Prevention of infective endocarditis
in developing countries – justifiable caution? SAMJ 2012;
102:652–4.
17. Koegelenberg CF, Doubell AF, Orth H, Reuter H. Infective
endocarditis in the Western Cape Province of South Africa:
a three- year prospective study. QJM. 2003; 96(3):217–25.
18. Koegelenberg CFN, Doubell AF, Orth H, et al.
Infective endocarditis: improving the diagnostic yield.
Cardiovascular Journal of South Africa 2004;15:14–20
Declaration: No conflict of interest declared. ●
References
1.Van der Bijl P, Van der Bijl P. Antibiotic prophylaxis for
infective endocarditis: new AHA and BSAC guidelines
and implications for practice in South Africa. SADJ 2008;
63:240-4.
2.Oliver R, Roberts GJ, Hooper L, Worthington HV.
Antibiotics for the prophylaxis of bacterial endocarditis
in dentistry. Cochrane Database of Systematic Reviews
2008; Issue 4, Art. No. CD003813.
3. Wray D, Ruiz F, Richey R, Stokes T. Guideline
Development Group. Prophylaxis against infective
endocarditis for dental procedures – summary of NICE
guideline. Br Dent J 2008; 204:555-7.
4.Owen CP, Huang WH. Antibiotic prophylaxis for dental
procedures: is it necessary? SADJ 2012; 67:413-9.
5. Gould FK, Elliott TSJ, Foweraker J, et al. Guidelines
for the prevention of endocarditis: report of the
Working Party of the British Society for Antimicrobial
Chemotherapy. J Antimicrob Chemother 2006;
57:1035–42.
6. Wilson W, Taubert KA, Gewitz M, et al. Prevention of
infective endocarditis: Guidelines from the American
Heart Association. JADA 2007; 138:739–60.
PAGE 23
Ethics
Periodontal treatment
and allegations of neglect
Prof. Sue Naidoo
A long-standing patient attended a practice and
said that she plans to report her practitioner
to the Health Professions Council for failing to
adequately treat her periodontal condition. At
her initial examination some ten years earlier,
she presented with advanced periodontal disease
and radiographs clearly showed the extent of the
severe bone loss throughout the patient’s mouth.
The practitioner did a thorough examination and
charting, and discussed at length both the shortand long-term treatment plans. The patient was
fully informed of the situation, given appropriate
advice and consented to undergo extensive
periodontal therapy. It was recommended that
she attend every three months for examinations,
scaling and oral hygiene instruction. She agreed to
the treatment plan and her progress was carefully
monitored and her periodontal status gradually
improved over the years.
Although the practitioner saw the patient regularly
and carried out such care and treatment as was
deemed necessary, the periodontal condition began
to deteriorate resulting in mobility of a number of
anterior teeth and the patient was then referred to a
periodontist for a second opinion. During the visit to
the periodontist, a perhaps inappropriate comment
was made to the effect that something could have
been done to save a number of these teeth had the
appropriate advanced treatment been instituted at
an earlier stage. The patient was naturally upset by
this statement and decided to make a complaint
against her dentist and oral hygienist.
PAGE 24
COMMENTARY
People are living longer and retaining their teeth
into later life. The percentage of individuals with
moderate to severe periodontitis, in which the
destruction of supporting tissue can cause loosening
and even loss of teeth, increases with age. The most
common form of adult periodontitis is described
as ‘general and moderately progressing’. It is
characterised by a gradual loss of attachment of
the periodontal ligament to both the gingiva and
bone, progressing to actual loss of the supporting
bone. It is most often accompanied by gingivitis.1
The severity of periodontal disease is determined
through a series of measurements, including the
extent of gingival inflammation and bleeding, the
probing depth of the pocket to the point of resistance,
clinical evidence of attachment loss of the periodontal
ligament and the loss of adjacent alveolar bone as
measured by radiographs.1 Severity is also determined
by the rate of disease progression over time and the
response of the tissues to treatment. The prevalence
and severity of periodontal disease increases, but
does not accelerate with age.2 The current view is
that the disease process may not be continuous but
rather progresses in random bursts in which short
periods of breakdown of periodontal ligament and
bone alternate with periods of quiescence. These
episodes occur randomly over time and at random
sites in the mouth. Part of the difficulty in determining
the pattern of progression reflects variation in the
sensitivity of the instruments used to measure the
loss of soft tissue and bone.3
While there is no doubt that the existence of
bacteria plays an important role in the aetiology of
periodontal disease, studies suggest that it is the
combination of the presence of these bacteria and
the host response of the individual that determines the
development and rate of progression of periodontal
disease.4 Thus the main risk factors of the disease are
often outside the control of the clinician. In addition,
familial history, genetic susceptibility, systemic
disease and smoking are known to play a part in the
aetiology and rate of progression of the disease.5
Again, the clinician cannot be held responsible for
the existence of these factors and patients need to
understand that their periodontal disease is also their
problem. However, it is an ethical responsibility of
the clinician to educate the patients, to make them
aware of the condition and assist them to reduce
the impact, giving advice, guiding, monitoring and
encouraging the patient to maintain the best levels
of oral hygiene they can achieve.
Complaints regarding undiagnosed and untreated
periodontal disease are on the increase.6 The most
common allegation is that the patient was unaware
of the presence of periodontal disease or that the
extent and implications of the disease had not been
adequately explained to them. In these instances,
two questions are usually posed: firstly, did the
oral health professional properly diagnose, treat
and monitor the periodontal disease and secondly,
was there adequate communication and discussion
regarding the diagnosis between the oral health
professional and the patient?
OHASA JOURNAL
Ethics
A patient-centred approach is in keeping with
the principle of respect for autonomy. Listening to
the patient enables the oral health professional
to decide what information the patient needs,
how this information should be transmitted to
the patient and what the patient’s preferences
are. Good communication makes it possible to
compile a complete and accurate patient history,
and makes the patient feel reassured and cared for.
Furthermore, good communication is a necessary
pre-requisite for responsible decision-making. In
order to exercise their right to informed consent,
patients must understand their diagnoses, the various
treatment options, and the possible consequences
of undergoing or refusing treatment.7 in the abovementioned case scenario, it is clear that the dentist
and oral hygienist acted in the best interests of
the patient. She was informed at her first visit that
her periodontal condition was compromised and
that periodontal disease can manifest by years
of quiescence and occasional bouts of sporadic
activity. Radiographic evidence did not show any
major deterioration until the final visit and when
a second opinion was required she was referred
to a specialist.
In many cases, the levels of periodontal disease
in a patient’s mouth are due to factors beyond the
oral health professional’s control and do not reflect
any fault or the part of the oral health professional.
However, it is easier to demonstrate that a high
standard of care was provided, if dental records
are comprehensively written up.
An oral health professional that is able to
communicate effectively and compassionately is
able to dissipate fear and allay anxiety. This, in turn,
leads to better patient satisfaction and to better
treatment adherence. Research has demonstrated
a relationship between communication skills
and complaints lodged against oral health care
workers. Oral health professionals who focus on
technical procedures or technology, who spend
little time talking to patients and who give minimal
explanations to patients are at higher risk of
litigation. Risk of litigation appears to be related to
“patients’ dissatisfaction with their physicians’ ability
to establish rapport, provide access, administer
care and treatment consistent with expectation
and communicate effectively”.
It is worth taking the time to schedule a faceto-face conversation with patients to discuss
complex disease like periodontal disease.5 Such
communication goes a long way to encourage
the patient to ‘internalise’ the problem, take
responsibility and importantly to adhere to oral
hygiene instructions and oral health education
messages. These discussions need to be carefully
documented in the clinical records, together with
copies of any written correspondence. Oral health
professionals who do not keep adequate records
are placed in an invidious position when a patient
makes a claim about the standard of care which
has been provided. It has been recommended that
a clinical audit be carried out to monitor patients
with moderate or severe periodontal disease. Any
gaps or weaknesses in record keeping should be
identified and improved upon. ●
4.Matthews JB, Wright HJ, Roberts A, Ling-Mountford
N, Cooper PR, Chapple ILC. Neutrophil hyperresponsiveness in periodontitis. Journal of Dental
Research 2007; 86 (8): 718–22.
5.McLeod DE. A practical approach to the diagnosis and
treatment of periodontal disease. Journal of American
Dental Association 2000; 131 (4): 483–91.
6.Dental Protection Limited (DPL). Exercises in risk
management: Periodontal monitoring -Riskwise 10,
2006.
7.Moodley K, Naidoo S. Ethics and the Dental Team. Van
Schaik Publishers, Pretoria, 2010.
8. Hickson GB, Federspiel CF, Pichert JW. Patient complaints
and malpractice risk. JAMA 2002; 287(22): 2951–7.
REFERENCES
1. Genco RJ. Current view of risk factors for periodontal
diseases. J Periodontol 1996 Oct; 67(10 Suppl): 1041–9.
2. Beck JD. Periodontal implications: older adults. Ann
Periodontol 1996; 7(1): 322–57.
3. Jeffcoat MK, Ready MS. Progression of probing
attachment loss in adult periodontitis. J Periodontol 1991;
62: 185–91.
PAGE 25
OHASA NEWS
Guidelines for
Authors
OHASA Journal has produced these guidelines to assist prospective authors. The Journal will
consider for publication full-length research papers, clinical case reports, review articles, short
communications, letters to the editor and professional issues.
PLEASE SUBMIT MANUSCRIPTS TO:
Natasha Swart
Managing Editor, OHASA Journal
PO Box 75715
Lynnwood Ridge
Pretoria
0040
Tel: +27 12 3192687
Fax: +27 12 3192146
Email:[email protected]
[email protected]
MANUSCRIPTS
Each manuscript should be sent either on a CD, or
electronically via email as an attachment.
COPYRIGHT
The submission of the manuscript by the authors
means that the authors automatically agree to
assign exclusive copyright to OHASA Journal if and
when the manuscript is accepted for publication.
PEER REVIEW
Upon receipt by the Editor, manuscripts are sent to
two independent referees approved by the Editor.
Manuscripts will not be returned to authors.
LENGTH OF CONTRIBUTIONS
For research papers and case reports authors
should ideally limit their work to 2,500 words.
Tables and figures must be allowed for in the final
count. (Approx. 100-500 words, depending on size).
TITLES
Titles must be descriptive and succinct.
ABSTRACTS
A structured abstract of research papers and case
reports is required. It should include objectives,
methods, results and conclusions and state the
purpose of the study, basic procedures, main
findings and principal conclusions. It may be up
to 200 words and should be able to stand alone.
TABLES
Tables should be numbered consecutively with Arabic
numerals. A caption should accompany each table.
ILLUSTRATIONS
Illustrations must be submitted in a format and
quality suitable for reproduction – i.e., in the case of
graphics, high resolution (300 dpi) - in the Journal.
The Editor and Publisher reserve the right to reject
illustrations or figures based upon poor quality of
submitted materials. Appropriate consent must have
been obtained by the author for any illustration
showing a patient.
EXAMPLES
Reference to a journal article
Lewis MAO, Lee SM, Potts AJC and Nutes SJ. Mucous
membrane pemphigoid in childhood. Dent Health
2000; 39 (3): 10-11.
LEGENDS
Legends should be typed double-spaced in
consecutive order on a separate page. They
should be brief and specific.
Reference to a book
Cawson RA and Odell EN. Essentials of Oral
Pathology and Oral Medicine. London: Churchill
Livingston, 1998.
ACKNOWLEDGEMENTS
Acknowledge persons who have made substantive
contributions to the study. Authors are expected to
disclose any commercial or other relationships that
could constitute a conflict of interest.
Reference to a chapter in a book
Bergenholtz G and Hasselgren G. Endodontics and
Periodontics. In: Lindhe J, Karring T and Lang NP
(eds.) Clinical Periodontology and Implant Dentistry,
pp 296-326, Copenhagen: Munksgaard, 1997.
REFERENCES
The author is responsible for the accuracy of the
reference list at the end of the article. All references
must be in the Vancouver style. Number references
consecutively in the order in which they appear
in the text and these numbers should appear
as superscripts each time the author is cited. All
OHASA
PAGE 26
references cited, and only these, must be listed
at the end of the paper. This should include the
names and initials of all authors unless they are
more than six when only the first three should be
given followed by et al. in italics. The authors’ names
are followed by the title of the article; the title of
the journal abbreviated according to the style of
Index Medicus or the Index to Dental Literature; the
year of publication; the volume number; first and
last page numbers in full. Titles of books should be
followed by the place of publication, the publisher
and the year.
The Editor reserves the right to edit material for
clarity of style and to suit the space available. A full
copy of Guidelines for Authors is available on request
from the Editor. ●
ANNUAL GENERAL MEETING
8 NOVEMBER 2014 | CAPE TOWN
OHASA JOURNAL
Continuous professional development
CPD
QUESTIONNAIRE
No. 3 2014
General
The association between periodontitis and pre-term birth and/or low birth
weight: a literature review
1. Pre-term birth and/or low birth weight contribute significantly to the
health care, economic and social burden imposed on the government,
communities and families involved.
a.True
b.False
2. Periodontitis can be modified by:
a.The type of organisms
b. Host immuno-inflammatory response
c. Environmental, genetic and systemic factors
d. b and c
e. a, b and c
3. Periodontitis can be regarded as a constant pathogenic and inflammatory
challenge at a systemic level because of the large epithelial surface that
could be ulcerated in the periodontal pocket.
a. True
b.False
4. The WHO defines pre-term birth as all live births before 36 weeks of
complete gestation.
a.True
b.False
5.In developed countries, low birth weight is usually caused by intra-uterine
growth restriction, whereas in developing countries it is more often as a
result of pre-term birth.
a.True
b.False
6.The rise and fall pattern of the hormones coincides with the onset and
peak of the gingival inflammation observed in pregnancy.
a.True
b.False
7. Pregnancy alters the rate and pattern of collagen production in the gingiva
but collagen repair may also be affected due to folate deficiency caused
by oestrogen and progesterone.
Instructions for completing the CPD questionaire will be
e-mailed to each OHASA member. If you do not receive your
e-mail, please contact the Editor.
8. Periodontal pathogens, their shed virulence factors and/or inflammatory
cytokines from the periodontal pocket may gain access into the bloodstream
and disseminate through the body.
a.True
b.False
9.Mechanisms through which an inflammatory response can affect PTLBW
are:
a.Damage to the placental tissue
b.Pre-eclampsia
c. Pre-term rupture of the membrane and contraction of the uterus
d. b and c
e. a, b and c
10.Scaling and root planing in pregnant women with periodontitis may result
in the increase of pre-term births.
a.True
b.False
Guidelines for the selection of tooth whitening products amongst those
available on the market
11. Peroxide is the chemical most frequently used as a tooth whitening agent
with two types being generally employed namely hydrogen peroxide or
carbamide peroxide.
a.True
b.False
12.The public sees the following aspects as important with regards to tooth
whiteners:
a. Effectiveness of the whitener
b. How long lasting is the effect
c.The cost of the treatment
d.All of the above
e. None of the above
13.There are two ways to measure the effect of tooth whiteners namely by
means of matching with a calibrated shade guide or numerically (colourimeter,
chromameter or spectrophotometer).
a.True
b.False
a.True
b.False
PAGE 27
Continuous professional development
14.The best results with the highest values according to Tables 1 and 2 were
with a 10% or 15% carbamide peroxide treatment over a relatively long
treatment period (two weeks 6/8 hours per night).
a.True
b.False
15.In general in-office treatments were far more successful than at-home
treatments with ~10% carbamide peroxide.
a.True
b.False
16.There is a major difference in the relapse after a four week or longer
period between at-home whitening and in-office whitening namely 13.1%
for at-home and 55.2% for in-office.
a.True
b.False
17.Opalescence PF was the most commonly tested product and showed 45%
improvement as reflected on the shade guide scale.
a.True
b.False
18.Tooth sensitivity during the whitening process does not disappear
spontaneously after the treatment period.
a.True
b.False
19.This article concludes that the whitening treatment of choice should be:
a.At-home whitening under supervision of a dentist/oral hygienist
b.Using a 10% carbamide peroxide
c. ~14 days and ~8 hours per night on average
d. a, b and c
23.The cumulative bacteraemia refers to bacteraemia resulting from common
daily activities and may cumulatively be several million times higher than
those resulting from single invasive procedures.
a.True
b.False
24.The most common pathogenic organisms in a South African setting are
oral streptococci and the antibiotic choice should therefore be no different
to that of the international guidelines.
a.True
b.False
25.The guidelines as set forth by the AHA, ESC and BSAC are appropriate and
apply also in the South African context.
a.True
b.False
Ethical
Periodontal treatment and allegations of neglect
26.The factors playing a part in the etiology and rate of progression of
periodontal disease are:
a.Bacteria
b. Genetic susceptibility
c. Practitioner’s neglect
d. a and b
e. a, b and c
27.Listening to the patient enables the oral health practitioner:
Infective endocarditis and antibiotic prophylaxis – an update for South
African dental practitioners
a.To decide what information the patient needs
b.To know how this information should be transmitted to the patient
c.To know what the patient’s preferences are
d.All of the above
20.The two factors challenging the concept of antibiotic prophylaxis in dentistry
are the lack of scientific evidence for linking infective endocarditis to dental
procedures and the uncertainty regarding the effectiveness of prophylaxis.
28.In order to exercise their right to informed consent, patients must understand
their diagnoses, the various treatment options and the possible consequences
of undergoing or refusing treatment.
a.True
b.False
21.According to the 2006 and 2007 guidelines the dental procedures requiring
prophylaxis are those involving manipulation of gingival tissues or the
peri-apical regions of the teeth or perforation of the oral mucosa.
a.True
b.False
22.The rationale of the NICE guidelines is:
a.The absence of a consistent association between interventional
procedures, dental or otherwise and the development of endocarditis
b.The potential mortality of anaphylaxis
c.Increased expense
d.All of the above
PAGE 28
a.True
b.False
29.Dental records that are comprehensively written up demonstrate that a
high standard of care was provided.
a.True
b.False
30.Oral health professionals who focus on technical procedures or technology,
who spend little time talking to patients and who give minimal explanations
to patients are at lower risk for litigation.
a.True
b.False
OHASA JOURNAL
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