Oral Pathology - School of Medicine

Transcription

“Benign” Oral Pathology
Michael D. Puricelli, MD
James C. Denneny, MD
Overview
•
•
•
•
•
•
Anatomy Review
Background
Potentially Malignant Lesions
Classification of oral lesions
Case
Differential diagnosis of leukoplakic lesions
Oral Cavity - Boundaries
• Anterior border: vermillion of
the lips
• Posterior border: circumvallate
papillae of the tongue, the
anterior tonsillar pillars
(palatoglossus muscles), and
the posterior margin of the
hard palate
• Superior: hard palate
• Inferior: mylohyoid muscles
• Lateral: buccomasseteric region
(buccal mucosa of the cheeks)
and the retromolar trigone
Poon, CS. Stenson, KM. Overview of the diagnosis and staging of head and neck cancer. UpToDate.
Anatomy Review
• What are the subsites of the oral cavity?
Oral Cavity - Subsites
•
•
•
•
•
•
•
Lips
Buccal mucosa
Anterior tongue
Floor of the mouth
Hard palate
Upper and lower gingiva
Retromolar trigone
http://training.seer.cancer.gov/head-neck/anatomy/
Anatomy Review
• What are the subsites of the oropharynx?
Oropharynx - Subsites
•
•
•
•
•
•
Palatine tonsils
Soft palate
Tonsillar pillars
Posterior/lateral pharyngeal wall
Tongue base
Valleculae
http://training.seer.cancer.gov/head-neck/anatomy/
Background
• Oral lesions are common but challenging to diagnose
– Vast processes that present similarly
– Epithelial turnover in the oral cavity ranges from 3 to 7 days
• Oral involvement precedes other symptoms in many conditions
• Most (84%) physicians [hospitalists] feel that performing an
intraoral examination is important
• In the same study, 80% of hospitalists failed to correctly
diagnose a clinical photo of early squamous cell carcinoma
• 56% of hospitalists did not feel confident examining the
oral cavity and 77% felt that they were inadequately
trained in this examination
• Many referrals to ENT clinic
Morgan, R, Tsang J, Harrington N, Fook L. Survey of hospital doctors' attitudes and knowledge of oral conditions in older patients. Postgrad Med
J. 2001;77(908):392.
Background
• Oral cavity cancer accounts for approximately 3% of all
malignancies and is a significant worldwide health
problem
– Approximately 25,000-30,000 cases of oral cancer are
diagnosed each year
• Particularly common in Asia
– Many oral SCCs develop from premalignant conditions of
the oral cavity
– Up to 80% of patients with oral SCC have used tobacco
products, and the risk of developing malignancy is 5-9
times greater for smokers than nonsmokers
• Paramount in consideration of benign lesions is
systematic consideration and exclusion of malignancy
Deschler, DG, Erman, AB. Chapter 119: Oral Cavity Cancer. Bailey’s Otolaryngology Head and Neck Surgery
Meyers, AD. Premalignant Conditions of the Oral Cavity http://emedicine.medscape.com/article/1491418-overview#aw2aab6b4
Background
• Unfortunately not as simple as benign and malignant
– Spectrum
•
•
•
•
Benign (always) / Malignant (never)
Benign (usually) / Malignant (rarely)
Benign (occasionally) / Malignant (sometimes)
Benign (never) / Malignant (always)
• Some lesions that are usually or occasionally benign
will progress to malignancy or harbor foci of tumor
– 5-18% of epithelial dysplasias become malignant
– Led to the adoption of classification system inclusive of
“Potentially Malignant Lesions”
Deschler, DG, Erman, AB. Chapter 119: Oral Cavity Cancer. Bailey’s Otolaryngology Head and Neck Surgery
http://www.oralcancerfoundation.org/cdc/cdc_chapter4.php
Overview
•
•
•
•
•
•
Anatomy Review
Background
Case
• Features:
– In longitudinal studies, areas of tissue with certain alterations in
clinical appearances identified at the first assessment as
precancerous’ have undergone malignant change during followup
– Some of these alterations, particularly red and white patches,
are seen to co-exist at the margins of overt oral squamous cell
carcinomas
– A proportion of these may share morphological and cytological
changes observed in epithelial malignancies, but without frank
invasion
– Some of the chromosomal, genomic and molecular alterations
found in clearly invasive oral cancers are detected in these
presumptive precancer or premalignant phase[s]
Warnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa. J Oral Pathol Med. Nov 2007;36(10):575-80
•
•
•
•
•
•
•
•
Leukoplakia
Erythroplakia
Palatal lesions in reverse smokers
Oral submucous fibrosis
Actinic keratosis
Lichen planus/Lichenoid reaction
Discoid lupus erythematosus
Hereditary
– Dyskeratosis congenita
– Epidermolysis bullosa
Oral Leukoplakia
• Most common premalignant oral mucosal
lesion
– Most cases are benign and remain so over time
– Rate of malignant progression is reported ranging
between 3.6% and 17.5% of lesions
• Greater at floor of mouth, lateral tongue, and lower lip
– Up to 19.9% of lesions have dysplasia with 3.1%
showing frank carcinoma
Wein, RO. O’Leary, M. Chapter 51: Stomatitis. Bailey’s Otolaryngology Head and Neck Surgery
Sclubba, JJ. Chapter 91: Oral Mucosal Lesions. Cummings Otolaryngology Head and Neck Surgery
Oral Leukoplakia
Erythroplakia
• “A fiery red patch that cannot be characterized
clinically or pathologically as any other definable
disease”
– Often red macule or patch with soft and velvety
texture
• High risk for malignancy
– 51% of erythroplakic lesions demonstrate invasive
squamous cell carcinoma
– 40% demonstrate carcinoma in situ
– 9% show mild to moderate dysplasia
Bing images
• Specific to populations who smoke with the
lighted end of the cigar, cigarette or cheroot
inside the mouth
– Resulting palatal lesion may appear clinically as a red,
white, melanotic patch or papule
• Defining⁄diagnosing this lesion is based upon
identification of the smoking habit
• Up to 84% of palatal lesions have been
demonstrated to harbor dysplasia upon histologic
analysis
J. J. Pindborg, F. S. Mehta, P. C. Gupta, D. K. Daftary, and C. J. SmithReverse Smoking in Andhra Pradesh, India: A Study of Palatal Lesions among 10,169 Villagers Br J
Cancer. Mar 1971; 25(1): 10–20.
Nicotine stomatitis in a reverse smoker. Notice the increased
hyperkeratosis, hyperplasia, and swelling of minor salivary glands
• Juxtaposition of atrophic epithelium and adjacent
fibrosis of the lining mucosa of the upper digestive
tract involving the oral cavity, oropharynx and
frequently the upper third of the esophagus
– Failure of collagen remodeling
– Loss of tissue mobility (oral opening and tongue mobility)
• Chief etiologic factor being the consistent and habitual
use of areca (betel) nut
– Malignant transformation rates as high as 7.6%
– Dysplasia has been seen in 7-26% of individuals
Betel Nut
Bing images
Actinic Keratosis
• Actinic keratosis is considered to represent a
potentially malignant condition of the lip
• A provisional diagnosis may be made on
clinical grounds, but definitive diagnosis
requires biopsy
Lichen planus
• Common chronic inflammatory disorder
demonstrating immune pathology
– White striaform lesions that are bilaterally
symmetric usually asymptomatic
• Other forms of oral lichen planus include the plaque
form, atrophic or erythematous form, and erosive form
which may be painful
– Cell mediated, T lymphocytes accumulate beneath
the epithelium of the oral mucosa and increase
the rate of differentiation of stratified squamous
epithelium
Lichen Planus
• Appear to be a small but bona fide risk of carcinoma
evolving from proven oral lichen planus
– More likely to be seen in conjunction with the atrophic or
erosive form of the disease rather than the far more
common reticular or striaform type
– Need for long-term follow-up also disputed
• Lichenoid dysplasia
– Significant degree of allelic loss in dysplastic oral lichenoid
lesions as well
• Degree of dysplasia in association with lichenoid features should
alert the clinician to either remove the balance of the altered
mucosa or follow the patient carefully
Erosive Lichen Planus
Irregularly marginated, intense erythema with patchy superficial erosions.
Atrophic Lichen Planus
Lichen Planus
• Chronic autoimmune disease of unknown
etiology
– Oral lesions present in about 20% of individuals
with discoid lupus
• There are conflicting data from the literature
as whether to regard oral DLE as a potentially
malignant disorder.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519212/?report=reader#!po=20.5882
Discoid Lupus
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519212/?report=reader#!po=20.5882
Hereditary disorders with increased
risk
• Two conditions that may have an increased
risk of malignancy in the mouth
– Dyskeratosis congenita (DC)
• Triad of abnormal nails, reticular skin pigmentation,
and oral leukoplakia
– Epidermolysis bullosa
• Characterized by blisters form after a minor injury
• Limited data available
Dyskeratosis congenita
Hematol Oncol Clin North Am. 2009 April ; 23(2): 215–231. doi:10.1016/j.hoc.2009.01.003
Epidermolysis bullosa
Premalignant Conditions
• “Benign” = “not malignant” + “not potentially
malignant”
– Challenge is that both erythroplakia and leukoplakia
are diagnoses of exclusion
• Best method of “ruling out” malignant and
potentially malignant lesions is having a
systematic approach to oral lesions
– Guides which patients need biopsy
• Two “schools of thought”
– Appearance
– Etiology
Overview
•
•
•
•
•
•
Anatomy Review
Background
Case
Approaches to Oral Lesions
Appearance
• Red/White lesions
• Vesiculobullous/Ulcerative
• Pigmented
Etiology
• Treatment Related
• Infectious
• Immunologic
• Systemic
• Nutritional
• Idiopathic
• Unique to Childhood
• Multifactorial
Approaches to Oral Lesions
Appearance
• Red/White lesions
• Vesiculobullous/Ulcerative
• Pigmented
Etiology
• Treatment Related
• Infectious
• Immunologic
• Systemic
• Nutritional
• Idiopathic
• Unique to Childhood
• Multifactorial
Red/White
•
•
•
•
•
•
•
Leukoedema
Oral leukoplakia
Oral hairy leukoplakia
Oral lichen planus
Submucous fibrosis
Verruciform xanthoma
Candidiasis
Vesiculobullous/Ulcerative
•
•
•
•
•
•
Pemphigus vulgaris
Mucous membrane pemphigoid
Herpes simplex
Recurrent aphthous stomatitis
Erythema multiforme
Traumatic (esosinophilic) granuloma
Pigmented
• Melanotic macule
• Melanoma
• Amalgam tattoo
Overview
•
•
•
•
•
•
Anatomy Review
Background
Case
Case
• A 55 year old is referred to your clinic for
evaluation of an oral lesion discovered on
routine dental examination.
• History?
Suggested History
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Time course surrounding the onset of symptoms
Location
Multiple vs singular
Duration
Pain
Induration
Other mucosal lesions
Cutaneous lesions
Systemic diseases
Medications (esp. recent changes)
Recognized triggers/palliating factors
Aggressiveness of oral hygiene and product use
Prodromal symptoms
Risk factors for malignancy
History
•
•
•
•
•
•
•
Incidentally discovered 3 weeks ago
Left buccal region
Singular
Pain - none
Other mucosal lesions - none
Systemic diseases - negative
Recognized triggers/palliating factors - none
Physical Examination
• A full head and neck examination is necessary
• Assess for synchronous findings beyond the oral
presentation
• Dentures should be removed and assessed for quality
of fit while asking the patient about the original date of
manufacture in addition to visits for modification
• Buccal mucosal lesions, the relationship of the
ipsilateral dentition and any amalgam that contacts the
mucosa in a closed mouth position should be identified
• Quality of salivary production should be assessed.
Photo
http://trialx.com/curetalk/wp-content/blogs.dir/7/files/2011/05/diseases/Leukoplakia_Oral-1.jpg
Next Steps
• Do I need tissue for diagnosis/adjuvant testing?
– Gram stain and culture
– Tzanck smear and viral cultures
– Complete blood count (CBC) with differential, erythrocyte
sedimentation rate (ESR), anti-nuclear antibody (ANA), and
cytoplasmic- antineutrophil cytoplasmic antibodies (cANCA) in addition to levels or iron, ferritin, total ironbinding capacity, folate, thiamine (B1), riboflavin (B2),
pyridoxine (B6), cobalamin (B12), zinc, and magnesium
– Anti-SSA and anti-SSB
– Immunofluorescence for deposition of IgG, IgA, and/or
complement C3
– Colonoscopy
Proposed Framework
• What is your differential diagnosis for this
lesion?
Proposed Framework
• Could this lesion be malignant?
• Could this lesion be potentially malignant?
–
–
–
–
–
–
–
–
Leukoplakia
Erythroplakia
Actinic keratosis
Lichen planus/Lichenoid reaction
Hereditary
• Dyskeratosis congenita
• Epidermolysis bullosa
• Do I need tissue for diagnosis/adjuvant testing?
Oral Leukoplakia
• Most common premalignant oral mucosal
lesion
• Definition/Diagnosis?
Pictorial Definition
Biopsy “Not Needed”
•
•
•
•
•
•
•
White sponge nevus
Morsicatio buccarum
Chemical injury
Acute pseudomembranous candidiasis
Leukoedema
Skin graft
Leukokeratosis nicotina palate
White Sponge Nevus
• White patches of tissue that appear as thickened, velvety, spongelike tissue
– Most commonly found on the buccal mucosa (bilateral)
– Rarely also present on nose, esophagus, genitals, or anus
– Can become infected with bacteria or cause annoyance due to texture
• Otherwise asymptomatic
• Usually first appears during early childhood
– Estimated to affect less than 1 in 200,000 individuals worldwide.
• Caused by mutations in the KRT4 or KRT13 gene for keratins,
specifically intermediate filaments
– Filaments do not fit together properly = irregular intermediate
filaments that are easily damaged promoting inflammation and
epithelial proliferation
– Autosomal dominant with reduced/incomplete penetrance
http://ghr.nlm.nih.gov/condition/white-sponge-nevus
White Sponge Nevus
1: Songu M, Adibelli H, Diniz G. White sponge nevus: clinical suspicion and diagnosis. Pediatr Dermatol. 2012 Jul-Aug;29(4):495-7. doi: 10.1111/j.15251470.2011.01414.x. Epub 2012 Feb 22. Review. PubMed PMID: 22352924.
White Sponge Nevus
White Sponge Nevus
Morsicatio buccarum
• Hyperkeratosis found in the line of the
occlusal plane on the tissue that contacts the
teeth.
• The mucobuccal folds are usually not affected
by the trauma
– Inner lip areas may also be irritated (morsicatio
labiorum) and traumatized by the incisor teeth.
• History of habitual chewing
Chemical Exposure
• Foods, chemicals, friction,
thermal/mechanical injury, metals, spices, and
oral care products have been documented to
cause irritant reactions in susceptible
individuals
• Most irritation in the oral cavity tends to
reverse quickly when the causative agent is
removed
Davis CC, Squier CA, Lilly GE. Irritant contact stomatitis: a review of the condition. J Periodontol. 1998 Jun;69(6):620-31. Review. PubMed PMID: 9660330.
Cinnamon Contact Stomatitis
Georgakopoulou EA. Cinnamon contact stomatitis. J Dermatol Case Rep. 2010 Nov 19;4(2):28-9. doi: 10.3315/jdcr.2010.1047. PubMed PMID: 21886744;
PubMed Central PMCID: PMC3157809.
7 Days Later
Georgakopoulou EA. Cinnamon contact stomatitis. J Dermatol Case Rep. 2010 Nov 19;4(2):28-9. doi: 10.3315/jdcr.2010.1047. PubMed PMID: 21886744;
PubMed Central PMCID: PMC3157809.
Candidiasis
• Opportunistic infection with several clinical forms: pseudomembranous
(thrush), erythematous, atrophic, and hyperplastic.
– Candida albicans, Candida tropicalis, Candida krusei, and Candida glabrata
• Shift from a commensal state to that of a “pathologic” state: overgrowth
• Symptoms of oral/oropharyngeal candidiasis range from none or minimal
ones to those that may include burning, dysgeusia, sensitivity, and
generalized discomfort.
• Diabetes mellitus, immunosuppression, topically delivered drugs
(corticosteroids), xerostomia (with loss or diminution of saliva’s protective
function), heavy smoking, and denture appliances
• Angular cheilitis is generally considered to be a candida related condition,
although supervening or coinfection with Staphylococcal species may be
noted
• Approximately 50% of adults (normal carriers) will have culture tests
positive for intraoral candidal organisms; thus the clinicopathologic
correlation becomes an important consideration.
Median Rhomboid Glossitis
• Associated with candida
infection and responds
to antifungal therapy
Common tongue conditions in primary care. Am Fam Physician. 2010;81(5):627-634.
Pseudohyphae
Candidiasis
• A wide spectrum of topical and systemic agents is
available
– Topical polyene compound (nystatin)
• The nonabsorbable polyene compound in liquid or cream
form may be useful for most mild to moderate infections
– Clotrimazole may be useful both topically and to a
lesser extent systemically
– Systemically administered triazoles including
fluconazole and itraconazole, as well as ketoconazole,
are effective in eradicating more severe forms of this
disease.
Leukoedema
• Diffuse and generalized mild surface opacification
that involves the buccal mucosa
• Normal variation of surface mucosal texture and
characteristics and can be identified in large
numbers within the population
– Most marked in those possessing higher levels of
cutaneous and mucosal pigmentation
• The appearance may be that of a diffuse filmy
grayish surface with white streaks, wrinkles, or
milky alteration
– Characterized by vacuolated spinosum
Leukoedema
Oral Skin Graft
Leukokeratosis Nicotina Palate
• Smoking history
with grey-white
palate
• Typically resolves
within several
weeks of
smoking
cessation
http://www.lsusd.lsuhsc.edu/Documents/TCI/TobaccoOralChanges0729081.pdf
Biopsy Considered: Overview
• Frictional keratosis that does not resolve with
removal of offending agent
• Hairy leukoplakia
• Lichenoid reaction
Frictional Hyperkeratosis
• History of trauma/chronic cheek biting
• Located along the occlusal plan
• Typically reversible on removal of the cause
Frictional Hyperkeratosis
Note occlusal wear
http://emedicine.medscape.com/article/1076089-overview
• “A diagnostic biopsy should be considered for
any mucosal lesion that persists for more than
14 days after obvious irritants are removed”
http://www.oralcancerfoundation.org/cdc/cdc_chapter4.php#sthash.OrfuvN7Y.dpuf
Oral Hairy Leukoplakia
• Relationship in the majority of cases with systemic
immunosuppression
• Epstein-Barr virus is considered the etiologic agent
• Characteristically arises along the lateral tongue margins bilaterally,
ranging from subtle white keratotic vertical streaks to thick
corrugated and then to shaggy surface alterations
– Other sites: dorsum of the tongue, buccal mucosa, and floor of the
mouth
• Diagnosis by routine microscopy and in situ hybridization to
demonstrate the presence of the Epstein-Barr virus is essential in
that the confirmed diagnosis almost always correlates with systemic
immunosuppression
• Management of hairy leukoplakia is not necessary
– Proven association of HIV-AIDS
– Disappearance of the usually accompanies antiretroviral therapy
Oral Hairy Leukoplakia
Differential Diagnosis
Oral Leukoplakia: Management
• Depends upon the histologic findings obtained by
incisional biopsy
– Benign or minimally dysplastic lesions
• Periodic observation vs excision (elective option)
– Premalignant lesions of moderate dysplasia or worse
• Excision
– Reported recurrence rates for premalignant lesions are as
high as 34.4%
• No proven and effective prevention strategy regarding
malignant transformation
– Retinoids, antioxidants, and cyclooxygenase (COX)-2
inhibitors are yet to be proven effective by randomized
trials
http://www.oralcancerfoundation.org/cdc/cdc_chapter4.php#sthash.OrfuvN7Y.dpuf

Oral Pathology - School of Medicine

Transcription

Similar documents

GLES CASE STUDY

saint john`s hospital - Hungarian Medical Care company for the

Neurotic Excoriation - Physicians Practice

Techniques in Head and Neck Surgery

PE041 Tonsil and Adenoid Surgery

Vanderbilt Otolaryngology Symposium

1-Mycobacteria 2-Chlamydia 3-Mycoplasam 4

Soothe-A

OVER 8 YEARS - Asaadi Plastic Surgery

Abdominal Sacrocolpopexy with possible removal of ovaries