1. Benign Mucosal Lesions of the Oral
Cavity
Grand Rounds
3/2/2006

2. Outline
 Case study
 Mucosal lesions
 Ulcerative lesions
 Conclusions

3. Case Study
 33 yo male admitted for throat pain, fever. Patient
developed a vesiculopapular rash, fever as high as
103F, and thick coating on tongue, and penile ulcers
following one week history of fevers and sore throat.
 Physical exam- Crusted lesions over face and neck,3
mm tender lesion on upper lip, tongue-tender, thick
white coating with 2 erythematous areas on tip,
numerous white lesions across uvula, hard and soft
palate, Neck- No lymphadenopathy
 ESR- 44

4. Leukoedema

5. Leukoedema
 Diffuse, filmy grayish surface with white
streaks, wrinkles, or milky alteration
 Symmetric, usually involving the buccal
mucosa, lesser extent labial mucosa
 Normal variation; present in the majority of
black adults, and half of black children
 At rest, opaque appearance. When stretched
dissipates

6. Oral Leukoplakia

7. Oral Leukoplakia

8. Oral Leukoplakia
 Clinically defined white patch or plaque that
has been excluded from other disease
entities
 Presence of dysplasia, carcinoma in situ, and
invasive carcinoma from all sites 17-25%
(Bouqot and Gorlin 1986)
 Etiology- associated with tobacco (smoking,
smokeless tobacco), areca nut/betel
preparations

9. Oral Leukoplakia
 May be macular, slightly elevated, ulcerative,
erosive, speckled, nodular, or verrucous
 Clinical shift in appearance from
homogenous to heterogenous, speckled, or
nodular, a rebiopsy is mandatory
 Correlation between increasing levels of
dysplasia and increases in regional
heterogeneity or speckled quality

10. Proliferative Verrucous Leukoplakia

11. Proliferative Verrucous Leukoplakia
 Uncommon variant of leukoplakia
 Multifocal, occurring more in women, and in
those without the usual risk factors
 Evolution from a thin, flat white patch to
leathery, then papillary to verrucous
 Development of squamous cell CA in over
70% of cases

12. Site of Leukoplakia
 Risk of dysplasia/carcinoma higher with floor
of mouth, ventrolateral tongue, retromolar
trigone, soft palate than with other oral sites

13. Epithelial Dysplasia

14. Treatment
 Trial of cessation of offending agent, follow-up
 Guided by microscopic characterization
 Benign, minimally dysplastic- periodic observation or
elective excision
 Complete excision can be performed with scalpel
excision, laser ablation, electrocautery, or
cryoablation
 Chemoprevention

15. Oral Hairy Leukoplakia

16. Oral hairy leukoplakia
 Asymptomatic, seen with systemic
immunosuppression
 EBV
 Lateral tongue bilaterally; subtle white keratotic
vertical streaks to thick corrugated ridges
 Diagnosis by microscopy and in situ hybridization
 Management includes establishing diagnosis and
treating immunosuppression

17. Oral lichen planus

18. Oral lichen planus
 0.2%- 2% population affected
 Usually asymptomatic, reticular from, white
striaform symmetric lesions in the buccal
mucosa
 T-cell lymphocytic reaction to antigenic
components in the surface epithelial layer
 Other variants: plaque,
atrophic/erythematous, erosive

19. Oral lichen planus
 Small risk of squamous cell carcinoma, more
likely seen in the atrophic or erosive types
 Studies show that dysplasia with lichenoid
features have significant degree of alleic
loss. Recommendation is to remove these
lesions/follow patient closely

20. Candidiasis

21. Candidiasis
 Opportunistic infection, Candida albicans
 Pseudomembranous (thrush), erythematous,
atrophic, hyperplastic
 Risk factors: Local- topical steroids,
xerostomia, heavy smoking, denture
appliances. Systemic- Poorly controlled
diabetes mellitus, immunosuppression

22. Candidiasis
 Symptoms: burning, dysgeusia, sensitivity,
generalized discomfort
 Angular cheilitis, coinfection with staph may
be present
 Acutely- atrophic red patches or white curd-
like surface colonies Chronic- denture
related form confined to area of appliance

23. Candidiasis
 Confirmation with KOH smear, tissue PAS or
silver stains
 Treatment- topical or systemic,
polyene,azoles

24. Oral ulcerative lesions
 Acute
 Chronic
 Recurrent

25. Acute ulcerative
 Bacterial
Acute necrotizing ulcerative gingivostomatitis
Poor oral hygiene, Punched-out ulcer at
interdental papillae, seen in young adults with
poor nutrition, heavy smoking
Streptococcal gingivostomatitis
B hemolytic strep, bright red gingivae
Oral tuberculosis
Gonococcal stomatitis

26. Syphilis

27. Acute ulcerative
 Syphilis
Congenital syphilis- Hutchinson’s incisors, “moon’s molars”
Primary-painless, indurated, ulcerated, usually involving the lips,
tongue
Secondary- mucous patches, split papules
Tertiary- Gummas, can involve palate, tongue
 Fungal
Oral Candidiasis
Histoplasmosis- disseminated form, oropharyngeal lesions may
present as ulcerative, nodular, or vegetative. Biopsy will provide the
diagnosis

28. Primary Herpetic Gingivostomatitis

29. Acute ulcerative
 Viral Infections
Herpes simplex- 600,000 new cases annually,
prodrome followed by small vesicles that ulcerate,
primary infection involves the gingiva, and can
involve the entire oral cavity
Recurrent herpes simplex- prodrome present,
herpes labialis, limited to keratinized epithelium and
can involve the gingiva and hard palate
Varicella zoster virus- distribution of trigeminal nerve
Coxsackie- prodrome, vesicular, pharynx,tonsils, soft
palate

30. Recurrent herpes simplex

31. Erythema Multiforme

32. Acute ulcerative
 Erythema multiforme
Mucocutaneous hypersensitivity reaction
Etiology- infectious (strong association with
HHV-1, viral, mycoplasma), drugs
(antiseizure medications, sulfonamides)
Clinically- target lesions develop over the
skin with erythematous periphery and central
area that can develop bullae, vesicles.

33. Erythema Multiforme
 Clinically- Oral mucosa and lips demonstrate
aphthous like ulcers and occasionally vesicles or
bullae may be present. Gingiva rarely involved;
common sites include labial mucosa, palate, tongue,
and buccal mucosa
Mucosal ulcers are irregular in size and shape,
tender and covered with fibrinous exudate
Sialorrhea, pain, odynophagia, dysathria
Severe EM are associated with involvement of other
mucosal sites- eyes, genitalia, and less common
esophagus and lungs

34. Erythema Multiforme
 Histopathology- Intense lymphocytic
infiltration in a perivascular distribution and
edema from submucosa into the lamina
propria, epithelium lack antibodies, blood
vessels contain fibrin, C3, IgM
 Treatment- with oral involvement only can
treat symptomatically/short course of
corticosteroids

35. Acute ulcerative
 Lupus erythematosus- chronic discoid and systemic
lupus erythematosus (SLE) forms
Discoid type- lip, intraoral lesions, most common site
is buccal mucosa; central depressed, red atrophic
area surrounded by slightly, raised keratotic border
SLE form- common site posterior hard palate,
superficial ulcerations that vary in size without
keratinization of the oral mucosa
Immunofluorescence shows staining of the
basement membrane with immunoglobulin, and
complement

36. Acute Ulcerative
 Reiter’s Syndrome- mainly young men 20 to
30. Classis triad of conjunctivitis, arthritis,
and urethritis. Oral lesions range from
erythema to papules to ulcerations involving
the buccal mucosa, gingiva, and lips. Lesions
on the tongue resemble geographic tongue
 Behcet’s Syndrome- recurrent oral and
genital ulcers, athritis, and inflammatory
disease of eyes and GI tract.

37. Acute ulcerative
 Drug reactions
Barbiturates, salicylates, phenolphthalein,
quinine, digitalis, griseofulvin, and dilantin

38. Chronic Ulcerative

39. Chronic ulcerative
 Pemphigus vulgaris- 0.1 to 0.5
patients/100,000; 70% present with upper
aerodigestive lesions
 Desmoglein 3 is the pemphigus antigen
 IgG, IgA
 Deposition of antibodies in the intracellular
spaces produces direct damage to the
desmosomes

40. Pemphigus vulgaris
 Clinical presentation- ulceration and pain with
collapse of vesicles
 Lesions extend from gingival margin to alveolar
margin
 Oropharyngeal lesions favor lateral aspects of soft
palate to lateral pharyngeal wall
 Lesions heal quickly without scarring
 Treatment- immunosuppression with steroids
supplemented with azathioprine
5% mortality with immunosuppression

41. Chronic Ulcerative
 Mucous Membrane (Cicatricial) Pemphigoid
Autoantibodies directed at molecular
components of the basement membrane
Most common Head and Neck sites-
oral, followed by ocular, nasal, and
nasopharynx sites
Ocular scarring- symblepharon, corneal
opacification, entropion

42. Mucous Membrane Pemphigoid
 Diagnosis is with immunofluorescence
showing linear immune deposits along the
basement membrane
 Site directed therapy. Oral cavity- topical vs.
systemic steroids.

43. Chronic Ulcerative
 Traumatic (Eosinophilic) Granuloma-
self-limiting, relatively long duration, deep mucosal injury, origin
unknown
Clinical presentation- 5th
to 7th
decade, painful rapid onset, 1 to 2
cm in diameter with crater center and firm periphery that is
white in appearance
Pathology- deep ulceration extending into skeletal muscle,
intense, diffuse inflammatory infiltrate of histiocytes, endothelial
cells, and eosinophils
Treatment- observation, topical or intralesional corticosteroids,
excision if clinical presentation in question

44. Major aphthous ulcer

45. Recurrent ulcerative
 Recurrent aphthous stomatitis (RAS)
Frequency range of 20-40% of population,
most common non-traumatic form of oral
ulceration
Data indicates a greater prevalence among
those in professional groups, higher
socioeconomic status, and non-smokers

46. RAS
 Seen in a variety of conditions
Crohn’s disease, Behcet’s syndrome, gluten-sensitive
enteropathy, food hypersensitivity (nuts, spices, chocolate)
Certain medications- NSAIDS, B-blockers, K+channel blockers
Sweet’s syndrome- acute febrile neutrophilic dermatosis
PFAPA- Periodic fever, aphthous ulcers, pharyngitis,
and adenitis
Familial variety

47. PAS
 Pathogenesis- No sign of vesicle or blistering
formation
Lesions over non-keratinizing mucosal
surfaces (labial, buccal, ventral, and lateral
tongue, floor of mouth, soft palate, tonsillar
pillars)

48. RAS
 Classification-
Minor <1.0cm, comprise 85% of all ulcers
usually anterior portion of oral cavity, ulcerative episode 7 to 10
days, no scarring
Major > 1.0 cm deeper, more painful, posterior aspect of oral
cavity, 6 weeks or longer in immunocompromised
Herpetiform- multiple pinhead-sized, pain greater than size of
lesion
Treatment- symptomatic, topical steroids, for larger lesions
intralesional steroids. Severe- short term systemic steroids.

49. Case Study
 Prodrome
 Rash present, major aphthous ulcers, genital
findings
 No eye findings
 No prior history

50. Conclusions
 Must rule out dysplasia, squamous cell
carcinoma with leukoplakia
 Duration of lesion, as well as location help to
narrow your differential diagnosis
 Biopsy of persistent lesions can help guide
management

51. References
 Cohen, Lawrence. Ulcerative Lesions of the
Oral Cavity. International Journal of
Dermatology Sept 1980, 362-373.
Sciubba, James. Oral Mucosal Lesions.
Cummings Otolaryngology Head and Neck
Surgery. Philadelphia, 2005, 1448- 91.