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 ORAL CAVITY LESIONS   Frederick Mars Untalan, MD
mouth ulcer Latin ulcus and from Greek "ἕλκος" - elkos, "wound"[ American English, canker sore open sore inside the mouth, or rarely a break in the mucous membrane or the epithelium on the lips or surrounding the mouth.  Causes:  physical abrasion, acidic fruit, infection, other medical conditions, medications, and cancerous and nonspecific processes.   Two common types : aphthous ulcers cold sores or fever blisters
Epidemiology Epidemiological studies show an average prevalence between 15% and 30%. women > men and  < 45 years.  >16-25 year olds, and  <over 55. The frequency of mouth ulcers varies from fewer than 4 episodes per year (85% of all cases) to more than one episode per month (10% of all cases) including people suffering from continuous RAS
ORAL CAVITY LIPS TEETH GINGIVA PALATE TONGUE ORAL MUCOUS MEMBRANES ORAL LYMPHOID TISSUES
Acute: small, recent onset, short duration, recurrent Trauma Recurrent Aphthous Stomatitis Behcet’s Herpesvirus Infection Herpangina
Trauma: Cheek Biting
Trauma: Ill-Fitting dentures
Trauma: Chemical Burns
Trauma: Abrasions from Teeth
Recurrent Aphthous Stomatitis(RAS) Most common ulcerative lesion of oral cavity Recurrent, painful ulcers Confined to soft mucosa Subdivided into three types: Minor aphthae Major aphthae Herpetiformaphthae
Recurrent Aphthous Stomatitis(RAS) Minor aphthae: Less than 1 cm Heal completely in 7-10 days without scarring Painful  Prodromal stage Shallow and round to oval Gray to yellow membrane Clusters of up to 5 ulcers Steroids
Recurrent Aphthous Stomatitis (RAS) Minor apthae
Recurrent Aphthous Stomatitis (RAS) Major Aphthae Uncommon Irregular, deep ulcers 1-3 cm in size Raised borders Heal in 4-6 weeks Extensive scarring and distortion BIOPSY!! Steroids
Recurrent Aphthous Stomatitis (RAS) Major apthae
Major aphthous ulcer
Recurrent Aphthous Stomatitis (RAS) Herpetiform Aphthae Uncommon Crops of up to 150 very small (<3mm) ulcers Heal completely in 7-10 days COMPLETELY UNRELATED TO HERPESVIRUS
Recurrent Aphthous Stomatitis (RAS) Herpetiform aphthae
Behcet’s Symptom complex of: Recurrent aphthous ulcers of the mouth Painful genital ulcers Uveitis or conjuctivitis
Behcet’s Affects persons of Mediterranean, Middle Eastern, or Japanese decent Easily confused with Stevens-Johnson syndrome or Reiter’s disease Need referral for systemic treatment
Acute Ulcerative Behcet’s Syndrome 	recurrent oral and genital ulcers 	arthritis 	inflammatory disease of eyes and GI tract.
Acute Ulcerative Reiter’s Syndrome mainly young men 20 to 30 Classis triad  Conjunctivitis Arthritis urethritis.  Oral lesions range from erythema to papules to ulcerations involving the buccal mucosa, gingiva, and lips.  Lesions on the tongue resemble geographic tongue
Herpesvirus Infection HSV-1 and/or HSV-2 Primary Infection Secondary Infection Varicella zoster virus (HHV-3)
Herpesvirus Infection Primary Infection Herpetic gingivostomatitis Younger patients Often asymptomatic May be associated with fever, chills, malaise Vesicles-ulcers-crusting Anywhere in the oral cavity
Herpesvirus Infection Primary Infection
Herpesvirus Infection Primary Infection
Herpesvirus Infection Secondary Infection Reactivation of latent virus Not associated with systemic symptoms Small vesicles  Occur only on the hard palate and gingiva Prodromal signs
Herpesvirus Infection Secondary infection
Herpesvirus Infection Varicella zoster virus (HHV-3) Latent infection Oral ulcers Dermatomal distribution
Herpesvirus Infection Varicella zoster virus
Herpesvirus Infection Varicella zoster virus
Herpangina NOT caused by Herpesvirus Coxsackie A virus Children < 10 years of age Common in summer and fall Often subclinical presentation Headache/Abdominal pain 48hrs prior to papulovesicular lesions on tonsils & uvula. Sore throat
Herpangina
Primary Herpetic Gingivostomatitis
Acute ulcerative Varicella zoster virus- distribution of trigeminal nerve Coxsackie- prodrome, vesicular, pharynx,tonsils, soft palate Recurrent herpes simplex- prodrome present,  	herpes labialis, limited to keratinized epithelium and can involve the gingiva and hard  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 palate
Recurrent herpes simplex
Chronic:  longer duration, well circumscribed, raised borders, indurated base with crater Trauma Infection Neoplasm Necrotizing sialometaplasia
Trauma: Ill-Fitting dentures
Infection Rare HIV/AIDS patients Bacterial Deep mycotic infection Candida
Infection Bacterial Usually secondary infection Primary infection:  syphilis, tuberculous, or actinomycosis
Infection Bacterial-Syphilis
Syphilis
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
Infection Bacterial-Syphilis
Infection Mycotic Blastomycosis Histoplasmosis
Infection Histoplasmosis
Acute ulcerative	 Histoplasmosis disseminated form, oropharyngeal lesions may present as ulcerative, nodular, or vegetative  	Biopsy will provide the diagnosis
Infection Candida Candida albicans Most common Normal flora Predisposing factors White creamy patches  KOH prep  Nystatin oral suspension
Infection Candida
Candidiasis
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
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
Candidiasis Confirmation with KOH smear, tissue PAS or silver stains Treatment- topical or systemic, polyene,azoles
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
Leukoedema
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
Oral Leukoplakia
Oral Leukoplakia
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
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
Proliferative Verrucous Leukoplakia
Site of Leukoplakia	 Risk of dysplasia/carcinoma higher with floor of mouth, ventrolateral tongue, retromolar trigone, soft palate than with other oral sites
Epithelial Dysplasia
Treatment	 Trial of cessation of offending agent, follow-up Guided by microscopic characterization Benign, minimally dysplastic- periodic observation or elective excision Complete excision  scalpel excision laser ablation electrocautery,  cryoablation Chemoprevention
Oral Hairy Leukoplakia
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
Neoplasm Squamous cell carcinoma (SCC) Most common Irregular ulcers with raised margins May be exophytic, infiltrative or verrucoid Mimic benign lesions grossly
Neoplasm Squamous cell carcinoma
Neoplasm Squamous cell carcinoma
Neoplasm Squamous cell carcinoma
Necrotizing Sialometaplasia Inflammatory condition Ischemia to minor salivary glands Deep ulcers of the hard palate Resolves in 6 weeks
Sialometaplasia
Sialometaplasia
Generalized:  broad classification encompassing a wide variety of causative agents or conditions Contact stomatitis Radiation mucositis Cancer chemotherapy
Dermatologic Disorders:  cutaneous and oral manifestations Erythema multiforme Lichen planus Benign mucous membrane pemphigoid Bullous pemphigoid Pemphigus vulgaris
Dermatologic Disorders Erythema multiforme Rapidly progressive Antigen-antibody complex deposition in vessels of the dermis Target lesions of the skin Diffuse ulceration, crusting of lips, tongue, buccal mucosa Self-limited, heal without scarring
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  central area that can develop bullae, vesicles.
Dermatologic Disorders Erythema multiforme
Erythema Multiforme
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 buccalmucosa Mucosal ulcers are irregular in size and shape, tender and covered with fibrinousexudate. Sialorrhea, pain, odynophagia, dysathria.  Severe EM are associated with involvement of other mucosal sites- eyes, genitalia, and less common esophagus and lungs
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
Dermatologic Disorders Lichen planus Chronic disease of skin and mucous membranes Destruction of basal cell layer by activated lymphocytes Reticular: fine, lacy appearance on buccal mucosa (Wickman’s striae) Hypertrophic: resembles leukoplakia Atrophic or erosive: painful
Oral lichen planus
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
Dermatologic Disorders Lichen planus
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
Dermatologic Disorders Lichen planus
Dermatologic Disorders Lichen planus
Dermatologic Disorders Benign mucous membrane pemphigoid Tense subepithelial bullae of skin and mucous membranes Rupture, large erosions, heal without scarring Sloughing (Nikolsky sign) Bullous pemphigoid Cutaneous lesions more common Both show subepithelial clefting with dissolution of the basement membrane IgG in basement membrane
Dermatologic Disorders Benign mucous membrane pemphigoid
Dermatologic Disorders Benign mucous membrane pemphigoid
Dermatologic Disorders Pemphigus vulgaris Severe, potentially fatal Jewish and Italians Intraepithelial bullae and acantholysis Nikolsky’s sign Loss of intracellular bridges Autoimmune response to desmoglein 3 Intraepithelial clefting
Dermatologic Disorders Pemphigus vulgaris
Dermatologic Disorders Pemphigus vulgaris
Quinn’s Rule for Stomatitis: “Call it aphthous stomatitis.   Treat it for two weeks.   If it is still there,  biopsy it.”
 ORAL CAVITY LESIONS   Frederick Mars Untalan, MD

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Oral cavity lesions

  • 1. ORAL CAVITY LESIONS Frederick Mars Untalan, MD
  • 2.
  • 3. mouth ulcer Latin ulcus and from Greek "ἕλκος" - elkos, "wound"[ American English, canker sore open sore inside the mouth, or rarely a break in the mucous membrane or the epithelium on the lips or surrounding the mouth. Causes: physical abrasion, acidic fruit, infection, other medical conditions, medications, and cancerous and nonspecific processes. Two common types : aphthous ulcers cold sores or fever blisters
  • 4. Epidemiology Epidemiological studies show an average prevalence between 15% and 30%. women > men and < 45 years. >16-25 year olds, and <over 55. The frequency of mouth ulcers varies from fewer than 4 episodes per year (85% of all cases) to more than one episode per month (10% of all cases) including people suffering from continuous RAS
  • 5. ORAL CAVITY LIPS TEETH GINGIVA PALATE TONGUE ORAL MUCOUS MEMBRANES ORAL LYMPHOID TISSUES
  • 6. Acute: small, recent onset, short duration, recurrent Trauma Recurrent Aphthous Stomatitis Behcet’s Herpesvirus Infection Herpangina
  • 8.
  • 10.
  • 13. Recurrent Aphthous Stomatitis(RAS) Most common ulcerative lesion of oral cavity Recurrent, painful ulcers Confined to soft mucosa Subdivided into three types: Minor aphthae Major aphthae Herpetiformaphthae
  • 14. Recurrent Aphthous Stomatitis(RAS) Minor aphthae: Less than 1 cm Heal completely in 7-10 days without scarring Painful Prodromal stage Shallow and round to oval Gray to yellow membrane Clusters of up to 5 ulcers Steroids
  • 15. Recurrent Aphthous Stomatitis (RAS) Minor apthae
  • 16. Recurrent Aphthous Stomatitis (RAS) Major Aphthae Uncommon Irregular, deep ulcers 1-3 cm in size Raised borders Heal in 4-6 weeks Extensive scarring and distortion BIOPSY!! Steroids
  • 17.
  • 18.
  • 19. Recurrent Aphthous Stomatitis (RAS) Major apthae
  • 21. Recurrent Aphthous Stomatitis (RAS) Herpetiform Aphthae Uncommon Crops of up to 150 very small (<3mm) ulcers Heal completely in 7-10 days COMPLETELY UNRELATED TO HERPESVIRUS
  • 22. Recurrent Aphthous Stomatitis (RAS) Herpetiform aphthae
  • 23. Behcet’s Symptom complex of: Recurrent aphthous ulcers of the mouth Painful genital ulcers Uveitis or conjuctivitis
  • 24. Behcet’s Affects persons of Mediterranean, Middle Eastern, or Japanese decent Easily confused with Stevens-Johnson syndrome or Reiter’s disease Need referral for systemic treatment
  • 25.
  • 26.
  • 27. Acute Ulcerative Behcet’s Syndrome recurrent oral and genital ulcers arthritis inflammatory disease of eyes and GI tract.
  • 28. Acute Ulcerative Reiter’s Syndrome mainly young men 20 to 30 Classis triad Conjunctivitis Arthritis urethritis. Oral lesions range from erythema to papules to ulcerations involving the buccal mucosa, gingiva, and lips. Lesions on the tongue resemble geographic tongue
  • 29. Herpesvirus Infection HSV-1 and/or HSV-2 Primary Infection Secondary Infection Varicella zoster virus (HHV-3)
  • 30. Herpesvirus Infection Primary Infection Herpetic gingivostomatitis Younger patients Often asymptomatic May be associated with fever, chills, malaise Vesicles-ulcers-crusting Anywhere in the oral cavity
  • 33. Herpesvirus Infection Secondary Infection Reactivation of latent virus Not associated with systemic symptoms Small vesicles Occur only on the hard palate and gingiva Prodromal signs
  • 35. Herpesvirus Infection Varicella zoster virus (HHV-3) Latent infection Oral ulcers Dermatomal distribution
  • 36.
  • 39. Herpangina NOT caused by Herpesvirus Coxsackie A virus Children < 10 years of age Common in summer and fall Often subclinical presentation Headache/Abdominal pain 48hrs prior to papulovesicular lesions on tonsils & uvula. Sore throat
  • 42. Acute ulcerative Varicella zoster virus- distribution of trigeminal nerve Coxsackie- prodrome, vesicular, pharynx,tonsils, soft palate Recurrent herpes simplex- prodrome present, herpes labialis, limited to keratinized epithelium and can involve the gingiva and hard 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 palate
  • 44. Chronic: longer duration, well circumscribed, raised borders, indurated base with crater Trauma Infection Neoplasm Necrotizing sialometaplasia
  • 46. Infection Rare HIV/AIDS patients Bacterial Deep mycotic infection Candida
  • 47. Infection Bacterial Usually secondary infection Primary infection: syphilis, tuberculous, or actinomycosis
  • 50. 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
  • 51.
  • 52.
  • 53.
  • 57. Acute ulcerative Histoplasmosis disseminated form, oropharyngeal lesions may present as ulcerative, nodular, or vegetative Biopsy will provide the diagnosis
  • 58. Infection Candida Candida albicans Most common Normal flora Predisposing factors White creamy patches KOH prep Nystatin oral suspension
  • 61. 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
  • 62. 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
  • 63. Candidiasis Confirmation with KOH smear, tissue PAS or silver stains Treatment- topical or systemic, polyene,azoles
  • 64. 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
  • 66. 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
  • 69. 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
  • 70. 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
  • 72. Site of Leukoplakia Risk of dysplasia/carcinoma higher with floor of mouth, ventrolateral tongue, retromolar trigone, soft palate than with other oral sites
  • 74. Treatment Trial of cessation of offending agent, follow-up Guided by microscopic characterization Benign, minimally dysplastic- periodic observation or elective excision Complete excision scalpel excision laser ablation electrocautery, cryoablation Chemoprevention
  • 76. 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
  • 77. Neoplasm Squamous cell carcinoma (SCC) Most common Irregular ulcers with raised margins May be exophytic, infiltrative or verrucoid Mimic benign lesions grossly
  • 81. Necrotizing Sialometaplasia Inflammatory condition Ischemia to minor salivary glands Deep ulcers of the hard palate Resolves in 6 weeks
  • 84. Generalized: broad classification encompassing a wide variety of causative agents or conditions Contact stomatitis Radiation mucositis Cancer chemotherapy
  • 85. Dermatologic Disorders: cutaneous and oral manifestations Erythema multiforme Lichen planus Benign mucous membrane pemphigoid Bullous pemphigoid Pemphigus vulgaris
  • 86. Dermatologic Disorders Erythema multiforme Rapidly progressive Antigen-antibody complex deposition in vessels of the dermis Target lesions of the skin Diffuse ulceration, crusting of lips, tongue, buccal mucosa Self-limited, heal without scarring
  • 87. 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 central area that can develop bullae, vesicles.
  • 90. 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 buccalmucosa Mucosal ulcers are irregular in size and shape, tender and covered with fibrinousexudate. Sialorrhea, pain, odynophagia, dysathria. Severe EM are associated with involvement of other mucosal sites- eyes, genitalia, and less common esophagus and lungs
  • 91. 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
  • 92. Dermatologic Disorders Lichen planus Chronic disease of skin and mucous membranes Destruction of basal cell layer by activated lymphocytes Reticular: fine, lacy appearance on buccal mucosa (Wickman’s striae) Hypertrophic: resembles leukoplakia Atrophic or erosive: painful
  • 94. 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
  • 96. 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
  • 99. Dermatologic Disorders Benign mucous membrane pemphigoid Tense subepithelial bullae of skin and mucous membranes Rupture, large erosions, heal without scarring Sloughing (Nikolsky sign) Bullous pemphigoid Cutaneous lesions more common Both show subepithelial clefting with dissolution of the basement membrane IgG in basement membrane
  • 100. Dermatologic Disorders Benign mucous membrane pemphigoid
  • 101. Dermatologic Disorders Benign mucous membrane pemphigoid
  • 102. Dermatologic Disorders Pemphigus vulgaris Severe, potentially fatal Jewish and Italians Intraepithelial bullae and acantholysis Nikolsky’s sign Loss of intracellular bridges Autoimmune response to desmoglein 3 Intraepithelial clefting
  • 105. Quinn’s Rule for Stomatitis: “Call it aphthous stomatitis. Treat it for two weeks. If it is still there, biopsy it.”
  • 106. ORAL CAVITY LESIONS Frederick Mars Untalan, MD