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Similar to desquamative ginigivitis
desquamative ginigivitis
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- 2. Contents Introduction History Epidemiology Classification Disorders associated withdesquamative gingivitis • Lichen planus • Pemphigoid • Pemphigus • Lupus erythematosus • Erythema multiforme • Miscellaneous Conditions mimicking desquamative gingivitis Diagnostic pathways Clinical significance and implications Conclusion References
- 3. Introduction Current classificationsystem Common characteristics Immunomediated pathogenesis Desquamative gingivitis
- 4. Introduction Gingivosis 75% cases –dermatologic genesis
- 5. History 1894 Prinz,1932 McCarthy et al, 1960 Glickman and Smulow, 1964
- 6. Epidemiologic features Highestprevalence - lichen planus and mucous membrane pemphigoid Rarer conditions Disorder Number of cases of desquamative gingivitis Mucous membrane pemphigoid 35-48% Oral lichen planus 24- 45% Pemphigus vulgaris 3-15%
- 7. Classification 1) Dermatoses a) Cicatricialpemphigoid b) Pemphigus c) Lichen Planus d) Erythema Multiforme e) Lupus Erythematosis f) Linear IgA disease 2) Hormonal influence a) Estrogen deficiency following oophorectomy & post menopausal women b) Testosterone imbalance c) Hypothyroidism 3) Abnormal response to irritation 4) Chronic infection a) Tuberculosis b) Chronic candidiasis c) Histoplasmosis 5) Aging 6) Idiopathic
- 8. Disorders associated withdesquamative gingivitis General clinical features • Predominantly affects women (Prinz 1932, Meritt 1993) • Occurs in 4th – 5th decade • Red, swollen & glossy gingiva • Multiple vesicle and superficial denuded areas • Difficult to eat hot, spicy food • Nikolsky’s sign may be positive • Types
- 9. Disorders associated withdesquamative gingivitis • Scattered, irregularly shaped areas • Denuded and red gingiva • Extremely painful • Elevation of epithelium → vesicle • Patchy distribution • Slight pitting with pressure • Burning sensation • Nikolsky’s sign • Labial > Lingual • Diffuse erythema • Painless
- 10. Disorders associated withdesquamative gingivitis Lichen planus Pemphigoid Pemphigus Lupus erythematosus Erythema multiforme Miscellaneous
- 11. Lichen planus Inflammatorymucocutaneous disorder Immunologically mediated - host T lymphocytes play a central role (Ishii et al, 1987) 0.1 - 4% of the population (Scully et al 1998) Female : Male – 2:1
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- 13. Oral lesions •Relapsing –remitting course • Papule arrangement • Wickhams striae • Various clinical forms Atrophic Erosive Reticular Bullous Lichen planus
- 14. • Painful erythematousareas • Sensitive to heat, acid, spicy foods • Asymptomatic • Bilateral interlacing white strands • Erythematous background Reticular Erosive Lichen planus
- 15. Gingival lesions •Keratotic lesions • Erosive or ulcerative lesions • Vesicular or bullous lesions • Atrophic lesions Lichen planus
- 16. Pathogenesis CD8+ T cellTNF-α Apoptosis CD4+ T cell IFN-γ, IL-2 ↑ immune response Keratinocytes IL-1,8,10,12; TNF-α Lichen planus
- 17. Histopathology • Pullon etal (1969) • Irregularity of nuclear membrane • Increased thickening and granularity of epithelial tonofibrils Lichen planus
- 18. Immunopathology • Direct immunofluorescence •Indirect immunofluorescence Lichen planus
- 19. Differential diagnosis • Lupuserythematosus • Chronic ulcerative stomatitis • Cicatricial pemphigoid • Pemphigus vulgaris Lichen planus
- 20. Diagnosis of lichenplanus Erosive/UlcerativeAsymptomatic No therapy Follow up 6-12 months Severe cases - injections of triamcinolone acetonide (10 to 20 mg) Topical steroids No resolution Resolution Refer to dermatologist Retinoids, Dapsone, Systemic steroids Wean off and monitor Treatment of Lichen planus
- 21. Recalcitrant cases -0.1% tacrolimus Antifungal therapy Risk for malignant transformation ~ 5% (Becker et al 2006) Lichen planus
- 22. Pemphigoid Cutaneous, immune-mediated, subepithelialbullous diseases characterized by separation of the basement membrane zone Bullous pemphigoid Cicatricial pemphigoid
- 23. Parapemphigus Oral involvement –1/3 of the patients Histologically, • No acantholysis • Subepithelial vesicles • Epithelium separation • Two major antigenic determinants Bullous pemphigoid 230- kDa protein plaque BP1 180-kDa collagen- like transmembrane protein BP2
- 24. Immunopathology Treatment • Primary treatment- moderate dose of prednisone • Steroid sparing strategies • Localized lesions - high potency topical steroids or tetracycline Bullous pemphigoid
- 25. Mucous membrane pemphigoid Oralcavity, conjunctiva, mucosa of the nose, vagina, rectum, esophagus, urethra Female predilection Five subtypes Cicatricial pemphigoid Oral pemphigoid Multiple antigens pemphigoid Ocular pemphigoid anti-BP antigen mucosal pemphigoid Anti-epiligrin pemphigoid
- 26. Oral lesions • Areasof erythema, desquamation, ulceration • Bullae - thick walled • Healing - 3 weeks or longer Ocular lesions Cicatricial pemphigoid Unilateral conjunctivitis Symblepharon Ankyloblepharon Bilateral conjunctivitis
- 27. BP 1, BP2, laminin5 and 6, uncein, α6β4integrin Cytokine release Sequestration of leukocytes Complement activation Production of autoantibodies Blister formation Cicatricial pemphigoid Release of proteases, collagenases, elastases
- 28. Histopathology • Non specific •Subepithelial vesiculation • Intact basal layer Immunopathology • Direct immunofluorescence - IgG and C3 • Indirect immunofluorescence - positive in <25% Cicatricial pemphigoid
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- 30. Diagnosis of cicatricial pemphigoid Asymptomatic Plaquecontrol Mild to moderate Topical steroids Severe Refer to dermatologist Prednisolone Azathioprine Dapsone Sulfonamide Tetracycline Treatment of Cicatricial pemphigoid
- 31. Pemphigus Cutaneous +mucous membranes blisters Types P. vulgaris P. vegetans P. foliaceous P. erythematosus Pemphigus vulgaris
- 32. 0.1 - 0.5cases /100,000 individuals/year Higher predilection in women (Robinson et al 1997) Potentially lethal: mortality rate < 10% (Black et al 2005) Etiology Idiopathic Drug induced pemphigus Paraneoplastic pemphigus Pemphigus vulgaris
- 33. Oral lesions • Siegelet al 1994 • Painful small vesicles → large bullae • Nikolsky’s sign Pemphigus vulgaris Soft palate > buccal mucosa > tongue > lower labial mucosa > gingiva
- 34. Pathogenesis Pemphigus vulgaris Harmanet al 2001
- 35. Histopathology Intraepithelial vesiculation ↓ Fluid filledbulla Pemphigus vulgaris Acantholysis ↓ Intercellular bridges are lost "Tombstone" appearance
- 36. Cytology • Tzanckcells • Tzanck test Immunopathology • Direct • Indirect
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- 38. Treatment Pemphigus vulgaris Diagnosis of pemphigusvulgaris Primary treatment Secondary treatment Prednisone Decrease dose →maintenance dose Azathioprine Cyclosporine Methyltrexate Plasmaphoresis Refer to dermatologist
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- 40. Systemic cutaneous •Predilection for females (10:1) • Affects vital organs – kidneys, heart • Classic cutaneous lesion • Oral lesions (36% of SLE patients) - ulcerative or lichen planus-like • Tendency to bleed, surrounded by red halo Lupus erythematosus
- 41. Laboratory test • LEcell inclusion phenomenon(Weiss and Swift et al 1955) Immunopathology • Direct - Perilesional and normal tissue: Ig and C3 deposits at dermal-epidermal interface Lupus erythematosus
- 42. Chronic cutaneous •Skin lesions – Discoid lupus erythematosus • Produce scarring and atrophy • Oral lesions - 9% of patients present lichen planus-like plaques Lupus erythematosus Soft palate > buccal mucosa > tongue > lower labial mucosa > gingiva
- 43. Immunopathology • Subacute cutaneous lupuserythematosus Lupus erythematosus
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- 45. Treatment Diagnosis of LE Cutaneouslesion Topical steroids Sunscreens Hydroxychloroquinine Mucosal lesion Topical steroids Systemic involvement Moderate- to-high doses of prednisone Lupus erythematosus
- 46. Erythema Multiforme Acute bullousand/or macular inflammatory mucocutaneous disease Types Etiology Erythema multiforme minor Erythema multiforme major/ Stevens-Johnson syndrome Mycoplasma infection Herpes simplex infection Drug reactions
- 47. Male predilection Symmetricdistribution of macules, papules or vesicles “target”, “iris” or “bulls eye” appearance Erythema multiforme
- 48. Oral lesions • 70%of patients with skin involvement (McCarthy 1980) • Multiple, large, painful ulcers with an erythematous border • Hemorrhagic crusting of vermilion border of lips Buccal mucosa > tongue > lower labial mucosa > floor of mouth > palate >gingiva Erythema multiforme
- 49. Steven Johnsons Syndrome •Severe bullous form • Abrupt occurrence of fever, malaise, photophobia and eruptions of oral mucosa, genitilia and skin • Oral lesions → rupture → surfaces covered with thick white or yellow exudate • Lips - ulceration with bloody crusting • ANUG Erythema multiforme
- 50. Histopathology • Epithelium • Laminapropria Immunopathology – negative Erythema multiforme
- 51. Treatment Diagnosis oferythema multiforme Spontaneous resolution Mild cases Systemic and local antihistamines + topical anesthetics + debridement of lesions Severe cases Systemic corticosteroids Erythema multiforme
- 52. Miscellaneous Chronic Ulcerative Stomatitis LinearIgA Disease Dermatitis Herpetiformis Drug eruptions
- 53. Drug eruptions • Stomatitismedicamentosa • Stomatitis venenata or contact stomatitis Etiology • Mercurial compounds • Toothpaste Clinical presentation Vesicular or bullous Pigmented or nonpigmented macula Erosions Deep ulceration with purpura
- 54. Conditions Mimicking Desquamative Gingivitis Factitiouslesions Candidiasis Graft versus host disease Wegeners granulomatosis Foreign body gingivitis
- 55. Diagnostic pathways Identification of desquamative lesion Immunopathologic assessment Histopathologic assessment Extraoral examination Intra oral examination Clinical history Diagnosis establishment General and periodontal management
- 56. Clinical history Onset Chief complaint Infections Topicalsubstances Drug intake Acute, subacute Symptoms Intraoral examination Location Clinical presentation Extraoral examination Other mucosae Skin Internal organsHistopathology Epithelial changes Basement membrane alterations Lamina propria Cell –cell attachment, Acantholysis, epithelial thickening Inflammatory infiltrate BM integrity and staining Immunopathology Serum Involved tissue DIF IIF
- 57. Clinical significance Painful oral lesions Impededaily oral hygiene procedures ↑ plaque and calculus ↑ inflammation and enhancement of symptoms Exacerbation of lesions Direct effect (Ramon et al 1999, Tricamo et al 2006) Indirect effect
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- 60. References Newman, Takei,Klokkevold, Carranza. 10th edition. Carranza’s Clinical Periodontology. W. B. Saunders Company. Lucio Lo Russo, Stefano Fedele, Rosario Guiglia,Domenico Ciavarella, Lorenzo Lo Muzio, Pio Gallo, Chiara Di Liberto, and Giuseppina Campisi. Diagnostic Pathways and Clinical Significance of Desquamative Gingivitis. J Periodontol 2008;79:4-24. Shafer, Hine and Levy. 4th edition, A textbook of Oral Pathology. W. B. Saunders Company. Burket L. Burket’s Oral Medicine – Diagnosis and Treatment. 9th edition. Lippincott. Michele D. Mignogna, Giulio Fortuna, Stefania Leuci, Elvira Ruoppo, Flavio Marasca and Sergio Matarasso. Nikolsky’s Sign on the Gingival Mucosa: A Clinical Tool for Oral Health Practitioners. J Periodontol 2008;79:2241-2246.
Editor's Notes
- #10 Nikolskys sign – seperation attributed to prevesicular edema causing disruption of epidermal-dermal junction
- #19 “Sawtooth” appearance of rete pegs. Hydropic degeneration of basal layer, with the appearance of a thin band of eosinophilic coagulum in this region. Epithelium becomes thin and atrophic or detaches off the underlying CT producing a Subepithelial vesicle. Colloid bodies or Civatte bodies are seen at the epithelium- CT interface.
- #32 Dapsone (ocular lesions). Side effects – intolerance and hematological side effects
- #41 Intravenoues human Ig has been shown to be successful in steroid resistant cases. (Yeh et al 2005)
- #46 Igg
- #56 Chronic Ulcerative Stomatitis – chronic oral ulcerations which present as painful solitary blisters and resemble erosive lichen planus Linear IgA disease – uncommon mucocutaneous disorder. Cud be trigerred by ACE inhibitors. Resemble erosive lichen planus clinically and histologically Dermatitis herpetiformis – cutaneous manifestaion of celiac disease with tissue transglutaminase as the predominant autoantigen. Characterised by painful ulceration preceeded by collapse of vesicles or bullae.