desquamative gingivitis

desquamative gingivitis

1. DESQUAMATIVE GINGIVITIS DR. BENITA MARIA REGI 1 ST MDS

2. contents History Introduction Chronic desquamative gingivitis Systemic approach for the diagnosis of chronic desquamative gingivitis Diseases clinically presenting as desquamative gingivitis * Lichen planus *Pemphigus *Pemphigoid * Linear IgA disease *Lupus erythematosus * Dermatitis herpetiformis *Chronic ulcerative stomatitis

3. Miscellaneous Conditions Mimicking Desquamative Gingivitis Diagnostic pathways and clinical significance Conclusion References

4. HISTORY Coined in 1932 McCarthy and colleagues (1960) Glickman and Smulow (1964)

5. Introduction DG is a clinically relevant entity….. DG can be associated with a wide range….. Because the majority of disorders causing DG…..

6. Chronic desquamative gingivitis is characterized by intense redness and desquamation of the surface epithelium of the attached gingiva. Chronic desquamative gingivitis

7. Etiology Dermatological diseases Endocrine disturbances Abnormal responses to bacterial plaque Chronic infections Idiopathic Aging (“ desquamtive gingivitis- a clinical sign in mucous membrane pemphigoid: report of case and review of literature: shamimul hassan ”)

8. Nisengard and Neiders & Rogers and his associates…

9. Epidemiological features “(Diagnostic Pathways and Clinical Significance of Desquamative Gingivitis Lucio Lo Russo et al”)

10. Diagnosis of desquamative gingivitis: Microscopic Examination Immunofluore-scence

11. Practitioner's experience, Systemic impact of the disease Systemic complications of the medications Management:-

12. Treatment Local treatment Plaque control Use of corticosteroid ointments and creams Systemic treatment High dose therapy Moderate dose therapy

13. Disorders associated with desquamative gingivitis

14. ORAL LICHEN PLANUS: Immunologically mediated mucocutaneous disorder - T cells play a central role. Middle aged & older women 2:1 ratio

15. Idiopathic S t r e ss Traumatism Malnutrition and infection Autoimmune Hereditary Gri n s p a ns syndrome Li c hen planus Etio l ogy

16. ORAL MANIFESTATIONS: Radiating white or gray , velvety, thread-like papules in a linear, annular or retiform arrangement forming typical lacy, reticular patches, rings and streaks over the buccal mucosa, lips, tongue and palate. Vesicle and bulla formation.

17. GINGIVAL LESIONS Atrophic Atrophic Keratotic lesion Erosive Re t i c ul a r

18. Histopathology

19. DI- Linear-fibrillar deposits of fibrin in the basement membrane zone. Scattered immunoglobulin-staining cytoid bodies in the upper areas of the lamina propria. Serum tests using indirect immunofluorescence are negative in lichen planus.

20. TREATMENT:- The keratotic lesions of oral lichen planus are asymptomatic and do not require treatment. The erosive, bullous, or ulcerative lesions of oral lichen planus are treated with high-potency topical steroid such as 0.05% fluocinonide ointment ( Lidex , three times daily). It can also be mixed 1:1 with carboxymethyl cellulose (Orabase) paste or other adhesive ointment.

21. SEVERE CASES - Intralesional injections of triamcinolone acetonide (10 to 20 mg) or short-term regimens of 40 mg prednisone daily for 5 days followed by 10 to 20 mg daily for an additional 2 weeks. Topical tacrolimus

22. PEMPHIGOID Cutaneous, immune-mediated, subepithelial bullous diseases that are characterized by a separation of the basement membrane zone, including bullous pemphigoid pemphigoid gestationis mucous membrane pemphigoid

23. Cicatricial pemphigoid. Chronic, vesiculobullous autoimmune disorder It predominantly affects women in fifth decade of life. Five subtypes:-

24. Symblepharon Ankyloblepharon Small vesicular lesions on conjunctiva – eventually produces scarring, corneal damage and blindness Ocular involvement

25. ORAL MANIFESTATIONS Desquamative gingivitis with areas of erythema, desquamation, ulceration, and vesiculation of the attached gingiva. Bullae- thick roof- rupture in 2-3 days leaving irregular shaped areas of ulceration; healing- 3 weeks or longer .

26. Separation of epithelium and C.T. occurs at the basement membrane zone. EM- shows spilt in basal lamina

27. Immunopathology Direct immunofluorescence IgG and C3 Indirect immunofluorescence positive in <25%

28. Topical steroids – main Rx for mucous memb . Pemphi . Fluocinonide(0.05%) and Clobetasol propionate (0.05%) in an adhesive vehicle can be used 3 times a day for 6 mnths .

29. BULLOUS PEMPHIGOID Chronic, autoimmune, subepidermal , bullous disease with tense bullae that rupture and become flaccid in the skin.

30. Oral Manifestations Oral lesions – less frequently in BP than in CP Presence of vesicles and areas of erosion and ulceration Lesion- painful Gingival tissues appear extremely erythematous…. Bullae on gingiva

31. Histologically, No acantholysis The epithelium separates from the underlying connective tissue at the basement membrane zone

32. IgG&C3 immune deposits along epithelial basement membrane and circulating IgG antibodies to the epithelial basement membrane. Direct immunofluorescence is positive in 90% to 100% of these patients, whereas indirect immunofluorescence is positive in 40% to 70% of affected patients

33. control signs and symptoms Primary Rx –moderate dose of systemic prednisone Steroid sparing strategies (Prednisone + immunomodulatory drugs)… For localized lesions of bullous pemphigoid,….

34. PEMPHIGUS - Grou p of a utoi m m une bullous di s ord e rs - cutaneous and/or mucous membrane blisters Types P. vulgaris P. foliaceous P. vegetans P. erythematosus

35. Lethal chronic condition Predilection in women(after 4 th decade of life)

36. Range from small vesicles to large bullae Rupture of bullae leads to extensive areas of ulceration Any area of oral cavity involved- Oral lesions confine less often to gingival tissues Nikolsky’s sign…. ORAL LESIONS:- Soft palate > buccal mucosa > tongue > lower labial mucosa > gingiva

37. HISTOPATHOLOGY Intraepithelial vesiculation Tombstone appearance of epithelial cells. Acantholysis

38. Intercellular deposits in epithelium ( IgG in most; C3 in some) of perilesional mucosa

39. TREATMENT Systemic corticosteroids with or without other immunosuppressive agents Steroid sparing therapies- pt not responsive to corticosteroid. Optimal oral hygiene Pts in maintenance phase- prednisone before oral prophylaxis and periodontal surgery to prevent flare ups.

40. CHRONIC ULCERATIVE STOMATITIS 1990 Condition presents with chronic oral ulcerations Predilection for women(4 th decade) Erosions and ulcerations in oral cavity- few cases with cutaneous lesions ORAL LESIONS Painful, solitary small blisters and erosions with surrounding erythema – mainly on gingiva and lateral border of the tongue ; hard palate may also present similar lesions.

41. HISTOPATHOLOGY Hyperkeratosis, acanthosis and liquefaction of the basal cell layer with areas of sub epithelial clefting . The underlying lamina propria exhibits a lymphohistocytic chronic infiltrate in a band like configuration. Immunofluorescence : - Direct (normal and perilesional tissues) – IgG with a speckled pattern - basal cell layer of the normal epithelium. Fibrin deposits at the epithelial- connective tissue interface.

42. TREATMENT Mild cases- topical steroids (fluocinonide, clobetasol propionate) and topical tetracycline Severe cases- systemic steroids Hydroxychloroquine sulfate 200-400 mg/ day – Rx of choice for complete, long lasting remission

43. LINEAR IgA DISEASE (LINEAR IgA DERMATOSIS) Uncommon mucocutaneous disorder with predilection in women C/F Pruritic Vesiculo bullous rash, during middle to late age..

44. ORAL LESIONS Vesicles , Painful ulcerations or erosions and erosive gingivitis/ chelitis Hard and soft palate commonly affected → tonsillar pillars, buccal mucosa, tongue and gingiva Rarely, oral lesion may be the only manifestation for several years; before cutaneous lesions

45. Chronic condition Young adults (20-30 years) Slight predilection for males. Bilateral and symmetric pruritic papules/vesicles… Oral lesions - Painful ulcerations preceded by collapse of ephemeral vesicles/bullae to erythematous lesions.

46. HISTOPATHOLOGY Focal aggregates of neutrophils and eosinophils amidst deposits of fibrin at the apices of the dermal pegs. IMMUNOFLUORESENCE Direct immunofluoresence show that IgA &C3 are present at the dermal papillary apices. There is clear association with celiac disease & circulatory anti endomysial and anti gliaden antibodies may be of diagnostic value.

47. TREATMENT Gluten free diet Oral Dapsone

48. It is an autoimmune disease with three different clinical presentations 1. Systemic Lupus Erythematosus 2. Chronic Cutaneous Lupus Erythematosus (CCLE) 3. Subacute Cutaneous Lupus Erythematosus (SCLE)

49. Predilection for females (10:1) Affects vital organs – kidneys, heart Classic cutaneous lesion …. Oral lesions (36% of SLE patients) - ulcerative or lichen planus-like

50. Skin lesions – Discoid lupus erythematosus Describes chronic scarring and atrophy producing.. Oral lesions - 9% of patients present lichen planus-like plaques .. Soft palate > buccal mucosa > tongue > lower labial mucosa > gingiva

51. SUBACUTE CUTANEOUS LUPUS ERYTHEMATOUS present cutaneous lesions that are similar to DLE but that lack the development of scarring and atrophy.

52. TREATMENT

53. ERYTHEMA MULTIFORME An acute bullous and/or macular inflammatory mucocutaneous disease young adults between the ages of 20 and 40 years;

54. EM minor- Stevens –Johnson syndrome/ Erythema multiforme major Toxic epidermal necrolysis

55. Target or iris lesions with central clearing 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

56. Buccal mucosa > tongu e >lower labial mucosa > floor of the mouth > palate > gingiva.

57. 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

58. TREATMENT

59. DRUG ERUPTIONS D r ug acts as an alle r gen either alon e or in co m bination, sensitiz es the tissues and then causing the allergic reaction. TYPES Stomatitis medicamentosa - mouth or parenterally Stomatitis venenata(contact dermatitis) – local use.

60. Mercurial compounds Toothpaste

61. Vesiculo bullous to pigmented or non-pigmented macular lesions. Erosions result in ulceration and purpuric lesions gingiva ORAL LESIONS

62. Factitious lesions Graft vs. Host disease Wegener's granulomatosis Foreign body gingivitis MISCELLANEOUS CONDITIONS MIMICKING DESQUAMATIVE GINGIVITIS

63. Candidiasis MISCELLANEOUS CONDITIONS MIMICKING DESQUAMATIVE GINGIVITIS Kindler syndrome

64. Summary of diagnostic pathways

65. “(Diagnostic Pathways and Clinical Significance of Desquamative Gingivitis Lucio Lo Russo et al”)

66. Clinical significance Painful gingival and oral lesions….. This can increase the inflammation associated with DG lesions,…. The potential direct effects of DG-associated disorders on periodontal status have been investigated rarely.

67. It seems that the presence of DG lesions…. In addition, systemic/topical….. Oral hygiene procedures should be performed avoiding trauma because many immune-mediated disorders associated with DG are characterized by the Koebner phenomenon ,

68. Systemic complications also are important….. Systemic corticosteroids and/ or other immune suppressive drugs…. A small but increased risk for malignant transformation of the oral mucosa…. “(Diagnostic Pathways and Clinical Significance of Desquamative Gingivitis Lucio Lo Russo et al”)

69. From a theoretic point of view, disorders causing DG may have potential harmful In fact, DG lesions are typically chronic and often associated to a wide range of oral symptoms…. In the instance of such an indirect effect…..

70. On the other hand, a direct effect of DG lesions on periodontitis ….. ( Kornman , 2008). Immune-inflammatory mechanisms are also critical for the pathogenesis of most of DG-associated disorders (Lo Russo et al, 2008), which often involves common molecules⁄cytokine networks [e.g. TNF-a for OLP ( Sugerman et al, 2002; Sugermann et al, 1996; Khan et al, 2003)].

71. ( Tricamo et al, 2006) showed that…... ( Akman et al, 2008)…..

72. (“Desquamative Gingivitis − Aetiology, Diagnosis and Management Lewis Winning et al”)

73. C0NCLUSION

74. references Carranza clinical periodontology 12 th edition Shafer's oral pathology 5 th edition Diagnostic Pathways and Clinical Significance of Desquamative Gingivitis J Periodontol 2008;79:4-24. Position Paper Oral Features of Mucocutaneous Disorders J Periodontol 2003;74:1545-1556. Desquamative Gingivitis: Investigation, Diagnosis and Therapeutic Management in Practice Perio 2005; Vol 2, Issue 3: 183–190 Periodontal Implications: Mucocutaneous Disorders Ann Periodontol 1996;1:401-438 Desquamative Gingivitis − Aetiology, Diagnosis and Management; Lewis Winning, Amanda Willis, Brian Mullally and Christopher Irwin Desquamtive gingivitis- a clinical sign in mucous membrane pemphigoid: report of case and review of literature: Shamimul Hassan