1. Desquamative Gingivitis

2. Contents Introduction Etiology Clinical Features Diagnosis
Diseases Clinically Presenting As Desquamative Gingivitis
Lichen Planus
Pemphigoid
Mucus Membrane Pemphigoid
Pemphigus
Chronic Ulcerative Stomatitis
Linear IgA Disease
Dermatitis Herpetiformis
Lupus Erythematosus
Erythema Multiforme
Drug Eruptions
Miscellaneous Conditions Mimicking Desquamative Gingivitis
Conclusion

3. Introduction Rare nonspecific manifestation of oral mucosa
Prinz (1932) - “chronic diffuse desquamative gingivitis” is a specific disease, characterized by erythema, desquammation and ulceration of the free and attached gingiva
McCarthy and Shklar (1960) - desquamative gingivitis is not a specific disease , but a gingival response associated with a variety of conditions

4. Etiology Certain dermatoses Hormonal influence Chronic infections
Idiopathic
Most important dermatoses
Lichen Planus
Cicatrical Pemphigoid (MMP)
Pemphigus Vulgaris

5. Clinical Features Gingivae - red, swollen and glossy in appearance
Occasionally multiple vesicles and superficial denuded areas
Nikolsky’s sign
Sensitive gingival tissue – difficulty in eating hot, cold or spicy food

6. Diagnosis of Desquamative Gingivits
Systematic Approach –
Clinical History
Clinical Examination
Biopsy
Microscopic Examination
Immunofluorescence

7. Clinical History - Onset
A Systematic approach is needed to diagnose disease associated with Desquamative gingivitis -
Clinical History - Onset
Symptoms
Treatment
Clinical examination -Unifocal ,multifocal lesions
Gingival inolvement
Nikolsky’s sign
Biopsy - Histopathological & immunofluoroscent tests of perilesional tissue

8. Management Practitioner’s experience 2. Systemic impact of the disease
3 factors
Practitioner’s experience
Direct and exclusive responsibility of the treatment
e.g., erosive lichen planus which is responsive to topical steroids
2. Systemic impact of the disease
Collaboration with another dectors.
e.g., cicatrical pemphigoid where the dentist treats the oral lesions and ophthalmologist deals with ocular lesions

9. 3. Systemic complications of the condition
Only medical practitioner treats the disease
e.g., pemphigus vulgaris

10. Diseases Clinically Presenting As Desquamative Gingivitis

11. 1. Lichen Planus
A muco cutaneous condition, an immunological disorder involving T- lymphocytes.
Females affected more than males

12. Clinical Features Adults - > 40 years F:M – 2:1
Small, angular, flat-topped papules only a few millimeters in diameter
Wickham’s striae – fine, grayish-white lines covering the papules
Commonly involved sites-
Flexor surfaces of wrist
Inner aspect of knees & thighs
Trunk

13. Types of Lichen Planus -
Chronic Dermatosis- violet papules with pruritis
Oral lesions- Reticular( Wickhams striae)
Atrophic
Bullous & Erosive
3. Gingival lesions- Keratotic
Erosive or Ulcerative
Vesicular or bullous

14. Oral Lesions Reticular type – Asymptomatic
Bilateral on the posterior region of buccal mucosa
Tongue, gingiva, palate, alveolar mucosa may also be affected
Interlacing white lines

15. Erosive type – Usually painful
Atrophic, erythematous and often ulcerated areas
Fine, white radiating striations bordering the atrophic and ulcerated zones
Sensitive to heat, acid and spicy foods

16. Erosive or Ulcerative lesions
Gingival Lesions
Keratotic lesions
Raised white lesions presenting as groups of individual papules, linear or reticular lesions, or plaque like configurations
Erosive or Ulcerative lesions
Extensive erythematous areas with a patchy distribution
Exacerbated by slight trauma (e.g., tooth brushing)

17. Vesicular or Bullous lesion
Raised, fluid-filled lesions which rupture quickly and leave ulceration
Atrophic lesions
Produce epithelial thinning resulting in gingival erythema

18. Differential Diagnosis
Lichenoid reactions
Leukoplakia
Candidiasis
Pemphigus
Cicatrical pemphigoid
Erythema multiforme
Syphilis
Recurrent aphthae
Lupus erythematosus
Chronic ulcerative stomatitis

19. Treatment Keratotic, asymptomatic lesions – no Rx. Regular follow-up
Erosive/bullous/ ulcerative lesions - topical steroids such as 0.05% fluocinonide ointment (Lidex TDS)
In more severe cases,
Intralesional injections of triamcinolone acetonide or
40 mg of prednisone OD for 5 days, followed by mg OD for an additional 2 weeks
Elimination of mechanical trauma or irritants such as sharp filling margins

20. Alternative to Corticosteroids -
Cyclosporine
Levamisole
Topical human interferon – β
Systemic isotretinoin
Dapsone
Non-Drug Therapy
Surgical excision
Cryosurgery
CO2 laser
Ultraviolet radiation
Magnetism

21. 2. Pemphigoid
A number of cutaneous, immune-mediated, subepithelial bullous diseases characterized by a separation of the basement membrane zone (BMZ)
Bullous Pemphigoid (nonscarring & confined to skin)
Mucous Membrane Pemphigoid (scarring & confined to MM)
Pemphigoid Gestationis

22. Bullo us Pemphigoid (BP)
Chronic, autoimmune, subepidermal, blistering skin disease that rarely involves mucous membranes
Oral involvement occurs in few patients

23. Clinical Features > 60 years of age
Generalized, nonspecific rash, commonly on the limbs which may persist for several weeks to several months
Appearance of the vesiculobullous lesions
Vesicles/bullae remain intact for some days or may rupture to leave a raw, eroded area which heals rapidly

24. Oral Lesions Vesicles and areas of erosion and ulceration
Gingival tissues - extremely erythematous and may desquamate as a result of even minor frictional trauma

25. Therapy Primary Rx - Moderate dose of systemic prednisone
When high doses of steroids are needed or the steroid alone fails to control the disease - Steroid-sparing strategies (prednisone plus other immunomodulator drugs)
For localized lesions of BP -
Topical steroids
Tetracycline with/without nicotinamide

26. Mucous Membrane Pemphigoid (Cicatrical Pemphigoid)
Chronic, vesiculobullous autoimmune disorder of unknown origin that predominantly affects the mucous membranes, including the mouth and the oropharynx, the conjunctiva, the nares and the genitalia

27. Subtypes Oral pemphigoid Antiepiligrin pemphigoid
Anti-BP antigen mucosal pemphigoid
Multiple-antigens pemphigoid
Ocular pemphigoid

28. Clinical Features Peak age - 40 and 50 years Ocular Lesions
Unilateral conjunctivitis that becomes bilateral within 2 years
Symblepharon - adhesions of eyelid to eyeball
Ankyloblepharon - adhesions at the edges of the eyelids
Narrowing of palpebral fissure

29. Oral Lesions
Desquamative gingivitis, with areas of erythema, desquamation, ulceration and vesiculation of the attached gingiva
Lesions - vesiculobullous in nature
- persist for 2-3 days
- rupture leaving a raw, eroded bleeding surface
Involvement of the oropharynx - dysphagia

30. Therapy
Fluocinonide (0.05%) & Clobetasol propionate (0.05%) in an adhesive vehicle TDS for up to 6 months
When confined to gingival tissues - topical corticosteroids
Meticulous oral hygiene
Minimize gingival irritation from any dental prosthesis
If ocular involvement is present - systemic corticosteroids are indicated

31. 3. Pemphigus Vulgaris
Autoimmune bullous disorders that produce cutaneous and mucous membrane blisters
Potentially lethal, chronic condition
10% mortality rate

32. Etiology Diet – controversial Drugs – Penicillamine Rifampicin
Diclofenac
Viruses – HSV
Other Factors – smoking, exposure to pesticides
Other Autoimmune diseases – Lupus Erythematosis, pernicious anemia

33. Clinical Features 50-60 years
Rapid appearance of vesicles & bullae varying in diameter from a few mm to cm
Rupture of bullae leave a raw, eroded surface
Nikolsky’s sign – loss of epithelium caused by rubbing unaffected skin

34. Oral Lesions Range from small vesicles to large bullae
Ill-defined, irregularly shaped, gingival, buccal or palatine erosions, which are painful and slow to heal
Gingival lesions - less common and usually comprise severe desquamative or erosive gingivitis
Soft palate – most commonly involved

35. Treatment
Topical or intralesional corticosteroids or other immunosuppressants
The treatment of desquamative gingivitis consists of-
Improving the oral hygiene
Minimizing irritation of the lesion
Alternative treatment to corticosteroids –
Chlorambucil, azathioprine, cyclophosphamide
Other drugs – gold, dapsone, prostaglandin E2
Plasmapheresis
Intravenous immunoglobulins

36. 4. Chronic Ulcerative Stomatitis
It clinically presents with chronic ulcerations and has a predilection for women in their fourth decade of life
Oral Lesions
Painful, solitary small blisters and erosions with surrounding erythema are present mainly on the gingiva and the lateral border of the tongue

37. Treatment For mild cases - For severe cases –
Topical steroids (fluocinonide and clobetasol propionate)
Topical tetracycline
For severe cases –
Systemic corticosteroids
Hydroxychloroquine sulfate mg/day

38. 5. Linear IgA Disease (LAD)
Subepidermal vesiculobullous disease that may be idiopathic or drug-induced
Most commonly caused by angiotensin converting enzyme (ACE) inhibitors
Children and adults are affected
Historically known as chronic bullous dermatoses of childhood

39. Oral Lesions
Vesicles, painful ulcerations or erosions and erosive gingivitis / cheilitis
The hard and soft palates are most commonly affected followed by tonsills, buccal mucosa, tongue and gingiva

40. Treatment Combination of sulfones and dapsone
Small amount of prednisone (10-30 mg/day) can be added if the initial response is inadequate
Alternatively, combinations of tetracycline (2 g/day) with nicotinamide (1.5 g/day) have been proved successful

41. 6. Dermatitis Herpetiformis
Rare, benign, chronic, recurrent, immune-mediated blistering dermatologic disease associated with gluten-sensitive enteropathy (GSE)
Approximately 25% of patients with celiac disease have dermatitis herpetiformis
Cutaneous manifestation of celiac disease

42. Clinical Features B/W 20 and 55 years
Pruritus and severe burning, followed by the development of erythematous papules, vesicles, bullae or pustules
Extremities, trunk and buttocks – most commonly affected
Vesicles - symmetrical and in groups
Vesicles or pustule eventually resolve and are followed by hyperpigmentation of the skin

43. Oral Lesions
Vesicles and bullae which rupture rapidly to leave areas of superficial ulceration at any intraoral site

44. 7. Lupus Erythematosus
Autoimmune disease with three different clinical presentations
Systemic lupus erythematosus
Chronic cutaneous lupus erythematosus
Subacute cutaneous lupus erythematosus

45. Systemic Lupus Erythematosus (SLE)
Etiopathogenesis
Not completely known
Genetics, hormones and the environment (e.g. sunlight, drugs) contribute to disease process
Greater production of autoantibodies immune complex formation and tissue damage

46. Clinical Features
Peak age of onset - 30 years in females but 40 years in males
Female:male ratio is 10:1
The cutaneous lesions are characterized by the presence of a rash on the malar area so called butterfly distribution

47. Oral Lesions Usually ulcerative or similar to lichen planus
In 36% of patients, oral ulcerations are present
In 4% of patients, hyperkeratotic plaques are present on buccal mucosa and palate

48. Chronic Cutaneous Lupus Erythematosus (CCLE)
Skin lesions – Discoid Lupus Erythematosus
Oral Lesions
Lichen planus-like plaques on the palate and buccal mucosa
The center of the lesion is slightly depressed and eroded and is covered with a bluish red epithelial surface
On the tongue - circumscribed, smooth, reddened areas in which the papillae are lost or as whitish patches resembling leukoplakia

49. Subacute Cutaneous Lupus Erythematosus
A group of patients who have a characteristic cutaneous lesion that has similarities to DLE but lacks the development of scarring and atrophy

50. Treatment
Cutaneous rashes - topical steroids, sunscreens & hydroxychloroquine
For arthritis and mild pleuritis – NSAIDs / hydroxychloroquine
For severe systemic organ involvement - moderate to high doses of prednisone
For severe cases of SLE or when side effects of prednisone develop, immunosuppressive drugs such as cytotoxic agents

51. 8. Erythema Multiforme
An acute bullous and macular inflammatory mucocutaneous disease
Subtypes
Erythema multiforme minor
Localized eruption of the skin with mild or no mucosal involvement
Erythema multiforme major & Stevens-Johnson Syndrome
More severe mucosal and skin lesions and are potentially life-threatening disorders

52. Etiology 3 most common etiologic factors - Herpes simplex infection
Mycoplasma infection
Drug reactions
The most common causative drugs –
Sulfonamides
Penicillins
Phenylbutazone
Phenytoin

53. ‘iris’, ‘target’ or ‘bull’s eye’
Clinical Features
Any age but the highest incidence – 2nd to 4th decades of life
Males > Females
Characteristic lesion is concentric ringlike in appearance -
‘iris’, ‘target’ or ‘bull’s eye’
Most commonly involved sites are –
Hands and arms
Feet and legs
Face

54. Oral Lesions
Multiple, large, shallow, painful ulcers with erythematous border
Difficulty in swallowing and chewing
Most frequently affected sites
Buccal mucosa
Tongue
Labial mucosa
Floor of the mouth
Hard and soft palate
Gingiva
Hemorrhagic crusting of the vermilion border of the lip

55. Treatment No specific treatment For mild symptoms –
Systemic and local antihistamines together with topical anesthetics
Debridement of lesions with an oxygenating agent
For severe symptoms – systemic corticosteroids

56. 9. Drug Eruptions Stomatitis medicamentosa
Eruptions in the oral cavity resulting from sensitivity to drugs that have been taken by mouth and parenterally
Stomatitis venenata or Contact stomatitis
Local reaction from the use of a medicament in the oral cavity
(e.g., aspirin burn, stomatitis resulting from topical penicillin)
Vesicular and bullous lesion
Gingival lesions may be caused by the mercurial compounds present in the dental amalgam

57. Tartar control toothpaste - Desquamative gingivitis
Pyrophosphates and flavoring agent present in the toothpaste -main causative agents
Cinnamon compounds in tartar control tooth paste may produce intense erythema of the attached gingival tissues
Management includes the elimination of the offending agent

58. Miscellaneous Conditions Mimicking Desquamative Gingivitis

59. Graft versus Host Disease
Candidiasis
Rarely it may be limited to the gingival tissues and may simulate desquamative gingivitis
Graft versus Host Disease
Recipients of allogenic bone marrow transplants
Oral lesions may occasionally resemble desquamative gingivitis

60. Wegener’s Granulomatosis
Classically, gingival tissues exhibit erythema and enlargement and are typically described as “strawberry gums”

61. Foreign Body Gingivitis
More common in women during their fifth decade of life
Most foreign bodies are of dental origin, more specifically abrasives and restorative material

62. Kindler Syndrome It consists of – Cutaneous neonatal bullae
Poikiloderma
Photosensitivity
Acral atrophy
Oral lesions clinically resemble desquamative gingivitis

63. Conclusion
Desquamative gingivitis, in most cases, represents a manifestation of systemic disease
Because it has no specific clinical features, laboratory, histopathologic and immunohistochemical examination, should be used to unmask the underlying disease so that the appropriate treatment can be provided

64. Thank You !!!