Periodontics

1. DESQUAMATIV
E GINGIVITIS
DIAGNOSIS AND
MANAGEMENT

2. INTRODUCTION
 Desquamative gingivitis is characterized by intense
erythema, desquamation &ulceration of the free &
attached gingiva.
 It demonstrate potentially painful gingival erythema,
hemorrhage, sloughing, erosion, and ulceration.
 Lesions may be generalized or localized and may
extend into the alveolar mucosa.
 Often similar lesions are found elsewhere in the oral
cavity.
 DG is most frequently caused by mucocutaneous
diseases with the most common being oral lichen
planus mucous membrane pemphigoid and pemphigus
vulgaris

3. Desquamative gingivitis

4. Characteristic features

5. Oral lichen planus
 Lichen planus is an idiopathic t-cell
mediated inflammatory condition.
 Etiology,
cell mediated ( unidentified
epithelial antigen)

6. Clinical features
 White papular lesions & red erythematous
or erosive areas can be a part of reticular,
papular, plaque like, bullous & ulcerative
patterns.
 Lesions confined only to gingiva (8-10%)
may be entirely erythematous with no
reticular or papular elements.

7. Investigation
Histopathology:
 Hypokeratosis, basal cell
degenaration,
subepithelial lymphocyte
inflammatory infiltrate
Direct immunofluoresence
(DIF):
 Fibrin, fibrinogen at
BMZ

8. Treatment
 Topical and systemic steroids
 Topical tacrolimus or cyclosporine or
systemic hydroxychloroquine for
unresponsive cases
 Survelliance for malignant transformation

9.  Diagnosis of lichen planus
rule out superimposed candidiasis.
if positive use antifungals
Asymptomatic symptomatic
No therapy erosive ulceration
Intralesional steroids for large
chronic ulcers retinoids
dapsone
Periodic exam topical steroids cyclosporine
resolution wean off & moniter photopheresis
no resolution refer to dermatologist systemic steroids

10. Mucous membrane pemphigoid
 Also known as Cicatricial pemphigoid
 Is a chronic, vesiculobullous
autoimmune disorder
Etiology
 Autoantibodies to basement membrane
adhesion complex
Desquamative lesions with
bleeding on the attached
gingiva associated with
MMP.

11. Clinical features
 Intact vesicles of gingiva or other mucosal
surfaces, but frequently appear as non
specific erosions, which spread slowly.
 Desquamative gingivitis is the only
manifestation of the disease.

12. Investigation
HP:
 Subepithelial vesicle formation,
vacuolation in the basal lamina

13. Treatment
 Topical and systemic steroids
 Immunosuppresive drugs like
azathioprine, cyclophosphamide.
 Appropriate referral for extraoral
involvement

14. Diagnosis of MMP
refer to ophthalmologist
Asymptomatic mild to moderate severe
Plaque control topical steroids refer to dermatologist dapsone
methotrexate
prednisone cyclosporine
cyclophosphamide
no resolution azathioprine
dapsone

15. Pemphigus vulgaris
 Are a group of autoimmune bullous disorder
that produce cutaneous and mucous
membranes blisters.
Etiology:
 Autoantibodies to glycoprotein adhesion
molecules present on desmosomes.

16. Clinical features
 Bullae on non-inflammed base, which
rapidly breaks to leave shallow irregular
ulcers seen on the buccal mucosa, palate end
gingiva
 Thin layers of epithelium peels away in an
irregular pattern leaving a denuded base
 Nikolsky’s sign positive
Positive Nikolsky sign associated
with PV. The epithelium could be
peeled away easily by slightly
scratching the surface of the
gingiva.

17. Investigation
 Acantholysis, supra basilar bullae,
acantholytic kerotinocytes ( tzanck cells)
DIF:
 IgG, IgA, IgM, complement within the
epithelial intercellular spaces.

18. Immunofluorescence of Pemphigus
Vulgaris showing IgG in the
intracellular spaces of the epithelium
and cellular separation.
PV histology and DI

19. Treatment
 Topical and systemic steroids
 Immunosuppresive drugs like
azathiooprine, cyclophosphamide
 Surveillance for relapses

20. Diagnosis of pemphigus vulgaris
refer to dermatologist
primary treatment secondary treatment
prednisone
Azathioprine cyclophosphamide cyclosporine methotrexate gold

21. Bullous pemphigoid
Etiology:
 Autoantibodies to BP 180 and BP 230
found in lamina lucida region on the
hemidesmosomes

22. Clinical features
 Bullae which breaks into ulcers seen in
buccal mucosa
 Gingival lesions consist of generalized
edema, inflammation & desquamation with
localized areas of discreate vesicle
formation
 Nikolsky’s sign positive

23. Investigation
HP:
 Subepithelial bullae formation (lamina
lucida) eosinophil rich inflammatory
infiltrate
DIF:
 IgG at BMZ

24. Treatment
 Topical & systemic steroids
 Immunosuppresive drugs like
azathioprine, cyclophosphamide
 Dapsone combination of tetracycline &
nicotinamide

25. Erythema multiforme
Etiology:
 Hypersensitivity reaction – common
inciting factors are HSV and drugs.

26. Clinical features
 Erosions and ulcerations, which are large
and confluent
 Severe crusting and bleeding on the lips.

27. Investigation
HP:
 Subepithelial or
intraepithelial vesiculation,
necrotic keratinocytes,
mixed inflammatory
infiltrate in a perivascular
distribution
DIF:
 Fibrin c3 and cytoid bodies
at BMZ

28. Treatment
 Topical and systemic steroids
 Acyclovir for HSV- associated erythema
multiforme

29. Linear IgA disease
 Also known as linear immunoglobulin A
dermatosis
 Predilection for women
 LAD may mimic lichen planus both
clinically & histopathologically
Etiology:
 Autoantibodies to basement membrane

30. Clinical features
 Blisters and ulcers of oral mucosa
accompained by desquamative gingivitis
 The hard &soft palate are affected more
often

31. Investigation
HP:
 subepithelial blister formation
DIF:
 IgA at BMZ (linear pattern)

32. Treatment
 Topical and systemic steroids
 Dapsone in severe cases

33. Lupus erythematosus
Etiology:
 Prototype of autoimmune disease
involving immune complexes

34. Clinical features
 White radiating striae interspersed with
erythematous lesions seen on gingiva,
buccal mucosa tongue and palate.

35. Investigation
HP:
 Kerotinocyte vacuolization, lamina
propria edema, subepithelial PAS +
deposits, thickening of vascular basement
membrane, lymphocytic perivascular
infiltrate.
DIF:
 IgM, IgG, &C3 at BMZ

36. Treatment
 Topical and systemic steroids
 Hydroxychloroquine for mild cases
 Surveillance for extraoral involvement.

37. Dermatitis herpetiformis
Etiology:
 Immune mediated disease associated with
gluten – sensitive enteropathy.

38. Clinical features
 Vesicles & bullae, which rupture rapidly
to leave areas of superficial ulceration at
any intraoral site

39. Investigation
HP:
 Neutrophil accumulation in dermal
papillae, papillary microabcesses form
and progress to subepidermal
vacuolization and vesicle formation.

40. Treatment
 Dapsone , sulfapyridine, gluten-free diet

41. Conclusion
 Although a definitive diagnosis is required
to provide proper treatment, it is almost
impossible to differentiate between the
diseases and disorders reported to cause DG
based solely on the clinical presentation.
 Since it is possible for the lesions to recur
after DG goes into remission, patients should
be observed for a long period of time.
Periodic follow-ups should be performed and
treatment started immediately when gingival
lesions recur.