By,Dr. Dandu Sivasai Prasad

ReddyIIyr Post Graduate

Mamata Dental College

Desquamative Gingivitis

IntroductionHistoryChronic desquamative gingivitisSystemic approach for the diagnosis

of chronic desquamative gingivitisClinical historyClinical examinationBiopsyImmunofluorescenceManagement

CONTENTS:

Diseases clinically presenting as desquamative gingivitisLichen planusPemphigusPemphigoidLinear IgA diseaseLupus erythematosusDermatitis herpetiformisChronic ulcerative stomatitis

MISCELLANEOUS CONDITIONS MIMICKING DESQUAMATIVE GINGIVITIS:

Conclusion

References

The International workshop for classification of periodontal diseases and conditions noted that the periodontist may be called upon to manage non-plaque related mucocutaneous disorders either alone or as a part of treatment team consisting of physicians, dentists or other allied health care professionals.

Introduction

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

Clinical features of desquamative gingivitis vary in

severity

Mild form

Moderate form

Severe form

Chronic Desquamative Gingivitis:

Mild form:

Erythema

Painless

Females - 17-23 yrs

Moderate form: Patchy distribution of bright

red and gray areas involving marginal and attached gingiva

Smooth and shiny. Slight pitting with pressure Massaging of the gingiva

with the finger results in peeling of the epithelium and exposure of the bleeding connective tissue

Occurs in 30 and 40 years of age

Severe form:Wide areas of the oral

cavity involvedSurface epithelium

appears shreddedBlowing of air causes a

bubble in gingival epithelium

Very painfulConstant dry, burning

sensation

1932 – Princz

1953- Glickman

1960- Mc Carthy

History:

Clinical history

Clinical examination

Biopsy

Microscopic examination

Immunoflouroscence

Direct

Indirect

Systemic approach to diagnosis of Desquamative gingivitis:

ORAL LICHEN PLANUS:

Chronic inflammatory disease that affects skin and mucous membrane.

Wilson – 1869

Diseases clinically presenting as desquamative gingivitis:

Epidemiology:

Prevalence – 1.5 %

Women > Men

Predominant in adults > 40 yrs

Pathogenesis:

Current data suggest that OLP is a T cell-mediated autoimmune disease in which auto-cytotoxic CD8+ T cells trigger apoptosis of oral epithelial cells.

However, the precise cause of OLP is unknown.

The skin lesions of OLP appear as small , angular, flat topped papules.

Clinical features:

Oral lichen planus presents as white striations , white papules, white plaques, erythema, erosions or blisters

Present in a variety of forms:

RETICULAR

ATROPHIC,

PAPULAR,

ULCERATIVE

BULLOUS FORMS.

Oral lesions:

RETICULAR:Wickham’s striae

Plaque like lichen planus:Slightly raised or flat white

area on the oral mucous

membranes.

Plaque type lesions may

clinically similar to

homogenous leukoplakia.

VESICULAR OR BULLOUS LESIONS

These lesions are uncommon & short lived on

the gingiva, quickly rupturing and leaving an

ulceration.

ATROPHIC LESIONSAtrophy of the gingival tissues with ensuing epithelial thinning results in erythema confined to the gingiva.

HISTOPATHOLOGY:

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.

IMMUNOPATHOLOGY:

Lichenoid reactions

Lupus erythematosus

Chronic ulcerative stomatitis

Cicatricial pemphigoid

Pemphigus vulgaris

Leukoplakia

DIFFERENTIAL DIAGNOSIS:

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 (three times daily).

It can also be mixed 1:1 with carboxymethyl cellulose (Orabase) paste or other adhesive ointment.

TREATMENT:

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.

Anti fungal therapy.

Hippocrates was the first to describe pemphigoid as a type of fever accompanied by blisters .

Types of pemphigoid that are as follows:

Bullous pemphigoid Cicatrical / mucous membrane pemphigoid Antiepiligrin pemphigoid

PEMPHIGOID:

Cicatricial pemphigoid.Chronic, vesiculobullous autoimmune disorderIt predominantly affects women in fifth decade

of life.

The percentage of involvement is: oral mucosal bullous lesion: 85-90%occularlesions:66%,nasal lesions: 15-23%,laryngeal involvement;8-21%

MUCOUS MEMBRANE PEMPHIGOID:

The two major antigenic determinants for cicatricial pemphigoid are bullous pemphigoid 1 and 2 (BP1 and BP2).

Most cases of Cicatricial pemphigoid are the result of an immune response directed against BP2 and less commonly against BP1 and epiligrin

PATHOGENESIS:

EXTRAORAL LESIONS :

Nasopharyngeal involvement is characterized by rupture of vesicles in nasal mucosa.

Dysphagia.

Dyspnea and laryngeal stenosis.

CLINICAL FEATURES:

Ocular involvement:

Symblepharon

Ankyloblepharon

Entropion

Trichiasis

ORAL MANIFESTATIONS:Vesiculo bullous lesions seen in gingivaSevere erythema may remain for months

HISTOLOGY:sub epithelial vesiculation

Separation of epithelium and C.T.

Chronic inflammatory infiltrate

IMMUNOFUORESENCEPositive immunofluorescence.

The main immunoreactants are IgG &C3.

Bullous pemphigoid.

Bullous lichen planus.

Pemphigus vulgaris.

DIFFERENTIAL DIAGNOSIS:

Localized lesions - Fluocinonide (0.05%) and clobetasol propionate (0.05%) in an adhesive vehicle can be used three times a day for up to 6 months.

If ocular involvement exists, systemic corticosteroids are indicated.

When lesions do not respond to steroids, systemic Dapsone (4-4'diaminodiphenylsulfone) has proven to be effective

TREATMENT:

SEVERE CASES –

Intravenous immunoglobulins are another effective but expensive treatment option in high-risk patients.

Chronic, autoimmune, subepidermal blistering skin disease that rarely involves mucous membrane.

BULLOUS PEMPHIGOID:

Oral lesions

Gingiva- Erythematous and Desquamate

Painful.

Negative Nikolsky sign

HISTOLOGY:No evidence of acantholysis.

Developing vesicles are subepithelial rather than intraepithelial.

The epithelium separates from the underlying connective tissue at the basement membrane zone.

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

IMMUNOFLUORECENCE:

The primary treatment is a moderate dose of systemic prednisone.

Steroidsparing strategies (prednisone plus other immunomodulator drugs) are used when high doses of steroids are needed or the steroid alone fails to control the disease .

For localized lesions of bullous pemphigoid, highpotency topical steroids or tetracycline with or without nicotinamide can be effective .

TREATMENT:

Derived from Greek word pemphix ( bubble or blister)

Pemphigus vulgaris is most common of pemphigus diseases, which also includes

P.foliaceousP.vegetens P.erythematosus

PEMPHIGUS VULGARIS:

PATHOGENESIS:

Circulating autoantibodies are responsible for disruption of intercellular junctions and loss of cell-to-cell adhesion.

Bullae.

Erosions.

Ulcers.

Nikolsky test is positive.

Clinical features:

Histopathology:

DIF- Chicken wire” or “fish net” appearance.

IMMUNOFLUORECENCE:

PemphigoidLichen planusLinear IgA diseaseChronic ulcerative stomatitis

DIFFERENTIAL DIAGNOSIS:

Systemic corticosteroid therapy with/without addition of other immunosuppressive agents.

Prednisolone- 120-80mg/day

Adjuvant drugs – Azathioprine 1-3mg/ kg , Oral cyclophosphamide 50–200 mg /day)

TREATMENT:

1990

Chronic ulcerations

Females>males

CHRONIC ULCERATIVE STOMATITIS:

Painful, solitary small blisters and erosions with surrounding erythema are present mainly on the gingiva and the lateral border of the tongue. The hard palate may also present similar lesions.

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.

Oral lesions:

IMMUNOFLUORESENCE:

For mild cases, topical steroids (Fluocinonide, Clobetasol Propionate) and topical tetracycline may produce clinical improvement.

SEVERE CASES- Hydrochloroquinine sulfate at a dosage of 200-400mg/day

TREATMENT:

Is an uncommon mucocutaneous disorder with predilection in women It clinically presents as a pruritic vesiculobullous rash during middle to late age.

ORAL LESIONS:

LINEAR IgA DISEASE:

HISTOPATHOLOGY Small, tense subepithelial bullae with

polymorphonuclear leukocyte infiltration as well as large mononuclear cells are manifested. Similar to those observed in erosive lichen planus.

IMMUNOFLUORESENCE Linear deposits of IgA are

observed at the epithelial connective tissue interface.

Erosive lichen planus

Chronic ulcerative stomatitis

Pemphigus vulgaris

Bullous pemphigoid

Lupus erythematosus

DIFFERENTIAL DIAGNOSIS:

Combination of Sulfones and Dapsone.

Small amounts of Prednisone (10-30mg/day) can be added.

Alternatively, tetracycline (2g/day) combined with nicotinamide (1-5g/day) have shown promising results.

TREATMENT:

Chronic condition

Young adults (20-30 years)

Slight predilection for males.

Bilateral and symmetric pruritic papules/vesicles

Painful ulcerations preceded by collapse of ephemeral vesicles/bullae.

DERMATITIS HERPATIFORMIS:

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.

Gluten free diet

Oral Dapsone

Treatment:

It is an autoimmune disease with three different clinical presentations

1. Systemic Lupus Erythematosus2. Chronic Cutaneous Lupus

Erythematosus (CCLE)3. Subacute Cutaneous Lupus

Erythematosus (SCLE)

LUPUS ERYTHEMATOSUS:

SYSTEMIC LUPUS ERYTHEMATOSUS:Females 10 : 1

Affects kidneys, skin and mucosa

Fever, weight loss and arthritis

Rash on malar area

Oral lesions are present in up to 40% of patients.

Discoid Lupus Erythematosus

CHRONIC CUTANEOUS LUPUS ERYTHEMATOSUS:

HISTOPATHOLOGY:

Cutaneous rashes are treated with topical steroids, sun screens and hydroxy chloroquine.

For arthritis & mild pleuritis, NSAID’S or hydroxychloroquine are used .

For severe systemic organ involvement moderate to high doses of Prednisone are effective.

Treatment:

Factitious lesions

Graft vs. Host disease

Wegener's granulomatosis

Foreign body gingivitis

Kindler syndrome

MISCELLANEOUS CONDITIONS MIMICKING DESQUAMATIVE GINGIVITIS:

In many cases of desquamative gingivitis it may not be possible to determine the basic etiology. However, local therapy together with deligence &patience will eventually improve the condition and the etiologic background may be discovered on the eventual appearance of other lesions or symptoms.

It is clear that dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.

Conclusion:

Carranza’s clinical periodontology 10th edition.

Carranza’s clinical periodontology 9th edition.

Carranza’s clinical periodontology 11th edition.

Shafer’oral pathology 7th edition.

Garant oral cells and tissue.

References:

EricT. Stoopler et al, Desquamative gingivitis: Eariy presenting symptom of mucocutaneous disease. Quintessence Int 2003:34:582-586

L Lo Russo, R Guiglia,Effect of desquamative gingivitis on periodontal status: a pilot study Oral Diseases 2010: 16:102–107.

Lucio Lo Russo & Crescenzio Gallo Periodontal clinical and microbiological data in desquamative gingivitis patients. Clin Oral Invest 2014 18:917–925

AK.Markopoulos, D.Antoniades Desquamative gingivitis: A clinical, histopathoiogic, and immunologic study. Quintessence Int 1996:27:763-76.

Thank you.,