Desquamative Gingivitis

By,
Dr. Dandu Sivasai Prasad Reddy
IIyr Post Graduate
Mamata Dental College

 Introduction
 History
 Chronic desquamative gingivitis
 Systemic approach for the diagnosis of chronic
desquamative gingivitis
 Clinical history
 Clinical examination
 Biopsy
 Immunofluorescence
 Management

 Diseases clinically presenting as desquamative
gingivitis
 Lichen planus
 Pemphigus
 Pemphigoid
 Linear IgA disease
 Lupus erythematosus
 Dermatitis herpetiformis
 Chronic 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.

 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

 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 involved
Surface epithelium
appears shredded
Blowing of air causes a
bubble in gingival
epithelium
Very painful
Constant dry, burning
sensation

 1932 – Princz
 1953- Glickman
 1960- Mc Carthy

 Clinical history
 Clinical examination
 Biopsy
 Microscopic examination
 Immunoflouroscence
 Direct
 Indirect

ORAL LICHEN PLANUS:
 Chronic inflammatory disease that affects skin and
mucous membrane.
 Wilson – 1869

 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.

 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.

 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 LESIONS
Atrophy of the gingival tissues
with ensuing epithelial
thinning results in erythema
confined to the gingiva.

 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.

 Lichenoid reactions
 Cicatricial pemphigoid
 Pemphigus vulgaris
 Leukoplakia

 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.

 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

 Cicatricial pemphigoid.
 Chronic, vesiculobullous autoimmune disorder
 It 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%

 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

 EXTRAORAL LESIONS :
 Nasopharyngeal involvement is
characterized by rupture of vesicles in nasal
mucosa.
 Dysphagia.
 Dyspnea and laryngeal stenosis.

Ocular involvement:
 Symblepharon
 Ankyloblepharon
 Entropion
 Trichiasis

 ORAL MANIFESTATIONS:
 Vesiculo bullous lesions seen in gingiva
 Severe erythema may remain for months

sub epithelial
vesiculation
Separation of
epithelium and C.T.
Chronic inflammatory
infiltrate

Positive
immunofluorescence.
The main immunoreactants
are IgG &C3.

 Bullous pemphigoid.
 Bullous lichen planus.
 Pemphigus vulgaris.

 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

 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.

 Oral lesions
 Gingiva- Erythematous and Desquamate
 Painful.
Negative Nikolsky sign

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

 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 .

 Derived from Greek word pemphix ( bubble or blister)
 Pemphigus vulgaris is most common of pemphigus
diseases, which also includes
 P.foliaceous
 P.vegetens
 P.erythematosus

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

 Bullae.
 Erosions.
 Ulcers.
 Nikolsky test is
positive.

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

 Pemphigoid
 Lichen planus
 Linear IgA disease

 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)

 1990
 Chronic ulcerations
 Females>males

 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.

 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

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

 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
 Pemphigus vulgaris
 Bullous pemphigoid

 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.

 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.

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

 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)

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

 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.

 Factitious lesions
 Graft vs. Host disease
 Wegener's granulomatosis
 Foreign body gingivitis
 Kindler syndrome

 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.

 Carranza’s clinical periodontology 10th edition.
 Shafer’oral pathology 7th edition.
 Garant oral cells and tissue.

 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.

Desquamative Gingivitis

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