Desquamative gingivitis

Contents
• INTRODUCTION
• DEFINITION
• HISTORY
• EPIDEMIOLOGY
• CLASSIFICATION
• PATHOGENESIS OF DG
• CLINICAL PRESENTATION OF DG
• DIAGNOSIS OF DG
• DISORDERS ASSOCIATED WITH DG: 1. LP
2. PEMPHIGOID
3. PEMPHIGUS

Introduction
• In our day-to-day practice, we sometimes encounter certain unusual
gingival manifestations that can put a clinician in a quandary, as to what
the diagnosis is. The free and attached gingiva may present as an intense
erythema, desquamation, and/ or ulceration and most often with pain,
glazing, and friability.
• Desquamative gingivitis is one such condition that presents as erythema,
ulcerations, or erosions on the gingiva and may be indicative of a bigger
underlying condition/disease. While examining the oral cavity, we often
forget that it is an integral part of the rest of the body, the oral mucosa,
particularly the gingiva, is the site where several systemic diseases and
conditions manifest.
Rogers RS 3rd, Sheridan PJ, Nightingale SH. Desquamative gingivitis: Clinical, histopathologic, immunopathologic, and therapeutic observations. J Am Acad
Dermatol 1982;7:729-35.

definition
• A peculiar condition characterized by intense erythema, desquamation, and
ulceration of the free and attached gingiva. – Prinz 1894.
• Mccarthy and colleagues 1960- desquamative gingivitis was not a specific
disease entity but rather a gingival response associated with a variety of
conditions.
• Desquamative gingivitis is defined as an unusual, unique, non plaque associated
gingivitis characterized by intense diffuse erythema and desquamation (peeling)
of the surface epithelium. It is often associated with ulceration of the marginal
and attached gingiva. It is not a specific disease entity but a clinical
manifestation of a variety of conditions. – carranza 12th edition.
Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza’s Clinical Periodontology 10th ed. St. Louis: Saunders, Elsevier; 2006. p. 411-
33.

history
Dermatol 1982;7:729-35.

Dermatol 1982;7:729-35.

Epidemiologic features
• Highest prevalence- lichen planus and mucous membrane
pemphigoid.
Dermatol 1982;7:729-35.

classification
• Based on the etiological considerations desquamative gingival lesions are
classified as under. This is a modification of the original classification
formulated by McCarthy and others
Dermatol 1982;7:729-35.

pathogenesis
• To understand the pathogenesis of
desquamative gingivitis, 1st we must
know the basic organization of the
oral mucosa.
• The oral mucosa consists of a
stratified epithelial layer and
connective tissue underneath. Some
areas are keratinized and some are
non-keratinized. The oral mucosa
consists of three layers: stratified
squamous cell epithelium, lamina
propria, and the basement membrane
that separates them.
• Electron microscopic:

• Some of the epithelial proteins assure inter-cell and cell-membrane
integrity. The autoimmune diseases target these proteins (considered to be
antigens) and auto-antibodies are formed against them.
• These proteins act as cementing material for the maintenance of
intercellular and cell-basement integrity.
• The autoimmune response against any of these epithelial proteins results in
the loss of cell to cell adhesion or loss of cell basement membrane
adhesion, leading to vesculation.
Dermatol 1982;7:729-35.

• In patients with pemphigus develop autoantibodies directed toward a
glycoprotein adhesion molecule (ICAM-intercellular adhesion molecule)
named desmoglein (DSG 1 in primarily found in the skin and DSG 3 is
usually detected in mucosal epithelium).
• In bullous pemphigoid patients the antigen is a normal protein, constituent
of the hemi desmosomes-basement membrane complex. They are called
bullous pemphigoid antigen (BP). The initial defect is found in the Lamina
Lucida region of the basement membrane
Dermatol 1982;7:729-35.

Clinical features of DG
• Desquamative gingival lesions are seen in about 1.5 to 2.5 % of population
with females being more affected than males.
• It is most common in the third or fourth decade of life but can be seen in
younger individuals. Patients may be asymptomatic; when symptomatic
their complaints range from burning sensation to severe pain.
• Approximately 50% of the cases are confined to gingiva but other intra oral
and dermatological involvement may be found.
• Lesions such as pemphigus vulgaris have systemic impact which
transcends the boundaries of the oral cavity and results in significant
morbidity and even mortality.
33.

• Glickman and Smulow have described three forms of Desquamative
gingivitis viz. mild, moderate, and severe.
33.

Diagnosis of DG
Management of desquamative gingivitis involves five important steps
1. A meticulous history
2. Careful clinical examination
3. Opinion from a dermatologist if necessary
4. Biopsy and other investigations
5. Local and systemic therapy.
33.

Clinical history
• A thorough clinical history is mandatory to begin the assessment of
desquamative gingivitis. Data regarding the symptoms associated
with this condition as well as its historical aspects (i.e., when the
lesion started, whether it has worsened, if there is a habit that
exacerbates the condition) provide the foundation for a thorough
examination. Information regarding previous therapy to alleviate the
condition should also be documented.
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders a review. Aust Dent J 2003;48:206-11.

Clinical examination
• Recognition of the pattern of distribution of the lesions (i.e., focal or
multifocal, with or without confinement to the gingival tissues) provides
leading information to begin the formulation of a differential diagnosis.
• In addition, a simple clinical maneuver such as Nikolsky’s sign offers
insight into the plausibility of the presence of a vesiculobullous disorder.
With a pledget of wet cotton roll the lesions may be gently scrapped to see
any peeling of the surface epithelium.
• The handle of a mouth mirror or periodontal probe may gently be pressed
on the lesion to observe any tissue blanching. Examination of the skin and
eyes may reveal features leading to diagnosis.

Biopsy
• Given the extent and number of lesions that may be present in an
individual, an incisional biopsy is the best alternative to use to begin
the microscopic and immunologic evaluation. An important
consideration is the selection of the biopsy site.
• A perilesional incisional biopsy should avoid areas of ulceration,
because necrosis and epithelial denudation severely hamper the
diagnostic process. Also biopsy is done best after initial scaling and
debridement so that plaque associated marginal gingivitis does not
confuse the picture.

• A perilesional biopsy should be taken avoiding areas of ulceration.
10% buffered formalin should be used to fix the solution for
conventional H and E Michelle’s buffer (ammonium sulfate buffer,
pH7) used as transport solution for immunofluorescence study.
Immunological markers are generally found in normal mucosa, with
the exception of lichen planus and subacute lupus erythematosus,
where it presents only in the lesional tissue. Formalin-fixed,
paraffin-embedded H and E stained tissue is evaluated under the
light microscope.

Lichen planus
• Lichen planus is a relatively common, chronic, dermatosis
characterized by the presence of cutaneous violaceous papules that
may coalesce to form plaques. The current evidence suggests that
lichen planus is an immunologically mediated mucocutaneous
disorder where host T lymphocytes play a central role.
• 0.1-4% of population
• Female:male ratio 2:1.
33.

ETIOLOGY

ORAL LESIONS
• Although there are several clinical forms of oral lichen planus (reticular, patch,
atrophic, erosive and bullous), the most common are the reticular and erosive
subtypes. The typical reticular lesions are asymptomatic, bilateral, and consist
of interlacing white lines on the posterior region of the buccal mucosa.
• Oral lichen planus lesions follow a chronic course and have alternating,
unpredictable periods of quiescence and flares.
• The erosive subtype of lichen planus is often associated with pain and clinically
manifests as atrophic, erythematous areas. Fine white radiating striations are
observed bordering the atrophic zones. These areas may be sensitive to heat,
acid, and spicy foods.
33.

GINGIVAL LESIONS

HISTOPATHOLOGY
• Hyperkeratosis
• Hydropic degeneration of basal layer
• Saw tooth rete pegs
• Lamina propria exhinbits dense, bandlile infiltrate primarily of t-
lymphocytes.
• Civatte bodies
Immunopathology:
• DIF: linear fibrillar deposits of fibrin in basement membrane zone.
• IIF: negative.

• D/D: The classic clinical presentation of oral lichen planus can be
simulated by other conditions mainly, lichenoid mucositis.
• When an erosive component is present, lupus erythematosus and chronic
ulcerative stomatitis should be included in the differential diagnosis. In the
event that oral lichen planus is confined to the gingival tissues (erosive oral
lichen planus), the identification of fine white radiating striations bordering
the erosive areas support a clinical diagnosis of oral lichen planus.

TREATMENT OF LP

Pemphigoid
33.

Bullous pemphigoid
• Bullous pemphigoid is a chronic, autoimmune, subepidermal,
bullous disease with tense bullae that rupture and become flaccid in
the skin.
• Oral involvement occurs in about a third of the patients.
• Although the skin lesions clinically resemble those of pemphigus,
the microscopic picture is quite distinct.
Neville BW, Damm DD, Allen C, Bouquot JE. Dermatological disease. In: Neville BW, Damm DD, Allen C, Bouquot JE, editors. Oral and Maxillofacial
Pathology. Philadelphia PA: Saunders; 1995.

h/p:
• no acantholysis
• Subepithelial vesicles
• Epithelium separation
• 2 major antigenic determinants- 230-kDa protein plaque (BP1), 180-kDa
collagen-like transmembrane protein (BP-2).
I/P:
• IgG, C3 immune deposits along the epithelial basement membranes and
circulating IgG antibodies to the epithelial basement menbrane. Direct
immunofluorescence is positive in 90%–100% of cases and indirect in
40%.

Gingiva of BP
Drug induced BP
Oral lesions BP

Oral lesions:
Oral lesions of bullous pemphigoid have been reported to occur secondarily in
up to 40% of cases. The clinical presentation includes an erosive or
desquamative gingivitis and occasional vesicular or bullous lesions.
Treatment:
• Primary treatment- moderate dose of prednisolone
• Steroid sparing strategies
• Localized lesions- high potency topical steroids or tetracyclines.

CICATRICIAL PEMPHIGOID
• Female predominance
• 5th decade
• Oral cavity, conjuctiva, mucosa of nose, vagina, rectum, esophagus,
urethra.
• 5 subtypes:
1. Oral pemphigoid
2. Multiple antigens pemphigoid
3. Anti-epiligrin pemphigoid
4. Anti-BP antigen mucosal pemphigoid
5. Ocular pemphigoid

ORAL LESIONS.
• The most characteristic feature of oral involvement is the presence of
desquamative gingivitis with typical areas of erythema, desquamation,
ulceration, and vesiculation, of the attached gingiva.
• Vesiculobullous lesions may occur elsewhere in the mouth.
• The bullae tend to have a relatively thick roof and rupture in 2 to 3 days,
leaving irregularly shaped areas of ulceration. Healing of the lesions may
take up to 3 weeks or longer.

H/P:
• non-specific
• Subepithelial vesicukation
• Intact basal layer
I/P:
• DIF: IgG and C3.
• IIF: +ve <25%

Pemphigus
• The pemphigus diseases are a group of autoimmune bullous
disorders that produce cutaneous and/or mucous membranes blisters.
• Types: p. vulgaris
• P. vegetans
• P. foliaceous
• P. erythematosus
33.

PEMPHIGUS VULGARIS
• 0.1-0.5 cases/1000000 individuals/year
• Higher-women
• Mortality rate <10% (black et al 2005)
• pemphigus vulgaris has also been reported in unusually young
children and even in newborns.

PATHOGENESIS OF PV
• Circulating autoantibodies are responsible for disruption of intercellular
junctions and loss of cell-cell adhesion.
• Auto-antibodies directed against desmoglein 3- oral; DSG1-cutaneous.
• Early studies implicated complement in the acantholu=ysis which follows
antibody binding (jordan et al 1974)
• Plasminogen activator production by keratinocytes has been implicated in
acantholysis (Hashimoto et al 1983)
• Pemphigus foliacues- antibodies directed against DSG1 (Hashimoto et al
1990)

INTRAORAL MANIFESTATIONS:
• Intraepithelial separation
• Bullae soon ruptures- painful erosions with ragged borders
• Gingival lesions can occur and along with other oral lesions may
represent the 1st manifestation of disease.
• +ve nikolsky’s sign.

H/P:
• Intraepithelial clefting
• Acantholysis and suprabasilar
bullae formation
• Basal cella lining the floor of
bullae- tombstone pattern
• Tzank cella
• Dense mononuclear lymphocyte
infiltration
I/P:
• DIF: intercellular deposits in the
epithelium IgG in all cases and C3
in most cases.
• Chicken wire or fish net
appearnce.
• IIF: less sensitive. Helpful in
monitoring the disease.

TREATMENT
• The main therapy for pemphigus vulgaris is systemic corticosteroid therapy
with or without the addition of other immunosuppressive agents. Initially,
when only steroids were employed, high initial and maintenance doses of
steroids were necessary to control the disease.
• Currently, if the patient responds well to corticosteroids, the dosage can be
gradually reduced, but a low-maintenance dosage is usually necessary to
prevent or minimize the recurrence of lesions.

Desquamative gingivitis
Dr P MIKITHA
II MDS
DEPT OF PERIODONTOLOGY
AECS MAARUTI COLLEGE OF DENTAL SCIENCES AND RESEARCH CENTRE

SESSION-2
• DISORDERS ASSOCIATED WITH DG: 4. LE
5. EM
6. CHRONIC ULCERATIVE STOMATITIS
7. DERMATITIS HERPETIFORMIS
8. DRUG ERUPTIONS
9. LINERA IGA DISEASE
• CONDITIONS THAT MIMIC DG
• OVERVIEW OF MANAGEMENT
• TREATMENT
• EFFECT OF DG ON PERIODONTAL STATUS
• PERIODONTAL MANAGEMENT
• CONCLUSION
• REFERENCES

Lupus erythematosus
• Lupus erythematosus is an autoimmune disease characterised by the
production of autoantibodies against several cell constituents, occuring
predominantly in women.
• They present with three different clinical presentations: systemic, chronic
cutaneous, and subacute cutaneous.
33.

1. Systemic Lupus Erythematosus.:
• Females 10:1
• Affects kidneys, skin, mucosa, heart, joints, lungs,
• Skin is involved upto 85% SLE cases.
• Fever, weightloss and arthritis
• Oral lesions are present in upto 40% pt.
• Malar area with a distribution rash.

ORAL LESIONS:
• Hyperkaratotic plaques reminiscent of lichen planus appear on the
buccal and palate.
Immunofluorescence:
IgG, C3 deposits at the dermal-epidermal interface.

CHRONIC CUTANEOUS LE
• Chronic cutaneous lupus erythematosus (CCLE) usually has no
systemic signs or symptoms, with lesions being limited to skin or
mucosal surfaces. The skin lesions are referred to as discoid lupus
erythematosus (DLE).
• Produces scarring and atrophy
• Oral lesions 9% of pt present LP like plaques.
33.

H/P:
• Hyperkeratosis, alternating
acanthosis and atrophy,
hydropic degenration of the
basal layer of epithelium.
• More diffuse and deeper
inflammatory infiltrate with
perivascular pattern.
Immunofluorescence:
• DIF: Ig, C3 deposits at dermal-
epidermal junction of lesional
or perilesional tissue.
• IIF: antinuclear antibodies in
more than 95% pt.

SUBACUTE CUTANEOUS LUPUS
ERYTHEMATOSUS
• Pt have cutaneous lesions similar to those of DLE but lack
development of scarring and atrophy.
• Arthritis, arthralgia, low-grade fever, malaise, myalgia seen in 50%
pt
• DIF reveals Ig, C3 deposits at dermal-epidermal junctions in 60%
cases and granular IgG deposits in the cytoplasm of basal cells in
30% cases.

TREATMENT

Erythema multiforme
• Acute mucocutaneous disorder, characterised by varying degrees of
blistering and ulceration.
• Disease is characterised by skin eruptions with or without oral or other
mucous membrane lesions.
• Target or iris- hallmark of EM
• Types: EM major, EM minor, SJS, Toxic epidermal necrolysis
• EM minor lasts aprox 4 weeks and exhibits moderate cutaneous and
mucosal involvement.
33.

• Stevens– Johnson syndrome can last a month or longer. It involves the skin,
conjunctiva, oral mucosa, and genitalia, and it requires more aggressive
therapy than erythema multiforme minor.
• Some researchers consider toxic epidermal necrolysis to be the most severe
form of erythema multiforme, but other investigators think they are
unrelated entities.
• The two most common etiologic factors for the development of erythema
multiforme are herpes simplex infection and drug reactions.
• The most common causative drugs are sulfonamides, penicillins,
quinolones, chlormezanone, barbiturates, oxicam nonsteroidal
antiinflammatory drugs, anticonvulsant drugs, protease inhibitors, and
allopurinol.

ORAL LESIONS:
• 70% pt with skin involvement
• Multiple large painful ulcers with an erythematous border
• Hemorrhagic crusting of lip

TREATMENT

Chronic ulcerative stomatitis
• Chronic ulcerative stomatitis, which was first reported in 1990,
manifests with chronic oral ulcerations and has a predilection for
women during the fourth decade of life.
• The erosions and ulcerations occur predominantly in the oral cavity,
with only a few cases exhibiting cutaneous lesions.
• Circulating specific IgG autoantibodies to ΔNp63α, an epithelial
nuclear transcription factor that modulates epithelial cell growth,
have been demonstrated.
33.

Oral lesions:
• Painful solitary small blisters and erosions with surrounding
erythema occur mainly on the gingiva and the lateral border of the
tongue. Because of the magnitude and clinical features of the
gingival lesions, a diagnosis of desquamative gingivitis is
considered.
• The buccal mucosae and hard palate also can have similar lesions.

Linear Ig A disease
• Uncommon, prediliction for women
• etiopathogenesis- drug-induced LAD triggered by ACE inhibitors.
• c/f- pruritic vesiculobullous rash, affects middle age or later
• Mucosal involvement including oral mucosa 50-100%
• Characteristic plaques with an annular manifestation surroundede by
peripheral rim of blisters affect skin of upper and lower trunks,
groin.
33.

ORAL LESIONS
• Vesicles, painful ulcerations or
erosions
• Hard and soft palate are
affected more often, buccal
mucosa, tongue, gingiva.

Dermatitis herpetiformis
• Seen in young adults 20-30 years. Men are commonly affected.
• Cutaneous manifestation of celiac disease.
• Manifests with bilateral and symmetric pruritic papules or vesicles
that are restricted to the extensor surface of the extremities.
• The oral lesions of dermatitis herpetiformis range from painful
ulcerations preceded by the collapse of vesicles or bullae to
erythematous lesions.
• A gluten free diet is essential for the treatment of celiac disease and
dermatitis herpetiformis.
• Oral dapsone is usually needed.
Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza’s Clinical Periodontology 10th ed. St. Louis: Saunders, Elsevier; 2006. p. 411-33.

Drug eruptions
• Stomatitis medicamentosa: eruptions in the oral cavity that result from
sensitivity to drugs that have been taken by mouth or parentrally.
• Stomtitits venenata: the local reaction from the use of a medicament in the
oral cavity (eg. Stomatitits as a result of topical penicillin use)
• Manifestations: vesiculobullous lesions
• Pigmented/non-pigmented macular lesions
• Erosion, deep ulcerations with purpuric lesions
• Seen in different areas of the oral cavity with gingiva often affected.
33.

• Development of gingival lesions caused by contact allergy:
mercurial compounds in dental amalgam
• Pyrophosphates and flavoring agents like cinnamon in tartar control
toothpastes.
• Intense erythema of the attached gingival tissues- comparitive of
plasma cell gingivitis.

Conditions that mimic DG
• CANDIDIASIS
• FACTITIOUS LESIONS
• GRAFT VERSUS HOST DISEASE
• WEGNER’S GRANULOMATOSIS
• KINDLER SYNDROME
• SCC
• FOREIGN BODY GINGIVITIS

Overview of management
• After the diagnosis is established, dentist must choose the optimum
management for the patient.
• Management of the lesions by:
• 1 elimination of potential factors
• 2 suppressing the inflammatory reaction
• 3 using specific therapies for the underlying diseases

Treatment
• KEY POINTS:
1. Institution and discussion of appropriate oral hygiene measures
should be performed for all patients
2. Systemic therapies should be instituted after failure of topical
therapy, for widespread disease or as first-line therapy in setting of
certain immunobullous diseases.
Markopoulos AK, Antoniades D, Papanayotou P, Trigonidis G. Desquamative gingivitis: A clinical, histopathologic, and immunologic study. Quintessence Int
1996;27:763-7.

Oral hygiene
1. Evaluation:
• All patients with DG should have a thorough inspection of the oral
cavity.
• The clinician should carefully inspect the gingiva and teeth for
accumulation of dental plaque, signs of gingival retraction,
evidence of dental root exposure, and tooth loss.
• Evaluation by a dental professional for the presence and
management of caries should also be conducted.

• All mucosal surfaces should be inspected for the presence of
microbial colonization, including evaluation for the white plaques of
oral candidiasis, punched-out erosions of herpes simplex virus, or
honey-colored crust of impetigo.
2. Plaque control: Subgingival and supragingival plaques should be
removed and proper teeth brushing with a soft brush in addition to
flossing should be recommended.

3. Decolonization: Reduced oral hygiene and treatment with local
immunosuppressant medications can lead to increased microbial
colonization in patients with DG. regular antifungal prophylaxis.
This can be performed with the twice-daily use of an antiseptic
mouth rinse containing hydrogen peroxide and daily use of
antifungal troches.
Chaikin BS. A treatment of desquamative gingivitis by the use of free gingival grafts. Quintessence Int 1980;9:105-11.

Topical therapies
• Topical therapies are an important component to the therapy of DG.
For some diseases, topical therapies alone can be sufficient to
control disease when mild to moderate, including EM, complex
aphthosis, OLP, and graft-versus-host disease.
• For immunobullous diseases, systemic therapies are generally
required, but topical modalities represent an important adjunctive
treatment.
• The most commonly used first-line topical therapy is a topical
corticosteroid.
1996;27:763-7.

CORTICOSTEROIDS
• Systemic and topical corticosteroids are used for the medical
treatment of DG.
• Topical corticosteroids are commonly used to treat DG.
• Corticosteroids impair immunological competence
• Suppress hypersenstisation and allergic phenomena
• Suppress recruitment of leucocytes at sites of contact with Ag.
1996;27:763-7.

• Topical corticosteroids: triamcinolone, fluocinonide, clobetasol gel,
beclomethasone diproprionate spray (inhaler).
• However, their effects are limited due to the saliva volume and the
tongue movements which decreases the effectiveness of the
treatment.
• Direct application of chlobetasole-17- propionate to the affected site
is recommended. Custom built silicone or acrylic carriers which
provide long term contact of the drug with the gingival lesion can be
prepared to increase the effectiveness of the topical treatment.
1996;27:763-7.

2. Immunosupressive agents: cyclosporine, griseofulvin, Azathioprine,
Methotrexate, Cyclophosphamide (Lever WF et al 1979)
3. Tetracyclines: systemic doxycyxline improves DG in LP(Ronbeck
1990)
4. IV IG: proved successful and safe in steroid- resistant PV(Mobini et
al 1995)
1996;27:763-7.

5. Hormonal therapy: Estrogen support for the treatment of DG has
been recommended based on the presence of estrogen-sensitive
receptors in the human gingiva and estrogen destruction. (Ziskin
1937) The idea of estrogen therapy has been rejected since the
estrogen receptors expressions in the gingival tissues are not related
to the presence or absence of estrogen as well as the side effects of
estrogen (Yih et al)
1996;27:763-7.

• Plasmapheresis: selective removal of large volumes of plasma which
includes antibodies. Used for treatment of bullous pemphigoid,
epidermolysis bullosa, LE
• Photopheresis: extracorpeal photopheresis involves the exposure of
the pt mononuclear cells to 8-methoxypsorlean and UV light to
induce apoptosis of T-cells.
1996;27:763-7.

Other treatments
• Proteinase inhibitors(Dobrev ET al 1996)
• Chimeric molecules for specific recognition and elimination of the
auto immune B cells (Proby et al 2000)
• Suggestions for a novel avenue for the development of a steroidal
treatment for using anti-acantholytic activity cholinergic agonists
(Grando 2000)
1996;27:763-7.

Effect of DG on periodontal status
• From a theoretic point of view, disorders causing DG may have
potential harmful outcomes on the development and progression of
plaque-related periodontal disease.
• These potential injuries may be related to both direct and indirect
relationships.
• Indirect effect: Symptoms associated with DG- prevent proper oral
hygiene- plaque – periodontal diseases.
• Direct effect: may also be plausible based on the possible shared
pathogenicity mechanisms/mediators.

• Ramon-Fluxia et al (1999) observed that no significant differences
were present between OLP group of patients and a control group
with regard to different periodontal indices.
• Akman et al (2008); periodontal status is worse in pt. affected by
pemphigus.

Periodontal management
• Though different protocols have been used for plaque control in
studies, some general principles should be applied for all patients
with DG.
• First, all patients should undergo a baseline tooth cleaning with a
dental professional comfortable in the management of patients with
DG.
• Second, patients should perform at-home dental cleaning with tooth
brushing twice daily.

• A soft toothbrush is recommended (either manual or electric) while
active erosions are present, using a modified Bass technique, where
the bristles are placed at a 458 angle to the tooth surface at the edge
of the gum, and strokes are performed to the tooth edge.
• Antiseptic mouth rinse should be performed twice daily, with
avoidance of alcohol-based rinses. Periodic teeth cleaning
procedures should be performed, and avoidance of local irritants,
such as ill-fitting prostheses or unsatisfactory restorations, is critical.

conclusion
• Desquamative gingivitis can be the clinical symptom of some dermatitis
and mucocutaneous diseases and the underlying primary cause should be
evaluated meticulously.
• Taking detailed patient history, performing a careful intraoral examination
and determining the presence or absence of similar lesions at other sites of
the body are the most important steps in clinical practice.
• Definitive diagnosis of DG should be made by incisional biopsy,
histopathological examination and DIF.
• Gingival lesions are controlled by improving oral hygiene and the use of
topical corticosteroids. If there is an underlying systemic disease, the case
should be consulted with the physician.

references
• Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza’s
Clinical Periodontology 10th ed. St. Louis: Saunders, Elsevier;
2006. p. 411-33.
• Neville BW, Damm DD, Allen C, Bouquot JE. Dermatological
disease. In: Neville BW, Damm DD, Allen C, Bouquot JE, editors.
Oral and Maxillofacial Pathology. Philadelphia PA: Saunders; 1995.
• Rogers RS 3rd, Sheridan PJ, Nightingale SH. Desquamative
gingivitis: Clinical, histopathologic, immunopathologic, and
therapeutic observations. J Am Acad Dermatol 1982;7:729-35.

• Markopoulos AK, Antoniades D, Papanayotou P, Trigonidis G.
Desquamative gingivitis: A clinical, histopathologic, and
immunologic study. Quintessence Int 1996;27:763-7.
• Scully C, el-Kom M. Lichen planus: Review and update on
pathogenesis. J Oral Pathol 1985;14:431-58.
• Robinson NA, Wray D. Desquamative gingivitis: A sign of
mucocutaneous disorders a review. Aust Dent J 2003;48:206-11.
• Chaikin BS. A treatment of desquamative gingivitis by the use of
free gingival grafts. Quintessence Int 1980;9:105-11.

Desquamative gingivitis

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