desquamative lesions of gingiva

Desquamative lesions of
gingiva
Presented by:
Sonal Goyal
Ist MDS
AECS Maaruti College of Dental
Sciences

INDEX
1. Introduction
2. History
3. Classification
4. Chronic desquamative gingivitis
5. Diagnosis
6. Diseases clinically presenting as desquamative gingivitis
 Lichen planus
 Pemphigoid
 Pemphigus Vulgaris
 Chronic ulcerative gingivitis

 Linear IgA disease
 Dermatitis herpetiformis
 Lupus erythematous
 Erythema multiforme
7. Drug eruptions
8. Conditions mimicking desquamative gingivitis
9. Conclusion
10. Reference

Introduction
 Desquamative gingivitis is a clinical term to describe red, painful,
glazed and friable gingivae which may be a manifestation of some
mucocutaneous conditions such as lichen planus or the
vesiculobullous disorders.
 The systemic involvement of desquamative gingivitis with oral and
extra-oral manifestations can cause high morbidity and occasionally
lethal complications.
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders– a review.
Aust dent j 2003;48:206-2011.

History
Coined in 1932 - Prinz to describe a peculiar condition characterized
by intense erythema, desquamation, and ulceration of the free and
attached gingiva.
McCarthy and colleagues (1960) concluded that desquamative
gingivitis was not a specific disease entity but a gingival response
associated with a variety of conditions.
Glickman and Smulow, 1964- DG is not a definitive diagnosis due to
it is a clinical association with several disorders.
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative Gingivitis:
Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral health 2015;7:88-92.

Classification
1) Dermatoses
a) Cicatricial pemphigoid
b) Pemphigus
c) Lichen Planus
d) Erythema Multiforme
e) Lupus Erythematosis
f) Linear IgA disease
2) Hormonal influence
a) Estrogen deficiency following oophorectomy & post
menopausal women
b) Testosterone imbalance
c) Hypothyroidism

3) Abnormal response to irritation
4) Chronic infection
a) Tuberculosis
b) Chronic candidiasis
c) Histoplasmosis
5) Aging
6) Idiopathic
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative
Gingivitis: Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral
health 2015;7:88-92.

Chronic desquamative gingivitis
 Widespread desquamation and/or erosion of the buccal side of
attached gingiva of anterior teeth.
 Can be confined to a limited multiple areas.
 These lesions can be more extensive gingival lesions with oral/and
or extra-oral involvement, in the primary phases or in disease
recurrence.
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative Gingivitis:
Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral health 2015;7:88-92.

• Long standing disease of indefinite duration with periods of
remission and exacerbation, which may terminate spontaneously
after months or years of involvement.
• Varies in appearance in different areas of the mouth and at different
times in the same patient.
Glickman I, Smulow JB. Chronic Desquamative Gingivitis - Its Nature and Treatment. In:
Clinical Periodontology.1:W. B. Saunders Company;1964:397-405.

Epidemiology:
Peak incidence – fourth and fifth decade.
Female predilection- 80%.
Approximately, 50% of the lesions are localized to gingiva,
although in some cases intraoral as well as extraoral sites may be
involved.
Newmann, Takei, Klokkevold et al. Desquamative gingivits. In: Carranza’s Clinical
Periodontology.11:Elsevier;2011:152-170.

According to Nisengard et al (1981, 1987) :
Approx. 75% of
desquamative
lesions are
dermatological
diseases.
95%- cicatricial
pemphigoid and
lichen planus.
25%- either
idiopathic or
associated with an
endocrine
imbalance, aging,
chronic infection or
abnormal response
to bacterial plaque.
Aust dent j 2003;48:206-2011.

Clinical features-
 Mild form :
Diffuse erythema.
Condition is painless
Age: 17 – 23 years
Common in females.
Aust dent j 2003;48:206-2011.

 Moderate form:
Patchy distribution of bright red and gray areas.
Surface is smooth and shiny and soft in consistency.
Slight pitting on pressure.
Nicolsky’s sign +ve
Remainder of the mucosa is also extremely smooth ad shiny.
Age: 30 – 40 years.
C/o of burning sensation and sensitivity to thermal changes.

Severe form:
• Scattered, irregularly shaped areas -striking red appearance.
• grayish blue areas giving an overall speckled appearance.
• Surface epithelium - shredded and friable and can be peeled
off in small patches.
• Areas of involvement seem to shift to different locations on
the gingiva.
• Patient cannot tolerate coarse food, condiments or
temperature changes.
• Constant dry and burning sensation throughout the oral
cavity,
Aust dent j 2003;48:206-2011.

Diagnosis
 Desquamative gingivitis is only a clinical term and not a diagnosis
per se.
 Once the presence of this condition is determined, a series of
investigations are used to arrive at final diagnosis.
Clinical examination
Biopsy
Microscopic Examination
Immunofluorescence
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative
Gingivitis: Review of the Literature and Clinical Guide for Dental Undergraduates. J int oral
health 2015;7:88-92.

Management
 Depends on:
1) Practitioner's experience,
2) Systemic impact of the disease, and
3) Systemic complications of the medications.
 Once oral treatment is provided, periodic evaluation is needed to
monitor the response of the patient.
 Initially, evaluation is done at 2 to 4 weeks after beginning of the
treatment

Diseases clinically presenting as Desquamative
gingivitis
1. Lichen planus
• Characterized by the presence of cutaneous violaceous papules
that may coalesce to form plaques.
• Immunologically mediated muco-cutaneous disorder- T cells
play a central role.
 Surface covered by characteristic, very fine grayish white lines
called Wickham’s striae.

White papules and striae on tongue
White striations on lower lip
Neville BW, Damm DD. Dermatological disease. In: Colour Atlas of Clinical Oral
Pathology.2:BC Decker;2003: 425-466.

 Skin lesions - flexor surfaces of wrist and forearms.
 ORAL MANIFESTATIONS:-
• Radiating white or gray, velvety, thread-like papules in a
linear, annular or retiform arrangement forming typical lacy,
reticular patches, rings and streaks over the buccal mucosa,
lips, tongue and palate.
• Vesicle and bulla formation.

Etiology
Lichen
planus
Idiopathic
Stress
Traumatism
Malnutrition
and infection
Autoimmune
Hereditary
Grinspans
syndrome

 A triad of lichen planus, diabetes mellitus and vascular
hypertension-GRINSPAN SYNDROME
 Immunologically mediated - host T lymphocytes play a
central role.
 0.1 - 4% of the population
 Female : Male – 2:1

 Forms of lichen planus :-
• Bullous :- Raised fluid filled blisters
• Erosive form- when bullae rupture; eroded or frankly ulcerated
lesions –irregular in size and shape and appear as raw, painful areas.;
characteristic radiating striae noted on the periphery of lesions.
• Atrophic form – smooth, red, poorly defined areas, often but not
always with peripheral striae present.
• Hypertrophic form- well –circumscribed, elevated white lesion
resembling leukoplakia

Erosive
Keratotic bullous
Atrophic

Histological features
• Hyper parakeratosis or hyper orthokeratosis
• Thickening of the granular layer
• Acanthosis with intercellular edema of the spinous cells
• Saw tooth appearance of rete pegs.

Pullon et al (1969)
• Irregularity of
nuclear membrane
• Increased
thickening and
granularity of
epithelial
tonofibrils

• Necrosis or liquefaction degeneration of the basal layer
• Infiltration of lymphocytes and occasionally plasma cells.
• Colloid bodies– present mostly in spinous and basal cell layers-
APPEAR as round , eosinophilic globules probably representing
degenerated epithelial cells or phagocytosed epithelial cell
remnants within macrophages.

Differential diagnosis
 Lupus erythematosus
 Chronic ulcerative stomatitis
 Cicatricial pemphigoid- if white striation are absent.
 Pemphigus vulgaris

Mild cases:
Delivery of therapeutic agent can be enhanced with use of vacuum-formed custom trays.
Rx: Lidex (0.05% fluocinonide) gel
Disp: One tube 1.5 g
Sig: Apply to affected area pc and hs.
Monitoring patient's oral cavity is warranted because candidiasis may develop after a
few weeks of topical steroid use; concomitant use of antifungal may be necessary.
Rx: Nystatin oral pastilles (100,000 IU)
Disp: 60 pastilles
Sig: Dissolve in mouth bid, then expectorate for 30 consecutive days.

Recalcitrant cases:
Rx: Protopic (0.1% tacrolimus) ointment
Disp: One tube 15 gm
Sig: Apply to affected area bid.
Severe or refractory cases:
Refer to dermatologist for management with systemic corticosteroids.

2. Pemphigoid
 Cutaneous, immune-mediated, subepithelial bullous diseases
characterized by separation of the basement membrane zone
Types of pemphigoid:-
1. Bullous pemphigoid
2. Cicatricial pemphigoid

 BULLOUS PEMPHIGOID
• Chronic, autoimmune, subepidermal, bullous disease with tense
bullae that rupture and become flaccid in the skin
• Oral involvement- 1/3 cases
• Age- elderly (over 60 yrs)

 Cutaneous lesions-
• Begin as generalized non specific rash, commonly on the limbs,
which appears urticarial or eczematous- which may persist for
several weeks to months before appearance of vesiculobullous
lesions
• Abdomen may also be affected
• Bullae are thick walled and remain intact for longer- don’t
necessarily rupture.

Oral manifestations:
• Vesicles and areas of erosion and ulceration.
• Gingival lesions similar to cicatricial pemphigoid- generally
involves most of gingival mucosa- exceedingly painful.
• Gingival tissues erythematous and desquamate even on minor
friction.
• Vesicles and ultimately erosions appear on gingiva and even on
buccal mucosa, palate, floor of mouth and tongue.

Histologically,
 No acantholysis
 Subepithelial vesicles
 Epithelium separation
 Two major antigenic determinants

 Treatment
Etiology unknown- control signs and symptoms.
Primary Rx –moderate dose of systemic prednisone.
Steroid sparing strategies (Prednisone + immunomodulator drugs)
used when steroids have to be used in large doses or steroids
alone not affective.
Local lesions- topical steroids.

Mucous membrane pemphigoid (cicatricial pemphigoid)
• Chronic, vesiculobullous autoimmune disorder of unknown cause.
• Predominant in women (5th decade of life).
• Rarely reported in children.
• Involvement- oral cavity, conjunctiva, mucosa of nose, vagina,
rectum, esophagus, and urethra; 20% cases skin involved.

Oral lesions
Areas of erythema, desquamation, ulceration
Bullae - thick walled
Healing - 3 weeks or longer
Ocular lesions
Adhesions of eyelids to eyeball
Adhesions at edges of eyelids
Small vesicular lesions on conjunctiva – eventually produces
scarring, corneal damage and blindness.

Desuamative ginigivitis Symblepharon
ankyloblepharon

 Histopathology
Striking subepithelial vesiculation with intact basal layer.
EM- shows spilt in basal lamina.
A mixed inflammatory infiltrate in connective tissue.
 Immunofluorescence-
+ve along the basement membrane (direct and indirect)- IgG and
C3.

Cicatricial
pemphigoid
• Pemphigus vulgaris
• Erythema multiforme
• Epidermolysis
bullosa acquisita
• Bullous lichen planus

 If acantholysis is present – pemphigus
 Acantholysis is absent – pemphigoid.
 EM- onset is acute
 labial involvement is severe
 gingiva is not affected.

 Epidermolysis bullosa –
 When biopsy is treated with salts,
 separation of dermis and epidermis occurs
 If the basement membrane immunoprotein is towards
epidermal side- pemphigoid
 If towards dermal side – epidermolysis bullosa

 Mild cases:
Rx: Lidex (0.05% fluocinonide) gel
Disp: One tube 1.5 g
Sig: Apply to affected area pc and hs.
Rx: Temovate (0.05% clobetasol propionate)
Disp: One tube 1.5 g
Sig: Apply to affected area qid.
 Severe or refractory cases:
Refer to a dermatologist for management with prednisone
(20-30 mg/day); concomitant use of azathioprine may be needed; dapsone,
sulfonamide, and
tetracycline are other alternatives.

3. Pemphigus Vulgaris
• Group of autoimmune bullous disorders that produce cutaneous
and/or mucous membrane blisters.
• Most common of pemphigus disease - pemphigus vulgaris,
pemphigus foliaceous, pemphigus vegetans, and pemphigus
erythematosus
• Lethal chronic condition.
• Predilection in women(after 4th decade of life)

 ETIOLOGY:
Mostly idiopathic
Drug-induced:- penicillamine and captopril (reversible)
Paraneoplastic pemphigus- genetically distinct from pemphigus-
associated with underlying malignancies.

 ORAL LESIONS:-
60% of the patients oral lesion is the 1st sign and may herald
dermatological lesion by a year or more.
Range from small vesicles to large bullae.
Rupture of bullae leads to extensive areas of ulceration.
Any area of oral cavity involved, Oral lesions confine less often to
gingival tissues

Paraneoplastic pemphigus-
crusting of lips
Erosive lesions on buccal mucosa
Multiple and coalescent areas
of ulceration are covered by
pseudomembranes of necrotic
epithelium.

 Histopathology:
Intraepithelial vesiculation begins as microscopic alteration and
gradually results in a grossly visible, fluid filled bulla
Occasionally – entire superficial layers of epithelium lost, leaving
only basal cells attached to underlying lamina propria-
TOMBSTONE appearance of epithelial cells.
Acantholysis characterized by round rather than polyhedral
epithelial cells- intercellular bridges are lost& nuclei are large and
hyperchromatic.

Mild to moderate chronic inflammatory infiltrate in underlying
connective tissue.
Intercellular deposits in epithelium
( IgG in most; C3 in some) of perilesional mucosa

 Primary treatment
 Prednisone
 Secondary treatment
 Azathioprine
 Cyclophosphamide
 Cyclosporine
 Methotrexate
 Gold
 Plasmaphoresis
 photophoresis

4. Chronic ulcerative gingivitis
 Condition presents with chronic oral ulcerations
 Predilection for women(4th decade)
 Erosions and ulcerations in oral cavity- few cases with
 Cutaneous lesions

 ORAL LESIONS
 Painful, solitary small blisters and erosions with surrounding
 Erythema – mainly on gingiva and lateral border of the tongue
 Hard palate may also present similar lesions.

Chronic and ulcerative lesions
Erythema and ulceration of gingiva

Histopathology
Hyperkeratosis, acanthosis, and liquefaction of the basal layer,
areas of subepithelial clefting
underlying lamina propria – lymphohistiocytic chronic infiltrate in
a band like configuration.

 Immunofluorescence :-
Direct (normal and perilesional tissues) –
IgG with a speckled pattern - basal cell layer of the normal
epithelium.
Fibrin deposits at the epithelial- connective tissue interface.
 DIAGNOSIS
Direct and Indirect Immunofluorescence required to arrive at
correct diagnosis

Nuclear deposits of IgG prominent in basal cell layer,
fades toward the superficial layer.

For mild cases- Lidex gel (0.05% flucinonide), applied to affected area qid. Temovate
(0.05% clobetasol propionate), apply to affected area qid.
For severe cases, a high dose of systemic corticosteroids is needed to achieve remission.
Reduction of the corticosteroid dose results in relapse of the lesions.
Hydroxychloroquine sulfate at a dosage of 200 to 400 mg per day seems to be the treatment
of choice to produce complete, long-lasting remission.
However, a long-term follow-up study demonstrated that combined therapy (small doses of
corticosteroids and chloroquine) may be required, because the initial good response to
chloroquine ceases after several months or even years of treatment .
Treatment:

5. Linear IgA disease
Uncommon mucocutaneous disorder with predilection in women
 Clinical features:
Pruritic vesiculobullous rash during middle to late age
plaques or crops with an annular presentation surrounded by a peripheral
rim of blisters .
skin of upper and lower trunk, shoulders, groin and lower limbs- face and
perineum may also be affected.

Oral lesions ( mucosal involvement in 50-100% of cases)
• Vesicles
• Painful ulcerations or erosions
• Erosive gingivitis/chelitis
• Hard and soft palate commonly affected → tonsillar pillars, buccal
mucosa, tongue and gingiva
• Occasionally oral lesion only manifestation for several years
before cutaneous lesions

linear deposits of IgA at epithelial-connective tissue interface
 D/D :- Erosive lichen planus
 Chronic ulcerative stomatitis
 Pemphigus vulgaris
 Bullous pemphigoid
 Lupus erythematosus

Treatment
• Combinations of dapsones and sulfones
• Small amounts of prednisone (10 - 30 mg/ day)

6. Dermatitis herpetiformis
 Dermatitis herpetiformis is a chronic condition that usually
develops in young adults (ages 20-30 years).
 Slight predilection for men.
 Dermatitis herpetiformis is a cutaneous manifestation of celiac
disease.

 Etiology of celiac disease is obscure; however, tissue
transglutaminase seems to be the predominant autoantigen in the
intestine, skin, and sometimes mucosae.
 Gluten enteropathy can be severe in about two thirds of patients
and mild or subclinical in the remaining third.

Clinical features:
 bilateral
 symmetric pruritic papules or vesicles
 primarily restricted to the extensor surfaces of the extremities.
 In severe cases, patients may complain of dysphagia, weakness, diarrhea,
and weight loss.
 clusters of vesicles or papules arise on the skin.
 These vesicles or papules eventually resolve and are followed by
hyperpigmentation of the skin, which ultimately wanes.

Oral lesions
presence of painful ulcerations preceded by the collapse of
ephemeral vesicles or bullae.
 Histopathology:
Focal aggregates of neutrophils and eosinophils among deposits of
fibrin at the apices of the dermal pegs.

 Immunoflurescence:
Direct immunofluorescence - IgA and C3 are present at the dermal
papillary apices.
Although no circulating autoantibodies to epithelial basement
membrane are present in dermatitis herpetiformis, almost 80% of
patients have antiendomysial and gliadin antibodies.

 Treatment:
A gluten-free diet is essential in the treatment.
Oral dapsone to alleviate oral symptoms.

7. Lupus erythematous
 An autoimmue disease
 has three different clinical presentations :
1. Systemic
2. Chronic cutaneous
3. Subacute cutaneous

Systemic lupus erythematous
 female predilection (10:1 female:male)
 affects vital organs such as kidney, heart, skin as well as mucosa.
 Oral lesions (36% of SLE patients) - ulcerative or lichen planus -
like
 Tendency to bleed, surrounded by red halo

 Cutaneous lesions:
 rash on the malar area with a butterfly distribution.
 Oral lesions:
Usually ulcerative
In about 4% of patients- hyperkeratotic plaque reminiscent of
lichen planus appear on buccal mucosa and palate.

Erythema on bridge of the nose with a “butterfly” pattern

 Direct immunofluorescence:
Perilesional and normal tissue
Ig and C3 deposits at the dermal-epidermal interface.
Antinuclear antibodies- 95% of cases.
DNA and extractable nuclear antigens (ENA) antibodies – 50%
cases.

Chronic cutaneous lupus erythematous
 No systemic signs or symptoms
 Lesions limited to skin or mucosal surfaces.
 Skin lesions- discoid lupus erythematous (DLE)
 DLE-
Chronic scarring, atrophy producing lesions that may develop into
hyperpigmentation or hypopigmentation of healing area

 Oral lesions-
Lichen-planus like lesions.
Palate and buccal mucosa
Gingiva maybe affected and clinically present as desquamative
gingivitis.

Intense erythema with ulceration is bordered
by white radial line
Speckled erythematous lesion with radiating white striae
•Multiple facial lesions with irregular
hyperpigmented borders.
•Central scarring with cutaneous
atrophy

 Direct immunofluorescence-
Reveals immunoglobulins and C3 deposits at the dermal-epidermal
junction of the lesional or perilesional tissue but not in normal
tissue.
This seems to differentiate SIE from DLL.
 Indirect immunofluorescence
ANAs in more than 95% of patients,
DNA- and INA-circulating antibodies are present in more than
50%.

Histopathology:
 hyperkeratosis or parakeratosis,
 Alternated acanthosis and atrophy, and
 hydropic degeneration of the basal layer of the epithelium.
 lamina propria exhibits a chronic inflammatory cell infiltrate
similar to that observed in lichen planus.
 a more diffuse and deeper inflammatory infiltrate with a
perivascular pattern is seen.

Subacute cutaneous lupus erythematous
 have a characteristic cutaneous lesion that has similarities to DLE
but lacks the development of scarring and atrophy.
 arthritis/arthralgia, low-grade fever, malaise, and myalgia may
present in up to 50% of SCLE patients.

 Direct immunofluorescence:
immununoglobulins and C3 deposits at the dermal-epidermal junction in
60% of cases
granular IgG deposits in the cytoplasm of basal cells in 30%.
About 80% of patients have Ro (SSA) antibodies to nuclear antigens,
whereas
25% to 30% have La (SSB) antibodies to nuclear antigens.
Rheumatoid factor (RF) is positive in about 30%
ANA is positive
Antiribonucleoprotein (anti-RNP) antibodies to nuclear antigens.

Lupus
erythemato
sus
Pemphigus
vulgaris
Erythema
multiforme
Erosive
lichen
planus

Treatment:
For patients resistant to topical therapy, systemic antimalarial drugs may be used.
For CCLE, topical steroids are effective to manage the cutaneous and oral lesions.
immunosuppressive drugs such as cytotoxic agents (cyclophosphamide and azathioprine)
and plasmapheresis alone or with steroids are useful.
For severe systemic organ involvement, moderate to high doses of prednisone are
effective.
For arthritis and mild pleuritis, a nonsteroidal antiintlammatory drug (NSAID) or
hydroxychloroquine is used.
Cutaneous rashes are treated with topical steroids, sunscreens, and hvdroxvciiloroquine.

8. Erythema multiforme
Acute bullous and/or macular inflammatory mucocutaneous
disease
 Types:
1. Erythema multiforme minor
2. Erythema multiforme major/ Stevens-Johnson syndrome

Male predilection
 Symmetric distribution of macules, papules or vesicles
 Etiology:
Mycoplasma
infection
Herpes simplex
infection
Drug reactions

•Hemorrhagic crusting of the vermillion border of lips common;
• Presence of crusting important in arriving at diagnosis
•Target or iris lesions with central clearing
•Multiple, large, shallow painful ulcers with an erythematous
borders
•Lesions –so painful that chewing and swallowing is impaired

Large, shallow and painful ulcers
involving the buccal and labial mucosa
Bull’s eye appearance

Steven Johnsons Syndrome
• Severe bullous form
• Abrupt occurrence of fever, malaise, photophobia and eruptions of
oral mucosa, genitilia and skin
• Oral lesions → rupture → surfaces covered with thick white or
yellow exudate
• Lips - ulceration with bloody crusting
• ANUG

Hemorrhagic and crusting of lips
and nostrils
Ulcers of oral mucosa

Histopathology:
• Liquefaction degeneration of upper epithelium and intraepithelial
microvesicles but without acantholysis
• Pseudoepitheliomatous hyperplasia and necrotic keratinocytes
• Degenerative changes- basement membrane
• Dense inflammatory cell infiltrate at the junction of epithelium and
lamina propria, which becomes indistinct.
• Edema of the lamina propria, vascular dilation, and congestion are
also present.

 Treatment
• No specific Rx, some cases resolve spontaneously
• bullous or ulcerative lesions require intervention-
 Mild symptoms- systemic and local antihistamines topical
anesthetics and debridement of lesions with an oxygenating agent.
 Intravenous human Ig (high dose)
 Severe symptoms- corticosteroids- but its use is not completely
accepted

Drug eruptions
 Eruptions in the oral cavity resulting from sensitivity to drugs that
have been taken by mouth or parenterally are termed stomatitis
medicamentosa.
 The local reaction from the use of a medicament in the oral cavity
(e.g., aspirin burn, stomatitis resulting from topical penicillin) is
referred to as stomatitis venenata or contact stomatitis.

Drug eruptions in the oral cavity are
multiform.
Vesicular and bullous lesions occur most
often,
But pigmented or nonpigmented macular
lesions are also frequently observed.
Erosions, often followed by deep ulceration
with purpuric lesions, may also occur.
The lesions are seen in different areas of the
oral cavity, with the gingiva often affected.

 Reported with the use of tartar control toothpaste.
 Pyrophosphates and flavoring agents have been identified as the
main causative agents of this unusual condition
 Oral reactions to cinnamon compounds (cinnamon oil, cinnamic
acid, cinnamic aldehyde) used to mask the taste of pyrophosphates in
tartar control toothpaste induce an intense erythema of the attached
gingival tissues characteristic of plasma cell gingivitis.

Plasma cell gingivitis-
Band of moderate to severe inflammation

Diagnosis and treatment:
 A thorough clinical history usually discloses the source of the
gingival disturbance.
 Elimination of the offending agent (e.g., tartar control toothpaste)
leads to resolution of the gingival lesions within a week.
 Challenge with the offending agent leads to recurrence of the oral
lesions.
 If removal of offending agent is not possible, topical
corticosteroids and topical tacrolimus are used.

Conditions mimicking desquamative
gingivitis

1. consciously and intentionally produced injuries without a clear
motive, although, guilt, seeking sympathy, or monetary
compensation may be the driving force behind this abnormal
behavior.
2. Graft-versus-host disease occur in recipients of allogenic bone
marrow transplants, whose oral lesions may occasionally
resemble desquamative gingivitis

 Wegener's granulomatosis is a systemic disease that may initially
present with striking alterations that are confined to the gingival
tissues. Classically, the gingival tissues exhibit erythema and
enlargement and are typically described as "strawberry gums”.

 Foreign body gingivitis is clinically characterized by red or red and
white chronic lesions that may be painful and are reminiscent of
desquamative gingivitis.
 women in the fifth decade of life.
 Microscopic analysis reveals small (<5 pm in diameter) foreign
bodies
 chronic inflammatory cell response that may exhibit granulomatous
and lichenoid characteristics.

 Kindler syndrome
cutaneous neonatal bullae,
poikiloderma,
photosensitivity, and
acral atrophy

Graft versus host disease Wegener’s granulomatosis-
“Strawberry” gums

Conclusion
 Desquamative gingivitis can be mistaken for plaque induced
gingivitis and this can lead to delayed diagnosis and inappropriate
treatment of serious dermatological diseases such as pemphigoid or
pemphigus.
 Correct identification of these conditions entails taking a careful
history and performing a thorough intra-oral examination, biopsy
and referral to an appropriate specialist.
Aust dent j 2003;48:206-2011.

Reference
1. Newmann, Takei, Klokkevold et al. Desquamative gingivits. In:
Carranza’s Clinical Periodontology.11:Elsevier;2011:152-170.
2. Neville BW, Damm DD. Dermatological disease. In: Colour Atlas
of Clinical Oral Pathology.2:BC Decker;2003: 425-466.
3. Robinson NA, Wray D. Desquamative gingivitis: A sign of
mucocutaneous disorders– a review. Aust dent j 2003;48:206-2011.

4. Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The
Differential Diagnosis of Desquamative Gingivitis: Review of the
Literature and Clinical Guide for Dental Undergraduates. J int oral
health 2015;7:88-92.
5. Glickman I, Smulow JB. Chronic Desquamative Gingivitis - Its
Nature and Treatment. In: Clinical Periodontology.1:W. B.
Saunders Company;1964: 397-405.

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