A concise review on some conditions that cause epithelial erosion in the oral cavity. This presentation covers some important lesions with clear diagrams for better comprehension.

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VIGNESH.R
BDS-2012
DESQUAMATIVE
GINGIVITIS

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• FIRST RECOGNISED AND REPORTED IN 1894.
• TERM COINED BY PRINZ IN 1932.
• CONDITION CHARACTERISED BY- intense
erythema,desquamation and ulceration of free and
attached gingiva.
• mostly ASYMPTOMATIC ,when symptomatic,ranges
from mild burning sensation to intense pain
CHRONIC DESQUAMATIVE GINGIVITIS

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• Approximately,50%-localized to gingiva.
• Mostly-women,4th-5th decades of life,suggestive of
hormonal derangement.
• In 1960,McCarthy et al.suggested that desquamative
gingivitis is not a specific disease entity,but a gingival
response associated with a variety of conditions.
• clinical and lab perimeters suggests-75% due to
dermatologic origin.
• among dermatologic conditions- cicatricial pemphigoid
and lichen planus- 95%.

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• Other dermatologic conditions include,bullous
pemphigoid,pemphigus vulgaris,linear immunoglobulin
A(IgA) disease,SLE.etc.
• other conditions like chronic bacterial,viral and fungal
infections as well as reaction to mouthwashes and
chewing gum.
• less commonly-Crohn’s disease,Sarcoidosis,some
leukemias.
• THEREFORE,IT IS OF PARAMOUNT IMPORTANCE TO
ASCERTAIN THE IDENTITY OF THE DISEASE
RESPONSIBLE TO ESTABLISH APPROPRIATE
THERAPEUTIC APPROACH AND MANAGEMENT.

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DIAGNOSIS;

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• CLINICAL HISTORY.
• CLINICAL EXAMINATION;
• Includes pattern of distribution(focal or multifocal,with or
without confinement to gingival tissues)- help in differential
diagnosis.
• BIOPSY;
• An incisional biopsy-best alternative to begin.
• site;perilesional incisional biopsy should avoid areas of
ulceration,because necrosis and epithelial denudation
severely hamper the diagnostic process.

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• MICROSCOPY;
• Buffered formalin(10%)-fixer
• hematoxylin&eosin-stain
• Michael’s buffer(ammonium sulphate)-transport
solution,for immunofluorescence assessment.
• sections of 5 microns of formalin fixed,paraffin
embedded tissue stained with H&E are obtained for
light microscopic examination.

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• IMMUNOFLOURESCENCE;
• Direct immunofluorescence;unfixed frozen sections
are incubated with a variety of fluorescein
labelled,antihuman serum(anti IgG,anti IgA,anti
IgM,anti-fibrin&anti C3)
• Indirect immunofluorescence;unfixed frozen sections
of oral and oesophageal mucosa from an
animal(monkey)are first incubated with a patient’s
serum to allow attachment of any serum antibodies to
mucosal tissue.Then it is incubated with fluorescein-
labelled antihuman serum.

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• MANAGEMENT;
• Once diagnosed,the dentist must chose the optimum
treatment plan.This is accomplished according to
three factors;
1. practitioners’ experience
2. systemic impact of the disease
3. systemic complications of the medications.

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• Inflammatory mucocutaneous
disorder of mucosal surfaces
and skin.
• mostly immune mediated.
• middle aged or older females.
• oral lichen planus-
reticular,patch,atrophic,erosiv
e&bullous.
LICHEN PLANUS;

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• ORAL LICHEN PLANUS.
• Mostly reticular-asymptomatic and bilateral,consist of white lines posterior region of
oral mucosa.
• can have erythematous background,a feature coexisting with candidiasis.
• GINGIVAL LESIONS;
• 10%of oral lesions.
• keratotic lesions-raised white lesions,groups of individual papules,linear or reticular,or
plaque like lesions.
• erosive/ulcerated-extensive,erythematous,patchy distribution,exacerbated by slight
trauma.
• vesicular/bullous-raised,fluid filled lesions,uncommon.
• atrophic lesions-atrophy of gingival tissues with epitheliel thinning.

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• Hyperkeratosis/parakerat
osis
• hydropic degeneration of
basal layer
• dense lymphocytic
infiltration in lamina
propria
• saw-tooth shaped rate
ridges
HISTOPATHOLOGY;

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• DIFFERENTIAL DIAGNOSIS;
• when erosive component-SLE &chronic ulcerative
stomatitis.
• if confined to gingival tissues-fine,white lines-lichen
planus.
• if white striae absent-cicatricial pemphigoid or
pemphigus vulgaris.

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• THERAPY;

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• Types-bullous,mucous
membrane,cicatricial…
• bullous-non-
scarring,mainly affects
skin.
• cicatricial-scarring
occurs,mainly affects
mucous membrane.
PEMPHIGOID

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• Cicatricial&bullous
pemphigoid-
sub-epithelial clefting with
epithelial separation from
underlying lamina
propria,leaving intact basal
layer.
HISTOPATHOLOGY

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• BIOPSY(DIRECT IMMUNOFLOURESCENCE)
• Linear deposits of C3,with or without IgG at
basement membrane zone in almost all cases.
• INDIRECT IMMUNOFLOURESCENCE;
• basement membrane zone(IgG)antibodies;
• 10%-cicatricial pemphigoid.
• 40-70%-bullous pemphigoid.

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TREATMENT;

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• Pemphigus diseases are a group
of bullous disorders that produce
cutaneous and mucous
membrane blisters.
• most cases are
idiopathic,however medications
like penicillamines and captopril
produce it.
• small vesicles-large bullae-,when
bullae ruptures,they leave large
areas of ulceration.
• most common-soft palate,buccal
mucosa.
PEMPHIGUS

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• Characteristic intra-epithelial
split,above the basal layer
• characteristic tombstone
appearance of epithelial
cells.
• acantholysis.
• mild-moderate chronic
inflammatory cell infiltration
underlying connective
tissue.
HISTOPATHOLOGY

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• BIOPSY;
• biopsy of peri-lesional tissue and uninvolved
mucosa shows;
• intercellular deposits in epithelium,IgG in all cases
and C3 in most cases.
• INDIRECT IMMUNOFLOURESCENCE;
• intercellular(IgG)antibodies in >90% of cases.

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TREATMENT

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• Autoimmune disease
• 3 clinical presentations-
systemic,chronic
cutaneous,and
subacute.
LUPUS ERYTHEMATOSUS

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condition histopathology
direct immunofluorescence
perilesional
tissues
uninvolved
areas
indirect
immunofluorescence

25. • DRUG ERUPTIONS;
• An increase in the incidence of skin and oral
manifestations of hypersensitivity to drugs has been
noted since the advent of
sulphonamides,barbiturates,and various antibiotics.
• the eruptive skin and oral lesions are attributed to the
drug,acting as allergens.Eruptions in the oral cavity
resulting from drugs-stomatitis medicamentosa.
• local reactions to drugs in oral cavity-stomatitis
venenata or contact stomatitis.

26. • In general drug eruptions in the oral cavity are
multiform,vesicular,bullous-occur most often.
• erosions,often followed by deep ulcerations with
purpuric lesions,may also occur.
• desquamative gingivitis has been reported with the
use of tartar control toothpastes.
• So,a thorough clinical history usually discloses the
source of gingival disturbance.Elimination of the
offending agent leads to resolution of gingival
lesions within a week.

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• TREATMENT;
• Depends on severity and extend of disease.
• cutaneous rashes-topical steroids,sunscreens.
• for arthritis and mild pruritis-NSAIDs
• moderate-severe condition-prednisolone

28. ERYTHEMA MULTIFORMAE
• Acute bullous-macular
lesion
• target/iris lesion-
characteristic
• mainly due to development
of immune complex
vasculitis,followed by
complement fixation leading
to leukoclastic destruction of
vascular wall and occlusion
of small vessels.

29. • Target or iris lesions with central clearing-
hallmark.
• minor-erythema multiforme-major or Steven-
Johnson syndrome,which are life threatening.
• minor-lasts for 4 weeks,exhibits cutaneous and
mucosal involvement.
• steven-johnson syndrome-for months,involves
skin,oral mucosa,conjunctiva and genitalia.

30. • three most common aetiology are;HSV infection
• mycoplasmic infection
• drug
reactions.(sulfonamides,penicillamines,phenytoin)

31. • Oral lesions;
• multiple large shallow,painful ulcers-with erythematous borders
• buccal mucosa and tongue-mostly.
• immunoflourescence-negative
• treatment-
• no specific treatment,some resolve spontaneously.
• mild cases-local antihistamines.
• severe cases-corticosteroids.

32. LINEAR IgA DISEASE
• Uncommon
• mostly in women.
• aetiology-unknown.
• pruritic vesiculobullous
rash,middle age to late age.
• plaques/crops with an
annular presentation
surrounded by a peripheral
rim of blisters.

33. • histopathology-resembles lichen planus.
• immunoflourescence-linear deposits of IgA
observed at epithelial-connective tissue interface.
• differential diagnosis-erosive lichen
planus,pemphigus vulgaris,bullous pemphigoid
and lupus erythematosus.
• treatment-combination of sulfones and dapsone.
• prednisolone-10-30 mg/day,can be added initially.

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• Carranza’s clinical periodontology,11th edition.
BIBLIOGRAPHY;

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