This document provides information on desquamative gingivitis, including its classification, diagnosis, and associated diseases. It classifies desquamative gingivitis into 7 categories including dermatosis, endocrine imbalance, aging, metabolic disturbances, abnormal response to irritation, chronic infection, and drug reactions. Key aspects of diagnosis include clinical history, examination, biopsy, and microscopic/immunofluorescence examination. Associated diseases discussed in detail include lichen planus, pemphigoid, pemphigus vulgaris, chronic ulcerative stomatitis, and linear IgA disease. Treatment varies depending on the underlying cause and severity of symptoms.

1. DESQUAMATIVE GINGIVITIS
Dr. D. Navya, MDS

2. DESQUAMATIVE GINGIVITIS
 Firstly recognized and reported
in 1894.
(Tomes et al, 1894)
 Term chronic desquamative
gingivitis coined in 1932 by
PRINZ.
 He described a peculiar
condition characterized by
intense erythema, desquamation
and ulceration of the free and
attached gingiva.

4. CLASSIFICATION
1. DERMATOSIS :
- Lichen planus
- Pemphigus
- Mucous membrane pemphigoid
- Bullous pemphigoid
2 ENDOCRINE IMBALANCE
- Estrogen deficiency in female
- In post menopausal state
- Removal of uterus
- Testosterone deficiency in male

5. 3. AGING :
- Senile ectopic gingivitis
4. METABOLIC DISTURBANCES
- Nutritional deficiency
- Vitamin deficiency
5. ABNORMAL RESPONSE TO IRRITATION
6. CHRONIC INFECTION
- Tuberculosis
- Chronic candidiasis
- Histoplasmosis
7. DRUG REACTIONS
- Toxic drug reactions
- Anti metabolites
- Allergy to antibiotics, NSAIDS, barbiturates.

6. DIAGNOSIS OF
DESQUAMATIVE GINGIVITIS
 CLINICAL HISTORY
A thorough clinical history is mandatory to begin the
assessment of desquamative gingivitis
 CLINICAL EXAMINATION
Recognition of pattern of lesions (i.e. focal or
multifocal, with or without confinement to gingival
tissues) provides leading information to begin the
formulation of differential diagnosis.

7.  BIOPSY
Incisional biopsy is the best option
 BIOPSY SITE
A perilesional incisional biopsy should avoid
areas of ulceration because necrosis and epithelial
denudation severely hamper the diagnostic
process.
 FIXATIVE
10% buffered formalin for H and E evaluation.
Michell’s buffer (ammonium sulfate buffer, pH 7)
for immunofluorescence assessment.

8.  MICROSCOPIC EXAMINATION
App. 5 um sections of formalin-fixed, paraffin-
embedded tissue stained with conventional H&E
are obtained for light microscopic examination.
 IMMUNOFLUORESCENCE
DIRECT IMMUNOFLUORESCENCE
Unfixed frozen sections are incubated with a
variety of flurescein-labelled,antihuman
serum(anti-IgG,anti-IgA,antifibrin and anti-C3)

9.  INDIRECT IMMUNOFLUORESCENCE
Unfixed frozen sections of oral and esophageal
mucosa from an animal such as monkey are first
incubated with patients serum to allow attachment
of any serum antibodies to mucosal tissue.The
tissue is then incubated with fluorescein-labeled
antihuman serum.

10.  MANAGEMENT
Accomplished by three factors
Practitioner experience
Systemic impact of disease
Systemic complications of medications
 PRACTITIONERS EXPERIENCE
Dentist takes direct and exclusive responsibility
for the treatment of patient.

11.  SYSTEMIC IMPACT OF DISEASE
Dentist collaborates with another health care
provider to evaluate and treat the patient
concurrently.
 SYSTEMIC COMPLICATIONS OF
MEDICATIONS
Patient is immediately referred to dermatologist
for further evaluation and treatment.

12. DISEASES CLINICALLY PRESENTING AS
DESQUAMATIVE GINGIVITIS
LICHEN PLANUS
 It is an inflammatory mucocutaneous disorder that
may involve mucosal surfaces ( e.g. oral cavity,
genital tract. other mucosae) and the skin
(including the scalp and the nails).
 It is an immunologically mediated mucocutaneous
disorder in which T lymphocytes play a central
role.

13.  Majority of patients with oral lichen planus
are middle aged and older females,with a
2:1 ratio of females to males.
 Children are rarely affected.

14. ORAL LESIONS
Clinical forms are-:
 Reticular
 Patch
 Atrophic
 Erosive
 Bullous
(Most common)
 Reticular
 Erosive subtypes

15.  RETICULAR LESIONS
These are asymptomatic and bilateral and consist
of interlacing white lines on the posterior regions
of buccal mucosa.
The lateral border and dorsum of the tongue, hard
palate, alveolar ridge and gingiva may also be
affected.
They have an erythematous background.

16.  EROSIVE LESIONS
They are associated with pain
and clinically manifest as
atrophic, erythematous and
often ulcerated areas.
Fine, white radiating striations
are observed bordering the
atrophic and ulcerated zones.
These areas are sensitive to
heat, acid and spicy foods

17.  GINGIVAL LESIONS
Upto 10% of patients with oral lichen planus have lesions
restricted to the gingival tissue which may have four
patterns.
1. KERATOTIC LESIONS:
These raised white lesions may present as groups of
individual papules, linear or reticulate lesions, or plaque
like configurations
2. EROSIVE OR ULCERATIVE LESIONS
These extensive erythematous areas with a patchy
distribution may present as focal or diffuse hemorrhagic
areas.
These lesions are exacerbated by slight trauma
(toothbrushing)

18. 3. VESICULAR OR BULLOUS LESIONS
These raised ,fluid filled lesions are uncommon
and short lived on the gingiva, quickly rupturing
and leaving an ulceration
4. ATROPHIC LESIONS
Atrophy of the gingival tissues with ensuing
epithelial thinning results in erythema confined to
the gingiva.

19. HISTOPATHOLOGY
Microscopically three main
features are:-
1. Hyperkeratosis or parakeratosis
2. Hydropic degeneration of basal layer
3. Dense band like infiltrate primarily
of T lymphocytes in the lamina
propria.
Classically, epithelial rete ridges
have a “ saw tooth” configuration
Colloid bodies (Civatte bodies) are
seen at the epithelialconnective
tissue interface.

20. TREATMENT
 KEROTOTIC LESIONS
- Asymptomatic
- Do not require any treatment
- Follow up of patient every 6-12 months
 EROSIVE,BULLOUS OR ULCERATIVE
LESIONS
- .05% fluocinonide ointment (LIDEX, three times daily)
- Intra lesional injection of triamcinolone acetonide
(10 to 20mg)

21.  40 mg prednisolone daily for 5 days
followed by 10 to 20mg daily for additional
2 weeks in severe cases.
 Other treatment modalities-
Retinoids, hydroxychloroquine cyclosporin,
free gingival grafts, antifungal therapy.

22. PEMPHIGOID
 Cutaneous, immune mediated, sub-epithelial
bullous disease.
 Characterized by separation of basement
membrane zone.
 Includes:-
- Bullous pemphigoid
- Mucous membrane pemphigoid
- Pemphigoid gestationis

23.  Bullous pemphigoid is preferred when the
disease is non scarring and mainly affects
the skin.
 Cicatricial pemphigoid is favoured when
scarring occurs and the disease is mainly
confined to mucous membranes.

24. BULLOUS PEMPHIGOID
 It is chronic, autoimmune,
subepidermal bullous disease with a
tense bullae that rupture and become
flaccid in the skin.
 Oral involvement occurs in about a
third of the patients
 No evidence of acantholysis and
developing vesicles are subepithelial
rather than intraepithelial.

25. HISTOPATHOLOGY
 No evidence of acantholysis and developing
vesicles are subepithelial rather than
intraepithelial.Microscopic studies show an actual
horizontal splitting or replication of the basal
lamina.
 The separating epithelium remains relatively
intact, and the basal layer is present and appears to
be regular.
 Two major antigenic determinants are 230-kD
protein plaque known as BP1 and the 180 –Kd D
collagen –like transmembrane protein BP2

26.  ORAL LESIONS
- Erosive or desquamative gingivitis presentation
- Occasional vesicular or bullous disease.
 THERAPY
- Etiology is unknown so treatment is designed to
control its signs and symptoms. Primary treatment-
moderate dose of systemic prednisone
- For localized lesions- high potency topical steriod or
tetracycline with or without nicotinamide

27. MUCOUS MEMBRANE PEMPHIGOID
 Other name is cicatricial pemphigoid
 Chronic ,vesiculobullous autoimmune disorder of
unknown cause.
 Mainly affects women in fifth decade of life, rarely seen in
young children.
SITES:-
 Oral cavity
 Conjuctiva
 Mucosa of the nose.vagina,rectum,oesophagus and urethra.

28.  The two major antigenic
determinants are bullous
pemphigoid 1 and 2( BP1 and
BP2).
OCULAR LESION
 The initial lesion is characterized
by unilateral conjuctivitis that
becomes bilateral within 2 years.
 There may be adhesions of eyelid
to eyeball (symblepharon).

29.  Adhesions at the edges of the eyelids
(ankyloblepharon) may lead to a narrowing
of the palpebral fissure.
 Small vesicular lesions may develop on the
conjuctiva, which may eventually produce
scarring,corneal damage, and blindness.

30. ORAL LESION
 Presence of desquamative
gingivitis with areas of
ulceration,erythema,
desquamation and
vesiculation of the attached
gingiva.
 Vesiculobullous lesions may
occur elsewhere in the
mouth.

31. THERAPY
 Topical steroids are the mainstay of treatment.
 Flucinonide(.05%) and clobetasol propionate(.05%)
three times a day upto 6 months
 Oral hygiene
 For lesions which do not respond to steriods,systemic
dapsone (4-4’ diaminodiphenylsulfone) should be
effective

33. PEMPHIGUS VULGARIS
 Group of autoimmune bullous disorders that
produce cutaneous and mucous membrane
blisters.
 Most common of pemphigus diseases include:-
- Pemphigus foliaceous,
- Pemphigus vegetants
- Pemphigus erythematosus.
 Potentially lethal chronic condition
 Predilection in women,usually after fourth decade
 Also seen in young children and new born.

34.  The epidermal and mucous membrane blisters
occurs when the cell to cell adhesion structures are
damaged by the action of circulating and in vivo
binding of auto ntibodies to the pemphigus
vulgaris antigens, which are cell surface
glycoproteins present in keratinocytes.
 These pemphigus vulgaris glycoproteins are
members of the desmoglein (DSG) subfamily of
the cadherin super family of cell cell adhesion
molecules ,present in desmosomes.

35. GENETIC BACKGROUND
 HLA class 2 allele associations in PV are found
with HLA-DR4
(DRB1*0402),DRw14(DRB1*1041) DQBI*0503.
 Two kinds of Dsg 3 derived peptides may be
presented by HLA-DR acc to HLA polymorphism

36.  The main antigen in pemphigus vulgaris is
Dsg3.
 The main antigen in pemphigus foliaceous
is Dsg1
 Dsg3 ,the gene coding for pemphigus
vulgaris, is located in chromosome 18.

37. ETIOLOGY
 Idiopathic
 Medications such as
penicillamine and captopril.
ORAL LESIONS
 Small vesicles to large bullae,
which when rupture leave
extensive areas of ulceration.
 Other sites include soft
palate(80%), buccal mucosa
(46%), or dorsum of ventral
aspect tongue(20%), lower
labial mucosa (10%).

38. HISTOPATHOLOGY
 Characteristic intraepithelial
separation, which occurs above
the basal cell layer.
 Characteristic “tombstone”
appearance to the epithelial cells.
 Acantholysis, a separation of the
epithelial cells of lower stratum
spinosum takes place
characterized by presence of
round rather than polyhedral
epithelial cells.
 Intercellular bridges lost and
nuclei large and hyperchromatic.

39. THERAPY
 Systemic corticosteroid therapy with or without
addition of other immunosuppressive agents.
 Patients not responsive to corticosteroids “steroid
sparing” therapies used, consisting of combination of
steroids and other medications like
azathioprine,cyclophosphamide, cyclosporine,dapsone
,gold methotrexate, photoplasmaphoresis and
plasmaphoresis.
 Optimal oral hygiene is essential.

41. CHRONIC ULCERATIVE
STOMATITIS
 First reported in 1990
 Clinically presents with chronic oral
ulcerations and has a predilection for
women in their fourth decade of life.
 Erosions and ulcerations are present in the
oral cavity with only a few cases exhibiting
cutaneous lesions.

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

43. HISTOPATHOLOGY
 Hyperkeratosis, acanthosis and liquefaction
of the basal layer with areas of subepithelial
clefting.
 The underlying lamina propria exhibits a
lymphohistiocytic, chronic infiltrate in a
band like configuration.

44. DIFFERENTIAL DIAGNOSIS
 Linear IgA disease
 Bullous pemphigoidErosive lichen planus
 Pemphigus vulgaris
 Mucous membrane pemphigoid
 Lupus erythematous

45. TREATMENT
 For mild cases: topical steroids (fluocinonide,
clobetasol propionate)
 Topical tetracyclines
 Recurrences are common
 For severe cases :high dose systemic
corticosteroids hydroxychloroquine sulphate(200 -
400 mg per day) is the treatment of choice to
produce complete long lasting remission.

46. LINEAR IgA DISEASE
(LINEAR IgA DERMATOSIS)
 Is an uncommon mucocutaneous disorder, more
prevalent in women.
 Clinically presents as pruritic vesiculobullous rash
usually during middle to late age.
 Characteristic plaques or crops with annular
presentation surrounded by peripheral rim of blisters-
affects skin of upper and lower trunk, shoulders, groin
and lower limbs.
 Face and perineum may be affected.
 Mucosal involvement including oral mucosa.

47. ORAL LESIONS
 Consists of vesicles, painful
erosions, ulcerations and erosive
gingivitis /cheilitis.
 Hard and soft palate are most
commonly affected.
 Tonsillar pillars,buccal
mucosa,tongue and gingiva
follows in frequency.
HISTOPATHOLOGY
 Similar to erosive lichen planus.

48. DIFFERENTIAL DIAGNOSIS
 Erosive lichen planus
 Chronic ulcerative stomatitis
 Pemphigus vulgaris
 Bullous pemphigoid
 Lupus erythematosus

49. TREATMENT
 Primary treatment is combination of sulphones
and dapsone
 Small amounts of prednisone(10-30mg/day) can
be added if initial response is inadequate.
 Alternatively,tetracyclines(2g/day)+nicotinamide(
1.5g/day) can be given.

50. DERMATITIS HERPETIFORMIS
 Chronic condition that usually develops in young adults
(20-30 yrs of age)
 Slight predilection for men
ETIOLOGY:-
 Although idiopathic, all patients have gluten enteropathy
which can be severe in 2/3rd of patients
CLINICAL FEATURES:
 In severe cases patient may complain of dysphagia,
weakness, diarrhoea and weight loss
 Clinically, it presents with bilateral and symmetric
pruritic pappules or vesicles predominantly restricted to
extensor surface of extremities

51.  SITES
Sacrum, buttocks and occasionally face and oral cavity
 The vesicles or pappules eventually resolve and are
followed by hyperpigmentation of skin which
ultimately wanes
 ORAL LESIONS- are characterized by painful ulcers
preceeded by collapse of ephemeral vesicles or
bullae.
 H/P:- reveals focal aggregates of PMNs &
eosinophils with deposits of fibrin at the apices of
dermal pegs.

52. LUPUS ERYTHEMATOSUS
 It is an autoimmune disease with 3 different clinical
presentations:-
A) SYSTEMIC LUPUS ERYTHEMTOSUS:-
SLE is a severe disease more common in females( 10:1)
- Affects vital organs like heart, kidneys and skin, mucosa.
- C/F:- fever, weight loss, arthritis are common
- Classic cutaneous lesions are characterized by presence of
rash on molar area with a butterfly distribution
ORAL LESIONS:- ulcerative or lichen planus like
hyperkeratosis plaque appear on palate & buccal mucosa

53.  SLE may have a genetic link.
 Lupus does run in families, but no single “lupus
gene” has yet been identified.Instead multiple
genes appear to influence a persons chance of
lupus developing when triggered by
environmental factors.
 The most important genes are located on
chromosome 6, where mutations may occur
randomly.
 People with SLE have an altered RUNX-1 binding
site which may either cause or contributor to the
condition.

54. PATHOGENESIS
 The exact mechanism for the development of SLE
is unclear since the pathogenesis is a multifactorial
event.
 Impaired clearance of dying cells is a potential
pathway for the development of SLE.
 This includes deficient phagocytic activity, scant
serum components in addition to increased
apoptosis.

55.  Monocytes isolated from whole blood of patients
with SLE show reduced expression of CD44
surface molecules involved in the uptake of
apoptotic cells.
 Most of the monocytes and tingible body
macrophages (TBM), which are found in germinal
centres of lymph nodes, even show a definitely
different morphology in patients with SLE. They
are smaller or scarce or die earlier.

56.  Serum components like complement
factors, CRP and glycoproteins re important
for efficiently operating phagocytosis, in
patients with SLE these components are
often missing,diminshed or insufficient.

57. B) CHRONIC CUTANEOUS LUPUS
ERYTHEMATOSUS ( CCLE)
Lesions are limited to skin or mucosal surface
 Skin lesions are referred to as DISCOID
LUPUS ERYTHEMATOSUS(DLE)
 Lesions are usually localized & at their
borders, numerous dilated B.V. in a radial
arrangement may extend into surrounding
tissue coupled with whitish, pinhead
pappules.
 In early stages, center of lesion is slightly
depressed & eroded & is covered with
bluish-red epithelial surface showing
recurrent scarring

58.  In older lesions, erythematous borders become less
elevated & is transformed into whitish or bluish white
peripheral zone of thickened epithelium
 White lines with same diverging radial arrangement
replace the dilated vessels
 On tongue, it occurs as circumscribed, smooth reddened
area in which papillae are lost or as patches with a whitish
sheen resembling leukoplakia.On lip, localized patches
may be present or entire lip may be involved
 Initially, lip is swollen, bluish-red & everted. At the
margins of patches dilated capillaries are fine, branching
radial lines may be seen

59. H/P:-
Consists of hyper/para keratosis, alternated
acanthosis & atrophy & hydropic degeneration of
basal layer of epithelium
Lamina propria exhibits chronic inflammatory cell
infiltrate

60. C) SUBACUTE CUTANEOUS LUPUS
ERYTHEMATOSUS( SCLE)-
 These are characteristic lesions similar to DLE but
lacks scarring & atrophy
 Arthralgia/ arthritis, low grade fever , malaise &
myalgia
D/D:-
 Erosive lichen planus
 Erythema multiforme
 Pemphigus vulgaris

61. TREATMENT
 Cutaneous rashes are treated with topical steroids,
sunscreens & hydroxychloroquinine
 For arthritis,& mild pruritis- NSAIDs
 For severe systemic organ involvement –
moderate to high doses of prednisone
 For severe SLE or in side effects of prednisone-
immunosuppresive drugs like cytotoxic drugs
(cyclophosphamide& azathioprine) &
plasmaphoresis

62. ERYTHEMA MULTIFORME
 Acute bullous &/or macular inflammatory mucocutaneous
disease
 This is followed by complement fixation leading to
leukocytoclastic destruction of vascular walls & small
vessel occlusion
 Target or ‘iris’ lesions with central clearings are the
hallmark of EM.
 TOXIC EPIDERMAL NECROLYSIS is the severest form
 ETIOLOGY:- Herpes simplex infection
Mycoplasma infection
 Drug reaction- Sulfonamides, penicillins,
phenylbutazone, phenytoin

63.  ORAL LESIONS
- Consists of multiple ,large shallow painful ulcers with
erythematous border
- Chewing & swallowing are difficult
- Buccal mucosa & tongue are most commonly affected
- Less commonly affected are- floor of mouth, hard & soft
palate, gingiva
- Haemorrhagic crusting of vermillion border of lips may be
seen

64. H/P:-
 Includes liquefaction degeneration of upper
epithelium & developmentof intra epithelial
microvesicles but without acantholysis.
 Acantholytic, pseudoepitheliomatous
hyperplasia & necrotic keratinocytes are seen.
 Degenerative changes also occur in basement
membrane.
 Edema of lamina propria, vascular dilation &
congestion are also present.

65. TREATMENT
No specific treatment
For mild symptoms, systemic & local anti-
histamines & topical anesthetics &
debridement of lesions with an oxygenating
agent.
For severe symptoms, corticosteroids are given

66. DRUG ERUPTIONS
 Eruptive skin & oral lesions occur as drug
act as allergens, either alone or in
combination sensitizing the tissues & then
causing allergic reaction
 Eruptions of oral cavity resulting from
sensitivity to drugs taken by mouth or
parentrally are called as STOMATITIS
MEDICAMENTOSA

67.  Local reaction from use of medicaments in
oral cavity is called as STOMATITIS
VENENATA or CONTACT STOMATITIS
 Vesicular or bullous lesions occur most
commonly but pigmented or non-pigmented
macular lesions are also seen
 Tartar control tooth paste, pyrophosphates &
flavouring agents
 intense erythema of attached gingival tissue
 TREATMENT:- elimination of offending
agentcauses resolution of gingival lesions
within a week

68.  MISCELLANEOUS:-
 Another group of
heterogenous lesions may
present as DG
 Eg- Factitious lesions
 Candidiasis
 GRAFT vs HOST
RESPONSE
 Wegener’s granulomatosis
 Foreign body gingivitis
 Kindler syndrome
 Squamous cell carcinoma

69. THANK YOU