Transcript Desquamative Gingivitis

Desquamative Gingivitis
Contents
Introduction
Etiology
Clinical Features
Diagnosis
Diseases Clinically Presenting As Desquamative Gingivitis
Lichen Planus
Pemphigoid
Mucus Membrane Pemphigoid
Pemphigus
Chronic Ulcerative Stomatitis
Linear IgA Disease
Dermatitis Herpetiformis
Lupus Erythematosus
Erythema Multiforme
Drug Eruptions
Miscellaneous Conditions Mimicking Desquamative Gingivitis
Conclusion
Introduction
Rare nonspecific manifestation of oral mucosa
Prinz (1932) - “chronic diffuse desquamative gingivitis” is a specific
disease, characterized by erythema, desquammation and ulceration of the
free and attached gingiva
McCarthy and Shklar (1960) - desquamative gingivitis is not a specific
disease , but a gingival response associated with a variety of conditions
Etiology
Certain dermatoses
Hormonal influence
Chronic infections
Idiopathic
Most important dermatoses
Lichen Planus
Cicatrical Pemphigoid (MMP)
Pemphigus Vulgaris
Clinical Features
Gingivae - red, swollen and glossy in
appearance
Occasionally multiple vesicles and
superficial denuded areas
Nikolsky’s sign
Sensitive gingival tissue – difficulty
in eating hot, cold or spicy food
Diagnosis of Desquamative Gingivits
Systematic Approach –
• Clinical History
• Clinical Examination
• Biopsy
• Microscopic Examination
• Immunofluorescence
A Systematic approach is needed to diagnose disease associated with
Desquamative gingivitis -
Clinical History -
Onset
Symptoms
Treatment
Clinical examination -Unifocal ,multifocal lesions
Gingival inolvement
Nikolsky’s sign
Biopsy -
Histopathological &
immunofluoroscent tests of perilesional tissue
Management
3 factors
1. Practitioner’s experience
Direct and exclusive responsibility of the treatment
e.g., erosive lichen planus which is responsive to topical
steroids
2.
Systemic impact of the disease
Collaboration with another dectors.
e.g., cicatrical pemphigoid where the dentist treats the oral
lesions and ophthalmologist deals with ocular lesions
3.
Systemic complications of the condition
Only medical practitioner treats the disease
e.g., pemphigus vulgaris
Diseases Clinically Presenting
As Desquamative Gingivitis
1. Lichen Planus
• A muco cutaneous condition, an immunological disorder
involving T- lymphocytes.
• Females affected more than males
Clinical Features
Adults - > 40 years
F:M – 2:1
Small, angular, flat-topped papules
only a few millimeters in diameter
Wickham’s striae – fine, grayishwhite lines covering the papules
Commonly involved sitesFlexor surfaces of wrist
Inner aspect of knees & thighs
Trunk
Types of Lichen Planus 1. Chronic Dermatosis- violet papules with pruritis
2. Oral lesions- Reticular( Wickhams striae)
Atrophic
Bullous & Erosive
3. Gingival lesions- Keratotic
Erosive or Ulcerative
Vesicular or bullous
Oral Lesions
Reticular type –
Asymptomatic
Bilateral on the posterior
region of buccal mucosa
Tongue, gingiva, palate,
alveolar mucosa may also be
affected
Interlacing white lines
Erosive type –
Usually painful
Atrophic, erythematous and
often ulcerated areas
Fine, white radiating striations
bordering the atrophic and
ulcerated zones
Sensitive to heat, acid and spicy
foods
Gingival Lesions
Keratotic lesions
Raised white lesions presenting as groups of individual
papules, linear or reticular lesions, or plaque like
configurations
Erosive or Ulcerative lesions
Extensive erythematous areas with a patchy distribution
Exacerbated by slight trauma (e.g., tooth brushing)
Vesicular or Bullous lesion
Raised, fluid-filled lesions which rupture quickly and leave
ulceration
Atrophic lesions
Produce epithelial thinning resulting in gingival erythema
Differential Diagnosis
Lichenoid reactions
Leukoplakia
Candidiasis
Pemphigus
Cicatrical pemphigoid
Erythema multiforme
Syphilis
Recurrent aphthae
Lupus erythematosus
Chronic ulcerative stomatitis
Treatment
Keratotic, asymptomatic lesions – no Rx. Regular follow-up
Erosive/bullous/ ulcerative lesions - topical steroids such as
0.05% fluocinonide ointment (Lidex TDS)
In more severe cases,
Intralesional injections of triamcinolone acetonide or
40 mg of prednisone OD for 5 days, followed by 10-20 mg
OD for an additional 2 weeks
Elimination of mechanical trauma or irritants such as sharp
filling margins
Alternative to Corticosteroids Cyclosporine
Levamisole
Topical human interferon – β
Systemic isotretinoin
Dapsone
Non-Drug Therapy
Surgical excision
Cryosurgery
CO2 laser
Ultraviolet radiation
Magnetism
2. Pemphigoid
A number of cutaneous, immune-mediated, subepithelial
bullous diseases characterized by a separation of the basement
membrane zone (BMZ)
Bullous Pemphigoid (nonscarring & confined to skin)
Mucous Membrane Pemphigoid (scarring & confined to MM)
Pemphigoid Gestationis
Bullo us Pemphigoid (BP)
Chronic, autoimmune, subepidermal, blistering skin disease that rarely
involves mucous membranes
Oral involvement occurs in few patients
Clinical Features
> 60 years of age
Generalized, nonspecific rash, commonly on the limbs which may persist for
several weeks to several months
Appearance of the vesiculobullous lesions
Vesicles/bullae remain intact for some days or may rupture to leave a raw,
eroded area which heals rapidly
Oral Lesions
Vesicles and areas of erosion and ulceration
Gingival tissues -
extremely erythematous and may
desquamate as a result of even minor frictional trauma
Therapy
Primary Rx - Moderate dose of systemic prednisone
When high doses of steroids are needed or the steroid alone fails to
control the disease - Steroid-sparing strategies (prednisone plus other
immunomodulator drugs)
For localized lesions of BP Topical steroids
Tetracycline with/without nicotinamide
Mucous Membrane Pemphigoid
(Cicatrical Pemphigoid)
Chronic,
vesiculobullous
autoimmune
disorder
of
unknown origin that predominantly affects the mucous
membranes, including the mouth and the oropharynx, the
conjunctiva, the nares and the genitalia
Subtypes
Oral pemphigoid
Antiepiligrin pemphigoid
Anti-BP antigen mucosal pemphigoid
Multiple-antigens pemphigoid
Ocular pemphigoid
Clinical Features
Peak age - 40 and 50 years
Ocular Lesions
Unilateral conjunctivitis that becomes bilateral within 2 years
Symblepharon - adhesions of eyelid to eyeball
Ankyloblepharon - adhesions at the edges of the eyelids
Narrowing of palpebral fissure
Oral Lesions
Desquamative gingivitis, with areas of
erythema, desquamation, ulceration and
vesiculation of the attached gingiva
Lesions - vesiculobullous in nature
- persist for 2-3 days
- rupture leaving a raw,
eroded bleeding surface
Involvement of the oropharynx dysphagia
Therapy
Fluocinonide (0.05%) & Clobetasol propionate (0.05%) in
an adhesive vehicle TDS for up to 6 months
When confined to gingival tissues - topical corticosteroids
Meticulous oral hygiene
Minimize gingival irritation from any dental prosthesis
If ocular involvement is present - systemic corticosteroids
are indicated
3. Pemphigus Vulgaris
Autoimmune bullous disorders that produce cutaneous and
mucous membrane blisters
Potentially lethal, chronic condition
10% mortality rate
Etiology
Diet – controversial
Drugs – Penicillamine
Rifampicin
Diclofenac
Viruses – HSV
Other Factors – smoking, exposure to pesticides
Other Autoimmune diseases – Lupus Erythematosis, pernicious anemia
Clinical Features
50-60 years
Rapid appearance of vesicles & bullae varying in diameter from a
few mm to cm
Rupture of bullae leave a raw, eroded surface
Nikolsky’s sign – loss of epithelium caused by rubbing unaffected
skin
Oral Lesions
Range from small vesicles to large bullae
Ill-defined, irregularly shaped, gingival, buccal or palatine erosions,
which are painful and slow to heal
Gingival lesions - less common and usually comprise severe
desquamative or erosive gingivitis
Soft palate – most commonly involved
Treatment
Topical or intralesional corticosteroids or other immunosuppressants
The treatment of desquamative gingivitis consists ofImproving the oral hygiene
Minimizing irritation of the lesion
Alternative treatment to corticosteroids –
Chlorambucil, azathioprine, cyclophosphamide
Other drugs – gold, dapsone, prostaglandin E2
Plasmapheresis
Intravenous immunoglobulins
4. Chronic Ulcerative Stomatitis
It clinically presents with chronic ulcerations and has a predilection for
women in their fourth decade of life
Oral Lesions
Painful, solitary small blisters and erosions with surrounding erythema
are present mainly on the gingiva and the lateral border of the tongue
Treatment
For mild cases Topical steroids (fluocinonide and clobetasol propionate)
Topical tetracycline
For severe cases –
Systemic corticosteroids
Hydroxychloroquine sulfate 200 - 400 mg/day
5. Linear IgA Disease (LAD)
Subepidermal vesiculobullous disease that may be
idiopathic or drug-induced
Most commonly caused by angiotensin converting enzyme
(ACE) inhibitors
Children and adults are affected
Historically known as
childhood
chronic bullous dermatoses of
Oral Lesions
Vesicles, painful ulcerations or erosions and erosive gingivitis /
cheilitis
The hard and soft palates are most commonly affected followed by
tonsills, buccal mucosa, tongue and gingiva
Treatment
Combination of sulfones and dapsone
Small amount of prednisone (10-30 mg/day) can be added
if the initial response is inadequate
Alternatively, combinations of tetracycline (2 g/day) with
nicotinamide (1.5 g/day) have been proved successful
6. Dermatitis Herpetiformis
Rare,
benign,
chronic,
recurrent,
immune-mediated
blistering dermatologic disease associated with glutensensitive enteropathy (GSE)
Approximately 25% of patients with celiac disease have
dermatitis herpetiformis
Cutaneous manifestation of celiac disease
Clinical Features
B/W 20 and 55 years
Pruritus and severe burning, followed by the development of
erythematous papules, vesicles, bullae or pustules
Extremities, trunk and buttocks – most commonly affected
Vesicles - symmetrical and in groups
Vesicles or pustule eventually resolve and are followed by
hyperpigmentation of the skin
Oral Lesions
Vesicles and bullae which rupture rapidly to leave areas of
superficial ulceration at any intraoral site
7. Lupus Erythematosus
Autoimmune
presentations
disease
with
three
different
Systemic lupus erythematosus
Chronic cutaneous lupus erythematosus
Subacute cutaneous lupus erythematosus
clinical
Systemic Lupus Erythematosus (SLE)
Etiopathogenesis
• Not completely known
• Genetics, hormones and the environment (e.g. sunlight, drugs)
contribute to disease process
• Greater production of autoantibodies
formation and tissue damage
immune complex
Clinical Features
Peak age of onset - 30 years in females but 40 years in males
Female:male ratio is 10:1
The cutaneous lesions are characterized by the presence of a rash on the
malar area so called butterfly distribution
Oral Lesions
Usually ulcerative or similar to lichen planus
In 36% of patients, oral ulcerations are present
In 4% of patients, hyperkeratotic plaques are present on buccal mucosa and
palate
Chronic Cutaneous Lupus Erythematosus (CCLE)
Skin lesions – Discoid Lupus Erythematosus
Oral Lesions
Lichen planus-like plaques on the palate and buccal mucosa
The center of the lesion is slightly depressed and eroded and is covered
with a bluish red epithelial surface
On the tongue - circumscribed, smooth, reddened areas in which the
papillae are lost or as whitish patches resembling leukoplakia
Subacute Cutaneous Lupus Erythematosus
A group of patients who have a characteristic cutaneous lesion that has
similarities to DLE but lacks the development of scarring and atrophy
Treatment
Cutaneous rashes
hydroxychloroquine
-
topical
steroids,
sunscreens
&
For arthritis and mild pleuritis – NSAIDs / hydroxychloroquine
For severe systemic organ involvement - moderate to high doses
of prednisone
For severe cases of SLE or when side effects of prednisone
develop, immunosuppressive drugs such as cytotoxic agents
8. Erythema Multiforme
An acute bullous and macular inflammatory mucocutaneous disease
Subtypes
Erythema multiforme minor
Localized eruption of the skin with mild or no mucosal involvement
Erythema multiforme major & Stevens-Johnson Syndrome
More severe mucosal and skin lesions and are potentially life-threatening
disorders
Etiology
3 most common etiologic factors 1. Herpes simplex infection
2. Mycoplasma infection
3. Drug reactions
The most common causative drugs –
Sulfonamides
Penicillins
Phenylbutazone
Phenytoin
Clinical Features
Any age but the highest incidence – 2nd to 4th decades of life
Males > Females
Characteristic lesion is concentric ringlike in appearance -
‘iris’, ‘target’ or ‘bull’s eye’
Most commonly involved sites are –
Hands and arms
Feet and legs
Face
Oral Lesions
Multiple, large, shallow, painful ulcers with
erythematous border
Difficulty in swallowing and chewing
Most frequently affected sites
Buccal mucosa
Tongue
Labial mucosa
Floor of the mouth
Hard and soft palate
Gingiva
Hemorrhagic crusting of the vermilion border of
the lip
Treatment
No specific treatment
For mild symptoms –
Systemic and local antihistamines together with topical anesthetics
Debridement of lesions with an oxygenating agent
For severe symptoms – systemic corticosteroids
9. Drug Eruptions
Stomatitis medicamentosa
Eruptions in the oral cavity resulting from sensitivity to drugs that have
been taken by mouth and parenterally
Stomatitis venenata or Contact stomatitis
Local reaction from the use of a medicament in the oral cavity
(e.g., aspirin burn, stomatitis resulting from topical penicillin)
Vesicular and bullous lesion
Gingival lesions may be caused by the mercurial compounds present in the
dental amalgam
Tartar control toothpaste - Desquamative gingivitis
Pyrophosphates and flavoring agent present in the toothpaste -main
causative agents
Cinnamon compounds in tartar control tooth paste may produce intense
erythema of the attached gingival tissues
Management includes the elimination of the offending agent
Miscellaneous Conditions
Mimicking Desquamative
Gingivitis
Candidiasis
Rarely it may be limited to the gingival tissues and may simulate
desquamative gingivitis
Graft versus Host Disease
Recipients of allogenic bone marrow transplants
Oral lesions may occasionally resemble desquamative gingivitis
Wegener’s Granulomatosis
Classically, gingival tissues exhibit erythema and enlargement and are
typically described as “strawberry gums”
Foreign Body Gingivitis
More common in women during their fifth decade of life
Most foreign bodies are of dental origin, more specifically
abrasives and restorative material
Kindler Syndrome
It consists of –
Cutaneous neonatal bullae
Poikiloderma
Photosensitivity
Acral atrophy
Oral lesions clinically resemble desquamative gingivitis
Conclusion
Desquamative gingivitis, in most cases, represents a
manifestation of systemic disease
Because it has no specific clinical features, laboratory,
histopathologic
and
immunohistochemical
examination,
should be used to unmask the underlying disease so that the
appropriate treatment can be provided