Desquamative gingivitis Logien Al Ghazal 10/11/2015

Chronic desquamative gingivitis Diagnosis of desquamative gingivitis Diseases presenting clinically as desquamative gingivitis lichen planus pemphigoid pemphigus vulgaris chronic ulcerative stomatitis linear iga disease (linear iga dermatosis) dermatitis herpetiformis lupus erythematosus erythema multiforme Drug eruptions

Chronic desquamative gingivitis Describe a peculiar condition characterized by intense erythema, desquamation, and ulceration of the free and attached gingiva. Desquamative gingivitis was not a specific disease entity, but a gingival response associated with a variety o f conditions. General information: Patients may be asymptomatic. when symptomatic range from a mild burning sensation to an intense pain. Approximately 50% of desquamative gingivitis cases are localized to the gingiva, although involvement of the gingiva plus other intraoral and even extraoral sites is common. Most cases were diagnosed in women in the fourth to fifth decades of life

Diagnosis of desquamative gingivitis Clinical History. A thorough clinical history is mandatory to begin the assessment of desquamative gingivitis. Data regarding the symptomatology associated with this condition, as well as its historical aspects (i.e., when did the lesion start, has it gotten worse, is there a habit that exacerbates the condition, etc.). Clinical Examination Recognition of the pattern of distribution of the lesions (i.e., focal or multifocal, with or without confinement to the gingival tissues). Nikolsky's sign offers insight into the plausibility of the presence of a vesiculobullous disorder. Biopsy

Differential diagnosis Lichen planus pemphigoid pemphigus vulgaris chronic ulcerative stomatitis linear iga disease (linear iga dermatosis) dermatitis herpetiformis lupus erythematosus erythema multiforme

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. Oral lichen planus lesions follow a chronic course and have alternating, unpredictable periods of quiescence and flares. Types of Lichen planus: Reticular Patch Atrophic. Erosive Bullous.

Skin lesions of lichen planus. Papules with delicate white striations.

Gingival Lesions Up to 10% of patients with oral lichen planus have lesions restricted to the gingiva

Four types of gingival lesions: 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. 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.

A variety of clinical appearances is characteristic of OLP A variety of clinical appearances is characteristic of OLP. These include: • Papular. • Reticular. • Plaque-like . • Atrophic. • Ulcerative. • Bullous.

Erosive lichen planus

Papular lesion of right buccal mucosa.

Reticular lesion of lower lip mucosa. The white striations are denoted Wickham striae.

Reticular lesion

Plaque-type lesion of maxillary gingiva.

Atrophic lesions of facial maxillary and mandibular gingiva Atrophic lesions of facial maxillary and mandibular gingiva. Such lesions were previously termed desquamative gingivitis.

Atrophic and reticular lesion of lower left canine region.

Bullous/reticular lesion of left palatal mucosa.

Treatment for lichen planus: The keratotic lesions of oral lichen planus are asymptomatic and do not require treatment once the microscopic diagnosis is established. Follow-up of the patient every 6 to 12 months is warranted to monitor clinical changes and the emergence of an erosive component. In contrast, the erosive, bullous, or ulcerative lesions of oral lichen planus are treated with high-potency topical steroid such as: 0.05% fluocinonide ointment (Lidex, three times daily). Lidex can also be mixed 1:1 with carboxymethyl cellulose (Orabase) paste or other adhesive ointment. Intralesional injections of triamcinolone acetonide (10 to 20 mg) . Short-term regimens of 40 mg prednisone daily for 5 days followed by 10 to 20 mg daily for an additional 2 weeks have also been employed in more severe cases.

Pemphigoid The term pemphigoid applies to a number of cutaneous, immune-mediated, subepithelial bullous diseases that are characterized by a separation of the basement membrane. Bullous pemphigoid, mucous membrane pemphigoid and pemphigoid. Among these conditions, bullous pemphigoid and mucous membrane pemphigoid (also known as benign mucous membrane pemphigoid and cicatricial pemphigoid) Bullous pemphigoid is preferred when the disease is nonscarring and mainly affects the skin. Cicatricial pemphigoid is favored when scarring occurs and the disease is mainly confined to mucous membranes

Bullous Pemphigoid Oral lesions. There is an erosive or desquamative gingivitis presentation and occasional vesicular or bullous lesions. Treatment: Control its signs and symptoms. The primary treatment is a moderate dose of systemic prednisone. Localized lesions of bullous pemphigoid, highpotency topical steroids or tetracycline with or without nicotinamide can be effective .

Mucous Membrane Pemphigoid (Cicatricial Pemphigoid). Effects women in 50s, and young children. Ocular lesions. In cases presenting first to the dentist (mainly desquamative gingivitis), the eyes are affected in approximately 25% of the patients. Oral lesions. The most characteristic feature of oral involvement is the presence of desquamative gingivitis with typical areas of erythema, desquamation,

Treatment Topical steroids are the mainstay of treatment for mucous membrane pemphigoid. when localized lesions are present. Fluocinonide (0.05%) and clobetasol propionate (0.05%) in an adhesive vehicle can be used three times a day for up to 6 months. Optimal oral hygiene is essential because local irritants on the tooth surface result in an exaggerated gingival inflammatory response. Gingival irritation from any dental prosthesis should also be minimized. Ocular involvement exists, systemic corticosteroids are indicated. When lesions do not respond to steroids, systemic Dapsone (4-4'diaminodiphenylsulfone) has proven to be effective

Pemphigus Vulgaris The pemphigus diseases are a group of autoimmune bullous disorders that produce cutaneous and/or mucous membranes blisters. (Intraepithelial bulla) Oral Lesions Oral lesions of pemphigus range from small vesicles to large bullae. When the bullae rupture, they leave extensive areas of ulceration The soft palate is more often involved (80%). Followed by the buccal mucosa (46%) ventral aspect or dorsum of tongue (20%) and lower labial mucosa (10%).

Histopathology. Lesions of pemphigus demonstrate a characteristic intraepithelial separation, which occurs above the basal cell layer. The intraepithelial vesiculation begins as a microscopic alteration. Oral lesions of pemphigus vulgaris Erosive lichen planus, Pemphigoid linear IgA chronic ulcerative stomatitis

Treatment of pemphigus vulgaris: Is systemic corticosteroid therapy with or without the addition of other immunosuppressive agents. They consist of combinations of steroids plus other medications such as azathioprine, cyclophosphamide, cyclosporine, dapsone, gold, methotrexate, photoplasmaphoresis, and plasmaphoresis.

Chronic ulcerative stomatitis Clinically, this condition presents with chronic oral ulcerations and has a predilection for women in their fourth decade of life. The erosions and ulcerations present predominantly in the oral cavity, with only few cases exhibiting cutaneous lesions. Oral Lesions. Painful, solitary small blisters and erosions with surrounding erythema are present mainly on the gingiva and the lateral border of the tongue. The hard palate may also present similar lesions.

Treatment. For mild cases, topical steroids (fluocinonide, clobetasol propionate) and topical tetracycline may produce clinical improvement; however, recurrences are common. For severe cases, a high dose of systemic corticosteroids is needed to achieve remission.

Linear IgA disease (LAD) as linear IgA dermatosis, is an uncommon mucocutaneous disorder with predilection in women. It clinically presents as a pruritic vesiculobullous rash usually during middle to late age. LAD may mimic lichen planus both clinically and histologically. Oral Lesions. Oral manifestations of LAD consist of vesicles, painful ulcerations or erosions, and erosive gingivitis cheilitis. The hard and soft palates are more commonl affected. Tonsillar pillars, buccal mucosa, tongue, and gingiva follow in frequency.

Dermatitis Herpetiformis Dermatitis herpetiformis is a chronic condition that usually develops in young adults (ages 20 to 30 years) Males. Severe cases patients may complain of: Dysphagia, weakness, diarrhea, and weight loss. Clinically, dermatitis herpetiformis presents with bilateral and symmetric pruritic papules or vesicles predominantly restricted to the extensor surfaces of the extremities.

Lupus Erythematosus. is an autoimmune disease with three different clinical presentations: Systemic ,Chronic cutaneous, and subacute cutaneous. Systemic Lupus Erythematosus. Females 10:1 Affects vital organs such as kidneys and heart, as well as the skin and mucosa. Extra-oral symptoms and signs: Fever. weight loss. Arthritis. The classic cutaneous lesions are characterized by the presence of a rash on the malar area with a butterfly distribution.

Antinuclear antibodies (ANA) are present in more than 95% of cases Oral lesions of SLE Usually ulcerative or lichen planus-like. Oral ulcerations. Hyperkeratotic plaques reminiscent of lichen planus appear on the buccal mucosa and palate Antinuclear antibodies (ANA) are present in more than 95% of cases

Chronic Cutaneous Lupus Erythematosus. Has no systemic signs or symptoms. Lesions being limited to skin or mucosal surfaces. Skin lesions are referred to as discoid lupus erythematosus (DLE) DLE merely describes the chronic scarring, atrophy-producing lesion that may develop hyperpigmentation or hypopigmentation of the healing area.

CCLE oral cavity lichen planus-like plaques on the palate and buccal mucosa. On the tongue the disease occurs as circumscribed, smooth, reddened areas in which the papillae are lost or as patches with a whitish sheen resembling leukoplakia. The lip is involved by direct extension from perioral skin lesions. Periods of activity and quiescence .

Subacute Cutaneous Lupus Erythematosus Subacute cutaneous lupus erythematosus (SCLE) has been used to describe a group of patients who have a characteristic cutaneous lesion that has similarities to DLE but lacks the development of scarring and atrophy.“ Systemic symptoms and signs Arthritis/arthralgia, low-grade fever, malaise and myalgia may present in up to 50% of SCLE patients.

Treatment. The therapy for SLE is dependent on the severity and extent of the disease Cutaneous rashes are treated with topical steroids, sunscreens, and hydroxychloroquinine. Arthritis and mild pleuritis, nonsteroidal antiinflamatory agents Severe cases of SLE or when side effects to prednisone

Genesis of ulcerative lesions affecting the skin Erythema Multiforme Genesis of ulcerative lesions affecting the skin immune complex vasculitis. complement fixation leukocytoclastic destruction of vascular walls and small vessels ischemic necrosis of the epithelium and underlying connective tissue

The three most common etiologic factors: (1) herpes simplex infection, (2) mycoplasma infection (3) drug reactions. The most common causative drugs are sulfonamides, penicillins, phenylbutazone, and phenytoin. Mild condition (erythema multiforme minor) or erythema multiforme major or Stevens-Johnson syndrome) Erythema multiforme Erythema multiforme minor (Mild) Erythema multiforme major (Stevens-Johnson syndrome)

Target or "iris" lesions with central clearing, are the "hallmark“ of erythema multiforme

Oral Lesions. The oral lesions consist of multiple,large, shallow, painful ulcers with an erythematous border. They may affect the entire oral mucosa in approximately 20% of erythema multiforme patients. The lesions are so painful that chewing and swallowing are Impaired. The buccal mucosa and tongue are the most commonly affected sites, followed by the labial mucosa. Less commonly affected are the floor of the mouth, hard and soft palate, and the gingiva. There are rare instances in which erythema multiforme may be confined exclusively to the gingival tissues,resulting in a clinical diagnosis of desquamative gingivitis.

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Treatment. There is no specific treatment for erythema multiforme. Some cases may even resolve spontaneously. In contrast, patients exhibiting bullous or ulcerative lesions require intervention. For mild symptoms, systemic and local antihistamines coupled to topical anesthetics and debridement of lesions with an oxygenating agent is adequate. In patients with severe symptoms, corticosteroids are considered the drug of choice although, its use is controversial and not completely accepted.

DRUG ERUPTIONS Hypersensitivity to drugs has been noted since the advent of the sulfonamides, barbiturates, and various antibiotics. 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., an aspirin burn or the stomatitis resulting from topical penicillin) is referred to as stomatitis venenata or contact stomatitis.

Lichenoid contact lesion of left buccal mucosa due to type IV hypersensitivity to mercury.

Diffuse gingivitis and cheilitis due to contact allergy to flavor additive in dentifrice.

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 and cinnamic aldehyde) used to mask the taste of pyrophosphates in tartar control toothpaste, include an intense erythema of the attached gingival tissues characteristic of plasma cell gingivitis. 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.

Miscellaneous Factitious lesions. Candidiasis. Graft vs. host disease. Wegener's granulomatosis. Foreign body gingivitis. Kindler syndrome. Squamous cell carcinoma.