Ch16 Part 1: Non-Infective Stomatitis PDF

Ch16 part1 : non infective stomatitis Laila Deek 122 aim is as ## Ulcers : - Definition: A break in the skin or mucous membrane with loss of surface tissue, necrosis of epithelial tissue, and often pus. - Healing: Most o...

Ch16 part1 : non infective stomatitis Laila Deek 122 aim is as ## Ulcers : - Definition: A break in the skin or mucous membrane with loss of surface tissue, necrosis of epithelial tissue, and often pus. - Healing: Most oral ulcers heal in a few days to 2 weeks. Healing is faster on the floor of the mouth or buccal mucosa compared to the palate or gingiva. - Recurrent oral ulcers: These occur repeatedly at the same or different sites. ### Traumatic Ulcers : - Causes: Biting, denture trauma, chemical trauma (e.g., dental etchant, hypochlorite, silver nitrate). - Common sites: Lips, buccal mucosa, or areas adjacent to denture flanges. - Features: Tender with a yellowish-grey fibrin slough and red margins. Inflammation and erythema vary based on cause and timing. No induration unless scarred from repeated trauma. May occur after dental anesthesia due to accidental biting. - Healing: Typically heals within days after removing the cause. If it persists for more than 10 days without improvement, biopsy is recommended. ### Eosinophilic Ulcer (Atypical or Traumatic Eosinophilic Granuloma): - Presentation: Deep ulcer or mass with ulcerated surface, resembling carcinoma, exceeding 10 mm in diameter, and often enlarging before stabilizing. - Causes: Likely an unusual response to trauma, though trauma history may be absent. - Common sites: Tongue, gingiva, and occasionally other areas. - Special cases: Riga-Fede disease in infants, caused by erupting lower incisors traumatizing the tongue or lower - Features: lip. an May persist for months, raising above the mucosa due to inflammatory infiltrate. Histologically can mimic lymphoma. - Healing: Typically resolves spontaneously within 3–10 weeks. Biopsy often accelerates healing. ps.wi ### Factitious Ulceration (Self-Inflicted Oral Ulcers): perceived benefit. ICI wy.im - Rare oral ulcers caused intentionally by patients, often linked to psychosocial disorders where patients gain a S I Tiot oiw. 4E s - Features: Non-healing ulcers, typically in the anterior mouth, caused by repeated trauma. Diverse methods of self-injury, including severe cases like self-extraction of teeth. May be associated with underlying emotional disturbances, which are often well-hidden. - Medical Context: Self-harm can occur in conditions such as autism, familial dysautonomia, Lesch-Nyhan syndrome, Tourette syndrome, and other learning disabilities. Minor unintended injuries, such as habitual gingival picking, are less severe and rarely lead to ulcers. - Diagnosis and Management: Biopsy may be needed to rule out organic disease. Diagnosing the underlying cause can be challenging due to concealed emotional issues. in II put at diagnosis Jim oo ulcers 11 ie ### Recurrent Aphthous Stomatitis (RAS): a j1Jo6Id - Prevalence: The most common oral mucosal disease, affecting up to 25% of the population. - Severity: Many cases are mild and go untreated. - Presentations: There are three clinical forms of RAS, each defined by its distinct presentation. - Differentiation: Ulcers similar to RAS may appear in other diseases or syndromes, though their classification as true RAS remains uncertain. clinical features jao.EC T1 Pathology : - Biopsy Role: Not typically used for diagnosis. Performed only to exclude carcinoma (in major aphthae) or viral infection (in herpetiform aphthae). - Findings if Biopsy is Performed: Prodromal phase shows lymphocytic infiltration of the epithelium. Followed by epithelial destruction with non-specific acute and chronic inflammation. - Clinical Feature: Aphthae are not preceded by vesicles. Management : 1. Reassurance and Education : Inform and reassure patients about the benign nature of the condition. 2.Corticosteroids :Triamcinolone dental paste for reducing inflammation. 3.Tetracycline Mouth Rinses Especially effective for herpetiform aphthae. Prepare by mixing 250 mg tetracycline capsule contents in water, used as a rinse for 2–3 minutes, three times daily. 4.Chlorhexidine:Antiseptic mouthwash used three times daily after meals, held in the mouth for at least 1 minute. 5. Topical Salicylates :Choline salicylate gels can be applied directly to the ulcers. 6. Local Analgesics : Lidocaine or benzocaine sprays and gels to provide pain relief. ### Major Aphthae: jez RAS It Walysis - Characteristics: Painful, persistent, and resistant to conventional treatment; can be disabling. May be associated with underlying diseases like HIV infection. - Treatment Options: Reportedly Effective: Azathioprine, Cyclosporin, Colchicine, Dapsone. Most Reliable: Thalidomide. ### Behçet s Disease (Behçet s Syndrome): - Definition: Rare disorder causing systemic blood vessel inflammation, leading to symptoms such as oral sores, genital ulcers, eye inflammation, and skin lesions. Can cause life-threatening complications like thrombosis, blindness, or brain damage. - Clinical Features: Affects mostly young adult males (20–40 years old). - Patterns of Disease: 1. Mucocutaneous: Oral aphthae (resembling common aphthous stomatitis). mucosa Genital ulcers and skin rashes (e.g., erythema nodosum, vasculitis). 2. Arthritic: Involves large weight-bearing joints. Joints Causes relapsing or constant pain, but no destructive arthritis. 3. Neurological: Late-stage vasculitis in the brain causing sensory/motor issues, confusion, fits, or thrombosis. May lead to raised intracranial pressure, blurred vision, or headaches. w 4. Ocular: Uveal inflammation, vasculitis, or retinal artery thrombosis. Rapidly leads to blindness if untreated. - Aetiology: Immune-Mediated Reaction: Circulating immune complexes, high cytokine levels, and lymphocyte/macrophage activation suggest immune involvement. Possibly triggered by an unknown infectious agent via immune cross-reaction with host heat shock proteins. Genetic Factors: Strongly associated with HLA-B51 , which is not diagnostic but predicts ocular lesions. - Management : - Approach: Requires a multidisciplinary team due to the complexity of the disease. - Main Treatments: Ciclosporin and tacrolimus. Corticosteroids for acute exacerbations. - For Oral Ulcers: Thalidomide or topical tacrolimus. - Emerging Therapies: Anti-TNFα drugs like infliximab show promise. - Complications: Blindness, large-vessel aneurysm rupture, thrombosis, and embolism. - Prognosis: Relapses may become less frequent over time, and the disease may eventually “burn out” if severe complications are avoided. É ### HIV-Associated Oral Ulcers: - Features: Severe recurrent aphthae, often major or herpetiform, resembling common aphthae. I - Diagnosis: Biopsy for non-healing ulcers to rule out opportunistic infections (e.g., lymphoma, Epstein-Barr virus, cytomegalovirus, deep fungal infections). - Treatment: Potent topical steroids. Severe cases may require systemic high-potency medications used for aphthous ulcers. Antiretroviral therapy reduces severity and frequency. ### Nicorandil-Induced Ulcers: - Cause: Potassium channel activator (nicorandil) used in angina treatment. - Features: Painful, sharply demarcated ulcers, often on the lateral tongue, buccal mucosa, gingivae, or fauces. May also occur on perianal or vulval skin. Commonly appear within weeks to 18 months of starting the drug, more frequent at higher doses. Scars may remain after healing. - Management: Ulcers heal after drug withdrawal, taking up to 9 weeks. ## Lichen Planus and Similar Conditions: - Chronic inflammatory condition of the oral mucosa, causing: White, lacy patches. Red, swollen tissues. Painful open sores with burning or discomfort. - Similar Diseases: Other conditions resemble lichen planus clinically or histopathologically, grouped as “lichenoid processes.” - Demographics: More common in middle-aged or older females. ## Lichen Planus: Prevalence: Affects 1%-2% of the population. I Demographics: Common in middle-aged or older individuals, slightly more frequent in females. Type: Chronic inflammatory disease of the skin and mucous membranes. - Aetiology and Pathogenesis: B.i T.gl - Cause: Unknown; multiple factors may lead to similar clinical and histological outcomes. - Mechanism: Cytotoxic T cells (CD8+) and helper T cells infiltrate basal layers of epithelium. Basal cells are destroyed by: 1. Direct Cytotoxicity: Perforin and enzymes. 2. Cytokine Secretion: TNFα and other cytokines. - Result: Basal cells undergo apoptosis. Epithelium thins, keratinizes, or ulcerates. Basement membrane becomes compromised, inhibiting repair and epithelial attachment. - Clinical Features: Lesion Distribution: Oral Lesions Only: 1/3 of cases. Skin Lesions Only: 1/3 of cases. Both Lesions: 1/3 of cases. Oral Lesions: Whitish keratotic lines called Wickham s striae are common. Skin Lesions: Purplish, 2-3 mm papules with Wickham s striae. Typically itchy and found on flexor surfaces of forearms and wrists. Skin lesions assist in diagnosis but can mimic drug-induced lichenoid reactions. - Course of Disease: Flare-ups triggered by stress, trauma, or dental treatment. Associated with hepatitis C. - Symptoms may fluctuate: Active Phase: Atrophic, ulcerated epithelium with non-specific inflammation. Recovery Phase: Basal cells regenerate, epithelium thickens, and keratinization increases, often leading to symptom resolution. - Management: Skin lesions respond well to steroids and often resolve within a few years. Important to inquire about past skin rashes during history-taking for diagnosis. lichenplanus EpibbW Cont. Oral Lichen Planus: 1. General Characteristics: 3196 in Oral lesions are difficult to treat and often persist for life. 1 The floor of the mouth and palate are usually not affected. If involved, consider misdiagnosis or a drug reaction. 2. Phases of Lichen Planus: Reticular: Characterized by a meshwork of fine, snowy white striae (keratinized lines) forming lacy, radiating, or annular patterns. May feel rough or dry if keratinization is thick. Atrophic: Epithelial thinning with red areas and visible inflamed submucosa. Often combined with striae. Ulcerated: Results from severe basal cell destruction, leading to shallow, irregular ulcers covered with a yellowish fibrin layer. Surrounded by atrophic areas and striae at the margins. Bullous: Blisters form due to separation of the epithelium caused by basal cell loss and weakened basement membrane. Most common on gingiva; blisters quickly rupture into ulcers. 3. Key Differentiation: Ulcerated lichen planus is distinct from erosive lichen planus and pemphigus. Bullous lichen planus must be differentiated from other immunobullous diseases. - Diagnosis: 1. Primary Approach: Diagnosis is based on patient history, lesion appearance, and distribution. Biopsy: - Mandatory for oral white lesions to rule out dysplasia. - Not typically needed for classic lichen planus but required for atypical or plaque-like lesions. 2. Differentiating Dysplasia: Dysplasia involves abnormal precancerous cell growth, more serious than hyperplasia (overgrowth of normal cells). - Management: 1. General Principles: No cure for the underlying disease; treatment is symptomatic. Reassure patients that lichen planus is not infectious. Education about the minimal risk of malignant transformation. 2. Treatment Approaches: Oral Hygiene: Essential for management. Topical Steroids: Low-potency: Hydrocortisone 2.5 mg adhesive tablets. Medium-potency: Triamcinolone gel, inhalers (beclomethasone), or betamethasone mouthwash. High-potency: Fluocinonide or clobetasol. Systemic Steroids: Prednisolone for severe cases. Chlorhexidine Mouthwash: To maintain hygiene and prevent infections. 3.Complications: Candidal Infections: Common due to keratinization and steroid use. Symptoms may worsen or switch to atrophic/ulcerated forms with superimposed candidosis. Diagnose with hyphae scraping; treat with antifungals to restore less symptomatic state. 4.Monitoring: Regular follow-up to track complications and manage flare-ups effectively. ## Vulvovaginal-Gingival Syndrome: Severe but uncommon form of lichen planus involving genital mucosa and gingiva. Buccal mucosa, tongue, scalp, esophagus, and eyes may also be affected. Leads to scarring and significant complications; resistant to treatment. Often requires high-potency steroids or topical tacrolimus for non-oral sites. ## Malignant Change in Lichen Planus: Rare but accepted risk of developing oral squamous carcinoma. - Challenges in risk assessment: 1. Non-specific clinical and histological features. 2. Dysplastic lesions may mimic striae. 3. Biopsy is often avoided in typical cases, making early dysplasia detection difficult. 4. Plaque-type lichen planus can resemble leukoplakia. ## Lichenoid Reactions: Lichen planus-like lesions triggered by known factors, often drugs. - Drug-induced Reactions: Wide range of drugs (e.g., colloidal gold) can cause skin or mucosal reactions. Reactions may persist for months or years post-drug administration. Treatment involves drug withdrawal and standard lichen planus management. - Restoration-induced Reactions: Caused by amalgam restorations (especially corroded ones). Lesions are localized to mucosa in contact with restorations. Healing occurs after restoration removal. ##Lupus Erythematosus (LE): - Autoimmune connective tissue disease with systemic and cutaneous forms. - Oral Lesions :Resemble lichen planus but with less defined striae. - Suggestive features: unilateral lesions, symmetrical ulcers with erythema, radiating striae, and palatal involvement. - Pathology: Histological features overlap with lichen planus. Systemic LE shows thickened basement membranes and fibrosis due to immune complex deposition. - Diagnosis: Based on clinical features, biopsy, and autoantibodies (e.g., anti-dsDNA, ANA, anti-Smith). - Management: Oral lesions respond to topical corticosteroids, but systemic lesions are resistant. ## Chronic Ulcerative Stomatitis (CUS): 1. General Characteristics: Rare mucosal disease often underdiagnosed. Primarily affects females over 40 years of age. 2. Clinical Features: Lesions: Shallow ulcers, erosions, or erythema, most commonly affecting the tongue, followed by buccal mucosa and gingiva. Resembles lichen planus both clinically and histologically, sometimes presenting with striae. Skin involvement is uncommon. 3. Diagnosis: Suspect in patients with severe, steroid-resistant lichen planus-like lesions. Confirmed via immunofluorescence or detection of circulating antibodies using ELISA. 4. ELISA: A diagnostic assay that measures antibodies, antigens, and proteins in biological samples to confirm CUS. l