"Other" Oral Inflammatory Conditions Flashcards
What is a granuloma?
- Focus of chronic inflammation.
- Microscopic aggregation of activated epithelioid macrophages fused to form giant cells, surrounded by lymphocytes +/- plasma cells +/- a rim of fibroblasts and connective tissue
What are orofacial granulomatosis?
- Unexplained granulomatous inflammatory lesions
* Non-specific diagnosis of exclusion
Subtypes of orofacial granulomatosis…
• Cheilitis granulomatosis - Limited to lips • Melkersson-Rosenthal Syndrome - Swells of face, oral mucosa, etc - Fissured tongue - Unilateral facial nerve paralysis
Clinical features of orofacial granulomatosis
- Lips affected more than other parts of face
- Swelling: nontender, persistent
- Rare lymphangioma-like vesicles
- Rare cervical lymphadenopathy
- Intraoral edema, ulcers, papules
- Gingival swelling, erythema, pain, erosions
- Buccal cobblestone
- Vestibular linear hyperplastic folds
Histology of orofacial granulomatosis
- Non-necrotizing granulomas
- Edema, dilated lymphatics, scattered lymphocytes
- Negative for micro-organisms and foreign substances
Diagnosis of orofacial granulomatosis
• Unexplained granulomatous inflammatory lesions
• OFG is diagnosis of exclusion - known causes of granulomatous lesions must be eliminated:
- Systemic:
• Chronic granulomatous disease
• Crohn's disease
• Sarcoidosis
• Infections (fungi, TB, etc)
- Local
• Chronic oral infection
• Foreign body reactions
• AllergyManagement for orofacial granulomatosis include…
- Special stains (for microorganisms)
- Polarize microscopy (for foreign material)
- Eliminate chronic inflammatory bowel disease
- Eliminate sarcoidosis
- Look for antigen
- Topical or intralesional corticosteroids
- Clofazimine (antileprosy agent)
- Surgical recontouring (but often recur)
Differential diagnosis for fissured tongue
- Normal variant
- Inherited condition
- Down syndrome
- Melkersson Rosenthal syndrome
- Erythema migrans-associated
- Plasma cell gingivitis
Causes of foreign body granulomas…
• Endogenous substances - Keratin - Bony sequestra • Exogenous - Usually birefringent (seen under polarized light) - Sutures - Dental materials
Clinical presentation of granulomatous gingivitis
- Solitary or multifocal lesions
- On interdental papilla or gingival margin
- Up to 2cm in diameter
- Red macules or enlargements
Diagnosis of granulomatous gingivitis…
• Rule out:
- Histologically distinctive/specific granulomatous conditions
• Foreign substances
• Deep fungal infections
• Acid fast bacilli
- Systemic granulomatous diseases
• Crohn's
• Wegener
• Sarcoid
• Diagnosis of nonspecific granulomatous gingivitis is made after r/o other diagnosesHistology of granulomatous gingivitis
• Foreign particles identified associated with:
- Granulomas = foreign body granulomatous gingivitis
- Nonspecific mucositis
- Lichenoid reaction
• Particles less than 1um may be undetected
• When there are granulomas without particles, diagnosis of nonspecific granulomatous gingivitis can be made after r/o all other diagnoses
Etiology of granulomatous gingivitis
- Trimming restorations near gingival margin
* Dental prophylaxis paste used too soon
Clinical features of Wegener granulomatosis
- Probably immune dysfunction
- Starts in upper respiratory tract
- Initially, nasal discharge or sinus pain
- Nasal septum and/or palatal destruction
- May affect lungs and kidneys
- May involve paranasal sinuses, TMJ, or gingivae
- Untreated disseminated cases survive only a few months
Treatment of Wegener’s granulomatosis
• Cytotoxic drugs
- Especially cyclophosphamide with prednisone
• can achieve long-term survival, even cure
Histology of Wegener’s granulomatosis
- Necrotizing vasculitis associated with granulomas
- Leukocytoclastic vasculitis
- Diagnosis involves identification of c-ANCA (serum antibodies against cytoplasmic components of neutrophils)
Discuss ANCAs as seen in Wegener Granulomatosis
• Circulating autoantibodies against a component of granules in cytoplasm of neutrophils
- Serum from patients with vasculities reacts with cytoplasmic antigens in neutrophils - Due to antineutrophil cytoplasmic antibodies - Cause IF patterns in ethanol-fixed neutrophils - One shows cytoplasmic localization of stain (c-ANCA) - Group of autoantibodies against enzymes mainly in azurophilic or primary granules in neutrophils - The most common target antigen is proteinase-3 (PR3), a component of a neutrophil granule
Autoantibodies present in Wegener granulomatosis…
- c-ANCA: autoantibodies against a component of granules in cytoplasm of neutrophils
- Titers correlate with disease activity
- May be important in pathogenesis
Etiology of sarcoidosis
• Abnormal immune response to unknown antigen
- Infectious agent
- Environmental factors
• Genetic predisposition
Clinical presentation of sarcoidosis
- Multisystem disease characterized by non-caseating granulomas in many organs
- Bilateral hilar lymphadenopathy or lung disease in 90% of cases
- Skin and mucous membranes (including nose and mouth)
- Eyes in 25% (blindness rare)
- Also lymph nodes, bone marrow, spleen, liver, kidneys, heart, CNS, parotid glands enlarged in 10-20% (cause of xerostomia)
Demographics of sarcoidosis
- Incidence varies wildly in countries throughout the world
* In U.S. it affects blacks more than whites, with peak incidence in the fourth decade.
Oral lesions in sarcoidosis…
• Soft tissue - Salivary gland enlargement --> xerostomia - Submucosal enlargements - Mucosal macules • Intraosseous - Radiolucencies
Histology of sarcoidosis
• Non-caseating granulomas
- Schaumann bodies (laminated calcifications in giant cells)
- Asteroid bodies in giant cells
Laboratory tests for Sarcoidosis…
• Elevated: - Angiotensin converting enzyme - Erythrocyte sedimentation rate - Serum calcium - Alkaline phosphatase - Vitamin D (Mnemonic: A SAVE) • Positive Kveim-Siltzbach skin test (but not often performed) • Transbronchial lung biopsy is often used
Pronosis for sarcoidosis
- Most patients recover
* 10-20% succumb to progressive fibrosis and cor pulmonale
Treatment for sarcoidosis
- Corticosteroids
- Steroid-sparing agents
- Antimalarial agents
Area mostly affected in Crohn’s disease
Mainly affects distal small intestine and proximal colon.
What is Crohn’s disease?
• Inflammatory GI (mainly) disease:
- Non-necrotizing granulomas
- Probably immunologically-mediated
• Abdominal cramping, nausea, diarrhea, etc.
Demographics of Crohn’s disease
Diagnosis in teens or in people over 60 years of age
Oral manifestations of Crohn’s disease…
• Initial manifestation in some cases
• Diffuse or nodular swellings
• Cobblestone
• Deep linear ulcers in vestibule
- Denture hyperplasia
• Mucogingivitis: patchy red macules and plaques
• Recurrent aphthous ulcers
• Pyostomatitis vegetans
- Manifestation of CIBD
- Multiple pustules
- Intraepithelial abscesses
• Eosinophils +++Reactions to physical & chemical agents include…
- Frictional keratosis
- Traumatic ulcers
- Eosinophilic ulcers
- Burns
- Submucosal hemorrhage
- Anticancer therapy
- Reactions to amalgam
- Tobacco
- Cervico-facial emphysema
- Hairy tongue
- Toxic metals
- Drug-related discolorations
What is frictional keratosis?
- Chronic mechanical irritation –> frictional keratosis
* Reversible
Clinical types of frictional keratosis
- Linea alba
- Morsicatio
- Toothbrush gingival abrasion
- Irritation including broken teeth, prostheses, and restorations
- Mastication on edentulous alveolar ridge
What is linea alba?
- Clinical type of frictional keratosis
- Very common
- White line on buccal mucosa (often bilateral) at level of occlusal plane
- Friction or sucking trauma
What is chronic mucosal chewing?
- “Morsicatio buccarum, linguarum, labiorum”
- White plaques with surface shedding
- +/- focal red erosions or ulcers
- Often bilateral
Histology of frictional keratosis
• Benign hyperkeratosis +/- other features:
- Ragged surface projections
- Bacterial colonies may coat surface
- Vacuolated spinous cells
Clinical features of traumatic ulcers
• Cause usually readily identified • Symmetrical or irregular • Shallow or deep • Base usually firm • Onset abrupt or gradual • Persist until cause is removed • Acute ulcers painful but chronic may be non-painful • Often exhibit a white or yellow surface - Removable, fibrinopurulent membrane
Describe an acute traumatic ulcer…
- Pain
- Yellow base, red halo
- History of trauma
- Heals in 7 to 10 days if cause eliminated
Describe a chronic traumatic ulcer…
- Little or no pain
- Yellow base, elevated margins (scar)
- History of trauma, if remembered
- Delayed healing if irritated, especially tongue lesions
- Clinical appearance mimics carcinoma and infectious ulcers
What are traumatic eosinophilic ulcer or ganuloma?
• Deep ulcer with indurated elevated border
• Clinical resemblance to SCC (or pyogenic granuloma)
• Pain and source of trauma may be lacking
• Most on tongue; may be multiple
• Traumatic eosinophilic granuloma is variant
- Discolored nodule, resembling pyogenic granuloma
Histology of traumatic eosinophilic ulcer or granuloma
- Ulcer bed: fibrin and inflamed granulation tissue
- Inflammation extends into underlying tissue
- Deeper inflammatory infiltrate eosinophils and histiocytes (some atypical)
- Inflammatory tissue replaces skeletal muscle
What is Riga-Fede disease?
- Variant of traumatic eosinophilic ulcer on anterior ventral tongue of infants
- Chronic mucosal trauma due to lower anterior teeth (natal or neonatal)
Types of burns
- Electric burns
- Thermal burns
- Chemical burns
