White and Red Oral Lesions PDF

White and Red oral lesions Done by Dr. Salsabeel Afifi Lecturer of Oral Medicine and Periodontology Classification Based on etiology Oral lichen planus and Lupus erythematosus lichenoid reaction Lichen planus It is a chronic...

White and Red oral lesions Done by Dr. Salsabeel Afifi Lecturer of Oral Medicine and Periodontology Classification Based on etiology Oral lichen planus and Lupus erythematosus lichenoid reaction Lichen planus It is a chronic inflammatory mucocutanous disease that can affect skin, hair follicles, scalp, nails, esophagus, genital areas as well as oral mucosa. It is, relatively, commonly seen clinical condition. Affects around 2% of the population. Oral lichen planus (OLP) occurs more frequently than the cutaneous form and tends to be more persistent and more resistant to treatment. Age: middle-age. Rare in children. Sex: Females more than males. Etiology A. Idiopathic lichen B. Lichenoid reaction planus Emotional stress Drug Induced Graft versus host Cell mediated immune disease (GVHD) response. Systemic diseases Dental materials Genetic factor. Cinnamon oil Oral Lichenoid reaction OLR Oral Lichenoid lesion OLL 1. Drug induced: Lichenoid lesions are similar or identical to lichen planus. Triggered by systemic drugs including gold, NSAIDs, beta blockers, sulfonylureas, some angiotensin converting enzyme (ACE) inhibitors, and some anti-malarials. Resolution of the lesions occurs when the offending drug is stopped or substituted with another drug. Drugs causing OLR Oral Lichenoid reaction OLR 2. Graft versus host disease (GVHD): Triggered by allogeneic bone marrow transplantation and it is associated with morbidity and mortality. It is an immunologically mediated reaction where lymphocytes in a donor graft mount an immunological reaction against the recipient tissue. Acute GVHD occurs within the first hundred days after transplant Chronic GVHD occurs in more than 100 days after BMT, and systemic organs and oral mucosa are involved. Oral Lichenoid reaction OLR 3. Systemic diseases: May occasionally be associated with autoimmune disorders such as primary biliary cirrhosis, chronic active hepatitis, ulcerative colitis, myasthenia gravis, and thymoma. Diabetes mellitus and hypertension (Grinspan syndrome: Triad of DM, hypertension and OLP). Hepatitis C & AIDS. Note: Epidemiological evidences from various studies worldwide strongly suggest that hepatitis C virus is associated with OLP.  Oral Lichenoid reaction OLR 4. Dental materials: Materials identified as triggering elements for OLR including; Amalgam restoration Polishing paste flavorings, especially cinnamon oil. Gold Cobalt Palladium Chromium Epoxy resins (composite) Prolonged use of denture wear (not proved) Most of the OLR associated to amalgam disappear in 3 to 15 months after that the restoration was changed. Oral Lichenoid reaction OLR 5. Cinnamon oil: Used as flavoring in polishing paste and some toothpastes. Food and some of food additives such as cinnamon aldehyde. Oral Lichenoid reaction OLR  Pathogenesis of OLP OLP is a T-cell mediated cytotoxicity reaction in which the cytotoxic CD8+ T cells trigger apoptosis of the basal cells of the oral epithelium. Activated CD8+ T cells induce keratinocyte apoptosis through various mechanisms such as: secretion of tumor necrosis factor (TNF)-alpha, secretion of granzyme B, or Fas/FasL interactions. Activated CD8+ T cells produce chemokines that attract additional inflammatory cells, therefore, promoting continued inflammation. Cell mediated immune process involving ⇒Langerhans cells, T-lymphocytes, &macrophages. Note: OLP may also be caused by genetic factor which influence the immune function. Mechanisms of basal cell damage Granzyme B TNF- α Fas/FasL interactions.  Clinical picture Patients may exhibit: 1. Skin lesions alone. 2. Oral lesions alone. 3. Both. In some cases, patients with OLP may present with concomitant lesions in the skin (15%), genital mucosa (25% of women and 2-4% of men), scalp (lichen planopilaris), nails, esophageal mucosa, larynx, and conjunctivae. Distribution: Bilateral Course: Frequent remission and exacerbation Duration: Persists for years (8-15years). Exacerbation may be associated with emotional upset. Clinical picture Skin lesion: 4 Ps  Papules and/or plaques.  Polygonal with angular border  Pink to Purple in color. May become brown.  Pruritic. With Koebner’s phenomenon  Have white striations on their surface (Wickham’s stria).  Symmetrical  Flexor surfaces of wrists, legs, trunk.  Face is usually unaffected. Some patients report genital involvement with features similar to skin lesions, scalp involvement (lichen planopilaris), and nail beds.  Koebner phenomenon (also called isomorphic response) Defined as appearance of new skin lesions on previously unaffected skin secondary to trauma or scratch. Koebner phenomenon Nail lesions:  In 10% of cases  Longitudinal fissuring  Nail bed discoloration  Lateral thinning  Complete loss of nail matrix  Scarring of proximal nail fold  Oral Lesions (Types of OLP) The oral lesions are bilateral/symmetrical anywhere in the oral cavity. Usually have Exacerbation and remission course Most commonly on buccal mucosa, tongue, lips, gingiva, floor of mouth and palate. May appear weeks or months before the appearance of cutaneous lesions. Clinical variants of OLP OLP has six classical clinical presentations: 1. Reticular 2. Plaque-like 3. Papular 4. Bullous 5. Erosive/ulcerative 6. Atrophic OLP may also be categorized into only three types: 1. Reticular/Plaque-like/Papular. 2. Bullous/Erosive/ ulcerative. 3. Atrophic. 1. Reticular/Papular/Plaque-like OLP Reticular OLP The most commonly seen form. Fine, intertwined lace-like pattern called “Wickham’s striae”. Get accentuated upon stretching at the periphery. Asymptomatic. Patient complaint is roughness of mucosa or change in color. Involves buccal mucosa in majority of cases. Reticular OLP Reticular OLP 1. Reticular/Papular/Plaque-like OLP Papular OLP Small white papules with fine striae at the periphery. Rarely observed. Usually associated with other forms. Asymptomatic. Papular OLP  Plaque-like OLP White homogeneous patch similar to leukoplakia. No change in the pliability or flexibility. Mainly involves the dorsum of the tongue followed by buccal mucosa. Plaque-like OLP 2. Atrophic OLP Diffuse red erythematous lesions. May be surrounded by the presence of white Wickham’s striae. Thin atrophic epithelium is more subjected to trauma and erosive areas would develop. Symptomatic. Patients complaint from burning sensation. Potentially malignant. 2. Atrophic OLP On the dorsum of tongue, atrophy of filiform & fungiform papillae occur, so the tongue appears smooth & erythematous. On the gingiva, in the form of Desquamative gingivitis. The full width of the attached gingiva appears bright red with marked edema and the gingival epithelium can be easily detached. 3. Bullous/Erosive/Ulcerative OLP Vesicles/bullae due to severe degenerative changes in the basal cells. Then rupture to form multiple shallow, irregular, well defined ulcers surrounded by red halo and white Wickham’s striae. May be as a complication of atrophic type as thin epithelium become abraded or ulcerated. Desquamative gingivitis may be an early manifestation of the disease. Symptomatic: burning sensation or soreness. Potentially malignant. Erosive lichen Planus Arrows point to vesicles in OLP  Desquamative gingivitis In atrophic and Erosive types Note: The triad constituted by erosive LP involving the vulva, vagina and desquamative gingivitis is termed as vulvovaginal–gingival syndrome. The different clinical forms of OLP is related to the magnitude of the subepithelial inflammation: Mild degree of Hyperkeratosis inflammation Partial/complete Intense deterioration of epithelium, inflammation (atrophy/ulceration). The central part Erythematous/ulcerative intensely inflamed, lesions surrounded by white whereas the periphery reticular/papular lesions is less affected  Diagnosis The history, classical oral lesions (bilateral, symmetrical white striae), and skin or nail involvement are usually sufficient to make a clinical diagnosis of OLP. Biopsy is recommended to differentiate it from other lesions. Differential diagnosis includes: 1. Lichenoid reactions to drugs, dental materials, GVHD. 2. Lupus erythematosus. 3. Leukoplakia (in plaque like OLP). Desquamative gingivitis Differential diagnosis includes: 1. Pemphigus vulgaris. 2. Mucous membrane pemphigoid. 3. dermatitis herpetiformis. 4. Linear IgA disease.  Histopathology of OLP 1. Liquefactive degeneration of the basal cells. Due to cell death by cytotoxic proteins (e.g. perforin, granzyme) released by Tc cells. 2. Apoptosis of keratinocytes Induced by T cells through various mechanisms. 3. Eosinophilic colloid bodies (Civatte bodies) in the lower half of the surface epithelium Represent degenerating keratinocytes. 4. A dense band-like lymphocytic infiltrate at the interface epithelial-CT junction Mainly T cells. B cells and plasma cells are uncommon findings. 5. Focal areas of hyperkeratinized epithelium Give rise to the Wickham's striae and papular form. Histopathology of OLP Specific features in each type: In papular/reticular/plaque OLP Hyperkeratosis. Acanthosis. Saw-teeth rete pegs (Rete pegs shortened and pointed). In bullous OLP Subepithelial vesicles/bulla due to extensive edema at epithelial-CT junction, following the degeneration of the basal cell layer. In atrophic OLP The epithelium is thin with absence of rete pegs. Little keratinization. Papular/reticular/plaque OLP Direct Immunofluorescent test: It helps in difficult cases of bullous OLP that may resemble other vesiculo- bullous diseases. DIF pattern: Shaggy band of fibrinogen and fibrin deposited in a linear pattern at B.M zone. Colloid bodies contain fibrin, IgM, C3, C4, and keratin. Oral Lichenoid lesions OLL Unilateral lesions OLLs are known to occur in all clinical varieties of presentation seen in OLP like reticular, atrophic, erosive, bullous, and keratotic with presence of Wickham’s striae. Potentially malignant with higher rate of transformation than OLP Drug induced OLL Amalgam related OLL Differentiating OLP & OLL  Management of OLP & OLL Remove the Patient cause education Therapeutic Other drugs modalities Surgical excision ⇒ is reserved to remove high-risk dysplastic areas only.  Management of OLP & OLL Remove the potential factors (in OLLs). i. Stop the offending drug. ii. Replace the offending dental material (amalgam, composite..etc). iii. Stop using suspected substances as cinnamon and its derivatives. iv. Control underlying systemic conditions. v. Consult a physician. Patient education: patients must be aware of: OLP is a persistent chronic condition with flare-up times and symptom-free periods. The hyperkeratotic striae will persist even in periods of remission. The aim of treatment is to relieve symptoms not curing the disease via: Prolong symptom-free times. Promote proper oral and dental hygiene (remove calculus, any source of trauma). Eliminate the local exacerbating factors (spicy food, cheek biting habit…etc) The potentially malignant nature of OLP and the risk of oral cancer in case of atrophic and erosive types. Remove the Patient cause education Therapeutic Other drugs modalities Therapeutic drugs 1. Corticosteroids (mainstay ttt of OLP). Topical Intralesional Systemic Combined 2. Immunosuppressive or immunomodulatory drugs. 3. Antifungal drugs (adjunctive) 4. Tranquilizers. 5. Anesthetic agents. Topical Systemic Intralesional Corticosteroids The mainstay treatment of symptomatic OLP (atrophic and erosive). Asymptomatic lesions (papular/reticular OLP) requires no treatment. Mechanism of action: Anti-inflammatory effect. Immunosuppressive effect. (through reducing the lymphocytic exudate, suppress T-cell function and stabilizing the lysosomal membrane). 1. Topical Corticosteroids Start with the weakest preparation, progressing to stronger one. All topical corticosteroids should be applied 4 times/day. Applied after meals and the last dose must be at bed time. Nothing should be taken by mouth for at least 1 hour after using topical steroids. When using mouth rinses; keep the solution in mouth for at least 2 minutes before spitting (mouth bath). Examples of topical corticosteroids: 1. Hydrocortisone muco-adhesive tablets 2.5mg. May be effective in mild cases. 2. Prednisolone 5 mg tablets dissolved in water and used as a mouth bath. 3. 0.1% triamcinolone acetonide ointment in orabase q.d.s. 4. 0.1%-0.2% triamcinolone acetonide mouth rinse used as a mouth bath. It is prepared by the pharmacist from injectable triamcinolone added to distilled water and the patient uses 5ml q.d.s. as mouth bath. 5. If triamcinolone fails; use betamethasone 0.1 mg in orabase. 6. Betamethasone valerate aerosol may be used in mild cases. 7. Clobetasol propionate 0.05% is used in severe refractory cases. In gingival lesions and Desquamative gingivitis: Steroid gels are applied in prefabricated silicone or plastic trays with high flanges to cover the gingiva. Used for 30 minutes at each application. Used 3-4 times/day. 2- Intralesional Corticosteroids 10 mg/ml of injectable triamcinolone acetonide is diluted with lidocaine 2% since steroid injection is very painful. May be required weekly (2-3 injection) for ulcerative lesions resistant to healing with topical &/or systemic steroids. 3. Systemic Corticosteroids Prednisolone 40 mg given 1.5 hour after arising for 7 successive days. Followed by 10-20 mg dose 1.5 hour after arising every other day for additional 2 weeks. Once the ulcers are resolved, control of the oral lesion is usually done by topical steroids alone. 4. Combined NSAIDs and low dose Systemic steroids Used if systemic steroids are contraindicated in high doses. 10-20 mg prednisolone is given 1.5 hour after arising +1200 mg Ibuprofen/day in divided doses for 2 weeks. NSAID has anti-inflammatory properties which augment the anti-inflammatory action of systemic steroids. Immunosuppressive or immunomodulatory drugs If corticosteroids are ineffective or contraindicated. They should be reserved for highly recalcitrant cases of OLP. Immunosuppressive or immunomodulatory drugs Topical application of cyclosporine, tacrolimus & retinoid has been suggested as a second line therapy for OLP. 1% topical cream of pimecrolimus has been successfully used as treatment for OLP. Mechanism of action: Cyclosporine and Tacrolimus are immunosuppressive drugs that inhibit calcineurin. (calcineurin is a protein phosphatase that is involved in the activation of IL-2, which stimulates the growth and differentiation of T-cell response) Pimecrolimus has significant anti-inflammatory activity and immunomodulatory capabilities with low systemic immunosuppressive potential. Retinoids has immunomodulatory effect. May be used systemic in severe cases of OLP. Antifungal drugs Topical or systemic anti-fungal drugs are used for 1 week out of every 4 weeks of Topical or systemic steroid therapy. Tranquilizers If the patient shows signs of anxiety or stress, tranquilizers may be prescribed. Examples include diazepam (e.g. valium) or chlorodiazepoxide (e.g. Librium) 5-10 mg 2-3 times/day. Advise the patient to consult a psychiatrist.  Anesthetic agents For relief of pain and discomfort 0.15% benzydamine hydrochloride mouth rinse. BBC spray. Lidocaine in orabase. Remove the Patient cause education Therapeutic Other drugs modalities Recent advances in OLP management 1. PUVA therapy 2. Photodynamic therapy (PDT) 3. Laser therapy 4. Cryotherapy  PUVA therapy It is a photochemotherapy with 8-methoxypsoralen and long wave ultraviolet light. Methoxypsoralen is given orally, followed by administration of 2 hours of UV radiation intraorally on the affected sites. Reserved for severe cases of OLP. Disadvantages Nausea and dizziness secondary to psoralen. 24-hour photosensitivity when this medicine is taken orally. Complicated geometry of the mouth, it is more applicable on skin over large, open surfaces. Photodynamic therapy (PDT) Uses a photosensitizing compound like Aminolevulinic Acid (ALA) or methylene blue, activated at a specific wavelength of laser light, to destroy the target cell via strong oxidizers. Mainly used in head and neck cancer. May have immunomodulatory effects and induce apoptosis in the hyperproliferating inflammatory cells which are present in psoriasis and lichen planus, reversing the inflammation of lichen planus. (under research) Laser therapy To destroy the superficial epithelium containing the target keratinocytes by protein denaturation. Deeper penetrating beam like the diode laser destroys the underlying connective tissue with the inflammatory component along the epithelium. Still under research. Cryotherapy Same concept as laser therapy