Red And White Lesions Of The Oral Mucosa PDF

Red And White Lesions of The Oral Mucosa Dr. Gillan El-Kimary BDS, MSc, PhD Lecturer of Periodontology & Oral Medicine...

Red And White Lesions of The Oral Mucosa Dr. Gillan El-Kimary BDS, MSc, PhD Lecturer of Periodontology & Oral Medicine Faculty Of Dentistry Alexandria University Outline Red and white tissue reaction Classification of red and white lesions 1- Infectious Diseases 2-premalignant Lesions 3- Immunopathologic Diseases 4- Allergic Reations 5-toxic Reactions 6- Reactions To Mechanical Trauma 7- Others Cause of white appearance 1) Increase production of keratin ( hyperkeratosis) 2) Abnormal but benign thickening of stratum spinosum (acanthosis) 3)Intra and extracellular accumulation of fluid in the epithelium 4) White pseudo-membrane Cause of red appearance 1) Atrophic epithelium characterized by a reduction in the number of epithelial cells 2) Increased vascularization Classification of Red & White Lesions 1)Infectious Oral Candidiasis Hairy Leukoplakia 2) Premalignant Oral Leukoplakia & Eryhtroplakia Oral Submucous Fibrosis 3) Immunopathologic Oral Lichen Planus Drug-induced Lichenoid Reactions Lichenoid Reaction Of Graft Versus Host Disease Lupus Erythematosus 1 4)Allergic Lichenoid Contact Reactions Reactions To Dentifrice & Chlorhexidine 5) Toxic Reactions Smokless Tobacco Smokers Palate 6) Reactions To Mechanical Trauma Morsicatio Frictional Hyperkeratosis 7) Others Benign Migratory Glossitis Leukodema White Spongy Nevus Hairy Tongue 1) Infectious Lesions a- Oral Candidiasis The most prevalent opportunistic infection affecting oral mucosa. Caused by Candida Albicans A superficial infection (upper layers of oral mucosal epithelium with formation of patchy white plaque or flecks on mucosa) It is composed of desquamated epithelial inflammatory cell, fibrin and yeast. Candida Albicans tissue invasion Epithelial Adherence Epithelial penetration “ Lipase” Predisposing Factors 1-changes in oral microbial flora followin administration of antibiotics 2-chronic local irritants as denture. 3-corticosteroids 4-radiation of head and neck 5-age(infancy-old age) 6-immune status 7-hospitalization 8- Smoking 9-Xerostomia 2 Classification Of Oral Candidiasis 1) Primary Oral Candidiasis Acute Pseudomembranous Erythematous Chronic Pseudomem. Erythematous Plaque-like Nodular Candida associated lesions Denture Stomatitis Angular Chelitis Median Rhomboid glossitis 2) Secondary Oral Candidiasis Accompanied by systemic mucocutaneous manifestations e.g AIDS, DiGeorge syndrome Pseudomembranous Candidiasis (Thrush) Acute form “Thrush” - primary oral candidiasis - predominantly affects patients medicated with antibiotics and immunosuppressant drugs Chronic form - associated with human immunodeficiency virus ( HIV patient) - Steroid inhalers Clinical presentation The infection typically presents with loosely attached membranes comprising fungal organisms and cellular debris, which leaves an inflamed, sometimes bleeding area if the pseudomembrane is removed. The clinical presentations of acute and chronic pseudomembranous candidiasis are indistinguishable. Erythematous Candidiasis “Atrophic” Clinical presentation Explained by increased vascularity Having diffuse border ,which help distinguishing it from erythroplakia, which has a sharper demarcation Infection is found in the palate, and dorsum of the tongue of patient using broad spectrum antibiotics, and smoking or using inhalation steroids 3 Chronic Plaque-Type and Nodular Candidiasis “ Candidal leukoplakia” Characterized by white irremovable plaque, indistinguishable from oral leukoplakia Has been associated with malignant transformation. Candida Associated Lesions 1- Denture Stomatitis The most prevalent site for denture stomatitis is the denture-bearing palatal mucosa ØThe denture serves as a vehicle that accumulates sloughed epithelial cells and protects the microorganisms from physical influences such as salivary flow. ØThe microflora is complex and may, in addition to C. albicans contain bacteria from several genera, such as Streptococcus, Lactobacillus, Prevotella, and Actinomyces-strains. ”Mixed Infection” Clinical presentation ØType I is limited to minor erythematous sites caused by trauma from the denture. ØType II affects a major part of the denture-covered mucosa ØType III has a granular mucosa (In addition to the features of type II) “Papillary Hyperplasia” 2- Angular Chelitis -It presents as infected fissures of the commissures of the mouth, often surrounded by erythema - The lesions are frequently coinfected with both Candida albicans and Staphylococcus aureus Etiology Loss of vertical dimension Vit. B deficiency Iron deficiencies DM, HIV, neutropenia 3- Median Rhomboid Glossitis MRG is clinically characterized by an erythematous lesion in the center of the posterior part of the dorsum of the tongue oval configuration. This area of erythema results from atrophy of the filiform papillae and the surface may be lobulated. A concurrent erythematous lesion may be observed in the palatal mucosa (kissing lesions) MRG is asymptomatic, and management is restricted to a reduction of predisposing factors. The lesion does not entail any increased risk for malignant transformation. 4 Management Of Oral Candidiasis Antifungal + remove predisposing factor The most commonly used antifungal drugs belong to the groups of polyenes or azoles polyenes such as nystatin and amphotericin B (well tolerated, not ass. with resistance) , they affect the yeast’s cell membrane integrity and also affect adherence of fungi. Azoles such as miconazole, fluconazole. (can be used systemically in deeply seated infections) There are several disadvantages with the use of azoles. They are known to interact with warfarin, leading to an increased bleeding propensity and development of resistance Type III denture stomatitis may be treated with surgical excision in an attempt to eradicate microorganisms present in the deeper fissures of the granular tissue. If this is not sufficient, continuous treatment with topical antifungal drugs should be considered NB: Chlorhexidine may also be used but can discolor the denture and also counteracts the effect of nystatin Antifungal (Systemic) In cases of inaccessible areas ”Oropharyngeal candidiasis” (soft palate, posterior third of tongue) C/I in liver and renal patients ( referral) Dosage (1st day 200mg then 100 mg daily for 1-2 weeks ) b- Oral Hairy Leukoplakia OHL is a common HIV-associated oral mucosal lesion. OHL has been used as a marker of disease activity since the lesion is associated with low CD4+ Tlymphocyte counts. The lesion is not pathognomonic for HIV disease since other states of immune deficiencies, such as caused by immunosuppressive drugs and cancer chemotherapy OHL is strongly associated with Epstein Barr virus (EBV) and with low levels of CD4+ T lymphocytes. Antiviral medication, which prevents EBV replication, is curative Clinical presentation Frequent site: lateral borders of the tongue as a vertical white folds ØThe lesions may also be seen as white and somewhat elevated plaque, which cannot be scraped off. ØOHL is asymptomatic. (unless superinfected with candidal strains) Dx & management ØDx of OHL is usually based on clinical characteristics, but histopathologic examination and detection of EBV can be performed to confirm the clinical diagnosis. ØCan be treated successfully with antiviral medication. ØIn addition, the disorder has also been reported to show spontaneous regression. ØOHL is not related to increased risk of malignant transformation 5 2) Premalignant Lesions The development of oral leukoplakia & erythroplakia as premalignant lesions involves different genetic events. Activation of oncogenes and deletion and injuries to suppressor genes and genes responsible for DNA repair will all contribute to a defective functioning of the genome that governs cell division. Following a series of mutations, a malignant transformation may occur Oral Leukoplakia Clinical presentation A) Homogenous Leukoplakia Ø Def: White plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer. Ø Clinically characterized as a white, often well-demarcated plaque with an identical reaction pattern throughout the entire lesion. The surface texture can vary from a smooth and thin to a leathery appearance with surface fissures “cracked mud” Ø Asymptomatic DDx.. OLP B) Non-homogenous Leukoplakia Other names: erythroleukoplakia & speckled leukoplakia white patches or plaques intermingled with red elements The clinical manifestation of the white component may vary from large white verrucous areas to small nodular structures. C) Proliferative Verrucous Leukoplakia (PVL) More aggressive proliferation pattern and high recurrence rate older women, and the lower gingiva is a predilection site. The malignant potential is very high, and verrucous carcinoma or squamous cell carcinoma may be present at the primary examination Oral Erythroplakia Clinical presentation A red lesion of the oral mucosa that excludes other known pathologies The lesion comprises an eroded somewhat submerged red lesion that is frequently observed with a distinct demarcation against the normalappearing mucosa. Asymptomatic DDx.. erythematous OLP Highest risk of malignant transformation Floor of the mouth Lateral borders of the tongue Retromolar area 6 Clinically.. loss of flexibility of the affected tissues and induration Predisposing factors.. SMOKING, alcohol, Candidiasis, mechanical trauma (chronic irritation) Oral leukoplakia/ Erythroplakia Diagnosis White or red patch (unexplained ) If trauma is suspected, such as a sharp tooth or restoration, should be eliminated. If healing does not occur in two weeks, a tissue biopsy is essential to rule out malignancy Diagnosis Biopsy : Histopathology reveals, A- No dysplasia: Hyperkeratosis, chronic inflammatory cells infiltration without any other features of a definable diagnosis is compatible with homogeneous OL. (cellular atypia) B- Epithelial dysplasia (mild to severe) Carcinoma in situ Defined as a lesion in which the full thickness of squamous epithelium shows the cellular features of carcinoma without stromal invasion Management tobacco and alcohol should be eliminated if no dysplasia is found, conservative treatment will be acceptable + Close Follow up topical antifungal is given 1-2weeks in case of dysplasia=surgical excision with or without grafting cryo-surgery, laser are preferred for rapid healing 7  Homogeneous OL are associated with a decreased risk for malignant transformation than nonhomogeneous leukoplakias and erythroplakias, and lesions not exceeding 2 cm appear to have a better prognosis than larger lesion Oral Submucous Fibrosis Oral submucous fibrosis is a chronic disease affecting the oral mucosa, as well as the pharynx and the upper two-thirds of the esophagus. Etiology 1- Chewing of areca nuts habit (dose dependence)...contain Alkaloids..modulate MMPs & collagenase..affect collagen metabolism …FIBROSIS 2- Genetic predisposition (Polymorphism of the gene, which is coding for tumor necrosis factor α (TNF-α) N.B.. Fibroblasts are stimulated by TNF-α, thereby participating in the development of fibrosis Clinical presentation Women-20s age Malignant transformation The 1st signs are erythematous lesions + petechiae …then , paler mucosa (white marbling)..Finally, fibrotic bands located beneath an atrophic epithelium.. loss of resiliency, which interferes with speech, tongue mobility, and a decreased ability to open the mouth burning sensation specially with spicy food Oral complications are most commonly observed on the lips, buccal mucosa, retromolar area, and soft palatal mucosa 3) Immunopathologic Diseases 1) Lichenoid Reactions “Delayed hypersensitivity reactions Type IV” oral lichen planus lichenoid contact reactions Lichenoid drug eruptions lichenoid reaction of graft versus host disease 2) Lupus Erythematosus Oral Lichen Planus Relatively common dermatosis occur on the skin, oral mucus membrane 50%of patient have oral and skin lesion Etiology ”multifactorial “ involves a cell mediated immunologically-induced degeneration of the basal cell layer of the epithelium / Stress Skin lesions Flat-topped, pruritic erythematous to violaceus papules with fine scaling on the surface Have a predilection for the trunk and flexor surfaces of arms and legs 8  The most frequent extra-oral mucosa site involved is the genital mucosa The patients report relief following intense scratching of the lesions, but trauma may aggravate the disease, (new skin lesions) which is referred to as “Koebner phenomenon” Clinical Types Reticular Papular Plaque-like Bullous (unusual) Erythematous Ulcerative - To establish a clinical diagnosis of OLP, reticular or papular textures have to be present. - OLP confined to the gingiva may be entirely erythematous, with no reticular or papular elements present, and this type of lesion has to be confirmed by a biopsy Reticular form characterized by fine white lines / striae (Wickham striae) The striae may form a network but can also show annular (circular) patterns. The striae often display a peripheral erythematous zone, which reflects a subepithelial inflammation. most frequent site: bilaterally in the buccal mucosa Asymptomatic Papular form usually present in the initial phase of the disease. It is clinically characterized by small white dots, which in most occasions intermingle with the reticular form Asymptomatic DDx ? Plaque-type OLP homogeneous well-demarcated white plaque that occurs in conjunction with striae Clinically,,very similar to homogeneous oral leukoplakias. Frequent in smokers (following cessation, the plaque may disappear and convert into the reticular type) overrepresented among OLP lesions transforming into oral SCC Asymptomatic Erythematous (Atrophic) characterized by a homogeneous red area. When this type of OLP is present in the buccal mucosa or in the palate, striae are frequently seen in the periphery of the lesion. Some patients may display erythematous OLP exclusively affecting attached gingiva. “Desquamative Gingivitis” DDx ? 9 Ulcerative type the most disabling form of OLP Clinically, the fibrin-coated ulcers are surrounded by an erythematous zone with white striae in the periphery Suspected to be ass. With malignant transformation DDx of OLP Other lichenoid reactions (same clinical & histo., must be diff. by history and upon cause removal, the lesions will disappear) Discoid Lupus Erythematosus (DLE) ” shows white radiating striae sometimes resembling those of OLP. The striae present in DLE are typically more prominent, with a more marked hyperkeratinization, and the striae may abruptly terminate against a sharp demarcation” Dx of LE is confirmed by Direct immunofluorescence for immunoglobulin IgM on biopsies of the clinically normal oral mucosa (Lupus Band Test) Plaque-like OLP is discriminated from homogeneous oral leukoplakia Erythematous OLP of the gingiva exhibits a similar clinical presentation as mucous membrane pemphigoid. Dx Reticular/popular forms are pathognomonic , except for erythematous OLP where biopsy is mandatory Histopathologic features 1- subepithelial band–formed infiltrate dominated by T lymphocytes and macrophages 2- degeneration of basal cells known as liquefaction degeneration “Civatte bodies” 3- hyperparakeratosis, thickening of granular cell layer 4- saw-toothed appearance of the rete pegs Management Unknown etiology. (Symptomatic Rx) Phase 1 therapy (esp. in Erythematous OLP) topical analgesic or antihistamine rinses & alkaline mouthwashes Topical & systemic corticosteroids to diminish inflammatory and hypersensitivity reaction ( 1mg/ Kg daily for seven days has been suggested, followed by a reduction of 10 mg each subsequent day maintenance dose with topical steroids may be commenced during the tapering of the systemic steroids) Topical antifungal Lichenoid Drug Eruptions mimics OLP clinically and histologically drugs or their metabolites may have the capacity to act as haptens, trigger a lichenoid reaction. (delayed hypersensitivity reaction) Penicillin, gold, NSAID, and sulfonamides Skin lesions similar to OLP Resolves upon discontinuance of the drug (symptomatic treatment with topical steroids) 10