Red and white lesions 2.pdf

Red and white lesions of the oral mucosa: RED AND WHITE TISSUE REACTION Red and white oral lesions are a group of conditions that a ect the lining of the mouth. They can be caused by a variety of factors, including trauma, infection, in ammation, and cancer. White lesion...

Red and white lesions of the oral mucosa: RED AND WHITE TISSUE REACTION Red and white oral lesions are a group of conditions that a ect the lining of the mouth. They can be caused by a variety of factors, including trauma, infection, in ammation, and cancer. White lesions of the oral mucosa can be caused by: 1. Increased production of Keratin ( Hyperkeratosis ) 2. Abnormal but benign thickening of the stratum spinosum ( Acanthosis ) 3. Epithelial edema: intra- and extracellular accumulation of uid in the epithelium may also result in clinical whitening 4. Microbes, particularly fungal infections (Fungi can produce whitish pseudomembranous) 5. Subepithelial super cial brosis, which with its decreased vascularity network causes a di use whitish appearance Red lesions of the oral mucosa can be caused by: 1. Decrease in thickness of epithelium ( Atrophy ) 2. loss of the super cial cell layers (super cial erosion) 3. Increased vascularization by dilatation of vessels and/or proliferation of vessels (in ammation) 4. cellular proliferation signifying a possible malignancy Consistency and texture are important to reach a diagnosis Palpation of white and red lesions is necessary in addition to inspection, as indurated lesions should draw additional suspicion for possible malignancy. Our clinical approach to di erential diagnosis should include Age, presence of pain, single versus multiple lesions, distribution in speci c areas, the borders toward the una ected tissue, onset, duration, change in shape and size, whether it is raised in comparison to surrounding mucosa, its relapsing nature, and reasons for improvement or exacerbation. A patient’s speci c systemic condition and associated medications are potentially very closely related to oral disease Infectious diseases: A. Oral Candiasis B. Hairy Leukoplakia A. ORAL CANDIDIASIS Oral candidiasis is the most prevalent opportunistic infection a ecting the oral mucosa Caused by various candida species. Predominantly C. albicans, C. tropicalis, C. glabrata C. Albicans is one of the components of normal oral micro ora More than 60% of people carry this organism. Candida is a dimorphic organism. It exist in two forms (hyphae and spores). Spores are nonpathogenic, hyphae are pathogenic. Candidal strains with better adhesion potential are more virulent than strains with poorer adhesion ability Its an opportunistic infection that usually happen to the very young, very old, and very sick. Candidiasis is when the candida cause lesion or symptoms. It’s usually super cial, can manifest as a red or a white lesion, and could be acute or chronic 1 of 20 ff ff fi fi fi fi ff fi fi fl ff fl ff fl fi fl  Predisposing factors for oral candidiasis A. Local Poor oral hygiene Hyperkeratosis (lichen planus) Smoking Xerostomia (drugs, radiotherapy, Sjogren’s Atrophic constitution syndrome) Corticosteroids (topical/inhalers) Broad spectrum antibiotics - Imbalance of Prolonged denture wearing oral micro ora High carbohydrate diet B. General Immunosuppressive disease (HIV) Impaired health status Immunosuppressive drug ( systemic corticosteroids, chemotherapy, biological agents) Hematological malignancies (leukemia and lymphomas) neutropenia Endocrine disturbances (diabetes mellitus, Addison’s disease, hypothyroidism, pregnancy) Nutritional de ciency (malnutrition and anemias) DIAGNOSIS Clinical examination Biopsy periodic acid Schi (PAS) stained smear culture of the saliva (cytology) Further examination might be needed (endocrinology - glucose tests, WBC, hemoglobin folic acid, vitamin B12, serum ferritin) if predisposing factor not clear Treatment Correction the predisposing factor, together with antifungal medication Topical agents for mild cases Nystatin (cream or suspension) , and Miconazole gel Chlorhexidine has some anti candida activity Systemic antifungals for severe or refractory cases Fluconazole (drug interaction with warfarin) Examples: 1. PSEUDOMEMBRANOUS CANDIDIASIS (ORAL THRUSH) The acute form of pseudomembranous candidiasis (thrush) is most common candidal infection. The infection predominantly a ects patients taking antibiotics, immunosuppressant drugs, or having a disease that suppresses the immune system. There is also a chronic form of pseudomembranous candidiasis, often associated with immunode ciency. Clinical: Thick creamy-white friable (loosely attached) plaques Can be wiped o with gentle scarping, which leaves an erythematous base underneath Symptomatic/metallic taste and burning sensation Main Predisposing Factors: - Dry mouth - Corticosteroids - Antimicrobials - Immune defect. Treatment: - Correcting predisposing factors + antifungal medication 2 of 20 fl fi fi ff ff ff  2. ERYTHEMATOUS CANDIDIASIS ACUTE ATROPHIC CANDIDIASIS (ANTIBIOTIC SORE MOUTH) Clinical: o Generalized mucosal redness o Often painful (burning sensation) o Lesions of erythematous candidiasis have a di use border, which helps distinguish them from erythroplakia, which usually has a sharper demarcation and often appears as a slightly submerged o The infection is also seen in the palate and the dorsum of the tongue of patients who are using inhalation steroids Main Predisposing Factors - Smoking - Corticosteroids - Antibiotics - Dry mouth Treatment: Address the underlying predisposing factors o e.g., stop causative antibiotic if possible o change to a narrower spectrum drug o rinse mouth after using steroid inhaler Topical antifungal therapy 3. CHRONIC ATROPHIC CANDIDIASIS (DENTURE-RELATED STOMATITIS) The most prevalent site for denture stomatitis is the denture-bearing palatal mucosa Denture stomatitis and angular cheilitis are referred to as Candida associated infections, as they are always associated with raised counts of intraoral Candida and since bacteria may cause these infections Nearly every patient will report wearing dentures overnight. Thus, denture stomatitis is the consequence of continuous irritation, both microbial and mechanical from the denture, on the underlying mucosal surface Cause: Candida +/- bacteria (BOTH) Clinical: Red area outlined by the shape of the maxillary denture Usually, asymptomatic Predisposes to angular cheilitis and in ammatory papillary hyperplasia Main Predisposing Factors: Continuous denture wearing Denture stomatitis is classi ed into three di erent types: Type I is localized erythematous sites caused by trauma from the denture Type II a ects a major part of the denture covered mucosa. Type III – in ammatory papillary hyperplasia Diagnosis: Mainly clinical and history smear of mucosa or denture can be done 3 of 20 ff fl fi fl ff ff 3. CHRONIC ATROPHIC CANDIDIASIS (DENTURE-RELATED STOMATITIS) (continues…..) Treatment: 1) Cease denture night wear 2) Improve denture hygiene 3) Store denture in an antiseptic at night e.g., commercial denture cleanser, chlorhexidine or diluted sodium hypochlorite solution 4) 1 teaspoon of sodium hypochlorite in a denture cup of water; keep for 15 minutes or at night; rinse for 2 minutes; can turn chrome cobalt dentures black 5) Apply miconazole gel B+F to the tting surface of denture 6) If recurrent, the most likely reason is failure to comply with treatment regime 4. ANGULAR CHEILITIS - Candida associated infections, as they are always associated with raised counts of intraoral Candida and since bacteria may cause these infections - Presents as infected ssures of the commissures of the mouth, surrounded by erythema. - The lesions are frequently infected with both candida albicans and Staphylococcus aureus. Cause: Candida +/- bacteria (Staph. aureus) (BOTH) Clinical: Red ssures at the corners of mouth Main Predisposing Factors: - Over closure of the mouth (loss of vertical dimension) - lip licking - intraoral candidiasis - anemia - drooling - denture wearing - (vit. B12 and iron def.) Treatment: 1. Miconazole gel (B+F) or fusidic acid cream 2. Treat intra-oral infection 3. Check for underlying causes (e.g. anemia) if recurrent or resistant to treatment Must treat intraoral infection simultaneously. This is always present even if not evident. 5. MEDIAN RHOMBOID GLOSSITIS (CENTRAL PAPILLARY ATROPHY) Clinical: Asymptomatic red rhomboid area on the midline dorsum of tongue Anterior to the circumvallate papillae Result from a trophy of the liform papillae Often with a matching "kissing" lesion on the palate Main Predisposing Factors: Tongue rests against the soft palate not a self-cleansing area Tobacco smoking, denture wearing, inhalation steroids, immune defect Treatment: Reassurance Anti-fungal treatment 4 of 20 fi fi fi fi 6. CHRONIC HYPERPLASTIC CANDIDIASIS (CANDIDAL LEUKOPLAKIA, CHRONIC PLAQUE TYPE, AND NODULAR CANDIDIASIS) Clinical: Leukoplakia-like lesion asymptomatic white plaque that cannot be rubbed o usually on anterior buccal mucosa Considered as a potentially malignant lesion A histologic feature is the penetration of candidal hyphae through the epithelial cells and the associated subepithelial chronic in ammatory response Main Predisposing factors: Smoking or immune defect Treatment: 1. Smoking cessation 2. Topical or systemic antifungal 3. Consider biopsy to assess for dysplasia 4. Consider excision/follow-up if persistent or dysplasia present 7. ORAL CANDIDIASIS ASSOCIATED WITH HIV More than 90% of AIDS patients have had oral candidiasis Oropharyngeal candidiasis is related to the degree of immunosuppression and is most often observed in patients with CD4 counts Di cult to eradicate Close follow-up is recommended 8 of 20 ff ffi fi fl  B. ERYTHROPLAKIA De nition: is a ery red patch or plaque that cannot be characterized clinically or pathologically as any other de nable disease or condition It’s a clinical diagnosis that require exclusion of other oral red conditions Tobacco, and alcohol use are risk factors Higher risk of malignant transformation 80% Less common than leukoplakia, but more serious prevalence in adults has been estimated to be in the range of 0.02% to 0.1% Clinically: well demarcated, red patch with a soft to velvety granular texture Usually, asymptomatic * Any red mucosal lesion without an apparent local cause or not tting into other known red lesions, and not regressing following removal of possible cause or two weeks of treatment, should be considered a cancer unless histologically proven otherwise Diagnosis and microscopic features : Exclusion of other oral red lesions DDx(non-speci c mucositis, erythematous candidiasis, erosive lichen planus LP, lupus erythematous) Histological evaluation of a biopsy specimen - Atrophic and non keratinized epithelium Almost all >90% of cases show dysplasia, carcinoma in situ, or carcinoma at initial presentation Treatment : Guided by histopathological changes Biopsy, complete excision for dysplastic lesion Aggressive treatment for SCCa Tobacco cessation Follow up BIOPSY Excisional biopsy is generally recommended if the leukoplakia diameter is less than 30 mm and the location allows Otherwise, in larger or suspicious lesions incisional biopsies should be undertaken, sometimes from several sites. Selecting the appropriate site that will best represent the most severe aspect is of paramount importance Following ve years of no relapse, self-examination may be a reasonable approach 9 of 20 fi fi fi fi fi fi  Examples: 1. CHRONIC HYPERPLASTIC CANDIDIASIS (CANDIDAL LEUKOPLAKIA) Etiology A white or red-white xed lesion caused by chronic C. albicans infection A form of chronic oral candidiasis The malignant potential is controversial and considered low Candida can induce hyperkeratosis and can produce chemical carcinogens (nitrosamines) Can be di cult to separate from oral leukoplakia secondarily superimposed with Candida (opportunistic infection) Clinical Well-demarcated white or red-white plaque Common on the labial commissure Leukoplakia- or speckled leukoplakia-like lesion Usually painless Cannot be rubbed o More common in smokers Microscopic Hyperkeratosis Candidal hyphae in the keratin layer (PAS stain) Epithelial dysplasia in rare, called 'leukoplakia' superimposed with candida Mild connective tissue chronic in ammation Diagnosis Biopsy is required to con rm candidal presence and to assess dysplastic changes if any The presence of candidial hyphae on biopsy, and the resolution of the lesion after antifungal therapy support the diagnosis Treatment Topical or systemic antifungal medications Smoking cessation Consider excision/follow-up if persistent or if dysplasia present treat as leukoplakia Prognosis: The risk of malignant transformation is controversial but low 2. ACTINIC CHEILITIS (ACTINIC CHEILOSIS; SOLAR CHEILOSIS) A premalignant alteration of the lower lip vermilion caused by chronic ultraviolet light exposure Etiology Chronic sun exposure Common among fair-skinned outdoor occupations Clinical Early lesions appear as blotchy, pale areas Indistinct mucocutaneous junction Rough plaques, scales, and crusts may develop later Persistent ulceration and nodularity may indicate malignancy Microscopic Hyperkeratosis Epithelial dysplasia in some cases Atrophic or acanthotic epithelium Signs of solar elastosis in the submucosa Diagnosis Treatment History of outdoor/chronic sun exposure Preventive measures Biopsy to rule out dysplastic changes (lip balm, sunscreen Indurated, thickened, or ulcered areas should be biopsied wide-brimmed hat when outdoors) 6-10% transformation rate Lip shave (vermilionectomy) for dysplastic 10 of 20 cases Long-term follow-up ffi ff fi fi fl  C. ORAL SUBMUCOUS FIBROSIS A chronic, precancerous, and debilitating condition characterized by progressive brosis of the oral cavity related to the habit of areca nut chewing Oral mucosa, pharynx, upper 2/3 of the esophagus may be a ected Causes There is dose dependence between an areca quid chewing habit and the development of this oral mucosal disorder Areca nuts contain alkaloids, of which arecoline seems to be a primary etiologic factor due to its ability to a ect collagen metabolism Epidemiology An addictive habit; mainly in the Indian subcontinent, and Southeast Asia Complications are most observed on the lips, buccal mucosa, retromolar area, and soft palatal mucosa prevalence in Indian population is 5% for women and 2% for men. Individuals less than 20 years old are commonly a ected due to commercials Conventional betel quid (Paan'): a mixture of fresh, dried, or cured areca nut, slaked lime, avors, and possibly tobacco, wrapped in betel leaf Gutkha’: a popular commercial product, contains crushed areca nut, tobacco, slaked lime, and avors Signi cance Fibrosis - caused by areca nut Dysplasia/carcinoma - linked to both tobacco and areca nut Clinical Trismus – restricted mouth opening Pale and white marbling mucosa with palpable brous bands underneath an atrophic epithelium 25% exhibit leukoplakia also erythroplakia could occur Diagnosis History and clinical appearance Biopsy suspicious areas Microscopic Atrophic epithelium Hyalinization of the subepithelial connective tissue Epithelial dysplasia in some cases Treatment 1) Cessation of chewing habit Stabilizes trismus and reduces the risk of malignant progression Early lesions may regress 2) Intralesional/ topical / systemic corticosteroids, hyaluronic acid, surgical splitting of brous bands, physiotherapy, skin grafting Not usually e ective; relapse is common Close clinical follow-up is essential Biopsy of suspicious red or white lesions 11 of 20 fl fl fi ff ff fi ff ff fi fi CRITERIA USED FOR DIAGNOSIS OF EPITHELIAL DYSPLASIA Loss of polarity of basal cells Presence of more than one layer of cells having a basaloid appearance Increased nuclear–cytoplasmic ratio Drop-shaped rete ridges Irregular epithelial strati cation Increased number of mitotic gures/ abnormal in form Presence of mitotic gures in the super cial half of the epithelium Cellular and nuclear pleomorphism Nuclear hyperchromatism Enlarged nuclei Loss of intercellular adherence Keratinization of single cells or cell groups in the prickle cell layer ORAL CANCER OSCC and oropharyngeal cancer represent the seventh most common cancer worldwide 4.2% of all cancers The number of new oral and oropharyngeal cancers estimated to be 300,000 cases world-wide/year High incidence in south central Asia Male: female 2.5:1 Five-year survival rate 64% -> Stage dependent ORAL SQUAMOUS CELL CARCINOMA Derived from the surface strati ed squamous epithelium The most common malignancy of the oral cavity (>90%) Globally, OSCCs account for 2-4% of all cancers Geographical variation exists around 45% of all cancers in India are oral SCC Has a multifactorial etiology Risk factors Smoking and smokeless tobacco use (80% of oral SCCas) Heavy alcohol consumption (tobacco and alcohol have a synergistic e ect) Betel quid chewing Fair skin and sunlight Presence of potentially malignant oral disorders (e.g., leukoplakia) High-risk HPV infection (HPV type 16) Poor diet (antioxidant protective e ects) Aging, immunosuppression, anemia, and patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) (20xrisk) Environmental pollution (heavy metals) Clinical Oldermenaremorecommonlya ected Clinical patterns: o Leukoplakia o Exophytic growth o Erythroplakia o Endophytic growth o Erythroleukoplakia Earlylesionsareasymptomatic Patients with advanced disease may develop pain, paresthesia, and cervical lymphadenopathy Sites: Lower lip vermillion (associated with actinic cheilitis) AC Lateral and ventral aspects of tongue (most common intra oral site-50%) Floor of the mouth - 35% Previous cancer increase the chance for a second cancer Note: In India, the buccal mucosa is the most common intra-oral site (quid) 12 of 20 fi fi fi ff fi ff fi ff  1. SQUAMOUS CELL CARCINOMAS OF THE LIP VERMILION In fair-skinned individuals with a history of chronic sun exposure Usually on the lower lip Male predominance Crusted, ulcerated, indurated lesion Tendtogrowrelativelyslowly Better prognosis than intraoral carcinoma Diagnosis History (risk factors, symptoms, etc.) and clinical features OSCC can be diagnosed de nitely only via biopsy and histopathologic assessment Clinical TNM staging Taking CT and/or MRI to determine the extent Histologic Dysplastic surface epithelium and invasive islands of malignant squamous epithelial cells Tumor Grading : well, moderate or poorly di erentiated - depending on how closely it resembles the parent tissue Most oral carcinomas are moderately or well-di erentiated lesions Treatment Guided primarily by the tumor stage Cancer treatment involves a team approach with di erent specialties A. Lip vermilion cancers Surgical excision Overall 5 year survival rate is 88% Often are diagnosed at an early stage B. Intraoral cancers Surgery Radiotherapy Combined surgery and radiotherapy Chemotherapy and/or targeted agents can be used as an adjunct Overall 5-year survival rate is 65% 2. VERRUCOUS CARCINOMA A low-grade variant of oral squamous cell carcinoma it has a much better prognosis with low mitotic activity and slow growth Tobacco use (smoking and smokeless) is the most common risk factor It is characterized by Typically appears as an exophytic broad-based lesion with a cauli ower-like warty surface Microscopically, verrucous carcinoma consists of liform projections lined by thick, well- di erentiated keratinized squamous epithelium Well-di erentiated carcinoma; little or no dysplasia Low chance of metastasis Surgery is the primary mode of treatment. Other options are Radiotherapy, Chemotherapy, combination, non-surgical techniques (usually for benign and precancerous lesions) such as Cryotherapy, and CO2 laser 13 of 20 ff ff fi ff ff fi ff fl  IMMUNOPATHOLOGICAL DISEASES 1) LICHENOID REACTIONS A. Oral lichen planus (OLP). B. Lichenoid contact Reactions (LCRs) will be discussed w/ allergic reactions. C. Drug-Induced Lichenoid Reactions (DILRs). D. Lichenoid reactions of graft-versus-host disease (GVHD). A. ORAL LICHEN PLANUS A chronic mucocutaneous in ammatory autoimmune disorder with no de ned autoantibodies, and with a genetic predisposition. - Prevalence: (0.5-2.2%) - Predilection: F>M - Age of onset: 30 and 60 yrs. old - Pathogenesis: Multifactorial process between stress and immune system represented by local destruction mediated by T-lymphocytes to basal keratinocytes in the basal layer of the epithelial cells (Liquefaction degeneration). Idiopathic cause. Low Potential for malignant transformation (0.04%-2.0%) Mostly in erosive and plaque subtypes, There is a higher chance for another autoimmune disease. The most common causes of desquamative gingivitis. Clinical types: Reticular (Wickham’s striae) (Most common) - a network of raised white lines or striae. Papular - white papules. Plaque-like - simulating leukoplakia. Bullous. Atrophic/Erythematous- simulating erythroplakia. Erosive/Ulcerative (Painful)-less common. * Variations depend on the extension of the sub- epithelial in ammation. (Mild in ammation represented by hyperkeratosis, whereas more intense in ammation will lead to deterioration of the epithelium (Atrophy, Erosion, or Ulceration). General Notes: - Reticular form Often bilaterally in buccal mucosa. - Plaque-like Mostly in smokers. Skin Lesions: Purple, Pruritic, Polygonal Papules (4 Ps). Frequently a ect the exor surfaces (inner aspect of elbow or wrist). HISTOPATHOLOGIC FEATURES: Hyperkeratosis and hypergranulosis Saw-toothed appearance to the rete ridges "Liquefaction degeneration," or necrosis of the basal cell layer, and formation of Civatte bodies. DIAGNOSIS: Papules or Reticular components need to be present to establish a correct clinical diagnosis. Di erential diagnosis with lichenoid appearance: 1) (OLP) 3) (DILRs) 5) Systemic Lupus 2) (LCRs) 4) (GVHD) Erythematous (SLE) Must DO biopsy for a de nitive diagnosis and to rule out malignancy. 14 of 20 ff ff fl fi fl fl fl fi fl A. ORAL LICHEN PLANUS (Continues…… MANAGEMENT Main strategy is to reduce or eliminate symptoms. Reticular form usually asymptomatic. Erosive and Ulcerative subtypes usually symptomatic and require treatment. Primary treatment choice: Topical steroids Second-line therapy: cyclosporine, tacrolimus, and retinoids Removing both sub and supragingival plaque and calculus is critical in Erythematous form. Oral hygiene should be optimized. B. Lichenoid contact Reactions (LCRs) will be discussed w/ allergic reactions. C. DRUG-INDUCED LICHENOID REACTIONS Etiology and Pathogenesis: Clinical and histopathologic appearances resemble a delayed hypersensitivity reaction. Some drugs such as: (Penicillin, NSAIDs, ACE inhibitors and sulfonamides) may act as haptens and trigger a lichenoid reaction. Poor drug metabolism due to genetic variation of the major cytochrome P-450 enzymes might be associated. Clinical Findings: Unilateral with an ulcerative reaction pattern. DILRs and OLP should be considered clinically indistinguishable. DIAGNOSIS: DILRs are often diagnostically challenged; however, A correct diagnosis is easier to establish when a patient develops a reaction after starting a new drug; however, DILR may not develop until several months where an another new drug might be started MANAGEMENT: Usually not associated with severe life-threatening reactions. Discontinuance of the drug and treatment with topical steroids for symptomatic lesions. Patient should be informed about the responsible drug for prevention. D. GRAFT-VERSUS-HOST DISEASE (GVHD) Occurs after a bone marrow or stem cell transplant, donated cells (graft) attack the recipient's body (host), and can a ect several organs: skin, liver, and intestines. Acute form in (20%–30%), (fever, rash, nausea, emesis, GI problems, and liver problems). Chronic form in (15%–50%), (xerostomia, keratitis sicca, skin problems, arthralgia, and fatigue). 33% of cases in identical sibling transplants, and 64% of unrelated donor transplants. Risk increases with age of the Bone marrow recipient. Clinical lichenoid reaction patterns are same as OLP (reticulum, erythema, and ulcerations); however typically associated with a broader involvement. Skin lesions often present with pruritic maculopapular and morbilliform rash, primarily a ecting the palms and soles. A toxic epidermal necrolysis–like epidermal desquamation in severe cases. 15 of 20 ff ff Etiology and Pathogenesis: Allogeneic hematopoietic cell transplantation is the major cause. Conditioning of the host by chemotherapy and radiation will generate host cell damage, release of cytokines, and up-regulation of (MHC). An interaction between the recipient’s Antigen presenting cells (APCs) and the donor’s T- lymphocytes, which will perceive the histocompatibility antigens, expressed by APCs as foreign, and lead to activation of the in ammatory cascade. DIAGNOSIS 1) Clinical evaluation: a thorough review of the patient's symptoms and history. Lichenoid eruptions have the highest positive predictive value of all reaction patterns. 2) Laboratory tests (CBC, Liver, bilirubin). 3) Imaging tests (Chest x-rays, CT- scans, and MRIs). 4) Skin biopsy 5) Biomarker testing MANAGEMENT: Supportive care: 1) Adequate nutrition 2) Infection prevention: (strict hygiene, prophylactic ABs, antifungal medications. 3) Symptom management: (pain and diarrhea) Immunosuppressive therapy: 1) Topical steroids 2) Calcineurin inhibitors Risk of developing malignancies, patients should be examined for oral malignancies regularly. There are some scoring systems such as Glucksberg score and Seattle staging that help assessing the overall severity, and treatment options. 2) LUPUS ERYTHEMATOSUS Etiology and Pathogenesis: An autoimmune disease involving both natural and adaptive (B and T lymphocytes) of the immune system with a genetic predisposition. Some environmental factors may aggravate the disease such as sun exposure, drugs, chemical substances, and hormones. Predominantly a ects women of a reproductive age. Signs and symptoms: Weight loss, fever, arthritis, fatigue/malaise. Kidney complications are very common. Malar (Butter y rash) in ~50% of patients. Discoid lupus on skin. 16 of 20 fl ff fl  2) LUPUS ERYTHEMATOSUS (Continues…. DIAGNOSIS According to the American College of Rheumatology (ACR) diagnosis of (SLE) is based on ful lling at least 4 out of 11 criteria: 1) Malar rash 5) Renal disorder 9) Neurological disorder 2) Discoid rash 6) Hematological disorder 10) Immunologic disorder 3) Photosensitivity 7) Oral ulcers 11) Positive antinuclear 4) Arthritis 8) Serositis antibody (ANA) test Management: Topical steroids for symptomatic intraoral lesions. CHX rinse (0.12%) If lesions do not respond appropriately to topical steroids in 2 weeks, consider systemic therapy. Mucosal ulceration can occur due to high intake of NSAIDs. 4. ALLERGIC REACTIONS A. Lichenoid contact reactions (LCRs). B Reactions to Dentifrice and Chlorohexidine (Contact stomatitis). A (or C). LICHENOID CONTACT REACTIONS A delayed hypersensitivity reaction to constituents derived from dental materials, predominantly amalgam llings and gold. Predilection: F>M LCRs usually con ned to the sites that are in a regular contact with the causative agent, such as the buccal mucosa and the border of the tongue. Etiology and pathogenesis: 1)Antigen presentation 3) Keratinocyte damage 2) T cell activation 4) Epidermal changes HISTOPATHOLOGICAL FEATURES Interface dermatitis, Acanthosis, Hyperkeratosis, and Basement membrane thickening. LCRs are diagnosed based on a combination of clinical features, histopathological ndings, and patch testing. Patch testing is a diagnostic test that is used to identify allergens. It involves applying small amounts of suspected allergens to the skin under adhesive patches. Patches then removed after 48 hours and the skin is examined for signs of an allergic reaction. MANAGEMENT Identify and avoid the causative agent is the rst step. Replacement of dental materials in direct contact with LCR will resolve the issue Most lesions will heal within 1-2 months. No need for replacement of restorative materials that are not in direct contact with the lesion. Healing does not depend on what type of dental material is used for replacement. No studies suggested a malignant potential B. REACTIONS TO DENTIFRICE AND CHLOROHEXIDINE (CONTACT STOMATITIS) Delayed hypersensitivity reactions to avor additives such as carvone and cinnamon or preservatives. These agents may be found in candy, chewing gum, or toothpaste. The clinical manifestations: Di use for toothpaste and localized for gum/candy. Healing of the lesions after withdrawal of the allergen-containing agent 17 of 20 fi ff fi fi fl fi fi 5. TOXIC REACTIONS A. Nicotinic Stomatitis (Smoker’s palate) B. Tobacco pouch Keratosis A. NICOTINIC STOMATITIS (SMOKER’S PALATE) It is related to: 1) Heavy cigarettes smoking, pipe and cigar smoking. 2) Reverse smoking (highly associated with malignant transformation). Red dots can be observed representing ori ces of accessory salivary glands, volcano-like papules with red central dots. Etiology: is caused by a synergistic e ect of high temperature and the chemical composition of the smoke, excess keratin, like a callous on skin. Asymptomatic Takes years to develop Cessation of smoking usually resolve the problem within 1-3 months. B.TOBACCO POUCH KERATOSIS SMOKELESS TOBACCO KERATOSIS; SNUFF POUCH A premalignant white lesion in individuals who habitually use smokeless tobacco, particularly snu. Irritation from the tobacco and other chemicals to the mucous membrane. Much less cancer risk than Leukoplakia. Clinical: Appears as white patches or plaques on the inner buccal mucosa, gingiva, or oor of the mouth ( location of smokeless tobacco) The risk of malignancy is relatively low: ~< (0.4%) lifetime risk. Stop habit: keratosis gone in 2-4 months. Histopathological features: Hyperkeratinization. Acanthosis. Epithelial vacuolizations No dysplasia 18 of 20 ff fl fi f  6. REACTIONS TO MECHANICAL TRAUMA A. Morsicatio Buccarum E. Chemical Trauma B. Frictional Hyperkeratosis F. Electrical Trauma C. Traumatic Eosinophilic Ulcer G. Anesthesia Necrosis D. Thermal Trauma A. MORSICATIO BUCCARUM (CHRONIC CHEEK BITING) Asymptomatic irregular, wide white buccal keratotic plaque (along the occlusal plane). From habit of light chewing on buccal tissues. More common in women. Usually bilateral Morsicatio labiorum: biting on labial mucosa Morsicatio Linguaraum: biting the tongue Management limited to assurance and awareness. Histopathological features: Hyperkeratosis and acanthosis. B-1: FRICTIONAL HYPERKERATOSIS A physiologic response to minor trauma Appears as a white keratotic line along occlusal plane of the buccal mucosa (Excess keratin). Bilateral/Unilateral From chronic frictional rubbing against teeth. If the diagnosis is doubtful, biopsy is mandatory to exclude premalignant lesions. The histopathologic features: hyperkeratosis without dysplasia and no or mild subepithelial in ammation. Smoking and alcohol are predisposing factors B-2: LINEA ALBA (WHITE LINE) A white keratotic line, a variation of normal. Bilateral on buccal mucosa. Trauma (biting) Often associated with smokers and nervous people (bruxing, grinding). Not a precancer Often regresses spontaneously. No need for treatment or biopsy. C. Traumatic eosinophilic ulcer; traumatic ulcerative granuloma with stromal eosinophilia (tugse) Deep, chronic ulceration or granulation tissue mass with eosinophils due to damaged muscle. Due to repetitive trauma Very slow to resolve: months /up to 1 year. Middle aged > 40 years of age Tongue is the most common site > gingiva > buccal mucosa > lip. Treatment: Biopsy and remove cause of trauma. Clinically similar to squamous cell carcinoma, must do biopsy. D. THERMAL BURN Usually from eating hot food (pizza burn) and beverages. Common on lip, palate and tongue. Appears as erythema and ulceration with remnants of necrotic tissue at the periphery. E. CHEMICAL BURN Aspirin Alcohol Tooth whitening agents Phenol Sodium perborate Formocreosole Hydrogen peroxide Acid etching liquids Silver nitrate. F. Electrical Burn : Common in children. 19 of 20 fl  G. ANESTHESIA NECROSIS Occurs at site on anesthetic injection. Necrosis/ischemia from epinephrine First: erythema, pain, then ulceration. Usually hard palate (vasoconstrictor is injected under great pressure). Heals after 1-2 weeks OTHER RED AND WHITE LESIONS A. Benign Migratory Glossitis C. White Sponge Nevus (Geographic Tongue) D. Hairy Tongue B. Leukoedema A. BENIGN MIGRATORY GLOSSITIS (GEOGRAPHIC TONGUE; ERYTHEMA MIGRANS) Involves dorsum of the tongue, and sometimes the ventrum. A ects mostly middle-aged. Asymptomatic (Some may complain of burning sensation from Candida). Color might change or lesion relocate. Etiology unknown (4% of psoriasis patients have it). Diagnosis mainly clinical. Management: Reassurance Zinc sulphate 200 mg (3x/day for 3 months) Topical rinse with 7% salicylic acid in 70% alcohol. B. LEUKOEDEMA A generalized gray-white lm di used throughout the buccal mucosa. Common in caucasians and blacks (~85%). Often Bilateral Disappears following stretching of the mucosa. Asymptomatic No Malignant potential. No treatment Histopathological features: Parakeratosis and acanthosis together with intracellular edema in epithelial cells of stratum spinosum. C. WHITE SPONGE NEVUS (CANNON DISEASE) Autosomal Dominant (AD). Asymptomatic white corrugated keratotic surface on buccal mucosa. Initiated following mutations in genes that are coding for epithelial keratin types K4 and K13. Benign Usually start during adolescence. It is rare 1:200,000 Bilateral No treatment D. HAIRY TONGUE (WHITE COATED TONGUE) Seen in patients with an imbalance in the micro ora due to: Antibiotics Oral candidiasis, Mouth breathers Immunosuppressive drugs Drinking alcohol Poor OH. Desquamation of the liform papilla. Determining the cause in order to avoid. Advising patients to brush the tongue or use a tongue-scraper, and improve oral hygiene 20 of 20 ff fi fi ff fl