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EnoughConsciousness

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Dr. Salsabeel Afifi

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oral lesions oral medicine candidiasis dental health

Summary

This presentation details various types of oral lesions, including classifications based on etiology, and covers infectious, reactive inflammatory, immunological, and idiopathic conditions. It provides information on causes, clinical manifestations, and management strategies for conditions such as acute and chronic candidiasis.

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White and Red oral lesions Done by Dr. Salsabeel Afifi Lecturer of Oral Medicine and Periodontology Classification Based on etiology Infective white and red lesions Oral hairy leukoplakia Oral Candidiasis ...

White and Red oral lesions Done by Dr. Salsabeel Afifi Lecturer of Oral Medicine and Periodontology Classification Based on etiology Infective white and red lesions Oral hairy leukoplakia Oral Candidiasis Acute Pseudomembranous Erythematous Chronic Erythematous Pseudomembranous Primary oral candidasis Hyperplastic Candida-associated Angular cheilitis lesions Denture stomatitis Median rhomboid glossitis Keratinized primary Leukoplakia lesions superinfected with Candida Lichen planus Lupus erythematosus Secondary oral Oral manifestations of systemic mucocutaneous candidasis candidiasis (CMC) Oral Candidiasis Acute Chronic Acute pseudomembranous Denture induced candidiasis (thrush) stomatitis Angular stomatitis Acute atrophic or Median rhomboid erythamatous candidiasis glossitis. (antibiotic stomatitis) Chronic hyperplastic candidiasis. Erythematous candidiasis Ch. Mucocutaneous candidiasis. Etiology It is a fungal infection caused by Candida species mainly Candida albicans. It occurs in extremities of age; the very young and the very old. Can be associated with one of these factors: i. Xerostomia. ii. Denture wearing. iii. Long-term antibiotic and/or steroid therapy. iv. Immunosuppressed patients (e.g. HIV/AIDs) v. Chemotherapy and/or radiotherapy to the head and neck region. vi. Uncontrolled diabetes. vii. Cancer (e.g. leukemia, lymphoma). Acute candidiasis 1. Acute pseudomembranous candidiasis (oral thrush) Painless Soft friable creamy plaque Whitish pseudomembrane consisting of sloughed epithelial cells or debris, fungal mycelium, and neutrophils, which are loosely attached to the oral mucosa. Can be Wiped off with difficulty Associated with bad taste or loss of taste sensation. To confirm diagnosis Take a smear and use Periodic acid Schiff stain (PAS stain) shows candidal hyphae. Biopsy: will show hyperplastic epithelium, inflammatory cells, edema. 2. Acute antibiotic stomatitis (atrophic or erythamatous) Follow overuse of broad spectrum antibiotics esp. tetracyclin. Due to Xerostomia (e.g. Sjogren syndrome, drug induced…etc.) The whole mucosa is red & glazed with Flecks of thrush. If lesions appeared on the dorsum of the tongue; typically will present as depapillated areas. Chronic candidiasis 1. Denture induced stomatitis Commonly seen in Upper denture. Due to well fitting denture cutting the washing effect of saliva. Mainly occurs in denture wearers with poor oral hygiene or continuous denture wearing. Painless red area. Ass. with angular stomatitis Clinical manifestations The mildest form of denture sore mouth appears as small, localized and asymptomatic red spots on the posterior palatal mucosa. As the condition worsens, large confluent areas turn crimson red. In later stages, hyperplasia of palatal mucosa occurs and produces the red, pebbly appearances of papillary hyperplasia. Management 1. Use topical antifungal drugs. 2. Sterilization of the denture with fungicide or chlorohexidine is indicated. 3. Good oral and denture hygiene should be maintained. Soak the denture in water and denture cleansing agent over night. 2. Angular stomatitis (Angular cheilitis) Leakage of infected saliva loaded with candida at mouth corners due to: 1. Low vertical dimension & loss of upper lip support. 2. Ptyalism. May be secondly infected with bacteria. Associated with other types of candidiasis.  It is inflammation of the oral commissures, characterized by fissures, erythema, and crusting.  Predisposing factors include: i. Loss of occlusal height. ii. Nutritional deficiencies (e.g iron, Vit B6, B12 and folic acid). iii. Poorly controlled diabetes. iv. HIV and immunosuppressed patients.  Most cases are caused by mixture of candidal infection together with bacterial infection (staphylococcus aureus or streptococci).  Mycolog (nystatin+triamcinolone) is effective in treatment of angular cheilitis.  Other topical antifungals as ketoconazole, miconazole and clotrimazole could be used. Angular Cheilitis 3. Median rhomboid glossitis Red patch of atrophic papillae in the central area of dorsum of tongue. Most of the cases are asymptomatic, some patients complain of persistent pain or irritation. Etiology Debatable May be Developmental defect resulting from an incomplete descent of tuberculum impar and entrapment of a portion between fusing lateral halves of the tongue. Some authors suggest chronic fungal infection as etiology because it responds to antifungal drugs (diagnosis ex juvantibus). 4. Chronic hyperplastic candidiasis (Candidal leukoplakia) Firm white leathery plaques or speckled. It usually occurs bilaterally in the commissural region of the buccal mucosa but may occur on other surfaces as cheek, lip, tongue, palate. Invasion of candida deeper in mucosa leads to proliferative response.  It is associated with smoking and carries a risk of malignant transformation.  Treat it with topical antifungal for two weeks, then take a biopsy if no resolution. To differentiate it from other types of leukoplakia: Take a smear and use Periodic acid Schiff stain (PAS stain) shows candidal hyphae. 5. Chronic mucocutaneous candidosis (secondary candidiasis) Defect in cell mediated immunity or iron deficiency Two categories: 1. Syndrome associated CMC i. Familial (Candidosis endocrinopathy syndrome) ii. Chronic ( Thymoma) 2. Localized (oral, skin &nails) and diffuse (widespread) 6. Chronic Erythematous candidiasis Red macules In HIV infection Mainly on hard palate , dorsum of tongue ,soft palate respectively Management of oral candidiasis Depends on the condition. Most candidal infections could be treated with topical preparations except if the patient is immunocompromised and/or there is a risk of systemic dissemination of infection (HIV, chemotherapy, immunosuppressed…etc). In this condition; systemic antifungal drugs are recommended. Topical antifungal drugs Nystatin oral suspension as a mouthwash four times daily. Clotrimazole lozenges four times daily. As a topical cream/ointment: ketoconazole, miconazole (e.g. Daktarin oral gel). Systemic antifungal drugs According to 2016 Guidelines of Infectious Diseases Society of America: 1. Echinocandin (e.g. caspofungin, micafungin, anidulafungin) is recommended as initial therapy. 2. Fluconazole, oral or IV, is a good alternative to Echinocandin as an initial therapy in patients who are not critically ill. 3. Amphotericin B is recommended if there is intolerance or resistance to other antifungal drugs. Idiopathic (true) leukoplakia: It is defined as “white lesion of questionable risk can’t be defined clinically and histopathologically as any other known lesion. It’s potentially malignant lesion”. Biopsy is required to confirm diagnosis. It will most often show hyperkeratosis with about 20%, however, will show dysplasia. It is Potentially malignant lesion. Idiopathic but may be predisposed by risk factors: Smoking Alcohol use (synergistic effect with smoking)  HPV infection  Ultraviolet radiation  Candidal infection Genetic makeup  Vitamin deficiencies (questionable) Clinical manifestations Age: old age Sex: males more than females Site: Mostly on buccal mucosa ,lower lip ,gingiva. Less common on palate, retromolar area ,floor of mouth & tongue 90% of dysplastic lesions are detected in tongue (ventral/lateral) & floor of mouth. Clinical variants of leukoplakia I. Homogenous leukoplakia II. Speckled leukoplakia III. Verrucous leukoplakia Non homogenous variants IV. proliferative Verrucous leukoplakia Homogenous Leukoplakia: Well defined white patch. Uniform in color. Elevated, fissured, wrinkled surface. Palpation: leathery or dry cracked mud like. Loss of flexibility and pliability. In floor of mouth: ebbing tide appearance. Speckled Leukoplakia: Mixed red & white Keratotic nodules on atrophic red base High risk of malignant transformation Verrucous leukoplakia: Thick with papillary surface. Heavily keratinized. In older patients. Clinically indistinguishable from verrucous carcinoma. Proliferative Verrocous leukoplakia (PVL): Extensive papillary plaque and/or involves multiple mucosal sites. More prevalent among elderly Females at age of 60 years and more. High rate of malignant transformation to SCC. PVL is a long-term progressive condition growing into a multifocal disease with exophytic and proliferative features. It has a high rate of both recurrence and malignancy.  Total excision with free surgical margins is critical combined with a lifelong follow-up. Differential diagnosis of PVL Verrrocous Squamous carcinoma cell papilloma Verrrocous carcinoma It is a rare, slow-growing tumor. They are chiefly exophytic, do not metastasize, but can invade and destroy deeper tissues. The lesser aggressive nature of VC establishes it as a low grade, well-differentiated variant of oral SCC. It has an excellent prognosis and indolent clinical behavior Squamous cell papilloma Exophytic masses caused by HPV Asymptomatic Occur between the ages of 30 and 50 years, and sometimes can occur before the age of 10 years. Most common sites are the hard palate and tongue. Surgical removal is the ttt of choice. Squamous cell papilloma Clinical signs of malignant transformation: Ulceration Bleeding Induration Lymphadenopathy Diagnosis of leukoplakia/erythroplakia: Tissue Biopsy is the gold standard. Toluidine blue staining: stain dysplastic & malignant cells , resist washing away by acetic acid. Cytobrush technique: firm bristle brush to obtain cells from full thickness of epith. for cytologic examination Exfoliative cytology of low benefit in these lesions. Management Depends on the histologic findings: If only hyperkeratosis and acanthosis with no dysplasia, removal of any apparent cause (e.g. smoking, alcohol drinking) and regular follow up. If the biopsy shows severe dysplasia or frank carcinoma total surgical excision is indicated. If mild dysplasia removal of any apparent cause (e.g. smoking, alcohol drinking) and regular follow up. Erythroplakia It is defined as “Red lesion of questionable risk can’t be defined clinically and histopathologically as any other known lesion. It’s potentially malignant lesion”. Idiopathic but may be predisposed by risk factors similar to that of leukoplakia. Erythroplakia Red bright velvety area Site: Ventral Tongue ,floor of mouth , soft palate ,tonsils. Size is variable. The texture may be normal or roughened. Asymptomatic More in elderly patients (60-70 years old) High malignant transformation. More than 90% of oral erythroplakias are dysplastic or malignant on the day of the biopsy. Diagnosis of leukoplakia/erythroplakia: Tissue Biopsy is the gold standard. Toluidine blue staining: stain dysplastic & malignant cells , resist washing away by acetic acid. Cytobrush technique: firm bristle brush to obtain cells from full thickness of epith. for cytologic examination Exfoliative cytology of low benefit in these lesions. Management Depends on the histologic findings: If the biopsy shows severe dysplasia or frank carcinoma total surgical excision is indicated. If mild dysplasia removal of any apparent cause (e.g. smoking, alcohol drinking) and regular follow up.

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