leukoplakia.pptx

Immunology

1. Oral Leukoplakia Presented by: Marij Noor Musfira eman Asmath khazeena Hoorain Ali

2. Introduction 01 Epidemiology and risk factor 02 Clinical manifestations 03 Diagnosis and Evolution 04 contents 04 Management and treatment

3. Introduction Oral leukoplakia is a condition characterized by the formation of thick, white patches on the mucous membranes inside the mouth.

4. Oral leukoplakia The patches cannot be scraped off and often develop on the tongue, gums, inner cheek lining, or the floor of the mouth. While oral leukoplakia is usually harmless and benign, it can sometimes indicate an underlying issue or even be a precancerous condition.

5. Pathophysiology Initiation: Exposure to risk factors, such as tobacco use, alcohol consumption, chronic irritation, or viral infections (e.g., human papillomavirus). Epithelial cells in the oral mucosa are exposed to these risk factors. Cellular Changes: Continuous exposure to risk factors leads to genetic and molecular alterations in the oral epithelial cells. DNA damage occurs, leading to mutations in oncogenes or tumor suppressor genes. The accumulation of genetic abnormalities disrupts normal cell cycle regulation and apoptosis. Hyperkeratosis: As a response to chronic irritation, the oral epithelium undergoes hyperkeratosis, resulting in thickening of the mucosal surface. Increased production and accumulation of keratinocytes occur.

6. Pathophysiology Dysplasia : In some cases, the genetically altered cells progress to dysplasia, characterized by abnormal cellular differentiation and architecture. Dysplasia may range from mild to severe, depending on the degree of cellular atypia and disorganized growth. Leukoplakia Formation: The accumulation of keratinocytes and dysplastic cells forms a white or grayish patch on the oral mucosa, known as leukoplakia. Leukoplakic lesions are predominantly found on the tongue, floor of the mouth, and buccal mucosa. Potential Progression: Leukoplakia may remain stable without further changes. However, in some cases, leukoplakic lesions can progress to oral squamous cell carcinoma (OSCC), a malignant form of oral cancer. Further genetic alterations and acquisition of additional mutations contribute to the transformation of dysplastic cells into invasive cancer cells.

7. Epidemiology 01

8. History

9. Prevalence

10. Global Prevalence: oral leukoplakia ranges from around 1% to 5% of the general population globally. Regional and Country-specific high rates of tobacco use, alcohol consumption, or betel quid chewing tend to have higher prevalence rates Southeast Asia (such as India, Sri Lanka, and Bangladesh) and certain countries in South America. High-Prevalence Areas: high rates of tobacco and betel quid use, have reported higher prevalence rates of oral leukoplakia.

11. Age and Gender Differences : Oral leukoplakia can occur at any age but is more commonly seen in older individuals. The risk of developing leukoplakia increases with advancing age. Men tend to be more commonly affected by oral leukoplakia than women

12. N ot a transmissible condition and does not have a specific transmission route. N ot caused by an infectious agent Mode of Transmission : D evelopment of oral leukoplakia is primarily associated with long-term exposure to risk factors such as: ( tobacco use, alcohol consumption, betel quid chewing, HPV infection, chronic irritation, and poor oral hygiene) primarily related to personal behaviors and lifestyle choices rather than transmission from one individual to another.

13. N ot a transmissible condition and does not have a specific transmission route. N ot caused by an infectious agent Mode of Transmission : D evelopment of oral leukoplakia is primarily associated with long-term exposure to risk factors such as: ( tobacco use, alcohol consumption, betel quid chewing, HPV infection, chronic irritation, and poor oral hygiene) primarily related to personal behaviors and lifestyle choices rather than transmission from one individual to another.

14. 3. Alcohol Consumption: Heavy Alcohol Consumption : Regular and heavy alcohol consumption, particularly when combined with tobacco use, is a significant risk factor for oral leukoplakia. 4. Betel Quid Chewing: containing areca nut, slaked lime, tobacco, and other ingredients, wrapped in a betel leaf. Chewing betel quid is a common practice in certain regions, primarily in South Asia and parts of Southeast Asia.

15. Human Papillomavirus (HPV) Infection: Certain strains of HPV, primarily HPV-16, have been associated with an increased risk of oral leukoplakia. Poor Oral Hygiene: Inadequate oral hygiene and oral health practices can increase the risk of oral leukoplakia . Nutritional deficiencies Genetic Disorders

16. Clinical Manifestation small and discreet or cover a larger area, asymmetrical to more defined outlines. White patches flat, slightly raised, or wrinkled Non-Removability firm attachment to the underlying tissue. Size and shape Texture texture of leukoplakic lesions can vary. Site of occurrence inside the mouth, floor of the mouth, or the roof of the mouth (palate) Sensitivity sensitive to touch, heat, spicy foods, or other irritants.

17. Oral Leukoplakia 4 3 2 1 5

18. Diagnosis and Evolution

19. Diagnosis The gold standard for diagnosis of leukoplakia is always a biopsy from the site of the lesion . Most often, doctors diagnose leukoplakia by examining the patches in the mouth, attempting to wipe off the white patches, discussing the patient's medical history and risk factors, and ruling out other possible causes Before a diagnosis of leukoplakia is made, other possible causes of the white patches are investigated The clinical diagnosis is primarily based on visual inspection and manual palpation

20. Here are some ways that leukoplakia can be diagnosed and evaluated: Visual examination A doctor can diagnose leukoplakia by examining the patches in the mouth and attempting to wipe off the white patches Medical history and risk factors A doctor may discuss the patient's medical history and risk factors to help diagnose leukoplakia

21. Biopsy A definitive diagnosis of leukoplakia is made when any etiologic cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder. Biopsy obtainment, repeated as necessary, is essential. A biopsy involves removing a small sample of tissue from the lesion and examining it under a microscope to determine if it is cancerous or precancerous. Oral brush biopsy This involves removing cells from the surface of the lesion with a small, spinning brush. This is a non-invasive procedure, but does not always result in a definitive diagnosis

22. Excisional biopsy This involves surgically removing tissue from the leukoplakia patch or removing the entire patch if it's small. An excision biopsy is more comprehensive and usually results in a definitive diagnosis. Toluidine blue dye This is a diagnostic aid that can help detect areas of abnormal tissue in the mouth. The dye is applied to the mouth and areas of abnormal tissue will absorb the dye and turn blue.

23. Salivary tests Salivary tests can help detect certain biomarkers that may be associated with oral cancer. These tests are not used to diagnose leukoplakia but may be used to monitor patients who are at high risk for developing oral cancer. It is important to diagnose and evaluate leukoplakia early, as treatment is most successful when a lesion is found and treated early, when it's small. Regular checkups and routine inspections of the mouth for areas that don't look normal are important

24. Within 15 years, about 3% to 17.5% of people with leukoplakia will develop squamous cell carcinoma, a common type of skin cancer . The statistical analysis from several studies piloted on the Indian subcontinent in general and in India concluded the prevalence of leukoplakia ranging from 0.2% to 5.2% and the malignant transformation of 0.13% to 10% . Leukoplakia is usually diagnosed late in the development of proliferative verrucous leukoplakia (PVL), as it takes time to spread to multiple sites . Treatment is a challenge and results are often mixed, but leukoplakia treatment is most successful when a lesion is found and treated early, when it's small. Evolution

25. Management and treatment Professional Evaluation: In any suspected case of oral leukoplakia, it is essential to seek professional evaluation from a dentist or oral surgeon. They will examine the lesion and determine the extent of the condition.

26. . 1.Biopsy: A biopsy may be recommended to confirm the diagnosis and rule out the presence of any cancerous changes. During a biopsy, a small piece of affected tissue is removed and examined under a microscope

27. . 1.Biopsy: A biopsy may be recommended to confirm the diagnosis and rule out the presence of any cancerous changes. During a biopsy, a small piece of affected tissue is removed and examined under a microscope

28. . TREATMENT: Topical Medications: Topical medications like retinoids (e.g., tretinoin ) or corticosteroids (e.g., fluocinonide ) may be prescribed to treat or manage oral leukoplakia. These medications are typically applied directly to the affected area.

29. . Surgical Treatment: Depending on the size, location, and severity of the leukoplakic lesion, surgical intervention may be necessary. Options include: Surgical Excision: The removal of the leukoplakic patch and a small margin of surrounding healthy tissue. Laser Surgery: The use of laser technology to vaporize or remove the affected tissue. Cryosurgery: Freezing the lesion with liquid nitrogen to destroy the abnormal cells. Electrosurgery : The use of electrical current to remove the leukoplakia.

30. . Follow-up Care: After treatment, regular follow-up appointments will be necessary to monitor for any recurrence or the development of new lesions. These appointments may include visual examinations and biopsies if required.

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