Dysplastic and Melanocytic Naevi .pptx

The "Dysplastic and Melanocytic Naevi" presentation by Bornface Kafute, BSc HB, MBChB provides a detailed exploration of two common types of skin moles, focusing on their characteristics, risks, and management. Key topics covered include:

Melanocytic Naevi (Common Moles):

Benign proliferations of melanocytes.
Typically small, round, and evenly colored, appearing during childhood and adolescence.
Dysplastic Naevi (Atypical Moles):

Unusual-looking benign moles resembling melanoma.
Larger than common moles, with irregular borders and varied coloration.
May appear during adulthood and often familial, indicating a higher melanoma risk.
Risk Factors and Monitoring:

Influenced by genetics and sun exposure.
Emphasizes the importance of regular self-examinations and dermatological check-ups.
Clinical Management:

Monitoring changes in moles' size, shape, color, or symptoms like itching or bleeding.
Biopsy or removal of suspicious moles.
This presentation is a valuable resource for understanding the differences between dysplastic and melanocytic naevi, their potential risks, and the importance of early detection and preventive measures in skin cancer.

1. Naevi Dysplastic and Melanocytic BORNFACE KAFUTE, BSc HB, MBCHB

2. Dysplastic Naevi

3. Introduction Dysplastic nevus or atypical mole is a nevus whose appearance is different from that of common moles. Dysplastic (dysplasia), refers to the presence of unusual cells in a tissue. Dysplastic tissue is not cancerous, but it has the potential to develop into cancer. When dysplastic tissue is multiple in number, this is a marker of an increased risk for melanoma

4. Etiology The condition has no known cause. However they are believed to be a response to ultraviolet exposure. People with fair skin,light hair and freckles are more likely to have UV damage leading to dysplastic and melanocytic nevi.

5. Risk Factors Atypical moles can affect people of all ages,sex and skin colour. Having dark skin doesn`t protect from atypical moles or skin cancer, but reduces the risks. People with the following factors are more likely to develop atypical moles; Fair skin,freckles,light eyes and hair. Family history of atypical moles,skin cancer or melanoma. History of excessive sun exposure,sunburns or an inability to tan. Sensitivity to UV light (photosensitivity).

6. Pathogenesis Pathophysiology of dysplastic nevi is not fully understood, however… Dysplastic nevi have been shown to harbor genetic mutations, indicating their position on a continuum between banal nevi and melanomas. (Scientists believe UV light exposure plays a role.) It was first proposed that morphologic stages in the development of dysplastic nevi and their eventual progression to melanoma (Fig. below), other workers have subsequently correlated these morphologic changes with the stepwise acquisition of oncogenic mutations and epigenetic changes

7. Pathogenesis cont ’ Genetic mutations in the NRAS and BRAF genes. inherited loss-of-function mutations in CDKN2A. (encodes several proteins including p16) Other affected families have mutations in the CDK4 gene that make the CDK4 protein resistant to inhibition by p16. Thus, it appears that RAS or BRAF activation and increased CDK4 activity contribute to the development of dysplastic nevi.

8. Clinical Features Asymmetry: irregular shape, with one half not matching the other half. Border irregularity: poorly defined or irregular, with notched or scalloped edges. Color variation: a mix of colors, including shades of tan, brown, black, pink, and red. Diameter: typically larger than common moles (usually exceeding 5 millimeters). Evolution: may change in size, shape, or color over time, although not all changes signify malignancy. Elevation: They may be flat or slightly raised above the skin surface. Pruritus or tenderness: Some dysplastic nevi can be itchy or tender to touch. Multiple lesions: often multiple atypical moles (typically more than 10) .

9. Dysplastic Nevi

10. Diagnostic Modalities Dermatoscopy This non invasive technique utilizes a dermatoscope, a specialized magnifying device, to visualize he nevus ‘s architecture and pigmentation patterns in greater detail Dermatoscopic features can aid in differentiating benign nevi from malignant melanomas Biopsy A small tissue sample is excised and subjected to microscopic examination Histopathological evaluation remains the gold standard for diagnosing melanocytic lesion

11. Melanocytic Naevi

12. Introduction The term mole or nevus (plural nevi) is used for any congenital skin lesion e.g birthmark Melanocytic nevus(pigment nevus or mole) is a benign neoplasm of melanocytes and most naevi are acquired.

13. Etiology The condition has no known cause. However they are believed to be a response to ultraviolet exposure. People with fair skin,light hair and freckles are more likely to have UV damage leading to dysplastic and melanocytic nevi.

14. Risk Factors Exposure to UV rays. Genetic factors such as dysplastic nevus syndrome(also known as familial atypical multiple mole melanoma syndrome, or FAMMM). Fair skin,freckling and light hair Family history of melanoma Personal history of melanoma or other skin cancers Having a weakened immune system Old age Male gender Xeroderma pigmentosum

15. Pathogenesis Melanocytic nevi are benign neoplasms derived from melanocytes, highly dendritic, pigment-producing cells that are normally interspersed among basal keratinocytes. Pathogenesis based on genetic mechanisms is as follows; 1.Activation of mutations in the RAS and BRAF pathways. 2. MAPK activation. 3. Proliferation (limited period) 4. Activation of CDK4 and CDK6, these however get inhibited by p16 and n4a hence occur for a very limited period. 5. Growth arrest. NB: The steps from 3 to 5 are collectively termed as oncogene induced senescence.

16. Pathogenesis cont ’

17. Clinical Features WHO CLASSIFICATION OF SKIN TUMORS (2018) ABCDE A – Asymmetry B – Border irregularity C - Color variation D – Diameter greater than 6mm E – Evolving Darker center

18. Clinical Features Cont’ Superficially spread Grows slowly from outer to deep layers of the skin If nodules are present – extremely aggressive & grows quickly in form of blue or black lump Nest-like clusters within lower epidermis, dermis or both Tan to brown, uniformly pigmented lesions Solid mass relatively flat (macules) Sometimes elevated skin (papules) with well defined rounded borders Lesions are more than 5mm diameter Have darker raised center and irregular flat periphery

19. Diagnostic modalities Visual inspection: using the nak Hbed eye or with the aid of a dermatoscope , a handheld device that magnifies the skin and provides better visualization of structures Dermoscopy : This non-invasive technique allows for a more detailed examination of skin lesions by magnifying them and visualizing specific structures not visible to the naked eye, aiding in the differentiation of benign and malignant lesions Biopsy: If a lesion appears suspicious, a biopsy may be performed to remove a sample of tissue for examination under a microscope. This helps in confirming the diagnosis and determining if the lesion is benign or malignant Histopathological examination: by assessing cellular characteristics, such as cell type, arrangement, and presence of atypical features, to determine if the lesion is benign (nevus) or malignant (melanoma) Molecular testing: In some cases, molecular testing may be used to analyze genetic mutations associated with melanoma, which can provide additional information about the aggressiveness of the lesion and guide treatment decisions.

20. Summary Dysplastic and Melanocytic nevi represent important clinical entities that require careful evaluation and management to mitigate the risk of melanoma development. Continued research and advancement in diagnostic techniques are essential to enhance our understanding of these lesions and improve patient outcome. Early detection , regular surveillance and patient education are key aspects of a comprehensive approach to managing dysplastic and melanocytic nevi. Ultimately by aiming to reduce the burden of melanoma and promote skin health.

21. REFFERENCES Kumar V, Abbas K. A, Aster C. J, Robbins And Cotran Pathologic Basis Of Disease 9 th Edition (2015 ), Elsevier Saunders, Canada