What Is a Dysplastic Mole?

Dysplastic nevus, also known as dysplastic nevus syndrome, BK syndrome, is often mistaken clinically for superficial disseminated malignant melanoma. The disease has a certain relationship with the occurrence of malignant melanoma, and tends to be familial. About 1/3 to 1/5 of stunted moles are histologically similar to malignant melanoma. The dysplastic nevus may have a certain genetic basis, and damage can occur anywhere on the body surface. Resection is the preferred treatment. [1]

Dysplastic mole

Basic information on dysplastic moles

Dysplastic nevus, also known as dysplastic nevus syndrome, BK syndrome, is often mistaken clinically for superficial disseminated malignant melanoma. The disease has a certain relationship with the occurrence of malignant melanoma, and tends to be familial. About 1/3 to 1/5 of stunted moles are histologically similar to malignant melanoma. The dysplastic nevus may have a certain genetic basis, and damage can occur anywhere on the body surface. Resection is the preferred treatment. [1]

Pathogenesis of stunted moles

(I) Causes of Onset
May appear in childhood. About 1/3 to 1/5 of stunted moles are histologically similar to malignant melanoma. The atypicalness and proliferation of cells have some correlation with sunlight exposure. In addition, studies have suggested that. Dysplasia moles are associated with partial deletion of chromosome 11 and testicular germ cell tumors. Familial malignant melanoma and dysplastic nevus are also associated with endocrine gland syndrome and autoimmune polyglandular syndrome. The above correlation cannot be fully determined.
The dysplastic nevus may have a certain genetic basis for differentiation. Endogenous hormones and the external environment promote the development of the disease. Genetic analysis of malignant melanoma-prone families is considered to be an autosomal dominant disease. Abnormal genes may be present in 1p35 or 9p21, resulting in cell cycle enzyme p16 / CDKN2A mutations that cause abnormal cell differentiation. In addition, excessive UV-induced photochemical products in dysplastic nevus can cause malignant transformation of cells.
(Two) pathogenesis
The pathogenesis is unclear. Abnormal genes may be present in 1p35 or 9p21 and cause cell cycle enzyme p16 / CDKN2A mutations to cause abnormal cell differentiation. In addition, excessive UV-induced photochemical products in dysplastic nevus can cause malignant transformation of cells. [2]

Clinical manifestations of dysplastic nevus

1. Damage can occur anywhere on the body surface, but it is most common on the trunk, followed by the limbs, and again the face.
2, single or multiple lesions, usually larger than nevus cell nevus, some can exceed 7mm in diameter. The center is often raised, hairless, of varying sizes, with irregular or unclear edges, and uneven shades.
3. Malignant melanoma can develop when multiple lesions occur, but if it is single, it has nothing to do with malignant melanoma.
In typical cases, pathological examination can be confirmed without difficulty, but it is difficult to determine when there is a tendency for superficial epidermal spread. [3]

Auxiliary examination of dysplasia

Tissue performance: The tissue configuration of the disease is more important than cytological features.
The tissue structures are as follows: The vast majority are compound moles, and a few are junctional. The melanocytes at the border junction expanded beyond the range of nevus cells in the central dermis. The nevus cells at the junction are fused in a "bridge" shape. The epidermal process extends, especially at the edge junction. There are nevus cell nests on the base and sides of the epidermal process. Melanocytes can be seen in the middle or upper part of the epidermal spinal cell layer, mostly in the form of nests. often mild to moderate inflammatory cell infiltration. Around the epidermal process is a thick and wide collagen band.
Cytological characteristics: The nucleus of melanocytes is large and deeply stained, with pleomorphism and irregularity, or obvious nucleoli, but no mitotic phenomenon is seen. [4]

Treatment of dysplastic moles

The disease should be closely observed for malignant changes. Follow-up should be carried out regularly, especially for those with familial malignant melanoma, adolescence, pregnancy and the use of sex hormone replacement therapy.
Resection is the preferred treatment. The extent of resection should reach 2 to 3 mm around the lesion. A single skin lesion can be removed, and multiple cases can be treated externally with fluorouracil or retinoic acid. Patients with or without familial malignant melanoma, if it is not easy to check the progress of skin lesions, preventive resection. The above treatments should be followed regularly throughout life, and biopsy if necessary. [5]

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