Skin Moles

Skin Moles Causes: There has been a continual debate as to the origin of skin moles. Although many theories have been proposed and some supporting data are available, the critical events leading to mole development remain a mystery. A number of hypotheses have been proposed. These include:
(1) transformation from epidermal melanocytes and subsequent deposition/migration into the dermis. Evidence for this hypothesis includes the demonstration of basement membrane around nevomelanocytes in the dermis based on routine, ultrastructural, and immunohistologic features, suggesting structural contiguity of dermal nevomelanocytes with epidermis. These studies would suggest that nevomelanocytes extend down from the epidermis along with the basement membrane.
(2) dual origin, i.e., nevomelanocytes in the epidermis and upper dermis being derived from epidermal melanocytes, and nevomelanocytes in the lower dermis being derived from Schwann cells of nerves. Evidence for this hypothesis is based on differences in differentiation of nevomelanocytes. This includes positive staining by a monoclonal antibody to the Schwann cell–associated antigen for nevomelanocytes in the lower dermis and negative staining for nevomelanocytes in the epidermis and upper and middle dermis. Moreover, nevomelanocytes in the epidermis and papillary dermis Typically resemble epithelioid cells, aggregate in nests, demonstrate tyrosinase activity but not cholinesterase activity, stain weakly for neuron-specific enolase, and contain melanin. Nevomelanocytes in the deep dermis tend to resemble fibroblasts or Schwann cells or form concentrically arranged and loosely layered structures becoming skin molesc corpuscles that resemble Meissner corpuscles, are usually disposed as single cells, demonstrate minimal tyrosinase activity, have abundant cholinesterase activity, and Typically stain positively for neuron-specific enolase. This hypothesis would suggest that the phenotypic differences in the nevomelanocytes are due to different origins (melanocytes and Schwann cells).
(3) hamartomatous change affecting many cell types. Evidence for this hypothesis includes changes in the associated epidermis, including lentiginous, seborrheic, or epidermal nevus type patterns, and aberrations of appendageal and neurovascular structures, particularly in congenital skin moles. These findings reinforce the notion that skin moles are benign hamartomas involving multiple tissue elements. The fourth hypothesis is based on the existence of defective melanoblasts that may lead to defective differentiation. Neural crest–derived melanoblasts migrate to the dermis and basal layer of the epidermis before 40 days of estimated gestational age. These cells are thought to take up residence in the epidermis and/or superficial dermis (or the deep dermis, panniculus, and adnexal structures in the case of congenital skin moles). Melanocytic “precursor” cells have been shown to be present in adult human skin. Theoretically, these cells could aberrantly proliferate and differentiate, giving rise to melanocytic neoplasms. Depending on the defect, timing, and local tissue influences, a variety of different melanocytic neoplasias could be created.
(4) benign neoplastic proliferation originating from a defect in melanoblast/neural crest cells.
This fourth hypothesis is supported by data showing that human acquired skin moles are clonal.