Skin Moles

The atypical mole is a special kind of dysplastic melanocytic nevus, with clinical and microscopic features suggestive of an intermediate form between the common acquired mole and melanoma. Atypical skin moles are important markers for both familial and non familial melanoma. As many as 50% of patients with “sporadic” melanoma have been observed to have atypical skin moles. The incidence of atypical skin moles in the general population has been estimated to be 1.8% to 10% and possibly as high as 19%. The presence of atypical skin moles has been established as an independent risk factor for melanoma, along with several other cutaneous traits, including red or blonde hair, solar lentigines, skin type 1 or 2, and increased numbers of common acquired melanocytic nevi. One study found the adjusted relative risk of melanoma to be 2 for a single atypical mole and 12 for 10 or more atypical skin moles. Another found a relative risk of 1.6 when one to four atypical skin moles were counted and 6.1 for five or more atypical skin moles. The risk ofmelanoma attributable to atypical skin moles may be further exacerbated by the coexistence of other melanoma risk factors, such as skin type 1 or 2. The increased risk for melanoma is particularly true in the setting of the atypical mole syndrome (AMS). AMS encompasses individuals with multiple atypical skin moles arising sporadically or in a setting of a family history of atypical skin moles or melanoma. AMS has been divided into a number of forms. Type A is sporadic atypical mole without melanoma; type B is familial atypical mole without melanoma; type C is sporadic atypical mole with a personal history of melanoma; type D-l is familial atypical mole with one family member with melanoma; and type D-2 is familial atypical mole with two or more family members with melanoma. Meticulous screening of family members may demonstrate that presumptive cases of sporadic AMS are actually familial. All patients with AMS have an increased risk for developing melanoma, although the magnitude of the risk varies among the AMS types. The relative risk of melanoma is least in patients with AMS types A and B, and has been estimated to be 7 with a cumulative lifetime risk of 6%. The relative risk of melanoma in type D-2 patients may be as high as 1000 or greater compared with the general population. Individuals with AMS also appear to be at an increased risk for multiple primary cutaneous melanomas.One study found a 35.5% cumulative 10-year risk of developing a second melanoma in those with AMS and a history of melanoma as compared with a 17% 10-year risk of developing a second melanoma in those with a history of melanoma but without AMS. Patients with AMS may also be at increased risk of conjunctival and intraocular melanoma. The recognition of AMS may allow early detection of melanoma and identification of those at risk and provide the opportunity for the initiation of preventive measures. A great deal of discussion has centered on the validity of the atypical mole as a distinct entity and its potential for progression to melanoma. Much disagreement over its nature stems from a lack of uniform clinical and microscopic criteria to define it. Atypical skin moles generally demonstrate both clinical and microscopic evidence of distorted and disordered architecture.  

Common features:
Typical acquired skin moles vary considerably in their gross features. In general, appearance to the naked eye is orderly; i.e., lesions have a homogeneous surface and coloration pattern, round or oval shape, regular outlines, and relatively sharp border. Typical acquired skin moles may be papillomatous, dome-shaped, pedunculated, or flat-topped and usually are flesh-colored, pink, or brown.
Clinico-pathological correlation:
More elevated acquired skin moles tend to be more lightly pigmented, and flatter acquired skin moles tend to be more darkly pigmented. More elevated and less pigmented lesions tend to have a prominent intradermal nevus component, whereas flatter and darker lesions have a more prominent junctional component and a less prominent dermal component. Skin moles on palms and soles, even compound skin moles, may not distort the skin surface, perhaps because of a thickened stratum corneum in these sites.
Special features:
Dark pigmentation:
Very dark brown and black are unusual colors for typical acquired skin moles in lightly pigmented people. In contrast, dark pigmentation is usual for Typical acquired skin moles in people who have darkly pigmented skin. Very dark brown and black in skin moles on acral and mucosal surfaces and nail apparatus should be viewed with suspicion regardless of normal skin color.
Other colors:
Blue, gray, red, and white areas in a mole are not typical features and ought also to be viewed with suspicion.
Hair quality:
The surfaces of skin moles may reveal hair that is less than, equal to, or greater than that of surrounding skin. Hair in skin moles may be coarser, longer, and darker than that in surrounding skin.
Site specific:
Lesions on palms and soles are usually hairless. Size, shape, skin markings, and hair quality of skin moles in darkly pigmented races are similar to those in whites.
Extent of lesion:
Skin moles of the nail apparatus may be a dark or light brown, extending from the nail matrix to the distal edge of the nail plate; extension of the pigmentation onto the skin of the nail fold or beyond the distal nail groove should be considered suspicious for melanocytic dysplasia or malignant melanoma.

Typical acquired skin moles have not been followed systematically from their progression to regression. Therefore, dynamic evolution of acquired skin moles must be suggested from static information or short-term follow-up studies. It has been stated that during the early years of life, virtually all skin moles are composed primarily of junctional moles, that nevomelanocytes in these junctional moles eventually push their way to the dermis and finally lose their epidermal contact as they continue to grow into the dermis and become intradermal skin moles, and that in the intermediate stage of this process there are junctional moles in the epidermis and sheets and nests of nevomelanocytes in the dermis (i.e., compound skin moles). This argument suggests that because skin moles in adults are primarily of the dermal type and because skin moles in children are primarily of the junctional type, skin moles evolve by a process of “dropping down” of nevus cells from the epidermis into the dermis. The precise nature of the “dropping down” process has not been defined. It is likely that acquired skin moles evolve through a life cycle, first becoming apparent after infancy in the vast majority of cases, peaking in number during the second and third decades of life, and then disappearing by the seventh to ninth decades. Regression of skin moles is believed to occur by degeneration. The formation of degenerative structures in aging skin moles suggests an end stage in differentiation and not a source of origin of intraepidermal skin moles. Transepidermal elimination of nevomelanocytes rarely occurs. Rarely, nevomelanocytes have been documented to show spontaneous disappearance. Skin moles also may involute during the course of inflammatory halo depigmentation (halo moles). There may be relatively sudden changes in skin moles that are unrelated to cancerous transformation. Any single mole that is noted to suddenly change independently should be a cause for concern. Causes of sudden changes in a mole (color, surface, or size, with or without pain, itching, ulceration, or bleeding) over days or weeks include cystic dilatation of a hair follicle, epidermal cyst formation, folliculitis, abscess formation, trauma, hemorrhage, and, in the case of a pedunculated mole, strangulation and thrombosis. These benign causes of sudden change may require close observation until resolution occurs over the course of 7 to 10 days (in the case of trauma or inflammation) or histopathologic examination. Cases have been described of the eruptive appearance of skin moles after blistering skin disease, immunosuppression, or chemotherapy. The vast majority of acquired skin moles are harmless, growing in proportion to body growth, with physiologic spurts of enlargement during early childhood and puberty.
A cancerous mole risk appears to be related to the number and size of skin moles; patients with numerous skin moles, atypical skin moles, and a personal or family history of a cancerous mole should be considered for periodic surveillance examinations.

Typical acquired skin moles develop after birth, slowly enlarge symmetrically, stabilize, and persist or regress later in life. The majority of Typical acquired skin moles appear to develop during the second and third decades of life, although some lesions may appear in the first 6 to 12 months of life.
A number of studies have measured the number of typical acquired skin moles in different age groups. The average number of skin moles per person peaked at 43 for males and 27 for females during the second and third decades, respectively, and decreased to very few in the sixth and seventh decades. A similar age-related prevalence rate for skin moles has also been documented. A difference in frequency distribution of skin moles according to gender is not clear, although most series show a close to equal prevalence in males and females. The prevalence of skin moles varies according to race. In blacks, the overall prevalence of skin moles (regardless of size) tends to be higher in those with lighter skin versus those with darker skin. When prepubertal whites were examined for skin moles, a significant association for excess skin moles was documented for pale skin, blue or green eyes, blond or light-brown hair, and a tendency to sunburn, but not a tendency to freckle. Other studies show variable relationships to these same parameters. Environmental exposure to UV light appears to be a critical exacerbating factor for the development of skin moles. Mole density has been shown to increase with increasing sun intensity of UV light. Further, the use of UV blocking sunscreens has been shown to decrease the number of new moles in children. Genetics plays a role in mole development. There is evidence that the size, frequency, and distribution patterns of acquired skin moles tend to aggregate in families. This observation is well documented for atypical skin moles in the setting of familial cutaneous melanoma and congenital skin moles.