Introduction
The skin is an essential organ in the human body made of a complex membrane of cells, tissues and pigments that hold the body together. Similarly, the skin color is determined by the amount of melanin, the location of melanin and melanocytes, and the presence of caretenoids (Ostler, et al., 2004). Further, the ratio between oxygenated blood and hemoglobin and exogenous or endogenous pigments, also affect the skin color. Melanin is a vital tissue in the skin and the malfunction of melanocytes system, can lead to pigmentation disorder (Rose, 2009).
The malfunction of melanocytes system can amount to melanocytic nevi, a condition under which proliferations of melanocytes are self-limited. In addition to this, Melanocytic nevi are benign tumors of the melanocytes, which are dendrites, pigment-synthesizing cells (Elder, 2010). The classification of melanocytic nevi is based on the location of the nests of the melanocytes; junction or compound nevi (Nordlund, et al., 2006). Similarly, clinical and histopathological criteria can also be used in classification, based on whether the nevi are; acquired or congenital, banal or atypical (dysplastic) (Nordlund, et al., 2006; Hearing and Leong, 2006). Other forms of nevi include; blue nevi, spitz nevi, giant pigmented nevi, Mongolian spot and recurrent nevi (Hearing and Leong, 2006).
Background
According to a research done by Rodenas, et al. (1997), it is affirmed that there is a core relationship between the development of Melanoma and melanocytic nevi, especially in the cutaneous malignant melanoma. In tandem to this, acquired melanocytic nevi contribute the strongest individual risk to the propagation of melanoma disease. Moreover, the acquired melanocytic nevi are attributed to exposure to the environment, or the interaction between constitutional and environmental facets (Gallagher and McLean, n.d). Elder (2010), also attests that acquired nevus cells, contain an indicative difference in their pathogenesis, and active mutations of the oncogene BRAF-gene responsible for sending signals in cells-and NRAS gene. English and Armstrong (1994) also affirmed that, the density of the nevus cells increased consistently with age. Sex was also a factor, boys being the most vulnerable group. They also noted that nevi were common on the lateral surface; face, neck and upper part of the limbs and the decrease of the skin pigment accelerated its development. Therefore, the understanding of acquired melanocytic nevi becomes an essential tool in treating and managing melanoma disease.
Epidemiology
Acquired melanocytic nevi are also tentatively referred to as melanocytic nevi or pigmented moles. The development of the nevi commences in early childhood as small pigmented macules, roughly 1-2 mm in length (Mallory, Bree and Chern, 2005). Further, the lesions slowly enlarge with age, increases in darkening, size and number at puberty. Most of the acquired nevi are found in sun-exposed areas, particularly in the torso. However, they can be found in any part of the body (Mallory, Bree and Chern, 2005).
Apart from junctional and compound nevi, dermal nevus is also a common form of acquired nevi, located within the dermis of the skin and dome in shape. Atypical mole syndrome and dysplastic nevi are associated with acquired nevi, and they are largely evinced in its pathogenesis (Mallory, Bree and Chern, 2005). Moreover, the prevalence of the acquired melanocytic nevi is higher in white skinned population compared to pigmented population. The adult population is also at higher risk of getting melanocytic nevi, since the number of nevus cells increase with increase in age (Gallagher and McLean, n.d).
Climate and UV radiations also determine the onset of melanocytic nevi, as confirmed in the study population of Australia (Harrison, MacKie and MacLennan, 2000). Subjects in Australia exhibit higher risks of developing melanocytic nevi than population in United Kingdom. Similarly, Harrison, MacKie and MacLennan (2000) also noted that in white population, nevi acquired through UV radiation, mature fast and later regress, causing the major risks to the development of melanoma. The major effects of melanocytic nevi on white skin include the development of moles or tumors, cancer and the propagation of melanocytic nevi to melanoma, since they are the strongest phenotypic risk factors (English and Armstrong, 1994).
Diagnosis
The principal mode of diagnosis is clinical presentation and differential diagnosis of the nevi (Mallory, Bree and Chern, 2005). In the same light, a variety of adjunct diagnostic devices have been established to aid in the differentiation of acquired melanocytic lesions and congenital lesions. Similarly, clinical examination for pigmented lesion is equivocal, and dermatoscopy should be employed, to check for any presence or suspicion of malignancy (Stockfleth, Rosen and Shumack, 2010). In relation to differential diagnosis, histological evaluation should be performed by a specialized dermatopathologist, in a comprehensive cancer centre. This is to differentiate between multiple types of melanoma, atypical nevi, congenital nevocellular, folliculitis and spitzoid lesions (Stockfleth, Rosen and Shumack, 2010).
Treatment
Most acquired melanocytic nevi do not require treatment, only if they are located on areas of irritation. Nevi can be surgically removed with an elliptical excision or deep saucerization. In line with this, the cosmetic result should be carefully evaluated to avoid further irritations or complications (Kerdel and Jimenez-Acosta, 2003). Further, medical care and surgical care are also remarkably essential. Patients diagnosed with acquired melanocytic nevi, are required to avoid excessive sun exposure. In tandem to this, they should use sunscreen. Mallory, Bree and Chern (2005), also affirm that nevi changes slowly with time and observation is an essential tool for treatment. Similarly, lesion with atypical histology should be excised wholly to monitor the malignant development and change. Destructive modes of therapy for instance laser and cryotherapy should also be avoided to prevent further complications.
Conclusion
Concisely, skin disorders are quite complicated and difficult to understand. The diagnosis of acquired melanocytic nevi and its treatment is involving and requires qualified dermatopathologist. Conversely, there are no therapies that enhance the prevention of disorder. Thence, it becomes difficult to prevent and educate the patients on the appropriate ways to prevent the disorder. Therefore, staying away from the sun and the use of broad-spectrum sunscreen becomes one of the best solutions to the prevention of acquired nevi. Similarly, all the health care providers should be imparted with the most appropriate knowledge for perfect diagnosis, treatment and reliable prevention measures.
References
Elder, E. D., 2010. Tumorigenic Melanocytic Proliferations. New York, NY: Demos Medical Publishing, LLC.
English, R. D. and Armstrong, K. B.,1994. Melanocytic Nevi in Children. American Journal of Epidemiology, 139 (4), pp. 390-401.
Gallagher, P. R. and McLean, I. D., n.d. The Epidemiology of Acquired Melanocytic Nevi: A Brief Review. [Online] Available at: <http://www.bccancer.bc.ca/NR/rdonlyres/E434689D-B2AB-4CFF-9182-8A7F56F99A14/1760/nevi.pdf > [Accessed 1september 2011].
Harrison, L. S. MacKie, M. R. and MacLennan. R., 2000. Development of Melanocytic Nevi in the First Three Years of Life. Journal of the National Cancer Institute, 92, pp. 1436-1438.
Hearing, J. V. and Leong, L. P. S. eds., 2006. From Melanocytes to Melanoma: The Progression to Malignancy. New Jersey: Human Press Inc.
Kerdel, A. F and Jimenez-Acosta, F., 2003. Dermatology: Just the Facts. New York, NY: The McGraw-Hill Companies, Inc.
Mallory, B. S. Bree, A. and Chern, P., 2005. Illustrated Manual of Pediatric Dermatology: Diagnosis and Management. Oxon, OX: Taylor & Francis Group.
Nordlund, J. J., et al., 2006. The Pigmentary System: Physiology and Pathophysiology. 2nd ed. Oxford: Blackwell Publishing Ltd.
Ostler, B. H., et al., 2004. Diseases of the Eye and Skin: A Color Atlas. Philadelphia, PA: Lippincott Williams & Wilkins.
Rodenas, J. M., et al., 1997. Melanocytic Nevi and Risk of Cutaneous Malignant Melanoma in Southern Spain. American Journal of Epidemiology, 145 (11), pp. 1020-1029.
Rose, T. P., 2009. Pigmenatry Disorder. Medical Clinics, 93, pp.1225–1239.
Stockfleth, E. Rosen, T. and Shumack, S. eds., 2010. Managing Skin Cancer. Berlin: Springer.
