Table 55 Causes of longitudinal melanonychia Racial variation

Laugier-Hunziker-Baran syndrome (Figure 5.34)

Inflammatory nail disorders

Drugs

Irradiation Fungal

Endocrine diseases

Trauma

Neoplasms

AIDS

Nutritional

Figure 5.33

Lateral band of longitudinal melanonychia.

Figure 5.33

Lateral band of longitudinal melanonychia.

Focal activation of the nail matrix melanocytes

This is the most common cause of LM, and is typified by the presence of melanocytes with long dendrites located among nail matrix basal layers. There is no atypia or theque formation.

Melanocyte activation occurs in 77% of African-Americans over 20 years of age and in almost 100% of those over 50 years old. It is observed in 10-20% of Japanese individuals as well as in people of Hispanic descent and other dark-skinned groups. It is uncommon in white populations. Normal variant in black population is due to the number and size of melanosomes produced. In white people melanosomes are small and aggregated in complexes. In black people melanosomes are greater in length, larger in diameter and distributed singly within keratinocytes.

Figure 5.34

Laugier-Hunziker-Baran syndrome—nail and lip hyperpigmentation.

Figure 5.34

Laugier-Hunziker-Baran syndrome—nail and lip hyperpigmentation.

Melanocyte activation may be induced by repeated trauma to the nail matrix. Patients who pick, break or chew the skin over the proximal nail fold frequently develop bands of LM. This is usually associated with nail plate surface abnormalities due to repeated nail matrix injury. Frictional LM is commonly observed in the toes of elderly individuals who have foot deformities and/or unsatisfactory footwear. The melanonychia typically appears at the site of friction with the tip of the shoes or under an overriding toe (see Chapter 9). Inflammatory disorders of the nail may also produce nail pigmentation. Post-inflammatory melanonychia has been described in lichen planus, Hallopeau's acrodermatitis and chronic radiodermatitis. Trichophyton rubrum and Scytalidium dimidiatum (Hendersonula toruloidea) nail infection may also occasionally lead to LM. Longitudinal melanonychia may be secondary to the inflammatory changes which induce activation of nail matrix melanocytes, or due to direct melanin production by the fungi.

Activation of nail matrix melanocytes is occasionally seen in endocrine disorders such as Addison's disease, in pregnancy and in patients with human immunodeficiency virus (HIV) infection, even in those not treated with zidovudine (azidothymine, AZT). Nail matrix melanocytes may also be activated by drugs such as AZT, cancer chemotherapeutic agents and psoralens. Drug-induced melanonychia usually involves several digits; it is reversible.

Melanocyte hyperplasia

Melanocyte hyperplasia is characterized by an increased number of melanocytes, which are scattered between nail matrix keratinocytes without 'nest' formation. The pathogenesis of melanocyte hyperplasia is unknown. We have found this pathological picture in patients with a single band of LM. Differential diagnosis from melanoma in situ may be difficult, and these bands should be completely excised in order to perform serial sections.

Nail matrix naevus

Congenital and acquired melanocytic naevi may occur in the nail matrix and present as LM. Nail matrix naevi are rare and only a few historically proven naevi of the nail matrix have been reported. Naevi of the nail matrix are most commonly of the junctional type. The architectural pattern of nail matrix naevi is similar to that of skin naevi. Naevus cells are usually seen arranged in nests at the dermo-epidermal junction. Single naevus cells can sometimes be found among nail matrix basal and suprabasal onychocytes. Dendritic melanocytes are only occasionally present.

Immunostaining with HMB-45 of nail matrix naevi shows a positive reaction in the cells of the epidermal and junctional component as usually seen in acquired skin naevi. Nail pigmentation due to congenital nail matrix melanocytic naevi may spontaneously regress. However, fading of the pigmentation may only relate to decreased activity of the naevus cells rather than regression of the naevus itself.

The frequency of progression from nail matrix naevi to nail matrix melanoma is not known but a few cases have been well documented. Surgical excision of nail matrix naevi is therefore a justified preventive measure.

Malignant melanoma

In the nail apparatus the most common initial sign of melanoma is acquired LM in white

Figure 5.35

Malignant melanoma.

individuals or broadening of an existing band in people of African or Asian descent. This tumour and its practical differential diagnosis from other chromonychias and nail dystrophies is described in this section; linear melanonychia from other causes is considered in Chapter 7.

Melanoma of the nail region is now better understood since the identification and analysis of acrolentiginous melanoma. It may be localized subungually or periungually with pigmentation and/or dystrophy of the nail plate (Figure 5.35). Initial lesions may be mistaken histologically for benign or atypical melanocytic hyperplasia, but serial sections usually reveal the true nature of the disease.

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