Keratin expression in the normal nail unit: markers of regional differentiation

Abstract

Differentiation within the nail unit was examined using a range of antikeratin monoclonal antibodies including the recently described antibody LHTric-1, specific to the acidic hair-type keratin Ha1. Keratinocytes of the nail matrix, nail bed and the digit pulp were characterized by different patterns of keratin expression. Nail matrix was the sole site of expression of Ha1, which colocalized in suprabasal matrix epidermis with epidermal keratins K1 and K10. Small amounts of K17 were found at the apex of the matrix in some cases. K6 and K16 were found where the epidermal surface folds forwards to become the ventral aspect of the proximal nail fold. The nail bed was distinguished by the absence of hair-type keratin Ha1 and the absence of markers of cornified epidermis and mucosal differentiation K1/K10 and K4/K13, respectively, while K6, K16 and K17 were detected. The basal keratin conformation marker, LH6, was expressed suprabasally throughout the nail bed. This complement of keratins exists in the nail bed in the absence of notable proliferative activity, and suggests a state of minimally developed differentiation which may be afforded by the physical or biological properties of the overlying nail. Keratins, K6, K16 and K17 were all found in the digit pulp in limited amounts, possibly in association with the epidermal component of the eccrine duct. The simple epithelial keratins, K7, K8 and K18, were found in small amounts in the specimens from younger individuals, mainly in epibasal cells of the apex of the matrix and in putative Merkel cells.

The human nail – Barrier characterisation and permeation enhancement

“…Although the majority of the protein in hair and nail is classified as 'hard' trichocyte keratins, both hard and soft keratins have been detected in the nail matrix and both forms of the protein have been found in the nail plate. Keratins 1 and 10 (soft) are found in the matrix together with the hard keratin Ha-1 (de Berker et al, 2000) and several further hard keratins have also been shown to be present in the nail matrix, nail bed and nail plate (Perrin et al, 2004;Perrin, 2007). Intermediate filamentassociated proteins and trichohyalin are also found within the nail (Cashman and Sloan, 2010).…”

The molecular basis of human keratin disorders

“…Keratins K6b and K17 which are mutated in pachyonychia congenita type II are found in the nail bed, hair follicle, eccrine glands and in palmoplantar skin McLean et al 1995). How mutations in these keratins cause hyperkeratosis of the nail is not entirely clear, presumably fragility of keratinocytes in the nail bed leads to release of cytokines that act upon proliferative cells of the nail matrix thereby causing overgrowth of the nail (De Berker et al 2000).…”

Nail matrix biopsy of longitudinal melanonychia: Diagnostic algorithm including the matrix shave biopsy

“…Traditional teachings suggest that matrix punch biopsies, 3 mm or less, are unlikely to cause a permanent dystrophy and that larger specimens are removed in a transverse orientation to facilitate repair and avoid dystrophic nail plate scarring. 1,2 More specifically, however, only 3-mm biopsies from the distal matrix are truly safe from permanent nail dystrophy; the proximal matrix, responsible for a majority of the nail plate production as well as the superficial nail plate, 3,4 is more susceptible to scarring or developing a split nail, even with a 3-mm punch. 2,5 Laterally based LM may be excised with lateral longitudinal excisions.…”