BACKGROUND: Vitiligo is probably the end result of different interacting processes. OBJECTIVE: To determine the possible roles of neural and apoptotic mechanisms in the pathogenesis of vitiligo. METHODS: Fifty-six biopsies from 28 patients with generalized vitiligo (28 from depigmented lesional areas and 28 from clinically nondepigmented skin at the periphery of the same areas) were examined; the panaxonal marker neuropeptide protein gene product 9.5 (PGP 9.5) and apoptosis were investigated using immunohistochemistry. RESULTS: Statistically significant differences were detected in the numbers of PGP 9.5-positive nerve fibers/axons in the papillary dermis between the center and periphery of the lesions (i.e. increased at the center in comparison with the periphery). A statistically significant inverse association was found between PGP 9.5 immunostaining in the dermis at the lesion center and the duration of the disease. When apoptosis and PGP 9.5 expression were compared, there was an identical distribution of PGP 9.5-positive nerve fibers/axons and apoptotic cells in the epidermis (i.e. basal in the lesion center; diffuse at the lesion periphery). CONCLUSIONS: There is a possible connection between the neural and apoptotic pathogenetic theories of vitiligo.
BACKGROUND: Vitiligo is probably the end result of different interacting processes. OBJECTIVE: To determine the possible roles of neural and apoptotic mechanisms in the pathogenesis of vitiligo. METHODS: Fifty-six biopsies from 28 patients with generalized vitiligo (28 from depigmented lesional areas and 28 from clinically nondepigmented skin at the periphery of the same areas) were examined; the panaxonal marker neuropeptide protein gene product 9.5 (PGP 9.5) and apoptosis were investigated using immunohistochemistry. RESULTS: Statistically significant differences were detected in the numbers of PGP 9.5-positive nerve fibers/axons in the papillary dermis between the center and periphery of the lesions (i.e. increased at the center in comparison with the periphery). A statistically significant inverse association was found between PGP 9.5 immunostaining in the dermis at the lesion center and the duration of the disease. When apoptosis and PGP 9.5 expression were compared, there was an identical distribution of PGP 9.5-positive nerve fibers/axons and apoptotic cells in the epidermis (i.e. basal in the lesion center; diffuse at the lesion periphery). CONCLUSIONS: There is a possible connection between the neural and apoptotic pathogenetic theories of vitiligo.