Poster Presentation ASPCR-ASDR Conference 2013

Transmission electron microscopy stereology of altered mitochondrial ultrastructure of melanocytes in perilesional vitiligo skin (#106)

Yan Lu 1
  1. 1st Affiliated Hospital, Nanjing Medical University , Nanjing, JS, China

Vitiligo is an acquired pigmentary disorder of unknown etiology that is clinically characterized by the development of white macules related to the selective loss of melanocytes. Recent data have suggested an altered functionality of mitochondria in vitiligo patients. To better understand whether a defective ultrastructure of mitochondria is involved in the pathogenesis of vitiligo, we have performed an ultrastructural study on normal and perilesional skin from 10 healthy volunteers and 20 patients with active or stable disease by on microscope. The resulting images of cells were analyzed using stereology to compare quantitatively mitochondrial morphology in the patient and control groups including volume density (Vv), surface density (Sv) and numerical density (Nv). We found that mitochondria were abundant with normal structure and cristae mitochondriales concentrated either in keratinocytes or melanocytes from volunteers. A large number of melanosomes in melanocytes of control group mainly stage Ⅲ and Ⅳ were detected. However, mitochondrial swelling and vacuolization as well as fragmentation of the mitochondrial cristae were commonly observed in vitiligo group. Stage Ⅲ melanosomes decreased significantly compared with normal group. Besides, no mitophagy was observed in the least, whereas autophagosomes could be occasionally noticed in normal melanocytes. The stereology results showed that Vv and Sv of mitochondria measured in vitiligo were significantly elevated compared with the normal, but Nv was markedly decreased. Remarkable differences were noted between active and stable stage of vitiligo for the Vv, Sv and Nv. These data provide further evidences for an altered mitochondrial ultrastucture and functionality in vitiligo patients, and the mitochondrial damage was closely correlated with active status of the disease.