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Progressive cytologic changes during the development of delayed feather amelanosis and associated choroidal defects in the DAM chicken line. A vitiligo model.

Newly hatched Gallus domesticus chicks of the delayed amelanotic (DAM) line have phenotypically normal down pigmentation. Functioning pigment cells are present in the down plumage, choroid, and retinal pigment epithelium. However, histologic and ultrastructural studies reveal that after hatching regenerating feather melanocytes synthesize melanosomes with abnormal, irregularly shaped surfaces and pigmented extensions. Eventually retraction of melanocytic dendrites and clumping of pigment occurs concomitantly with intracellular compartmentalization of the abnormal melanosomes. Melanocyte degeneration is accompanied by the appearance of mononuclear leukocytes (MNLs) in the pulp of the regenerating feathers. Concurrently, melanocytes cease to migrate into the regenerating feather epithelium, and the result is amelanosis. Changes in choroidal melanocytes are first evident as swelling of cell bodies and associated dendrites. Ultrastructurally, the choroidal melanocytes demonstrate increased cytoplasmic material, melanosomal irregularities, retraction of dendrites, melanosome compartmentalization, and eventual necrosis. Concurrently, MNLs arrive and remove the pigment from the choroid. The authors conclude that a basic melanocyte defect precedes the arrival of immunocytes in the delayed cutaneous and choroidal amelanosis in the genetic DAM vitiligo model of the chicken.