Pathogenesis of acne.

摘要: Acne vulgaris is a skin disorder of the sebaceous follicles that commonly occurs in adolescence and young adulthood. The major pathogenic factors involved are hyperkeratinization, obstruction resulting from abnormal keratinization infundibular epithelium, stimulation gland secretion by androgens, microbial colonization pilosebaceous units Propionibacterium acnes, which promotes perifollicular inflammation. clinical presentation acne can range mild comedonal form to severe inflammatory cystic face, chest, back. At ultrastructural level, follicular keratinocytes comedones be seen possess increased numbers desmosomes tonofilaments, result ductal hypercornification. activity glands elicited androgen causes proliferation P. an anaerobe present within retained sebum ducts. organism possesses ribosome-rich cytoplasm relatively thick cell wall, produces several biologically active mediators may contribute inflammation, for instance, promoting leukocyte migration rupture. In inflamed lesions, numerous neutrophils macrophages infiltrate around hair sometimes phagocytose acnes. To examine participation neurogenic pathogenesis acne, we quantitatively assessed effects neuropeptides on morphology vitro using electron microscopy. Substance P, stress, promoted development cytoplasmic organelles cells, stimulated germinative induced significant increases area glands. It also size individual cells number vacuoles each differentiated cell, all suggests substance P both differentiation this review, introduce general concept including typical microscopic findings recent evidence stress-induced exacerbation neurological point view. An improved understanding should lead rational therapy successfully treat disease.