title: Pathogenesis of acne.
abstract: Acne vulgaris is a skin disorder of the sebaceous follicles that commonly occurs in adolescence and in young adulthood. The major pathogenic factors involved are hyperkeratinization, obstruction of sebaceous follicles resulting from abnormal keratinization of the infundibular epithelium, stimulation of sebaceous gland secretion by androgens, and microbial colonization of pilosebaceous units by Propionibacterium acnes, which promotes perifollicular inflammation. The clinical presentation of acne can range from a mild comedonal form to severe inflammatory cystic acne of the face, chest, and back. At the ultrastructural level, follicular keratinocytes in comedones can be seen to possess increased numbers of desmosomes and tonofilaments, which result in ductal hypercornification. The increased activity of sebaceous glands elicited by androgen causes proliferation of P. acnes, an anaerobe present within the retained sebum in the pilosebaceous ducts. The organism possesses a ribosome-rich cytoplasm and a relatively thick cell wall, and produces several biologically active mediators that may contribute to inflammation, for instance, by promoting leukocyte migration and follicular rupture. In inflamed lesions, numerous neutrophils and macrophages infiltrate around hair follicles and sometimes phagocytose P. acnes. To examine the participation of neurogenic factors in the pathogenesis of acne, we quantitatively assessed the effects of neuropeptides on the morphology of sebaceous glands in vitro using electron microscopy. Substance P, which can be elicited by stress, promoted the development of cytoplasmic organelles in sebaceous cells, stimulated sebaceous germinative cells, and induced significant increases in the area of sebaceous glands. It also increased the size of individual sebaceous cells and the number of sebum vacuoles for each differentiated sebaceous cell, all of which suggests that substance P promotes both the proliferation and the differentiation of sebaceous glands. In this review, we introduce the general concept of pathogenic factors involved in acne, including typical electron microscopic findings and recent evidence of stress-induced exacerbation of acne from a neurological point of view. An improved understanding of the pathogenesis of acne should lead to a rational therapy to successfully treat this skin disease.
authors.affiliation: Department of Dermatology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Toyoda
authors.forename: M
authors.initials: M
authors.lastname: Morohashi
mesh_terms: D000152:Acne Vulgaris / Q000209:etiology* / Q000382:microbiology / Q000473:pathology; D000210:Acute-Phase Reaction / Q000473:pathology; D000818:Animals; D002478:Cells, Cultured; D004848:Epithelium / Q000473:pathology / Q000648:ultrastructure; D018859:Hair Follicle / Q000382:microbiology / Q000473:pathology / Q000648:ultrastructure; D006801:Humans; D008855:Microscopy, Electron, Scanning; D020932:Nerve Growth Factor / Q000494:pharmacology; D009479:Neuropeptides / Q000494:pharmacology; D011425:Propionibacterium acnes / Q000648:ultrastructure; D012627:Sebaceous Glands / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D012629:Sebum / Q000378:metabolism; D013312:Stress, Physiological / Q000150:complications; D013373:Substance P
chemical_list: D009479:Neuropeptides; D013373:Substance P; D020932:Nerve Growth Factor