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.

The role of neuropeptides in the multifactorial pathogenesis of acne vulgaris

“…30 There are very surprising and interesting differences of MC-1R immunoreactivity in the PSU between acne patients and healthy individuals in the ductus seboglandularis, the anatomical structure which play a crucial role in the pathogenesis of acne due to increased cellular turnover or keratinization. 44 In contrast to SZ95 sebocytes in which α-MSH does not augment proliferation, 45 this NP can increase the metabolic activity in HaCaT keratinocytes. 46 Benign and malignant adnexal neoplasms of the skin display prominent MC-1R immunoreactivity independently of their apocrine, eccrine, sebaceous or follicular differentiation as well as a non-neoplastic hyperproliferative skin disease, acanthosis nigricans, characterized by increased keratinocyte turnover and excessive hyperkeratosis, which supports the potential role of MC-1R as a mediator of increased cellular turnover of the cells situated in the ductus seboglandularis of acne patients.…”

Human Neutrophils Convert the Sebum-derived Polyunsaturated Fatty Acid Sebaleic Acid to a Potent Granulocyte Chemoattractant

“…Although fatty acids in sebum are initially present in the form of triglycerides, they are subsequently freed by bacterial lipases so that in skin surface lipids they are present principally in the free form (42,43). Furthermore, sebaceous glands have been reported to possess 5-LO activity (34), which, along with inflammatory cells, could convert sebaleic acid to 5-HODE.…”

Investigation of Frequency of Allergic Contact Dermatitis Due to Cosmetics in Patients with Acne Vulgaris

“…. Emosyonel stres, hormonlar, ›s›, nem, ultraviyole ›fl›nlar›, bas›nç, sürtünme, afl›r› ovma veya y›kama ve ya¤l› veya t›kay›c› özellikteki kozmetikler akneyi tetikleyen faktörlerdir 11,12 . Kozmetik ürünler ayn› zamanda AKD'nin en önemli nedenleri aras›nda yer almaktad›r 13 .…”