Acne vulgaris is a common dermatological disorder of the pilosebaceous unit that has a complex pathophysiology and can be triggered by a number of factors
Acne vulgaris primarily affects the face but in severe cases may affect the chest, neck, and back, with a clear detrimental psychosocial effect on the patient’s quality of life
Major factors in acne development include increased sebum production, increased androgen activity, abnormally increased keratinocyte production, microbial colonization of Propionibacterium acnes, inflammation, and immune reactions
Increased sebum production and androgen activity result in cells released into the follicles, leading to a sebum-rich, oxygen-poor environment ideal for the proliferation of Cutibacterium acnes (formerly Propionibacterium acnes)
The draining duct widens, the sebaceous gland grows larger due to accumulated material, and Cutibacterium acnes produces enzymes that hydrolyze triglycerides in the sebum, leading to hyperkeratinization and inflammation
3. Comedo may be closed (no obvious follicular opening, referred to as whiteheads) or open (dilated follicular opening, keratin plug darkens due to oxidized lipids and melanin, referred to as blackheads)
Including growth hormone, insulin-like growth factor, and peroxisome proliferator-activated receptors regulate sebaceous glands contributing to acne development
Closed comedo becomes larger and packed due to debris and inflammation, leading to the pore wall breaking and contents leaking into the surrounding skin, activating inflammatory cells
Deep, fibrous lesions that are hard to touch, more painful, severe, and deep red or purple in color, large in size (> 5 mm wide) and not filled with pus