In basic terms, acne is formed by the blocking of the skin duct surrounding hair follicles. Sebum and dead skin cells combine to block the skin duct, resulting in the formation of various types of non-inflammatory comedones (e.g., whiteheads and blackheads) that may then develop into inflammatory lesions (e.g., superficial papules and pustules). Subtypes of comedones respond differently to therapy.1

Sometimes inflammatory lesions extend deeper into the skin to form nodules or deep pustules, which often cause scars. However, even superficial acne can cause scarring and temporary or permanent hyperpigmentation.1

Formation of Comedones

The formation of comedones (e.g., blackheads and whiteheads) is caused by abnormal proliferation and differentiation of skin cells in the pilosebaceous duct. What this means is that there is an overproduction and conversion of skin cells to dead skin cells (corneocytes) inside the hair follicle that are then retained and clog up the pilosebaceous duct.1

The mechanisms that lead to this abnormal regulation of skin cells are not completely understood. However, research indicates that androgens, decreased levels of linoleic acid in sebum, inflammatory proteins, and bacteria are all factors.1


Layton, A.M. Disorders of the Sebaceous Glands. [ed.] D.A. Burns, et al., et al. Rook’s Textbook of Dermatology. 8th. Oxford: Blackwell Publishing Ltd., 2010, Vol. 2, 42. ISBN: 978-1-4051-6169-5.
Technically known as hypercornification.
Specifically, keratinocytes.
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