Pathogenesis of Acne

Sebaceous gland biology:

• These are exocrine glands attached to hair follicles (thus being part of the pilosebaceous unit).

• In mammals, the glands secrete lipids that are fluid at room temperature.

• Lipid secretion is via a holocrine mechanism; that is, cells are continuously produced from a basal layer, synthesize lipid, and undergo programmed cell death, releasing their cellular contents into the follicle.

• The glands are responsive to androgens and progesterone in particular, and lipid secretion to the skin surface increases markedly at puberty.

• Sebaceous glands are a component of the pilosebaceous unit, of which there are three types: (1) terminal, (2) vellus, (3) sebaceous

• Sebaceous follicles have very large glands with very small associated hairs, and are found in the acne distribution (face, chest, back).

• As far as is known, acne vulgaris occurs only in sebaceous follicles, terminal follicles (such as those of the beard in men) being unaffected.

• Despite this association, the role of sebaceous secretion in acne is not clear.

• A practical corollary is that removing skin surface lipid has no role in treating acne.

• Sebaceous glands have no known physiologically significant function in humans.

• Despite "common knowledge" to the contrary, they are not important in "lubricating" the skin, or conversely, preventing dry skin.  People do not require better barrier function after puberty, at least for the skin.

• A role in waterproofing animal fur and in particular, feathers of aquatic birds seems more clearly established for sebaceous type glands.

There are three major factors thought to be important in the pathogenesis of acne vulgaris:

• "Over-production" of sebum.
  
  • Sebum is lipid produced by sebaceous glands and is liquid at room temperature.
  • It consists almost entirely of triglyceride and hydrolysis products of triglyceride, wax esters (esters of long chain fatty acids and long chain fatty alcohols) and squalene (a long chain hydrocarbon precursor of cholesterol).
  • The role of this lipid in normal physiology and in the pathogenesis of acne vulgaris is not clear, but it is known that acne patients, as a group, produce more sebum than controls.

• Abnormal follicular keratinization
  
  • The upper part of the follicle produces a stratum corneum, similar to that found on normal skin, which must "desquamate" (that is, lose cell to cell cohesion) in an orderly way.
  • This seems to not occur in acne patients and leads, at least in part, to the formation of the follicular plug. This is the sine qua non of acne vulgaris.

• Presence of follicular bacteria, specifically Proprionibacterium acnes
  
  • This is a normal colonizer of human follicles but seems to be present in excessive numbers in patients with acne and plays a role in the induction of inflammation in association with the follicular plugs.
  • The relation and importance of the above three factors has not been worked out. There is still hot debate over the role sebum may play in the formation of comedones or inflammation, and it is known that reduction in sebum will be associated with improvement in acne.
  • On the other hand, improvement in acne can be seen from topical treatments that do not alter sebum production but do alter follicular keratinization.