Pathogenesis of Acne
Sebaceous gland biology:
- These are exocrine glands attached to hair follicles (thus being part of the
- In mammals, the glands secrete lipids that are fluid at
- 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
- 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
- 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
- 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