What is the pathogenesis of acne?
Acne is polygenic and multifactorial. Four main pathogenetic factors contribute to the disease:
- Sebaceous gland hyperplasia and excess sebum production. Sebaceous follicle size and number of lobules per gland are increased in patients with acne. Androgens stimulate sebaceous glands to enlarge and produce more sebum, which is most prevalent during puberty.
- Abnormal follicular differentiation. In normal follicles, keratinocytes are shed as single cells into the lumen and then excreted. In acne, keratinocytes are retained and accumulate due to their increased cohesiveness.
- Propionibacterium acnes colonisation. These gram-positive, non-motile rods are found deep in follicles and stimulate the production of pro-inflammatory mediators and lipases. While there may be increased numbers of P acnes in acne, bacterial counts often do not correlate with acne severity.
- Inflammation and immune response. Inflammatory cells and mediators efflux into the disrupted follicle, leading to the development of papules, pustules, nodules and cysts.
External factors occasionally contribute to acne, including mechanical trauma, cosmetics, topical corticosteroids and oral medicines (corticosteroids, lithium, iodides, some antiepileptics). Endocrine disorders (such as polycystic ovary disorder) can also be involved.
How does this relate to treatment?
A consensus recommends that treatment of acne should target at many of the pathogenic factors as possible.