The Science of Acne: Understanding What’s Going On In the Skin

 

by

Michael H. Berkson, M.D.

 

Even though it can be complicated, understanding a bit about the science of what’s happening at the microscopic level in the skin of people with acne can help explain the corresponding changes that are seen on the skin surface in the various phases and forms of acne.  Basic insight into the science also sheds light on the ways in which the various acne treatments have a beneficial effect and which treatments are likely to yield the best results depending on the type and severity of acne.

 

The anatomic site of acne is the pilosebaceous  follicle. “Pilo” means hair and sebaceous refers to an oil called sebum which is produced by the sebaceous gland. The pilosebaceous follicle is actually a large hair follicle that produces a small, often invisible hair.  The sebaceous gland connects to the follicle thru a duct through which the sebum produced by the sebaceous gland is secreted into the follicle.

The production of sebum is triggered by androgen hormones that act on receptors on the surface of the sebaceous gland. Sebum has a several functions, the most important of which is to help prevent water loss from the epidermis.  Pilosebaceous follicles are most numerous on the face, neck, and upper torso which are the same areas where acne tends to occur.

There are four major pathophysiological factors involved in the pathway that leads to acne including increased sebum production, comedogenesis, proliferation of bacteria within the pilosebaceous follicle, and inflammation.

 

Increased Sebum Production

 

Sebum production begins in earnest in prepubescent children at adrenarche, a developmental stage during which androgen hormones such as DHEAS start being produced by the adrenal glands.  Later, at the beginning of puberty, another androgen, testosterone is produced by the testicles and ovaries. The circulating androgens then get converted to dihydrotestosterone (DHT) which interacts with special receptors on the sebaceous glands, causing the sebaceous glands to enlarge and begin producing sebum which accumulates in the sebaceous follicle.

Although sebum is not the cause of acne, and the amount of sebum produced does not correlate with the severity of acne, sebum production is a necessary prerequisite for the development of acne.

 

 Comedogenesis

 

Comedogenesis refers to a process that occurs in the lumen of the sebaceous follicle.  The lumen is a tunnel like structure that originates from the depths of the follicle and opens as a pore at the surface of the epidermis. During comedogenesis, the cells that line the lumen of the sebaceous follicle begin to turnover (replicate) at an abnormally high rate. These cells are unusually sticky and tend to aggregate together forming an impaction (blockage) above the level where the sebaceous duct enters the lumen of the follicle. The follicle enlarges and dilates below the blockage resulting in a microcomedone.  If the process continues, the microcomedone can enlarge to the point where it becomes visible.

Closed comedones, or whitetheads, appear as small flesh colored bumps. Open comedones, or blackheads, appear as flesh colored bumps with a dark central opening. The dark part of the blackhead is composed of oxidized epithelial cells and melanin (pigment) that are trapped in the upper part of the follicle. Contrary to a popular misconception, blackheads do not result from trapped dirt from the outside. Microcomedones, and less frequently closed comedones can sometimes progress to inflammatory acne lesions such as papules and pustules (pimples) and nodules. Although many of the factors that cause comedogenesis are still unknown, there is now good evidence that inflammation can start and promote the process.

 

Bacterial Growth and Proliferation

 

As sebum production ensues, the sebaceous follicle becomes colonized by several types of bacteria that normally inhabit the skin.  Propionibacteria acnes ( P. acnes), which has recently been renamed Cutibacterium acnes, is one such bacteria.  P. acnes thrives in the sebum rich environment of the sebaceous follicle.  The comedone creates an oxygen poor environment which is even more conducive to the growth of P. acnes.  Among other things, the presence of large numbers of P. acnes within the sebaceous follicle elicits a potent immune response which in turn triggers inflammation.

 

Inflammation

 

Inflammation is perhaps the most important factor in the acne pathway.  Inflammation in acne is mediated by the immune system. Specifically white blood cells and other immune cells that produce chemicals called cytokines stimulate increased blood flow resulting in edema ( swelling) in and around the sebaceous follicle and an influx of more inflammatory cells and cytokines.  All of this action results in the formation of more comedones as well as the inflammatory lesions of acne including papules, pustules and nodules. The inflammatory response in acne is complex and can be triggered by a number of factors including sebum and the immune response to the P. acnes bacteria that are present within the sebaceous follicle.

 

This basic understanding of what’s happening in the skin of people with acne will now allow a better appreciation for what’s happening on the surface of the skin.

 

 

References:

 

From pathogenesis of acne vulgaris to anti-acne agents.  Cong TX, Hao D, Wen X, Li XH, He G, Jiang X.  Arch Dermatol Res. 2019 Mar 11

Acne vulgaris.  Williams HC, Dellavalle RP, Garner S.   Lancet. 2012 Jan 28;379(9813):361-72.

The evolution of healthy skin to acne lesions: a longitudinal, in vivo evaluation with reflectance confocal microscopy and optical coherence tomography.  Manfredini M, Bettoli V, Sacripanti G, Farnetani F, Bigi L, Puviani M, Corazza M, Pellacani G.  J Eur Acad Dermatol Venereol. 2019 Apr 26.

Recent advances in acne pathogenesis:  Implications for therapy.  Das S, Reynolds RV.  Am J Clin Dermatol. 2014 Dec;15(6):479-88.

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