Acne Information
and Treatment

Understanding Acne

Acne vulgaris is a very common skin disorder that affects most people at some point before their 21st birthday.[1] The disease often persists, and sometimes arises in, adulthood, affecting over half of adult women and nearly half of men.[2] However, only 3% of adults have a significant degree of acne.[2]

Aside from the possibility of physical scarring, acne also has psychological consequences, such as depression and anxiety, and can result in lower self-esteem and social withdrawal.[3,4] It may also result in decreased employability in adulthood.[3,4] Acne, therefore, is an affliction that should be taken seriously.

The purpose of this page is to provide a summary of what is currently known about acne. Unfortunately, for all that is known, much remains unknown. Nonetheless, because the subject is clouded with lore and misconceptions, this page may provide some perspective.

Where Acne Begins: The Sebaceous Follicles

A discussion of acne requires a basic introduction to its home--sebaceous follicles. These are specialized follicles, not normal hair or beard follicles, though they do contain a very small hair. People have literally thousands of sebaceous follicles, and they are located primarily on the face and trunk. Very basically, and as relevant here, sebaceous follicles consist of a duct, near the bottom of which are glands, called sebaceous glands, that release an oil called sebum into the duct. The other end of the duct opens to the surface of the skin. When functioning normally, the sebum travels up through the duct onto the skin's surface.[5]

The sebum(oil)produced by the sebaceous glands consists largely of triglycerides and free fatty acids.[7,9] A few types of organisms live within sebum. The most prominent is Proprionibacterium acnes, or P.acnes, which is a bacteria generally referred to as anaerobic (living without oxygen), though they are capable of surviving in the presence of oxygen, so they are sometimes called semi-anaerobic.[3,6] Another semi-anaerobic propionibacteria, called P.granulosum, also resides in sebum, as do aerobic bacteria, staphylococci and micrococci,as well as lipholyic yeasts.[3]

The wall of the sebaceous follicle duct contains keratinized cells, which are constantly cycling, with new cells replacing old ones, and the old, dead cells being discarded into the sebum.[5] Keratin is a hard, protein-rich substance also found in hair and fingernails.

How Acne Forms

Acne results from a number of factors, though the exact causes of these factors and the mechanisms by which they interact are not entirely clear. The basic factors are abnormal keratinization in the walls of sebaceous follicle duct, sebum production, and the colonization of P.acnes. A combination of these factors affect the process of acne formation, which occurs in stages.[5]

The first stage is the microcomedone, which is essentially a clog of the sebaceous follicle duct. This is generally tied to abnormal keratinization of the skin cells in the duct wall.[4] Instead of keratinized skin cells being shed in small pieces, they break off in larger sheets. The mixture of these keratin sheets, sebum, and bacteria ultimately leads to a comedone. It's unclear what causes abnormal keratinization in the ducts. P.acnes may play a role in instigating this process,[10,3] since antibacterial treatments reduce the number of comedones.[3]

Below a comedone, sebum becomes trapped in the duct. This creates an anaerobic environment ideal for P.acnes to proliferate. The accumulation of sebum and bacteria may cause the duct to balloon below the comedone, and the ductal wall may break down and eventually rupture, exposing the bacteria-laden sebum directly to surrounding skin tissue.[5]

Multiple contents of the duct, particularly keratin and P.acnes may induce immune responses.[6,11] This is key to acne inflammation, as white blood cells swarm to the area and, figuratively speaking, create a warzone, which manifests itself with redness and pus. While debatable, P.acnes are widely suspected as the primary inducer of inflammation.[3,6]

What Causes Acne

The factors generally understood to precipitate acne are described above. However, the cause(s) of these factors are not fully known.

Perhaps the central cause is excess sebum production.[5] Sebum provides the environment for P.acnes, and both sebum and P.acnes may affect keratinization of the ductal wall.[12] Acne sufferers generally have larger sebaceous glands than persons without acne, and those glands produce more sebum.[5, 16]. However, sebaceous glands do not act uniformly, with individual glands functioning at different times and producing sebum at different rates.[16]

Just as sebum is necessary to the production of acne, androgens (male hormones such as testosterone found in both men and women) are necessary to sebum production.[6] This is why acne onsets around puberty, when androgen levels increase.[13]. However, acne sufferers, as a group, do not have higher androgen levels in their blood than persons without acne. That said, individuals with elevated androgen levels often suffer from acne.[13] While acne suffers do not have higher androgen levels, androgens may nevertheless play a role in excessive sebum production, and hence, acne. This may be due to local (sebaceous follicle) metabolism of androgens or possibly hypersensitivity to androgens.[8]

Regarding androgen metabolism, a substance called Type 1 5α-reductase may affect androgen metabolism in acne-prone skin, increasing the severity of acne.[8] This 5α-reductase converts testosterone into a more potent androgen called dihydrotestosterone, or DHT.[3] Keratin cells and sebaceous glands both have androgen receptors that react to both testosterone and dihydrotestosterone.[13] It is theorized that the more potent dihydrotesterone may stimulate excessive sebum production by the sebaceous glands in acne sufferers. It may also affect the characteristics of keratin and the ductal wall.[14]

Another potential "cause" of acne is acne sufferers being hypersensitive to P.acnes, though this is more particularly tied to inflammation. As mentioned above, P.acnes can induce immune responses resulting in inflammation. Inflammatory acne sufferers have higher levels of P.acnes antibodies, and levels of P.acnes antibodies correlate with the level of inflammation.[15]

The general theory is that acne sufferers' bodies react differently to P.acnes. Specifically, their immune system's reaction to P.acnes is more significant than non-acne-sufferers', leading to the inflammation that is associated with the most distressing manifestations of acne (pustules, papules, & nodules) and ultimately scarring.[6,]

References:

1. Smithard A, Glazebrook C, Williams HC. Acne prevalence, knowledge about acne and psychological morbidity in mid-adolescence: a community-based study. Br. J. Dermatol. 2001;145(2):274-79.
2. Goulden V, Stables GI, Cunliffe WJ. Prevalence of facial acne in adults. J Am Acad Dermatol. 1999; 41(4):577-80
3. Gollnick H. Current Concepts of the pathogenesis of acne: implications for treatment. Drugs. 2003;63(15)1579-96.
4. Oberemok SS, Shalita AR. Acne Vulgaris, I: pathogenesis and diagnosis. Cutis. 2002;70(2):101-05.
5. Kligman AM, An overview of acne. J. Invest Dermatol. 1974;62(3):268-87.
6. Webster GF, Inflammation in Acne Vulgaris, 1995;33(2):247-53
7. Cotterill JA, Cunliffe WJ, Williamson B, Buluso L, Age and Sex Variation in Skin Survace Lipid Composition and Sebum Secretion Rate. Br. J. Dermatol. 1972;87:333-40.
8. Leyden JJ. Therapy for acne vulgaris. N Engl J Med. 1997;336(16):1156-62
9. Nikkari T. Comparative chemistry of sebum. J Invest Dermatol. 1974; 62(3):257-67.
10. Cunliffe WJ. Acne Vulgaris: pathogenesis and treatment. Br. Med J. 1980;280:1394-96.
11. Norris JF, Cunliffe WJ. A histological and immunocytochemical study of early acne lesions. Br. J. Dermatol. 1988; 118(5):651-59
12. Lavker RM, Leyden JJ, McGinley KJ. The relationship between bacteria and the abnormal follicular keratinization in acne vulgaris. J. Invest Dermatol. 1981;77(3)325-30
13. Shaw JC. Acne: Effect of hormones on pathogenesis and management. Am J Clin Dermatol. 2002;3(8):571-78.
14. Sansone G, Reisner RM. Differential rates of conversion of testosterone to dihydrotestosterone in acne and in normal human skin--a possible pathogenic factor in acne vulgaris. J Invest Dermatol. 1971;56(5):366-72
15. Webster GF. Inflammatory acne represents hypersensitivity to Propionibacterium acnes. Dermatology. 1998;196(1):80-81.
16. Plewig G. Acne Vulgaris: Proliferative cells in sebaceous glands. Br J Dermatol. 1974;90(6):623-30.