The skin on the face and upper body contain more and larger skin oil glands compared with other parts of the body, and these glands produce more skin oil than elsewhere on the body. More skin oil normally leads to more acne. Also, higher amounts of androgens (male hormones that are present in both males and females) in the skin of acne-prone areas such as the face and upper body may further contribute to the development of acne.
Some areas of the skin are more prone to acne than the skin on the rest of the body. These include:
- Upper back
- Upper arms
There are a few biological reasons that these parts of the body are more prone to acne:1-16
- More and larger sebaceous glands (skin oil glands): Increased production of skin oil usually means more acne, and acne-prone parts of the body are abundant in sebaceous glands.1-5
- Hormones: Higher amounts of androgen hormones (male hormones that are present in both males and females) in the skin result in more acne. Acne-prone individuals, both males and females, often have higher amounts of androgens.6
- Bacteria: Acne-prone skin is more likely to foster high levels of bacteria, specifically a type of bacteria called P. acnes, which exacerbates acne.7
- Skin cells: When skin cells are over-produced, they tend to clog the pore.8
- Inflammation: Acne is an inflammatory disease. The skin cells lining the pores of acne-prone skin become inflamed easily.9
Structure of the Skin
To understand why certain areas of skin are prone to developing acne, let’s begin with a quick review of the skin’s structure. The skin covering the human body is made of three layers. The outer layer is called the epidermis; the middle layer is called the dermis, and the deepest layer is called the hypodermis.15,16
Now let’s look at the biological reasons that some areas of skin are more prone than others.
Sebaceous (Skin Oil) Glands
The middle layer of the skin, the dermis, contains sebaceous glands. These glands produce sebum, an oily substance that helps protect the skin from bacteria and sun exposure, aids in wound healing, transports antioxidants to the skin, and helps to regulate moisture levels in the skin.2Sebaceous glands exist in most areas of skin on the body but are found in highest concentrations on the face, forehead, and on the scalp. They are also more numerous on the upper body, where acne commonly forms. The area with the highest concentration is the t-zone, which is on the face and includes the forehead, the bridge of the nose, and the fold between the nose and the lips. There are many sebaceous glands in the t-zone—as many as 400 to 900 glands per square cm!1-3
Research shows that most individuals with acne have larger sebaceous glands and higher sebum production on their facial skin than individuals without acne.3 Scientists don’t fully understand the role of sebum in acne formation. However, scientists currently hypothesize that the sebum produced by sebaceous glands increases inflammation around pores, leading to acne lesions.4
In addition to enlarged sebaceous glands in acne-prone areas of the skin, it is possible that the composition of sebum produced by acne-affected skin is different from that which is produced by non-acne-affected skin. One study found that skin with acne produces sebum containing a larger amount of certain fats and oils compared to skin without acne.5
A 1970 study published in the Journal of Investigative Dermatology examined 65 specimens of sebum from the face, neck, chest, and backs of men and women with acne. The authors confirmed a difference in composition, demonstrating that sebum from skin with acne has more substances called free fatty acids and triglycerides.5
While circulating androgen hormones in the blood are important for acne formation, and people with acne tend to have elevated levels of circulating androgen hormones, this is not the entire story. Androgen hormones can also reside in the skin, and acne-prone skin areas also tend to contain higher amounts of androgens.
Early studies demonstrated that androgens, such as testosterone, impact acne formation. However, androgen levels in the blood don’t appear to tell the full story, and they don’t always correlate with the severity of acne.6 An article in the American Journal of Epidemiology shows us that it is not just hormone levels in the blood that are completely responsible for acne formation:
As researchers from a study published in 2005 in the American Journal of Epidemiology explain, “It is not clear why acne spontaneously improves and disappears in most people. While acne recedes in late adolescence, androgen levels remain high until late adulthood, indicating that androgens alone cannot be responsible for the presence of acne.”7
Scientists hypothesize that one important factor is the way skin interacts with androgens in the bloodstream. The skin has enzymes that convert androgens in the blood to forms of the hormone that are active in the skin. An example of one of these hormones is dihydrotestosterone (DHT). DHT attaches itself to receptors in the sebaceous glands, causing them to enlarge and increase sebum production.8-11 Increased sebum production is then associated with acne. A 1971 study describes this process.10
In a 1971 study published in the Journal of Investigative Dermatology, researchers examined skin specimens taken from 32 individuals. Samples were taken from individuals with and without acne and from affected and unaffected skin. The results showed that skin with acne produced 2 to 20 times more DHT than normal skin. The study showed also that the rate at which the skin created DHT from the androgen, testosterone, in the bloodstream differed depending on the location of the skin. The face and the upper back—common locations for acne—converted testosterone to DHT at higher rates than skin on other parts of the body. These results suggest that skin exhibits acne-prone characteristics because of the rates at which it processes androgens in the bloodstream.10
Normal skin contains a variety of microorganisms, such as bacteria. The type and amount varies based on skin characteristics. As we have learned, acne-prone skin areas, such as the face, neck, and upper back, have a high density of sebaceous glands and produce more sebum. For this reason, these areas tend to host organisms that can feed on sebum. An example of such an organism is P. acnes, the bacteria known to contribute to the characteristic redness and soreness of acne. In fact, P. acnes is the dominant bacteria in acne-prone skin areas where there is a high density of sebaceous glands.12
When skin cells are over-produced and fail to shed from the skin as they should, they can clog the pore and contribute to acne formation. This tends to happen more in the pores of acne-prone skin areas.
The stratum corneum is the outermost layer of skin—the topmost layer of the epidermis. The purpose of the stratum corneum is to form a barrier to protect underlying tissue from infection, dehydration, chemicals, and abrasion. It is made of dead skin cells called corneocytes, which start out as live cells called keratinocytes that are formed at the base of the skin. These keratinocytes slowly move up toward the surface and die, becoming corneocytes, and eventually shed off in a process called desquamation.
In normal skin, it takes about 2 weeks for keratinocytes to form, move up into the stratum corneum, and shed from the skin. However, skin cells are over-produced in acne-prone skin areas, and it can take twice as long for these cells to reach the surface and shed. This slowdown can clog pores and cause acne to form.13
Scientists believe that acne is, at its core, an inflammatory disease. Research shows that inflammation associated with an immune substance called interleukin-1 may be central to the development of acne.
A recent study found that acne-prone areas of the skin may be more sensitive to interleukin-1 than other areas of the skin and may therefore be more likely to develop inflammation and acne.14
In a 2013 study published in The Journal of Clinical and Aesthetic Dermatology, researchers looked at the number of interleukin-1 receptors in the skin on different parts of the body. The results showed that the epidermis of the face and upper arms had elevated levels of interleukin-1 receptors. This may help to explain why these acne-prone areas of the skin may be more easily inflamed and more likely to develop acne.14
As this article highlighted, the face and upper body are more prone to acne because of several factors occurring on those areas of the skin. These factors include: (1) more and larger sebaceous glands, (2) higher levels of androgens, (3) elevated levels of the P. acnes bacteria, (4) improper production and maturation of skin cells, and (5) the susceptibility of pores to inflammation.
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- Ebling, F. J. The sebaceous glands. J. Soc. Cosmetic Chemist. 16, 405-411 (1965).
- Makrantonaki, E., Ganceviciene, R. & Zouboulis, C. An update on the role of the sebaceous gland in the pathogenesis of acne. Dermatoendocrinol. 3, 41–49 (2011).
- Thiboutot, D. & Del Rosso, J. Q. Acne Vulgaris and the Epidermal Barrier: Is Acne Vulgaris Associated with Inherent Epidermal Abnormalities that Cause Impairment of Barrier Functions? Do Any Topical Acne Therapies Alter the Structural and/or Functional Integrity of the Epidermal Barrier? J. Clin. Aesthet. Dermatol. 6, 18–24 (2013).
- Kellum, R. E. & Strangfeld, K. Acne vulgaris. Studies in pathogenesis: fatty acids of human surface triglycerides from patients with and without acne. J. Invest. Dermatol. 58, 315–318 (1972).
- Nicolaides, N., Ansari, M. N., Fu, H. C. & Lindsay, D. G. Lipid Composition of Comedones Compared With That of Human Skin Surface in Acne Patients. J. Invest. Dermatol. 54, 487–495 (1970).
- Shaw, J. C. Acne: effect of hormones on pathogenesis and management. Am. J. Clin. Dermatol. 3, 571–578 (2002).
- Galobardes, B., Davey Smith, G., Jeffreys, M., Kinra, S. & McCarron, P. Acne in adolescence and cause-specific mortality: lower coronary heart disease but higher prostate cancer mortality: the Glasgow Alumni Cohort Study. Am. J. Epidemiol. 161, 1094–1101 (2005).
- Ebede, T. L., Arch, E. L. & Berson, D. Hormonal treatment of acne in women. J. Clin. Aesthet. Dermatol. 2, 16–22 (2009).
- Knutson, D. D. Ultrastructural observations in acne vulgaris: the normal sebaceous follicle and acne lesions. J. Invest. Dermatol. 62, 288–307 (1974).
- Sansone, G. & Reisner, R. M. Differential rates of conversion of testosterone to dihydrotestosterone in acne and in normal human skin--a possible pathogenic factor in acne. J. Invest. Dermatol. 56, 366–372 (1971).
- Blauer, M. et al. Location of androgen receptor in human skin. J. Invest. Dermatol. 97, 264–268 (1991).
- Grice, E. A. & Segre, J. A. The skin microbiome. Nat. Rev. Microbiol. 9, 244–253 (2011).
- Tagami, H. Location-related differences in structure and function of the stratum corneum with special emphasis on those of the facial skin. Int. J. Cosmet. Sci. 30, 413–434 (2008).
- Tanghetti, E. A. The role of inflammation in the pathology of acne. J. Clin. Aesthet. Dermatol. 6, 27–35 (2013).
- Arda, O., Goksugur, N. & Tuzun, Y. Basic histological structure and functions of facial skin. Clin. Dermatol. 32, 3–13 (2014).
- Amirlak, B. Skin anatomy. <https://emedicine.medscape.com/article/1294744/-overview>.