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What Is Acne?

An Introduction to How Acne Is Formed and the Different Types

Last updated: August 23, 2018

Article Summary

Acne lesions are caused when a skin pore gets clogged, skin oil builds up inside the pore, and bacteria feeds on the skin oil and multiplies. All acne starts as a clogged pore, which can then develop into acne that falls into two categories: (1) non-inflammatory and (2) inflammatory. Non-inflammatory acne includes whiteheads and blackheads. Inflammatory acne includes papules, pustules, nodules, and cysts.

Human skin, especially on the face, neck, back, and chest, is covered in hundreds of thousands of microscopic hair follicles, often called pores.

For reasons no one completely understands, these follicles sometimes overproduce cells and become blocked. Sebum (skin oil) which normally drains to the surface gets trapped and bacteria begins to grow.1, 2-11

The Sebaceous Follicle
All acne lesions start out as a microcomedone.1,12-13

Early Stages of Clogged Pore Development: Microcomedone


Non-inflammatory Acne

Microcomedones can spontaneously become unplugged and heal or they become non-inflamed skin blemishes called comedones – either a whitehead or a blackhead.12-13

Whitehead. When the trapped sebum and bacteria stay below the skin surface, a whitehead is formed. Whiteheads may show up as tiny white spots or they may be so small that they are invisible to the naked eye.1,13

Clogged Pore Development: Comedone (Whitehead)
Blackhead. A blackhead occurs when the pore opens to the surface and the sebum, which contains the skin pigment melanin, oxidizes and turns a brown/black color. It is not dirt and cannot be washed away. Blackheads can last for a long time because the contents very slowly drain to the surface.1,13

Clogged Pore Development: Open Comedone (Blackhead)


Inflammatory Acne

A blackhead or whitehead can release its contents to the surface and heal or the follicle wall can rupture and inflammatory acne can ensue. This rupture can be caused by random occurrence or by picking or touching the skin. This is why it is important to leave acne-prone skin relatively untouched.1,12-13

Papule.papule occurs when there is a break in the follicular wall. White blood cells rush in and the pore becomes inflamed.13

Pustule.pustule forms several days later when white blood cells make their way to the surface of the skin. This is what people usually refer to as a "zit" or a "pimple."13

Inflamed Acne: Papules and Pustules
A papule or pustule can completely collapse or explode, severely inflaming the surrounding skin and may engulf neighboring follicles. These lesions are called nodules or cysts.1,13

Rupture of Follicular Wall
Nodule. When a follicle breaks along the bottom, total collapse can occur, causing a large, inflamed bump that can be sore to the touch.13

Severe Acne: Nodules
Cyst. Sometimes a severe inflammatory reaction can result in very large pus-filled lesions.1,13

Severe Acne: Cysts

The Experts at Acne.org

Our team of medical doctors, biology & chemistry PhDs, and acne experts work hand-in-hand with Dan (Acne.org founder) to provide the most complete information on all things acne. If you find any errors in this article, kindly use this Feedback Form and let us know.

References:

  1. Questions and Answers About Acne. National Institute of Arthritis and Musculoskeletal and Skin Diseases Jan. 2006. National Institutes of Health (2001).
  2. Kligman, A. M. & Plewig, G. Acne and Rosacea (Springer, Berlin, 2000).
  3. Bek-Thomsen, M., Lomholt, H. B. & Kilian, M. Acne is not associated with yet-uncultured bacteria. J. Clin. Microbiol. 46, 3355-3360 (2008).
  4. Zouboulis, C. C. Propionibacterium acnes and sebaceous lipogenesis: A love-hate relationship? J. Invest. Dermatol. 129, 2093-2096 (2009).
  5. Pappas, A., Johnsen, S., Liu, J. C. & Eisinger, M. Sebum analysis of individuals with and without acne. Dermatoendocrinol. 1, 157-161 (2009).
  6. Akaza N, et al. Effects of Propionibacterium acnes on various mRNA expression levels in normal human epidermal keratinocytes in vitro. J. Dermatol. 36, 213-223 (2008).
  7. Picardo, M., Ottaviani, M., Camera, E., & Mastrofrancesco, A. Sebaceous gland lipids. Dermatoendocrinol. 1, 68-71 (2009).
  8. Pappas, A. Epidermal surface lipids. Dermatoendocrinol. 1, 72-76 (2009).
  9. Youn, S. W. The role of facial sebum secretion in acne pathogenesis: Facts and controversies. Clin. Dermatol. 28, 8-11 (2010).
  10. Dessinioti, C. & Katsambas, A. D. The role of Propionibacterium acnes in acne pathogenesis: Facts and controversies.Clin. Dermatol. 28, 2-7 (2010).
  11. Makrantonaki, E., Ganceviciene, R. & Zouboulis, C. C. An update on the role of the sebaceous gland in the pathogenesis of acne. Dermatoendocrinol. 3, 41-49 (2011).
  12. Bettoli, V., Layton, A. M. & Thiboutot, D. Fast Facts-Acne (HealthPress Limited, Oxford, UK, 2004).
  13. Fry, L. The Encyclopedia of Visual Medicine Series: An Atlas of Dermatology (The Parthenon Publishing Group,  New York,1997).

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