Acne In-depth: How Dead Skin Cell Accumulation Can Lead to Acne
The Production of Too Many New Skin Cells Results in Dead Skin Cell Accumulation and A Clogged Pore
The Essential Information
Skin cells play an important role in the formation of acne.
Healthy Skin: In healthy skin, the body produces just the right number of skin cells. Once these skin cells grow old, they shed from the skin.
Acne-prone Skin: In acne, skin cells are over-produced. And when these skin cells get old, they tend to stick together, resulting in an accumulation of dead skin cells inside pores, which clogs the pore.
The skin renewal process of healthy skin goes awry in acne-prone skin, leading to clogged pores. Here's how:
Healthy Skin: In healthy skin, new skin cells (called keratinocytes) are constantly being produced in the deepest layers of the skin. As these skin cells age, they move towards the surface of the skin. Over the course of a couple of weeks, these skin cells will die (then called corneocytes). The corneocytes remain in the skin's pores for a few weeks before shedding from the pore.1
Acne-prone Skin: In acne-prone skin, the skin cell renewal process does not occur as it should. Skin cells are produced too fast, about 1.5 times as fast as in healthy skin.2 These skin cells are also stickier than they should be because they contain too much of a sticky protein called keratin. Once these skin cells die, the sticky keratin keeps them stuck together and they do not shed from the skin as they should, instead accumulating inside skin pores. This accumulation gives rise to clogged pores, which can develop into full-fledged acne lesions.
This article will explore each of these two causes of skin cell accumulation in more detail. First, let's examine what causes the production of excess skin cells.
What Causes the Overproduction of Skin Cells?
There are three main factors that may stimulate the production of new skin cells.
- Increase in skin oil (sebum): Acne-prone skin produces too much skin oil, called sebum, which is thought to stimulate skin cell production.
- Different makeup of sebum: Sebum is made of a mixture of lipids (oils, waxes, and fatty acids). One main lipid present in sebum, called linoleic acid, seems to be lower in people with acne-prone skin. The low levels of linoleic acid in acne-prone skin may lead to the production of more skin cells.
- Increase in bacteria: A strain of bacteria found in acne lesions, called P. acnes, grows inside clogged pores and feeds on sebum. It is thought that the presence of too many P. acnes bacteria can trigger the production of more skin cells. However, it is important to note that this factor differs from the other two factors since the P. acnes bacteria only triggers the production of new skin cells after a pore has already clogged. Because P. acnes triggers the production of new keratinocytes after a clogged pore is formed, it is thought that this may strengthen the clog in an existing clogged pore and worsen the acne lesion.2-5
Once there are too many cells, the other problem is that these cells stick together and don't shed as they should. Let's look next at what causes skin cells to stick together.
What Causes Skin Cells to Stick to Each Other?
In healthy skin, skin cells don't stick together inside the pore, but in acne-prone skin, two main factors cause this to happen.
- Increase in keratin: In acne-prone skin, there is more of a sticky protein called keratin in the skin. The abundance of keratin makes the skin stickier, which results in dead skin cells sticking together inside the pore.
- Increase in bacteria: When the P. acnes grows inside the pore, it produces a sticky film all its own that further leads to skin cells sticking together instead of shedding as they should.2,3
In healthy skin, the body produces just enough skin cells. As these skin cells die, they shed from the skin. However, acne-prone skin overproduces skin cells, and these skin cells are more likely to stick together inside a pore. This results in an accumulation of skin cells inside the pore, which clogs the pore and leads to acne.
- Aldana, O. L., Holland, D. B. & Cunliffe, W. J. Variation in pilosebaceous duct keratinocyte proliferation in acne patients. Dermatology 196, 98 - 99 (1998). https://www.ncbi.nlm.nih.gov/pubmed/9557240
- Knaggs, H. E., Holland, D. B., Morris, C., Wood, E. J. & Cunliffe, W. J. Quantification of cellular proliferation in acne using the monoclonal antibody Ki-67. J Invest Dermatol 102, 89 - 92 (1994). https://www.ncbi.nlm.nih.gov/pubmed/8288915
- Das, S. & Reynolds, R. V. Recent advances in acne pathogenesis: implications for therapy. Am J Clin Dermatol 15, 479 - 488 (2014). https://www.ncbi.nlm.nih.gov/pubmed/25388823
- 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). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051853/
- Duckney, P. et al. The role of the skin barrier in modulating the effects of common skin microbial species on the inflammation, differentiation and proliferation status of epidermal keratinocytes. BMC Res Notes 6, 474 (2013). https://www.ncbi.nlm.nih.gov/pubmed/24245826