We will be starting our series on acne and today’s post is on Acne 101 AKA general information. We’ll cover papules, comedones, treatments, etc in the subsequent posts. This series will include photos, so please be prepared!
What is acne?
Acne or acne vulgaris is a self-limiting skin disease of the pilosebaceous unit (the hair follicle and the accompanying sebaceous gland). It presents as comedones, papules, pustules, and nodules with varying extent and severity. Although the acne is self-limiting, it can be a lifelong (*sob*) process with formation of scarring
What causes acne?
a. Follicular epidermal hyperproliferation
Follicular epidermal hyperproliferation means that the thin tissue (epithelium) of the upper hair follicle (known as the infundibulum) becomes hyperkeratotic.
TIME OUT – SKIN 101
So I decided not to write a skin 101 series (yet) because there is already a great guide available here. For completeness sake, I will create a skin 101 series in the future, but I felt that since there was already some great information out there, I didn’t want to re-create the wheel (yet). But please feel free to read through the basics guide first to have a better understanding of how your skin works!
Hyperkeratotic. What does that mean?
So the outermost layer of your skin, the epidermis is made up of a few different types of cells. The most common type of cell in your epidermis are called keratinocytes. So hyperkeratotic means there’s an excess (hyper) amount of keratinocytes (keratotic).
So if you take a look at the above picture section A. We can see the keratinocytes are getting clumped together in the upper part of the hair follicle near the epithelial tissue. The keratinocytes stick together and results in a plug. This plugging of the hair follicle causes sebum, bacteria, and keratin (a protein that protects the epithelial cells from damage or stress) to accumulate in the follicle producing what’s known as a “microcomedone”
The reason for the increase in keratinocytes and why they stick together and cause follicular epidermal hyperproliferation is unknown, but they do have a couple theories:
- Androgen stimulation
- Androgens are a group of hormones that primarily influence the growth and development of the male reproductive system
- These hormones can play a role in increased sebum production (bullet b) and can also increase the amount of keratinocytes in the hair follicle because these hormones have an effect on the sebaceous gland
- To further prove their point that androgens can cause acne, they’ve found that people with complete androgen insensitivity do not develop acne (lucky ducks!)
- Decreased linoleic acid
- Linoleic acid is an essential fatty acid in the skin
- They have found that people with acne have lower levels of linoleic acid and it is proposed that these lower levels cause follicular keratinocyte hyperproliferation as well as inflammation
- Increased interleukin-1-alpha activity
- Interleukin-1-alpha is a type of protein that your cells produce in order to communicate with other cells (cool, right?) and is responsible for regulating your immune response, inflammatory reactions, and creating new blood cells
- Unfortunately, they believe that an increase in interleukin-1-alpha can cause follicular keratinocyte hyperproliferation
- Effects of Propionibacterium acnes (P. acnes)
- See subsequent bullet points to understand how these
devilsbacteria affect your skin and can cause acne
- See subsequent bullet points to understand how these
b. Excess sebum production
Sebum is the oily secretion of the sebaceous glands (a small gland found in the hair follicle). Aside from ruining lives by causing acne, sebum serves its purpose by lubricating the skin and hair. So honestly, sebum is good because it’s our body’s natural moisturizer. 🙂
However, people with acne produce more sebum than those without acne. Sebum is made up of triglycerides and lipoperoxides. The triglyceride component is broken down into free fatty acids by P. acnes and unfortunately these free fatty acids further increase the amount of bacteria on your skin and cause them to clump together which can promote inflammation and may cause formation of a comedone.
The microcomedone that we saw earlier can also turn into a comedone as the infundibulum continues to expand due to all the keratin, sebum, and bacteria being packed into it which will then eventually rupture. This rupturing of the microcomedone to become a comedone also causes an inflammatory response since all the bacteria, sebum, and keratin have broken free into the dermis (yuck).
We’ve already started talking about inflammation in point B. And aside from the mechanisms of inflammation we’ve already talked about, there’s unfortunately a whole host of other ways your body can freak out and cause inflammation further wreaking havoc on your skin.
We won’t go through all the other mechanisms of inflammation because it involves talking more about different interleukins, tumor necrosis factor, la dee da that doesn’t need to be covered.
Bottom line: inflammation promotes acne. People with acne have higher inflammatory markers in their skin than people who don’t have acne. Section C and D in the figure shows that further inflammation causes increased rupture, damage to the skin, and these later stages are called papules, postules, and nodules.
d. Propionibacterium acnes
P. acnes is a gram-positive anaerobic (lives without oxygen!) and microaerobic (lives with a bit of oxygen) bacteria found in the sebaceous follicle. Essentially, it prefers no oxygen (anaerobic) but can tolerate some oxygen.
Of course as with the other sections we’ve read so far, people with acne have higher concentrations of P. acnes compared to those without acne. Section b already covers P. acnes.
Bottom line: P. acnes causes inflammation and can also be part of the mess of stuff (bacteria, keratin, and sebum) that gets stuck under the “plug” of keratinocytes in the hair follicle.
NOTE: any of these four causes can be interrelated and can be influenced by your hormones or immune system
Can your diet cause acne?
The medical world says maybe, but more research is needed on this subject. The theory is that carbohydrates, sugars, and diary increase insulin-like growth factor (IGF)-1 which has proacne effects and also increases androgen activity.
Diet and acne deserves its own blog post as there are a couple studies that I would like to read through before presenting this information and accepting a new mantra of NO CHOCOLATE! NO SUGAR! NO MILK! (like that would ever happen anyway). I also would need to explain what IGF-1 is and that will be for another day.
Questions? Ask in the comments!
Reference: Fitzpatrick’s Dermatology in General Medicine 8th Edition. Chapter 80: Acne Vulgaris and Acneiform Eruptions