Acne Lesions

Ah, the pimple. It’s the bane of many a school picture and wedding day. Pimples help keep photo retouchers in business. But for many people, pimples aren’t simple nuisances that pop up at inopportune times. Instead, they’re a daily reminder that seemingly uncontrollable forces are at work in the skin.

I outline the events that are required to make acne lesions. (A lesion is dermatologist lingo for any abnormality or mark of the skin. A pimple is a lesion. A blackhead is a lesion. Your nose isn’t a lesion, unless you have two of them.)

I take you through many of the conditions necessary for a lesion to form and evolve: blocked hair follicles, overworked oil glands, and bacteria. Then I help you categorize your acne in order to understand when and why different treatments are used on the various types.

Paying the High Price for Oil

Acne lesions originate and mature in the hair follicle, the epicenter of our acne story. (To get a visual of what a normal, healthy follicle doing its job looks like, take a peek at Figure 1.)

Figure 1: A normal follicle.

Ultimately, in order for acne to develop, a follicle must be blocked. A blocked follicle isn’t the only condition necessary for acne to form (I detail the others in the sections that follow), but it’s a big one. So, to talk about the roots of acne, you need to go directly to the hair follicle.

Technically, the hair follicle and sebaceous gland are called the pilosebaceous unit (PSU). The hair follicle (actually the PSU) is made up of three components:

  • Sebaceous gland: This gland resembles a cluster of grapes and produces and pumps out a beneficial oily substance called sebum (pronounced see-bum) that coats and conditions the hair and skin. The oily sebum is composed of a rich blend of different lipids (fatty chemicals).

Sebum rises to the surface of your epidermis to keep your skin lubricated and protected. It also helps makes your skin waterproof. Plus, sebum helps carry dead skin cells out of the hair follicle and to the exterior skin so that the body can get rid of them.

In people with acne, there is an excessive production of sebum. Along with its producer, the sebaceous gland, its fellow cast member, the hair follicle, and its director testosterone (an important hormone), sebum plays much more than a bit part in the acne story.

  • Sebaceous duct: This tiny tube steers the sebum (and the dead skin cells it carries) from the sebaceous gland into the hair canal, the part of the follicle through which sebum travels onto the hairs before it is carried out to the exterior of your skin.
  • Hair: I’m talking about the actual hair that sprouts out of your pores (follicular orifices, or the holes in your skin that your hair grows out of). Hairs are sometimes called strands or hair shafts. Hairs are found all over our bodies; well, almost all over. There’s no hair on your palms, I hope. Hairs help carry sebum to our skin.

Hormones and acne

Hormones play a central role in the acne drama. Hormones are the body’s chemical messengers. Without hormones, you wouldn’t have acne, but you’d be in pretty bad shape, because hormones control just about every bodily function, from regulating your metabolism to ensuring that you can mature and have children.

In both males and females, a particular group of hormones, called androgens, are primarily associated with the formation of acne. The term androgen is a general term for hormones that have more masculinizing features.

Androgens are responsible for the development of secondary sex characteristics in males (facial hair, increased muscle mass, the ability to reproduce, and so on). The androgen testosterone is the main male hormone. However, if you’re female, you have androgens too, but they’re produced in smaller quantities and are much weaker than in your male counterparts.

Estrogen and progesterone are the primary female hormones that control menstrual cycles and regulate pregnancy. Both of these hormones can have an affect on acne as well — albeit less than androgens — by their periodic monthly fluctuations. The androgenic hormones help us regulate how much sebum our sebaceous glands produce.

People who get acne aren’t producing any more of these androgens than anyone else; it’s just that their sebaceous glands are very sensitive to the hormone’s message to increase production. The glands respond by pumping out excessive amounts of sebum.

Your face, chest, and back contain the highest concentrations of sebaceous glands; that’s why you’re more likely to have acne on these areas. Adolescence is generally the worst time for acne because androgens are increasing steadily during the teen years, and they signal your sebaceous glands to get larger and to generate more sebum, as shown in Figure 2.

Figure 2: The sebaceous gland overreacts to androgen stimulation.

As adolescence ends, the amount of androgen secretion diminishes and acne tends to disappear for most teens by age 18 or 19. But for various reasons some women (and much less commonly, men) retain a heightened sensitivity to their androgens and continue to have acne beyond adolescence. Some women even get acne for the first time as adults.

Hair canal

Every day, millions of skin cells die off. You continually make new skin cells and get rid of dead ones. Your body has ingenious ways of getting rid of these dead cells. In the case of your skin, sebum carries the dead skin cells to the outside of the body where they flake off.

Sometimes, though, as sebum ferries dead cells from the inside of your hair follicle along the oily sebaceous ducts and out through the hair canal, the exit route of the follicle is blocked by the excess oil.

This blockage causes the opening of your hair canal to narrow, and your pores, the tiny openings in your skin that serve as exits for your hairs, get clogged (see Figure 3).

Figure 3: The clogging of pores and the narrowing of the hair canal.

The exit of oil is also often impeded by a process called abnormal follicular keratinization. That’s a fancy way of saying that instead of flaking off with the sebum when they reach the skin’s surface as they normally do, the dead skin cells and keratin clump together with the oil to further clog the sebaceous ducts and hair canals.

Acne is not caused by forgetting to wash the oil off, or even by eating loads of greasy French fries and junk food. It’s not the oil in your tummy or on your skin; it’s the oil in your skin.

Blackheads and whiteheads

The trapped sebum, cells, and keratin form a very sticky mixture — a real traffic jam that blocks the exit route. This plug acts just like a cork in a bottle, locking in all that stuff inside with nowhere to go, so that it can’t exit onto the surface of the skin (see Figure 4).

Figure 4: The microcomedo forms and becomes either a blackhead (A) or a whitehead (B).

The plug is called a microcomedo (pronounced my-kro-cahm-e-doe). You can’t see a microcomedo with the naked eye; it’s too small. Over time, the increasing amount of trapped sebum builds up a lot of pressure and the hair follicle blows up like a balloon and becomes a visible comedo (pronounced cahm-e-doe; the plural of comedo is comedones). There are the two types of comedones (which you can see in Figure 4):

  • Blackheads: If the comedo enlarges and pops out through the surface of the skin, the tip looks dark and it’s called a blackhead. The dark color is not due to dirt; it’s the result of a buildup of melanin, a dark pigment in the skin that turns black when exposed to oxygen in the air. Blackheads are also known as open comedones.
  • Whiteheads: If the comedo stays below the surface of the skin, it’s light in color and looks like a small whitish bump; it’s called a whitehead. Whiteheads are also called closed comedones.

Comedogenesis is the medical term for the process that forms whitehead and blackheads.

Battling bacteria

The microcomedo may develop into, and remain, a comedo. But sometimes it becomes an inflammatory lesion. Inflammation is a reaction of the skin to disease or injury; in the case of acne, the inflammation is a reaction to the bacteria known as Propionibacterium acnes.

Signs of an inflammatory lesion include swelling, redness, heat, and sometimes pain. The presence of these bacteria does not mean that poor hygiene is a cause of your acne. Here’s a list of common inflammatory acne lesions:

  • Papule: A small, firm red bump, commonly referred to as a pimple or zit. It’s made up of inflammatory blood cells and doesn’t contain obvious pus.
  • Pustule: A papule that contains pus, a whitish, goopy substance that’s really just a bunch of white blood cells. Pustules are also known as “pus pimples.”
  • Nodule: A large and often tender, lumpy, inflamed, pus-filled papule or pustule that’s lodged more deeply in the skin. The term cyst is often used interchangeably to mean “nodule” because of the resemblance of a nodular acne lesion to a cyst.

One other common acne lesion is sometimes formed late in the life cycle of a lesion from the remains of an inflammatory lesion:

  • Macule: A macule is a flat red, purple, or brown spot that forms where a papule or pustule used to be. A macule remains for a while after an acne lesion has healed or is in the process of healing. For more details on how your skin heals.

P. acnes jumps in

In order for comedones to move up the inflammation chain into a full-blown lesion, they need the help of a certain bacteria. You know how people add yeast to make a cake rise? Well, the bacterium known as Propionibacterium acnes helps make the zits rise. From now on, I just call him (or is it her?) P. acnes, for short. P. acnes is an anaerobe.

That means that it prefers to live in areas that have very little oxygen such as in the low oxygen environment that exists in a hair follicle. P. acnes generally minds its own business.

These usually “friendly” and harmless bacteria are present on everybody’s skin, but in the proper environment (like a nice roomy, oily, hair follicle), they can cause trouble: In some kids and adults who are predisposed to have acne, P. acnes invade the plugged hair follicles (the comedones) and multiply.

These P. acnes never become bored or go hungry because they continuously munch on the oily, fatty sebum that serves as a food supply for them. They accomplish this culinary feat by producing chemicals known as enzymes.

Enzymes are proteins that cause a chemical change in other substances without being changed themselves. P. acnes enzymes are like our knives and forks that help us to chop up our food into smaller pieces so that it’s digestible.

The P. acnes produces the enzyme lipase, which can split apart certain fats (triglicerides) into smaller pieces (free fatty acids) so they can digest them. P. acnes eating breakfast, lunch, and dinner, combined with the force of the trapped sebum, can cause ruptures or leaks in the wall of the comedo, allowing the free fatty acids into the surrounding dermis.

Calling all white blood cells!

When the bacteria start to use their lipases to produce free fatty acids, this causes other chemical 911 signals to be sent to your white blood cells. That’s because the free fatty acids are very irritating to the skin.

Your body responds to the irritation by recruiting an army of red and white blood cells to seal off the area where the free fatty acids and bacteria are located. White blood cells are your body’s natural defense system. They rush to the scene accompanied by red blood cells to try to clean up the mess.

Despite their good intentions, sometimes these helpful little cells overdo it and produce inflammatory acne lesions. The cleanup attempt results in red, swollen pimples or pustules that may even lead to even larger lumps, papules, and nodules. See Figure 5.

Figure 5: The microcomedo becomes an inflammatory papule (A), pustule (B), or nodule (C).

Acne scars are the visible reminders of where the body’s inflammatory battle against an acne lesion took place. The deeper an acne lesion is lodged in the skin, the greater the chance for scarring.

Classifying Acne

It’s important for us dermatologists to be able to describe acne in various categories. It helps us to better understand what our patients have to say and it helps us to communicate with one another. It also helps us to follow the progress or lack of progress in our treatments.

Here are the basic categories of acne terms:

  • Non-inflammatory acne: This category of acne is identified when a person’s lesions are primarily whiteheads and blackheads. It’s sometimes called comedonal acne, because it’s characterized by comedones.
  • Inflammatory acne: In this type of acne, papules or pustules, red or purple macules, and nodules, often termed “cysts,” are predominant.

A single patient can have a combination of both non-inflammatory and inflammatory acne. Typically, this combination is seen in teenagers rather than adults. Adults more often have inflammatory acne. The way acne is treated often depends on which type you have:

  • For acne that is primarily comedonal with blackheads and whiteheads, we use agents known as retinoids, such as Retin-A, Differin, or Tazorac to treat them. These drugs are comedolytic, which means they break up comedones.
  • If you have inflammatory acne, we tend to rely more often on benzoyl peroxide and/or topical and oral antibiotics.
  • If you have a combination of both types of acne, we tend to use benzoyl peroxide in combination with the retinoids.