The visibility of the lesions of acne vulgaris and acne rosacea as we present ourselves to the world and interact with others is a source of anguish to many. The hidden lesions of acne inversa (hidradenitis suppurativa) may interfere even with the most basic social interactions.
The most profound effect of the acnes is on the psyche, so that aspect will be discussed “up front,” but first we need to know what we are talking about.
Vulgaris is a Latin word, an adjective that means common. It is not a pleasant term, but it is descriptive (even a little vulgar). It is also highly accurate because the lifetime risk of acne in developed countries with “Western” diets is 85–90% of the population. Indeed, acne vulgaris is so common that even senior dermatologists (who should know better) have stated, “Children as young as 7 years of age can present with mild, usually comedonal disease, which most often is a normal physiologic occurrence.”
To avoid embarrassing the author, no reference is provided. If I agreed with the statement that acne is “normal” (or “physiologic”), there would be no point to this book. My purpose in writing it is to draw together numerous threads of information, from very old to very new. I want to define the problem. Then I want to explain how this disorder (and its relatives) arises. Only then can we sort out how to treat it (and its various types) in as logical a fashion as possible. So let’s get started—at the beginning. Acne occurs when a plug forms in the follicular portion of the little oil gland and hair follicle organs on the skin called, in the older literature, pilosebaceous units.
Here they will be called folliculopilosebaceous units (FPSUs), for reasons discussed in the Introduction. There are other small organs that develop from the underside of the skin: The eccrine sweat glands over most of our skin surfaces produce ordinary sweat. The apocrine sweat glands in our armpits and groin areas produce a different kind of sweat, plus a peculiar class of chemicals called pheromones.
The mammary glands that form the breasts are derived in the same way, but obviously grow bigger than the others. These are all referred to as skin appendages. They all have their own diseases, and some may be related to acne.
The first plugs that lead to acne occur in the structurally quiet, non-inflamed, and non-infected follicular portion of the FPSU. The story starts with a stimulus to the development of a structure named the Follikel-Filament the first tiny accumulation of the lining cells, the keratinocytes, in the follicular duct .
These cells produce the tough linear protein called keratin that makes up the surface of our skin. When formed into a long thin fiber, keratin makes hair, and when produced in thick flat compact sheets, keratin becomes nail. Thin sheets of keratin, made of individual terminal keratinocytes, form the surface of skin and line the follicular portion of the FPSU. The process of formation of keratin
by keratinocytes in the follicular canal and on the skin surface is called keratinization. Normally, as these cells mature they separate from each other toward the center of the follicular duct, and the loose cells are released into the ductal canal where they are pushed to the top of the duct by the flow of sebum. Accumulation of these flat cells in the follicle leads to the microcomedo .
This growth progresses next with larger and larger masses of these lining keratinocytes, leading to the physical plugging of the duct. Next come microbial colonization and overgrowth of preexisting bacterial and yeast colonies. This continues at the same time as the increased plugging. The increase in intrafollicular mass causes expansion, leaking, and then rupture of the follicular unit. The pilar unit is unaffected in early acne.
It just keeps doing its job, which is to make hair, some of which may become trapped in the plugged and dilated follicular unit. That hair normally becomes increasingly coarse during the teen years, especially in boys, and has the effect of keeping the larger FPSUs open and uninvolved in the acne process. The sebaceous unit is also growing and producing more sebum. At body temperature, that sebum is a liquid. It quietly percolates to the surface, through and around the plugs, and is responsible for von Jacobi– Pringle’s “peculiar seborrhoeic condition,” the oily skin of acne that we all recognize .
It also happens to be the preferred food for the organisms that come to live in the follicular unit, so that encourages their growth. Much more on them later . The leaking and rupture of the follicular unit of the FPSU are intimately involved with inflammation. This is a huge and very complex area. Hundreds of papers have been written on the subject. As of this writing, there have been 619 papers since 1952.
I don’t plan to review them all here, but you need to know that there is serious debate as to what starts the process. Does the plugging of the follicular unit come first, with pressure-induced leakage leading to inflammation ? Or does very early inflammation actually stimulate the plugging of the duct to produce excessive numbers of ductal cells ? My personal belief is that hormones plug the pore, and that causes the expansion that leads to the leaking
which leads to the inflammation. My reasoning is simple: the organisms said to trigger the inflammation that triggers the keratinization are present in almost everyone, throughout life, and are in no greater number in acne patients than in normal persons . If these organisms were the cause, we would all have acne, all the time.
There has to be a factor that comes on at puberty, and generally leaves at the onset of maturity, in order to explain the timeline of acne in our population. More on that later (Section 2.6). There also needs to be a trigger that links the overproduction of the keratinocytes in the follicular duct to the onset of inflammation. That may be a recently described simple product of the pressure and hypoxia that build up in the follicular duct.
More on that as well later. Whether inflammation starts the plugging process or is a response to early leakage of materials from the FPSU, inflammation is seen as a target for therapy. For hundreds of years, physicians have been treating acne by trying to suppress the inflammation. I will try to convince you in this book that treating the inflammation is like chasing the horse after he has left the burning barn.
Far more important is preventing the fire in the first place. The “inflammatory process” doesn’t just cause inflammation. It is often forgotten that its main chore is to repair the damage caused. Sometimes, the inflammatory process stops with simple healing of the wall of the follicular unit. In the absence of repair, the inflammatory reaction just keeps burning. Unfortunately, that leads to much more destruction. The contents of the dilated follicles leak or explode into the tissue under the skin surface.
That causes more inflammation and leads to scarring. This prolonged destructive inflammatory activity is the cause of the tender nodules that are so ugly. Untreated, resolution occurs over a long time period, often years. This is referred to as “burning out” of acne. It leads to loss of parts of the FPSU, or the entire FPSU can be destroyed. It also leaves serious scarring behind