He major difference, recently demonstrated, is the location of the break in the funicular wall and the sequence of destructive events that follow. There has been a series of papers published recently that tell us more about this area than we ever knew before. The important features are the following:

There is apparently a defect in the support Structure of the FPSU, with no support (or very weak support) right at the spot where the sebaceous glands originate from the follicular unit, just above the upper level of the pilar unit . Inflammation appears in areas where the support structure is thin or missing. That pinpoints the area where the breakdown occurs. The inflammation consists of all the regular series of inflammatory cells one would expect . The sebaceous glands have been shown to almost disappear, blown off by inflammation.

In areas where the sebaceous glands are gone, there is visible inflammation and scarring. The destructive inflammatory process leaves behind little stumps where the sebofollicular junction previously existed. Just below the sebofollicular junction in the pilar unit of the FPSU is a group of cells that produces a visible bulge, so it is called the bulge region. This is a segment of the pilar unit between the attachment site of the arrector pili muscle to the pilofollicular structure below, and the beginning of the sebofollicular junction at the isthmus above .

The arrector pili muscles make the hair on the back of your arms stand up in a chill. More importantly, that bulge area is where Stem Cells come from. The main job of these stem cells is to make sure the hair follicle and hair root are stimulated to grow and replace themselves, to be sure that the FPSU continues to grow hair even if it is damaged, and to repair all portions of the FPSU if and when damaged.

Thus, stem cells can turn into all sorts of cells. When the sebofollicular area ruptures, the break occurs right next to the area occupied by the stem cells, and the closest stem cell variety to the sebofollicular junction is the Lgr6 series. The inflammation appears to allow (or perhaps stimulates) the stem cells to break loose, and they float off into the surrounding mixture of inflammatory cells and fluid. A population of “stemlike cells” has been identified in this inflammatory material by Gniadecki, and it is hypothesized that they are the source of the characteristic material found in AI/HS lesions [17]. These stem-like cells and accompanying inflammatory (and reparative) cells exist in a gelatinous soup. It is rich in nutrients because the body makes sure that the environment for healing is as good as possible.

The hormones needed to stimulate the growth of hairs and indeed the entire androgen-driven FPSU are surely present. The stem-like cells appear to be quite capable of living life on their own, and newly created islands of actively growing and dividing cells appear (Figures 1.20 and 1.21) floating in the gelatinous mass. Indeed, the “stem-like” cells are suggested to initiate the growth of these islands by changing themselves into more specialized structures, which is exactly what stem cells are programmed to do. All this needs proof, of course, and the technology is improving every day.

In summary, it is beginning to look like AI/HS is caused by the coincidental physical proximity of a congenital weakness in the follicular wall right next to the congenital strength of the stem cell line. Quite the coincidence! When these islands come together in the invasive proliferative gelatinous mass (IPGM), genetic programming appears to get to work. Because the source of these activated keratinocytes appears to be from stem cells and stem cells are tasked to perpetuate and repair the folliculopilar structure, they attempt to create a hollow structure whose first product is a protective PAS+(periodic acid–Schiff positive) basement membrane equivalent, most likely fabricated by the basal cells it is protecting on the outside, and lined on the inside, as these structures mature, with squamous epithelium.

This presumed genetic stimulus, carried by the stem cells, almost certainly pushes the little round collection of cells to become the little islands (Figure 1.22) that continue to grow and coalesce, making groups of hollow structures that join together (Figure 1.23). This seems likely, barring another explanation, to be the source of the extensive network of interconnecting sinuses that extend under the skin in AI/HS (Figures 1.24, 1.25, and 1.26). Importantly, there is no histological evidence that these epithelialized sinuses originate as down-growths from the plugged and ruptured follicles, as has been suggested. To the contrary, the residual upper part of the FPSU retires from the field of battle and becomes the receptacle in which the open tombstone comedo occurs The proliferative gelatinous mass in which ‘stemlike’ cells

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