It has been known for decades that the formation of keratinous plugs in the outlet of the sebaceous follicles is the first step in the process of acne vulgaris. These ‘comedones’, (called ‘open comedones’ (blackheads) if the opening of the pore is wide and the plug is visible; and ‘closed comedones’ (whiteheads) if it is tiny and the plug buried under the surface), precede the development of inflammatory lesions (what we call pimples). It has also been known for a long time that individuals who develop more than their fair share of acne have oily skin. Or, more precisely, they tend to have high rates of sebum production.
Downing and colleagues linked these two observations together and proposed that comedones are the result of essential fatty acid deficiency in the follicular orifice. Deficiency of the essential fatty acid, linoleic acid, produces a dermatitis characterized by scaling, redness or erythema, and a defective permeability barrier. This is because linoleic acid is a critical constituent of some of the ceramides that are required for the skin barrier. Sebum is rich in other fatty acids, but it lacks linoleic acid. Therefore, the epidermal cells lining the follicle, which are continually bathed in this deficient lipid mixture, could develop a form of localized essential fatty acid deficiency. The more sebum being produced, the greater this dilutional effect. Little has been done to test the Downing hypothesis since it was first espoused twenty five years ago. A first step in that direction would be to determine whether or not there is a barrier defect in the follicular epithelium.
In the studies reported here, we examined the barrier integrity of different regions of the hair follicle in biopsies of non-inflamed, open comedones, using a water-soluble tracer that can be seen with an electron microscope. While normal follicles show an intact barrier from the skin surface all the way down to the opening of the sebaceous gland, follicle walls surrounding open comedones leaked abundant tracer.
Bottom Line: These studies indicate that an barrier defect in the hair follicle wall is present in the earliest lesions of acne. It raises the possibility that treatments aimed at restoration of the barrier in early acne lesions might prevent the later development of inflammatory acne.