RESPONSE OF SEBACEOUS GLAND TO EXPERIMENTAL STRESS 193 directly to the sebaceous gland, and the hair or hairs, if they are found, are vestigial structures (Fig. 1). In reality these are "sebaceous follicles." All of the fat-laden cells of the sebaceous glands are derived from the mitot- ically active basal cells of the sebaceous gland, and the later cell layer is a continuation of the basal cell layer of the epidermis and follicular canal. The fully differentiated, fat filled sebaceous cells in the center of the seba- ceous glands are cast off to form sebum. This is called holocrine secretion. On histological examination, keratin-like trabeculae are also seen in many mature sebaceous cells. In other words, they are bipotential and still can produce keratin. On the other hand, the surface epidermal cells produce keratin as their main product, but also produce lipid material which is part of the surface lipid film. The following were among the experimental stresses studied in relation to changes in the sebaceous glands (1). 1) contact dermatitis, 2) occlusion of the surface with adhesive tape, 3) plucking of the hair, 4) puncturing of the follicle with a fine needle, 5) removal of the entire epidermis and upper dermis with a motor driven wire brush (dermabrasion), 6) destruction of Figure 1.--Normal pilosebaceous follicle from the cheek of a young adult male (X34). The dilated follicular canal is normal for this area. The sebaceous glands are very large and the follic- ular canal leads directly to them. On the left there is a small veilus-type telogen hair with evi- dence of new hair forming beneath this. The dark staining material in the follicular canal is made up of clumps of propionibacteria. ß .':.• .. .,,)' ::•.. • .•:.:.-..% %:.: ß zg• •--,• • •.. .. 3'- •.•.• - .:.. . .•,•.•...'•..•.• ,•.• :•' ? •: .. "% .... .. 3•: •"• '?'• .• ..... ... ', Figure 2.•Cheek 9 days after der- mabrasion (X52). This is the proto- typical example of replacement of the gland by primitive undifferentiated epithelial cells.

194 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS the follicular mouth by electrocoagulation and 7) production of local in- flammation by the injection of irritants into the dermis. Regardless of the type, any injury, sufficiently severe to result in tissue destruction, destroys the sebaceous glands. Furthermore, injuries just short of that producing total destruction result in marked atrophy of the sebaceous gland. These responses in no way are different than that seen in any tissue. Except for minor variations, all of the other changes in the sebaceous gland are stereotyped involving a replacement of the fat-ladened cells by cells similar to those found in the gland before it shows any sebaceous differentiation. These cells are undifferentiated and look like ordinary basal or prickle cells there is a true failure of sebaceous maturation. The mature sebaceous cells do not participate in the response. They are merely replaced by new undifferentiated cells derived from the basal cell layer of the sebaceous gland. The replacement of the gland by the un- differentiated epithelial cells may be incomplete, and varying percentages of cells may show partial or complete replacement with lipid. The pro- totypical example of this is seen after the entire epidermis and upper portions of the dermis and cutaneous appendages are removed in derma- brasion. By five days many of the mature sebaceous cells are replaced by these "undifferentiated cells," by nine days the change is almost complete (Fig. 2). Actually these cells are a major contributor to the formation of a new epidermis and without them this plastic procedure probably would be doomed to failure. After dermabrasion the changes are reversible and by four weeks the sebaceous glands are normal. Variations of the basic response are common, resulting in proliferation of the undifferentiated epithelial cells into the surrounding dermis, and also complete transformation of the sebaceous gland into a stratified squamous epithelial membrane producing keratin as its product (squamous meta- plasia). However, since these changes occur principally after the pro- duction of dermal inflammation they will be discussed subsequently. While minor injury to the skin (contact dermatitis) produced no changes in the sebaceous gland, any stimulus great enough to promote a profound response of any portion of the pilosebaceous unit, even if the gland itself is not injured produces changes in the sebaceous gland. What happens after a hair is plucked is an example of this (Fig. 3). Plucking of anagen hairs produces great damage to the pilosebaceous apparatus. Except for a few cellular remnants the matrix is removed completely as is the internal root sheath and the lower one-third of the external root sheath. Never- theless, the sebaceous gland itself is not directly injured. Five days after an injury such as this the follicular infundibulum is already distended with keratinized squamae produced by the upper portion of the external root sheath. At the same time what is left of the lower portion of the hair