Follicular hyperkeratinization

The pilosebaceous follicles are the target sites for acne. The pathophysiology of acne centers on interplay of follicular hyperkeratinization, increased sebum production, action of Propi-onibacterium acnes (P. acnes) within the follicle, and production of inflammation (Table 11.1). 

Tretinoin (Retin-A, others) has been used in the treatment of acne vulgaris for almost four decades. A primary use for tretinoin is to reduce the hyperkeratinization that leads to microcomedone formation, the initial lesion in acne. Follicular comeocytes become less cohesive as a result of shedding of desmosomes, decreasing tonofila-ments and increasing keratinocyte autolysis and intracellular deposition of glycogen. 

It seems probable that xerosis of the skin with hyperkeratinization, so-called toad skin or phrynoderma, also represents vitamin A deficiency in man. The relationship of vitamin A to mild skin changes such as localized areas of keratinization of the hair follicles, follicular hyperkeratosis, is less well documented. Vitamin A deficiency may be responsible for the lesions in some instances but certainly not in all. Unequivocal follicular keratotic changes have not been produced experimentally in man. ... 

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