The anagen induction and catagen inhibition in rapidly cycling infantile mice by PTH (7-34) may reflect an acceleration of the unknown "biologic clock" that drives hair cycling, PTH (7-34) could either be replacing the natural anagen initiation signal or counteracting PTHrP as a "brake" on anagen development. Alternatively, PTH (7—34) may directly antagonize the natural catagen initiation signal(s). That PTH (7-34) prolonged anagen and inhibited catagen in adolescent anagen-induced mice further supports the concept that PTHrP is a key signal for hair follicle regression because the follicles in these older mice were relatively slow cycling, which makes interference with the intrinsic generator of follicle cycling a less likely explanation. During its development and its postnatal cyclic remodeling, the hair follicle is essentially an epithelial—mesenchymal interactive system whose development depends on a tightly choreographed series of messages exchanged between the dermal and epidermal cells (Paus et al, 1990, 1991, 1994a, 1994b, 1994c). It has been hypothesized that the hair cycle is controlled by an inhibition/disinhibition system whereby a locally generated mitotic inhibitor ("chalone") that gradually accumulates during anagen causes entry of the follicle into catagen when present in sufficient concentrations (Chase, 1954). This "chalone hypothesis" further stipulates that the gradual loss of activity or the dispersal of the inhibitor during telogen eventually disinhibits follicle growth, a process that may be accelerated by the depilation of telogen hair shafts. It is now recognized that while human cultured keratinocytes and keratino-

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