30. Bulge activation hypothesis

 
Quotation from the 9th edition of Lever's:
 
"Recent experimental data in rodents suggests that the primary site that gives rise to new hair germ during follicular regrowth is the bulge region of the follicle where a population of normally slow-cycling, relatively undifferentiated cells with features of stem cells reside. Stimulation of the bulge region, which persists throughout telogen, then gives rise to new hair germ and the developing anagen follicle (bulge activation hypothesis)."
 
Reference in the 9th edition to concepts contrary by A. Bernard Ackerman et al. (ABA): None.
 
Statements contrary by ABA:
 
"For many years, speculation has abounded concerning the origin of cells responsible for formation of a new follicle at the end of telogen. It long was an article of faith that matrical cells were primordial in that regard. During the last decade of the 20th century, the "bulge-activation hypothesis" gained acceptance, the supposition being that the bulge of a follicle, which serves as a site for attachment of a muscle of hair erection, serves also as a reservoir for stem cells that, at the outset of anagen, give rise to a new inferior segment of a follicle. Our studies of sections of tissue of normal follicles, cut in both vertical and horizontal directions, have led us to a different conclusion. For one, the bulge is very different structurally from that pictured and described by proponents of the "bulge-activation hypothesis," i.e., it is not a single knobby protuberance that emanates from a discrete locus on one side of a follicle, but rather numerous finger-like projections that emerge along more than half the circumference of it. For another, bulges are irrelevant to the follicular cycle; the cells that become germinative, form a follicular germ, and soon transform into matrical cells en route to producing a new lower segment in anagen, derive from cells left behind at the base of the isthmus at the end of catagen, those cells lying dormant throughout telogen, only to be reawakened by a call from mesenchymal cells that reside immediately below and that come together to form a new follicular papilla. Each of the bulges is attached to a fascicle of smooth muscle whose sole purpose is to enable hairs to become erect."
 
Ackerman AB, Böer A, Bennin B, Gottlieb GJ. Histologic Diagnosis of Inflammatory Skin Diseases, 3rd Edition. New York: Ardor Scribendi, 2005.
 
Other works of ABA in which the ideas contrary are expressed:
 
1. Ackerman AB, Holecek BU. The bulge-activation hypothesis: is it valid? Am J Dermatopathol. 15(3):235-247 (June) 1993.
 
2. Ackerman AB. Bulge-activation hypothesis. Part 1. A hair is not a follicle. Dermatopathology: Practical & Conceptual 1(1):53-55, 1995.
 
3. Radonich M, Misciali C, Ackerman AB. Bulge-activation hypothesis. Part II. The bulge is not a bulge. Dermatopathology: Practical & Conceptual 1(2):77-94, 1995.
 
4. Ackerman AB, Misciali C, Radonich M. Bulge-activation hypothesis. Part III. A mouse is not a man. Dermatopathology: Practical & Conceptual 1(3):146-153, 1995.