Although hair forms (straight, curly, wavy, etc.) are present in apparently infinite variations, each fibre can be reduced to a finite sequence of tandem segments of just three types: straight, bent/curly, or twisted. Hair forms can thus be regarded as resulting from genetic pathways that induce, reverse or modulate these basic curvature modes. However, physical interconversions between twists and curls demonstrate that strict one-to-one correspondences between them and their genetic causes do not exist. Current hair-curvature theories do not distinguish between bending and twisting mechanisms. We here introduce a multiple papillary centres (MPC) model which is particularly suitable to explain twisting. The model combines previously known features of hair cross-sectional morphology with partially/completely separated dermal papillae within single follicles, and requires such papillae to induce differential growth rates of hair cortical material in their immediate neighbourhoods. The MPC model can further help to explain other, poorly understood, aspects of hair growth and morphology. Separate bending and twisting mechanisms would be preferentially affected at the major or minor ellipsoidal sides of fibres, respectively, and together they exhaust the possibilities for influencing hair-form phenotypes. As such they suggest dialectic for hair-curvature development. We define a natural-dialectic (ND) which could take advantage of speculative aspects of dialectic, but would verify its input data and results by experimental methods. We use this as a top-down approach to first define routes by which hair bending or twisting may be brought about and then review evidence in support of such routes. In particular we consider the wingless (Wnt) and mammalian target of rapamycin (mTOR) pathways as paradigm pathways for molecular hair bending and twisting mechanisms, respectively. In addition to the Wnt canonical pathway, the Wnt/Ca(2+) and planar cell polarity (PCP) pathways, and others, can explain many alternatives and specific variations of hair bending phenotypes. Mechanisms for hair papilla budding or its division by bisection or fission can explain MPC formation. Epithelial-to-mesenchymal (EMT) and mesenchymal-to-epithelial (MET) transitions, acting in collaboration with epithelial-mesenchymal communications are also considered as mechanisms affecting hair growth and its bending and twisting. These may be treated as sub-mechanisms of an overall development from neural-crest stem cell (NCSC) lineages to differentiated hair follicle (HF) cell types, thus providing a unified framework for hair growth and development.

The hair diameter major-axis has been shown to decrease normally toward the scalp in individual fibres. In this report sharp increases, rather than decreases, of hair-shaft major-axis diameters during pregnancy are described. Mean major-axis hair diameters of 15-20 fibres from each of 12 pregnant and 13 nonpregnant women were measured from the scalp distally at regular 6-mm intervals. Sample diameters were normalized relative to putative times of conception or a distance from the scalp equivalent to full term pregnancy, for the pregnant and nonpregnant women, respectively, and averaged. Major-axis diameter increases toward the scalp in hair of pregnant women were found to start at the beginning of pregnancy with a slope measuring 0.58%/cm, which is highly significant (r = 0.99, P < 0.0001). Hair diameters of the nonpregnant women, on the other hand, decreased toward the scalp during analogous times to the pregnancy, with a slope measuring -0.66%/cm, also highly significant (r = -0.97, P < 0.0001), and in good agreement with previously published data. To our knowledge this is the first description of hair diameter increases during a normal physiological process.

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Shed head-hair fibres of young (16-20-year-old), nonalopecic women (n = 25), exhibiting both exogen clubs and anagen tips (EA) were studied. Such fibres are shown, for the first time, to comprise approximately 44% of shed hair and to form a uni-modal, positively skewed distribution with a mean length of 16.7 +/- 4.9 cm, which is also correlated with the length of the haircut. As individual fibres exit the skin in early anagen VI, their major-axis diameters increase rapidly to maxima at about 25% of their total potential length and subsequently decrease to their exogen clubs, at a rate of 1.31% per cm (n = 28). EA diameters are further correlated with their lengths. Maximal and proximal diameters increase by 1.40% per cm and 1.02% per cm increments in fibre lengths, respectively (P < 0.0001 each; n = 14), these changes being also different from each other (P < 0.001). Besides identifying and characterizing a new class of normal hair (EA) which will probably feature prominently in future hair research, this study reveals several other important aspects of hair growth: (i) the classically described concept of hair miniaturization in androgenetic alopecia (AGA) is excessively broad and should therefore be revised; (ii) female AGA need not necessarily require a mechanism for rapid miniaturization as recently proposed; and (iii) the putative large variability of normal hair diameters is significantly overestimated, which further opens the field of hair diameter evaluation as a biological indicator of disease and physiological function.