PMID- 24617997 OWN - NLM STAT- MEDLINE DCOM- 20150408 LR - 20140721 IS - 1469-185X (Electronic) IS - 0006-3231 (Linking) VI - 89 IP - 3 DP - 2014 Aug TI - Hair curvature: a natural dialectic and review. PG - 723-66 LID - 10.1111/brv.12081 [doi] AB - 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. CI - (c) 2014 The Authors. Biological Reviews (c) 2014 Cambridge Philosophical Society. FAU - Nissimov, Joseph N AU - Nissimov JN AD - Trapezoid Hair Research, PO Box 1487, Jerusalem, 91014, Israel. FAU - Das Chaudhuri, Asit Baran AU - Das Chaudhuri AB LA - eng PT - Journal Article PT - Review DEP - 20140312 PL - England TA - Biol Rev Camb Philos Soc JT - Biological reviews of the Cambridge Philosophical Society JID - 0414576 SB - IM MH - Animals MH - Hair/*anatomy & histology/*growth & development MH - Humans MH - *Models, Biological OTO - NOTNLM OT - EMT/MET OT - Wnt/hippo pathways OT - hair bending/curling OT - hair follicle adipocytes OT - hair twisting OT - mTOR pathway OT - mesenchymal budding OT - neural crest stem cells (NCSC) OT - papilla bisection OT - papilla fission EDAT- 2014/03/13 06:00 MHDA- 2015/04/09 06:00 CRDT- 2014/03/13 06:00 PHST- 2012/12/12 00:00 [received] PHST- 2013/12/18 00:00 [revised] PHST- 2014/01/01 00:00 [accepted] PHST- 2014/03/13 06:00 [entrez] PHST- 2014/03/13 06:00 [pubmed] PHST- 2015/04/09 06:00 [medline] AID - 10.1111/brv.12081 [doi] PST - ppublish SO - Biol Rev Camb Philos Soc. 2014 Aug;89(3):723-66. doi: 10.1111/brv.12081. Epub 2014 Mar 12.