![]() The mandible-inferior alveolar nerve preparation is derived from the lower jaw and transferred to an organ bath consisting of an external solution and a mini-tube that is connected to a temperature-controlled application system. ( Top) Illustration of mouse head with jaws and their innervation. Thus, the cold transduction molecules and site of transduction in teeth remain unresolved. The physiological significance of the observed cold transduction in odontoblast and fibroblasts is still unclear, because the specific contributions of TRPA1 and TRPM8 to cold-induced tooth pain in vivo were not observed ( 16) and electrophysiological models to directly examine the relevance of these channels in the tooth sensory system are missing. In rat odontoblasts in vitro, cold sensitivity is controversial ( 14, 15). However, acutely isolated native human odontoblasts express TRPM8 but not TRPA1 ( 12), in contrast to these cells in more prolonged culture ( 10, 13). In addition, cultured human odontoblast-like cells ( 10) and cultured dental pulp fibroblasts ( 11) exhibit cold-induced increases in intracellular calcium in vitro, which is partly explained by their TRPA1 and TRPM8 channels. TRPM8 and TRPA1 mRNA and protein are present in high density in the trigeminal ganglion (TG) and in the sensory axons of the tooth pulp ( 7– 9). In the skin, TRPM8 and TRPA1 act synergistically and represent the key sensors of environmental cooling as well as painful cold ( 5, 6). Certain transient receptor potential (TRP) ion channel subtypes are strongly activated by cooling, acting as molecular sensors in the skin and mucous membranes where they depolarize nerve terminals to elicit action potentials ( 5). The lack of functional evidence for cold sensing in teeth is unexpected given the progress in our understanding of molecular cold-sensing molecules ( 5). Functional experimental evidence for this theory is lacking. In this theory, dentinal microcanals (tubules) act as a hydraulic link between the physical stimulus and the nerve terminals, which are sited at the pulp-dentin boundary (fig. ![]() In Brännström’s hydrodynamic or fluid movement theory, the transduction of thermal and other physical stimuli to activate dentinal nerve endings has been attributed to a fluid dynamic–induced mechanosensory process. On the basis of the functional anatomy, in which ceramic-like enamel and dentin insulate nociceptive terminals from temperature changes ( 3), the tooth pulp’s sensory plexus of Raschkow is widely accepted as mechano- and nociceptive. ![]() Inflamed teeth are extremely cold sensitive, perceived as a short, sharp intense neuralgic pain ( 2). Worldwide, 2.4 billion people have untreated caries in permanent teeth ( 1). Dental caries is a chronic disease in which a bacterial biofilm on the tooth surface, in combination with fermentable carbohydrate substrates, causes demineralization and eventually tooth decay. Insults to the tooth’s dentin produces inflammation, most commonly during tooth decay. Lennerz, and Katharina Zimmermann +21 authors +19 authors +14 authors fewer Authors Info & Affiliations Pfeifer, Fabien Ectors, Andreas Dahl, Marc Freichel, Viktorie Vlachova, Sebastian Brauchi, Carolina Roza, Ulrich Boehm, David E. Laura Bernal, Pamela Sotelo-Hitschfeld, , Christine König, Viktor Sinica, , Amanda Wyatt, Zoltan Winter, Alexander Hein, Filip Touska, Susanne Reinhardt, , Aaron Tragl, Ricardo Kusuda, Philipp Wartenberg, Allen Sclaroff, John D.
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