Topical review. Dental pain and odontoblasts: facts and hypotheses.

摘要: Dental pain arises from exposed dentin following bacterial, chemical, or mechanical erosion of enamel and/or recession gingiva. Thus, tissue and more specifically patent dentinal tubules represent the first structure involved in sensitivity. Interestingly, architecture could allow for transfer information to underlying dental pulp via odontoblasts (dentin-forming cells), their apical extension bathed fluid running tubules, a dense network trigeminal sensory axons intimately related odontoblasts. Therefore, external stimuli causing movements nerve complex responses may unique mechanosensory system bringing new role as sensor cells. How cells sense signals how latter are transmitted main questions be resolved. However, several lines evidence have demonstrated that express mechano- thermosensitive transient receptor potential ion channels (TRPV1, TRPV2, TRPV3, TRPV4, TRPM3, KCa, TREK-1) likely heat cold within tubules. Added this, voltage-gated sodium confer excitable properties vitro response injection depolarizing currents. In vivo, co-localize with terminals at pole correlate spatial distribution stretch-activated KCa channels. This highlights terminal web pivotal zone pulp/dentin sensing stimuli. Crosstalk between take place by release mediators gap space view nociception-transducing receptors on afferent fibers expression putative effectors Finally, guided target which kind signaling molecules is extensively discussed this review.