Molecular and neurovascular mechanisms of thermal sensitivity in teeth.

The perception of dental pain and thermal stimuli is governed by the specialized structural and physiological organization of the dentin - pulp complex. Teeth are subjected to rapid thermal changes during normal oral functions, while the dental pulp - an intensely vascularized and innervated tissue - is confined within rigid mineralized structures. Under these anatomical conditions, even mild thermal stimuli - especially cold - can induce rapid and intense pain sensations. The mechanisms underlying thermal sensitivity of dentin have been explained by several theories. The direct neural theory proposes that external stimuli directly activate trigeminal nerve endings, whereas the hydrodynamic theory suggests that temperature changes induce dentinal fluid movement within tubules, generating mechanical forces that stimulate pulpal afferent fibers. Increasing experimental evidence supports an integrated model in which odontoblasts (ODs) function as mechanosensory transducers. In this concept, thermal stimuli generate dentinal fluid movement and mechanical stress that activate ion channels and enzymes in ODs, leading to the release of signaling molecules such as ATP, glutamate and possible other mediators including nitric oxide. This thermomechanical coupling mechanism, linking dentinal fluid dynamics, odontoblast mechanotransduction, and neuronal activation, is the most widely accepted explanation for thermal pain and dentin hypersensitivity. Understanding these mechanisms provides important insights into dental nociception and may guide the development of more accurate clinical diagnosis and improved strategies for managing thermal dentin hypersensitivity.