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When tooth dentin is exposed, it may trigger dentin hypersensitivity, resulting in unexpected, strong dental pain that often prevents patients from eating and drinking. Osmotic stimuli are known to cause dentinal fluid movement, which in turn produces dentin hypersensitivity. TRPM8 is activated by several stimuli, including hyperosmotic stimuli (Sato et al. 2013; Quallo et al. 2015). The presence of osmo-sensors on other TRP channels such as TRPM7, TRPV1, and TRPV2 in hyperosmotic stimuli-induced nociception in neurons was shown by the results of the recent studies (Lee et al. 2020). TRPM8 channels were found to be molecularly and functionally expressed in some dental primary afferent neurons in a study by Lee et al. (2020). Hyperosmolar stimulation induced a response in neurons expressing TRPM8, and the TRPM8 antagonist (AMTB) prevented calcium transients produced by hyperosmolar sucrose solution. They concluded that TRPM8 in dental primary afferent nerve functions as a hyper-osmosensor in adult mice, contributing to oral nociception. In the talk, I will give a summary of the few reports that are available on hyperosmotic stimuli-induced nociception in dental afferents. [ABSTRACT FROM AUTHOR]