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Thermal stimulation of dentinal tubules
Published in J. Belinha, R.M. Natal Jorge, J.C. Reis Campos, Mário A.P. Vaz, João Manuel, R.S. Tavares, Biodental Engineering V, 2019
Paulo A.G. Piloto, Joana F. Piloto
The pain produced under thermal stimuli may be attributed to the activation of thermal sensitive receptors (TRPV1 – warm receptor and TRPM8 – cold receptor) (Le Fur et al. 2017, El Karim et al 2011). This activation seems to be caused by the threshold temperature around the warm receptors (Lin et al, 2011) and caused by the high rate of temperature variation in the unexposed surface of dentine for the cold receptor (assuming positive correlation between neural discharge and time derivative of dentinal temperature in the unexposed surface, Td). The pain produced under heating may be attributed to the attainment of a threshold temperature limit. The neural response to cold stimulus differs from the neural response to hot stimulus. Relative long latency is expected in case of hot stimulus, because nerve fibres are less sensitive (Le Fur et al. 2017). The theory used for dentine sensitivity induced by thermal stimulus is still under development. Dentine sensitivity is increased when it is directly exposed to thermal stimulus. The transmission of the stimuli in this region generate nerve impulses that have been registered during several experimental investigations (Le Fur et al. 2017). The neural theory dictates that pulpal nerves are activated by external thermal stimuli and produce electrical signals that are collected by nociceptive receptors (Le Fur et al. 2017). Among them, according to El Karim et al. (2011), the TRPM8 is cold sensitive with a threshold value of 22 ± 3°C and the TRPV1 (warm receptor) is hot sensitive with threshold temperature value of 43 ± 2°C.
Toxicity of Terpenoids in Human Health
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Ritobrata Goswami, Dijendra Nath Roy
Menthol in cigarettes does not have any remarkable impact on smoking behavior and exposure biomarkers (Strasser et al. 2013). A study showed that there is no evidence that menthol smokers are more dependent than non-menthol smokers (Frost-Pineda et al. 2014). There is no further evidence of any association of increased incidences of cigarette smoking in menthol cigarette smokers (Curtin et al. 2014). Whether menthol can cause DNA damage has also been ascertained. The expression of transient receptor potential melastatin 8 (TRPM8) was found to be menthol dependent (Kijpornyongpan et al. 2014). Cytosolic calcium level is increased in the presence of menthol and depends on the induced expression of TRPM8 (Kijpornyongpan et al. 2014). However, menthol did not induce cytotoxicity in a non-TRPM8–expressing cell line (Kijpornyongpan et al. 2014). Menthol has the capacity to augment TRPM8 expression (Yudin and Rohacs 2012). The toxic effects of menthol have been studied in animals as well. Cat gustatory nerve fibres displayed increased activity in the presence of menthol (Hellekant 1969). Low-dose menthol can enhance TRPM8-mediated lacrimation, and a very high dose of menthol, 50 mM, can augment lacrimation and nocifensive responses that are TRPM8 independent (Robbins et al. 2012). Proliferation and motility in DU145 cells are inhibited by menthol (Wang et al. 2012). Similarly G-361 cells, a melanoma cell line, displayed cell death in the presence of menthol (Yamamura et al. 2008). In prostate cancer epithelial cells, TRPM8 is an important endoplasmic reticulum Ca2+ release channel that could be involved in a number of Ca2+- and Ca2+-storage–dependent processes (Thebault et al. 2005).
L-menthol administration facilitates breathing comfort during exhaustive endurance running and improves running capacity in well-trained runners: A randomized crossover study
Published in European Journal of Sport Science, 2022
Yoshiko Tsutsumi, Haruki Momma, Satoru Ebihara, Ryoichi Nagatomi
BC, facilitated by L-menthol administration, which was observed in the exhaustive running exercise, may have been mediated through afferent feedback. The activation of the TRPM8 in sensory afferents is known to lead to analgesia in rats with neuropathic pain by inhibiting the sensitization of dorsal horn neurons (Proudfoot et al., 2006). The brain regions that have been associated with perceived dyspnea are the insular and anterior cingulate cortices and amygdala (von Leupoldt et al., 2009). The unpleasantness of dyspnea induced by inspiratory resistive load is specifically associated with activation of the right insular cortex and amygdala (von Leupoldt et al., 2008; Schön et al., 2008). Based on these findings, L-menthol may facilitate BC by attenuating or inhibiting the activity of specific brain regions, such as the insular cortex and amygdala. Interestingly, elite adventure racers during inspiratory breathing loading showed better cognitive task performance when right insular cortex activation was attenuated, which may have contributed to their extreme endurance performance (Paulus et al., 2012). Facilitation of BC by L-menthol administration may benefit endurance athletes as well as those who do not habitually exercise by facilitating the continuation of exercise through reduction of breathing unpleasantness. Even in a lower-intensity exercise, breathing discomfort reportedly increases during exercise (Kearon et al., 1991a). Administration of L-menthol solution during exercise may also be advantageous for those who have health benefits from exercise.