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Studies suggest that extracellular Ca2+concentration regulate dentin formation. We have previously reported that sensory denervation reduces dentin formation. The Ca2+-sensing receptor (CaSR) is expressed in perivascular sensory nerves in mesenteric arterioles and in dorsal root ganglion. Our study was aimed to (1) identify CaSR in dental pulp (DP), sensory axons and trigeminal ganglion (TG) and (2) to investigate whether increased extracellular Ca2+ increases tooth blood flow. Pulpal blood flow (PBF) was measured by laser-Doppler flowmeter. The distribution of CaSR in jaws, DP and TG was studied by immunohistochemistry. RT-PCR and Western blot were used to assess CaSR expression. Abundant expression of the CaSR was found in sensory axons and cells in the jaws, TG and DP. Activation by 5 mM Ca2+ and NPS R-467 resulted in increased PBF, suggesting that extracellular Ca2+ regulates tooth blood flow. Iberiotoxin inhibited relaxation caused by extracellular Ca2+. RT-PCR showed the presence of the CaSR message in TG and DP. Western blot analysis indicates expression of glycosylated and nonglycosylated forms of the receptor in TG and DP. It is concluded that the CaSR is present in the DP, sensory nerves and TG, and that increase in extracellular Ca2+ concentration in the DP causes vasodilatation, which may provide a mechanism to regulate dentin mineralization. [ABSTRACT FROM AUTHOR]

Aims: To investigate whether acute dental pain due to pulpal or periapical inflammation is associated with increased expression of cortisol and inflammatory markers and mediators in the saliva, as well as changes in salivary flow rate., Methods: Patients experiencing pain (n = 42) were recruited when seeking emergency dental treatment. A 0 to 10 numeric rating scale (NRS) was used as a measure of the severity of pain, and the number of days with pain sensation was also recorded. Unstimulated saliva was collected for 3 minutes (salivary flow measured in mL/minute) and stored at -80°C. Saliva was analyzed for the biomarkers cortisol, C-reactive protein (CRP), and cytokines interleukin-1β (IL-1β) and interleukin-6. In addition, the participants completed a simple questionnaire about stress-inducing factors such as insomnia, dental anxiety, or home/workplace stress. Patients received a dental examination and diagnosis (eg, symptomatic pulpitis/apical periodontitis or acute apical abscess), which was confirmed during dental treatment. The control group (n = 39) consisted of participants without any pain and no known medical or dental problems., Results: Patients experiencing acute pain due to pulpal or periapical inflammation had a mean NRS score of 7.0 ± 2.59. The mean duration of pain was 6.5 ± 7.9 days. There was no significant difference in pain level between male and female subjects, tooth type affected, or diagnosis. Higher levels of cortisol, IL-1β, and IL-6 and increased salivary flow were detected in patients with pain when compared to controls (P < .05). CRP was higher in patients with acute pain compared to control participants without pain, but this difference was not statistically significant. Stress at home or the workplace was reported by 79% of patients experiencing pain and by 28% of control participants., Conclusion: Acute dental pain due to pulpal or periapical inflammation was associated with an increase in salivary cortisol, IL-1β, and IL-6 levels and in salivary flow rate. Stress arising from home or the workplace may aggravate a symptom-free pulpal or periapical inflammation to an acute phase. Inflammation in the pulp and periapical region can have effects in regions remote from the disease site.

Objectives: Apical periodontitis is an inflammatory disease characterized by bone resorption, and sympathetic nerves are known to modulate bone resorption and bone remodeling. Higher numbers of osteoclasts and larger periapical lesions have been observed after sympathectomy in rats, but the mechanisms underlying the inhibitory effect of sympathetic nerves on osteoclasts are unknown. This study aimed to test the hypothesis that sympathetic nerves inhibit the production of the bone-resorbing pro-inflammatory cytokines IL-1 alpha and TNF-alpha in rat periapical lesions., Methods: Rats were unilaterally sympathectomized and apical lesions were induced by exposing the dental pulp of molar teeth to the oral microflora. We quantified the cytokines IL-1 alpha and TNF-alpha by enzyme-linked immunosorbent assay, and immunohistochemical analysis was done for qualitative localization. Pulp from intact incisor teeth was tested as a control., Results: We showed that IL-1 alpha was increased, but not TNF-alpha, in the periapical lesions on the sympathectomized side. Both IL-1 alpha and TNF-alpha were expressed in unexposed pulp. TNF-alpha was significantly decreased in the denervated incisor pulp, whereas the level of IL-1 alpha remained unchanged., Conclusions: This study suggests that sympathetic nerves have an inhibitory effect on IL-1 alpha in periapical lesions and a stimulatory effect on TNF-alpha in the intact rat pulp.