Abstract
A rat model of pulpitis/periapical periodontitis was used to study mechanisms underlying extraterritorial enhancement of masseter response associated with tooth inflammation. Periapical bone loss gradually increased and peaked at 6 weeks after complete Freund’s adjuvant (CFA) application to the upper molar tooth pulp (M1). On day 3, the number of Fos-immunoreactive (IR) cells was significantly larger in M1 CFA rats compared with M1 vehicle (veh) rats in the trigeminal subnucleus interpolaris/caudalis transition zone (Vi/Vc). The number of Fos-IR cells was significantly larger in M1 CFA and masseter (Mass) capsaicin applied (M1 CFA/Mass cap) rats compared with M1 veh/Mass veh rats in the contralateral Vc and Vi/Vc. The number of phosphorylated extracellular signal-regulated kinase (pERK)-IR cells was significantly larger in M1 CFA/Mass cap and M1 veh/Mass cap rats compared to Mass-vehicle applied rats with M1 vehicle or CFA in the Vi/Vc. Pulpal CFA application caused significant increase in the number of Fos-IR cells in the Vi/Vc but not Vc on week 6. The number of pERK-IR cells was significantly lager in the rats with capsaicin application to the Mass compared to Mass-vehicle treated rats after pulpal CFA- or vehicle-application. However, capsaicin application to the Mass did not further affect the number of Fos-IR cells in the Vi/Vc in pulpal CFA-applied rats. The digastric electromyographic (d-EMG) activity after Mass-capsaicin application was significantly increased on day 3 and lasted longer at 6 weeks after pulpal CFA application, and these increase and duration were significantly attenuated by i.t. PD98059, a MEK1 inhibitor. These findings suggest that Vi/Vc and Vc neuronal excitation is involved in the facilitation of extraterritorial hyperalgesia for Mass primed with periapical periodontitis or acute pulpal-inflammation. Furthermore, phosphorylation of ERK in the Vi/Vc and Vc play pivotal roles in masseter hyperalgesia after pulpitis or periapical periodontitis.
Highlights
Orofacial persistent pain following trigeminal nerve injury or orofacial inflammation is known to cause various motor as well as sensory disorders in the orofacial regions such as mastication or swallowing dysfunction [1]
It has been reported that the chronic orofacial pain associated with pulpitis and/or periapical periodontitis is one of the most frequent referred pain in the orofacial region, and pulpitis or periapical periodontitis is known to be involved in the referred pain in various intraoral structures [3,4]
Referred pain in non-inflamed orofacial areas associated with pulpitis or periapical periodontitis is often accounted for misdiagnosis or inappropriate clinical treatment
Summary
Orofacial persistent pain following trigeminal nerve injury or orofacial inflammation is known to cause various motor as well as sensory disorders in the orofacial regions such as mastication or swallowing dysfunction [1]. Electrical stimulation of the tooth pulp produces Fos protein expression in many neurons in the transition zone between the subnucleus interpolaris (Vi) and Vc (Vi/Vc) and the caudal Vc and upper cervical cord [5]. These two areas are thought to play differential roles in processing noxious information from the tooth pulp as well as orofacial skin or muscles [7,8]. It is highly possible that nociceptive neurons in the Vi/Vc and Vc enhance their firings following pulpitis or periapical periodontitis and play a role in orofacial cutaneous and/or Mass nociception as well as processing tooth pulp or periapical inputs. We hypothesized that Vi/Vc and Vc neurons are involved in masseter muscle hypersensitivity associated with tooth pulp and periapical inflammation
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