Abstract

Baroreceptor and chemoreceptor reflexes modulate inflammatory responses. However, whether these reflexes attenuate periodontal diseases has been poorly examined. Thus, the present study determined the effects of electrical activation of the carotid sinus nerve (CSN) in rats with periodontitis. We hypothesized that activation of the baro and chemoreflexes attenuates alveolar bone loss and the associated inflammatory processes. Electrodes were implanted around the CSN, and bilateral ligation of the first mandibular molar was performed to, respectively, stimulate the CNS and induce periodontitis. The CSN was stimulated daily for 10 min, during nine days, in unanesthetized animals. On the eighth day, a catheter was inserted into the left femoral artery and, in the next day, the arterial pressure was recorded. Effectiveness of the CNS electrical stimulation was confirmed by hypotensive responses, which was followed by the collection of a blood sample, gingival tissue, and jaw. Long-term (9 days) electrical stimulation of the CSN attenuated bone loss and the histological damage around the first molar. In addition, the CSN stimulation also reduced the gingival and plasma pro-inflammatory cytokines induced by periodontitis. Thus, CSN stimulation has a protective effect on the development of periodontal disease mitigating alveolar bone loss and inflammatory processes.

Highlights

  • Baroreceptor and chemoreceptor reflexes modulate inflammatory responses

  • The rats were divided into four groups: I: SHAM + Control; II: SHAM + carotid sinus nerve (CSN); III: periodontal disease (PD) + Control; IV: PD + CSN

  • In rats with PD plus CSN stimulation, decreased alveolar bone resorption was observed compared to the PD control group (Fig. 3A)

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Summary

Introduction

Baroreceptor and chemoreceptor reflexes modulate inflammatory responses. whether these reflexes attenuate periodontal diseases has been poorly examined. It is reasonable to expect that simultaneous baroreflex and chemoreflex activation produces a significant antiinflammatory response, inhibiting innate immune system, attenuating the release of pro-inflammatory cytokines and decreasing osteoclastogenesis in other inflammatory diseases, such as periodontitis. Our laboratory developed a technique to simultaneously stimulate the carotid baroreflex and chemoreflex in unanesthetized ­rats[30] This electroceutical approach allows the investigation of autonomic modulation without the undesirable effects of anesthesia under different protocols, those involving inflammatory ­models[24]. The present study determined the modulatory effects of long-term (9 days) carotid baroreflex and chemoreflex activation on bone resorption, histological damage and inflammatory mediators in rats submitted to ligature-induced periodontitis

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