Polarization of macrophages in the trigeminal ganglion of rats with pulpitis

Abstract

Background Dental pulp tissues are rich in pain‐related afferent nerve fibers, which originate from primary sensory neurons in the trigeminal ganglion (TG). The mechanisms of central nervous system (CNS) underlying ectopic pain following peripheral inflammation have been reported that the macrophages as inflammatory and immunologic mediators in the TG play an important role in the process of pulpitis and hyperalgesia. Objective(s) To observe the polarization response and dynamic distribution of macrophages in the TG during the development of dental pulp inflammation. Methods A rat model of pulpitis was established using complete Freund's adjuvant (CFA). Hematoxylin‐eosin (HE), immunohistochemistry (IHC), immunofluorescence (IF), toluidine blue (TB) staining, and RT‐qPCR were performed to observe the expression of macrophage‐related factors in the TG. Results The results of IHC staining showed that M2 macrophages labeled with CD206 were observed in the TG of both the control and CFA groups. The statistical analysis indicated that the number of CD206‐positive macrophages in the TG increased significantly at 24 h after CFA‐induced pulpitis, reached a peak at 2 weeks, and then returned to the normal level after 6 weeks. The ratio of M2/M1 in the CFA groups was significantly lower than that in the control group from 24 to 72 h, and this pattern was reversed at 2 weeks after CFA‐induced pulpitis; then, the ratio increased significantly and was maintained at a high level for 4 weeks. RT‐qPCR results showed that the expression of IL‐10 in the TG increased significantly from 1 to 4 weeks after CFA‐induced pulpitis. Conclusion The trend of M2 macrophages was opposite to that of M1 macrophages in the TG during the process of pulpitis induced by CFA, which is consistent with the expression of macrophage‐related cytokines. Macrophage polarization in the TG may participate in the neuroinflammation response induced by dental pulpitis.

Sympathectomy Ameliorates CFA-Induced Mechanical Allodynia via Modulating Phenotype of Macrophages in Sensory Ganglion in Mice

“…This result is consistent with those observed in previous studies. 5,55,56 Minimal changes were observed between sympathectomy and sham surgery group before CFA treatment, suggesting sympathectomy has no significant effect on macrophage phenotypic transition. Prior sympathectomy significantly reduced M1 macrophage infiltrated in TG from 1 to 14 dpi, suggesting that the SNS may promote M1 polarization in the TG during orofacial inflammation.…”

Multifunctional Exosomes Derived from M2 Macrophages with Enhanced Odontogenesis, Neurogenesis and Angiogenesis for Regenerative Endodontic Therapy: An In Vitro and In Vivo Investigation

“…The enhanced M1 polarization would exacerbate pulpitis progression [27], while M2 macrophages exerted a pivotal impact on the attenuation of reversible pulpitis and recovery of pulp tissue [28]. Concentrating on the relationship between macrophage phenotypes and nerve regeneration, Gao et al [29] found that in the early acute stage of pulpitis, the ratio of M2 to M1 macrophages was considerably reduced in trigeminal ganglion. However, as pulp inflammation subsided, this ratio was reversed entirely, indicating that the phenotypic transformation of macrophages from M1 to M2 facilitated nerve repair in pulpitis.…”

Non-Psychoactive Cannabinoid Modulation of Nociception and Inflammation Associated with a Rat Model of Pulpitis

“…Similarly, PPARγ has been linked to reduction in neuroinflammation via microglia in models of neuropathic pain [19]. Importantly, recent research has demonstrated that macrophages and microglia participate in neuroinflammation in the trigeminal ganglia following pulp exposure, suggesting that this may play a critical role in the development of inflammatory pain associated with pulpitis [20]. The present study does not investigate the receptor mechanism involved in the β-CP suppression of AIF gene expression; however, mounting evidence suggests that CB2 receptor/PPARγ cross-talk is the critical target for β-CP's antiinflammatory effects [21].…”