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Abstract:
This study explores the regulatory role of nociceptors in the immune response during bone regeneration, confirming that neutrophil-mediated nociceptor hyperplasia can exert a negative feedback regulatory effect on bone healing inflammation. It clarifies the mechanism by which specific neutrophil subpopulations drive nociceptor growth and promote inflammation resolution, reveals the regulatory relationship between neural immunity and the balance of inflammation and regeneration in bone repair, and elucidates the intrinsic association between abnormal pathways in diabetic bone tissue and bone healing disorders.
01 Research Background
Nociceptive pain is a major characteristic of traumatic and inflammatory bone diseases, but whether nociceptors actively regulate the immune response during bone regeneration and the specific regulatory mechanisms have not been clearly elucidated.
02 Main Content
Explore the negative feedback regulatory effect of neutrophil-induced nociceptor hyperplasia on inflammation during bone healing; clarify the mechanism by which specific neutrophil subpopulations drive nociceptor growth and promote inflammation resolution; analyze the molecular mechanism by which nociceptor-derived calcitonin gene-related peptide regulates the synthesis of inflammatory resolution mediators by osteoblasts; analyze the associated characteristics of nociceptive nerves, autophagy, inflammation, and bone formation in diabetic bone tissue.
03 Research Design
Conduct mechanism research centered on the regulation of nociceptors, neutrophils, immune inflammation, and bone regeneration, analyze the molecular pathways of neural immunity interaction using cell and animal models, and simultaneously detect relevant indicators in human diseased bone tissue to verify the actual relevance of the experimental mechanism.
04 Results
During bone healing, nociceptor hyperplasia induced by neutrophils can negatively regulate inflammation; specific Il4ra+Ccl2 high neutrophil subpopulations can drive TRPV1+ nociceptor growth and achieve inflammation resolution by promoting the production of lipoxin A4 by osteoblasts; nociceptor-derived calcitonin gene-related peptide activates osteoblast autophagy and inhibits the nuclear translocation of 5-lipoxygenase, thereby promoting the biosynthesis of lipoxin A4; in alveolar bone of diabetic patients, the weakened nociceptive nerve innervation, decreased autophagy level, aggravated inflammatory response, and impaired bone formation are significantly associated.
05 Extension of Thoughts
Based on the core mechanism of neural-immune interaction regulating the balance of inflammation and regeneration during bone repair, it is possible to further expand the research on the multi-dimensional regulatory network among nerves, immunity, and bone cells, providing new basic research directions for analyzing the pathological mechanisms of various bone diseases; focusing on the regulatory pathways of nociceptive nerves, it is possible to deeply explore related molecular regulatory targets and further improve the theoretical framework of the regulatory mechanism of bone regeneration.
Original Source: 1. Bone Research
2. Publication Date: January 1, 2026
3. DOI: 10.1038/s41413-025-00481-6
4. Authors: Xuanyu Qi, Guangzheng Yang, Zeqian Xu, Mingliang Zhou, Tejing Liu, Jiahui Du, Sihan Lin, Xinquan Jiang
