颞下颌关节骨关节炎 z-bio 2025-02-24 363

　　Figure 2 Schematic diagram of the mechanism of TMJ-OA condylar neurovascularization and targeted blockade strategy

　　Under the support of the National Natural Science Foundation of China (Grant No. 82471000, 82170978, 82325012) and other programs, Professor Jiao Kai's team from the Fourth Military Medical University of the Chinese People's Liberation Army has made progress in the research on the neural regulation mechanism of the temporomandibular joint, and a series of research achievements have successively published two papers: (1) titled "Effect of regional cross sensory nerve interaction on the regulation mechanism of temporomandibular joint osteoarthritis pain", on 2025 It was published in the International Journal of Oral Science (English) on January 7, 2006. Original link: https://www.nature.com/articles/s41368-024-00336-6 (2) titled "Neurovasculalization inhibiting dual response hydrogel for accelerating the progress of osteoarthritis", published in Nature Communications on February 6, 2025. Original link: https://www.nature.com/articles/s41467-025-56727-8 .

　　Temporomandibular joint osteoarthritis (TMJ-OA) is the main manifestation of severe temporomandibular joint disorder, which can lead to persistent oral and maxillofacial pain and limited joint function. Although current treatment methods can temporarily relieve pain, they cannot stop disease progression. It is urgent to deeply analyze its pathological mechanism and develop new intervention strategies. The research team constructed a TMJ-OA pain model and found that the sympathetic nervous system in the subchondral bone of the condyle releases norepinephrine (NE), synergistically activating neuroactive factors such as netrin-1 and prostaglandin E2 (PGE2), inducing abnormal growth and activation of sensory nerves, thereby exacerbating pain signal transduction. This indicates that the temporomandibular joint, as a "neural joint", is more susceptible to regulation and innervation by peripheral nerves (Figure 1). On this basis, the research team found that negatively charged extracellular nucleic acids (exRNAs) in subchondral bone can recruit positively charged proteins such as VEGF and Netrin1 to form nucleic acid protein aggregates, driving neurovascular invasion into the osteochondral junction, thereby revealing the molecular mechanism of TMJ-OA condylar neurovascularization. In response to this mechanism, the team proposed a dual blocking strategy: specific clearance of local exRNA in the condyle and sustained release of bevacizumab to inhibit VEGF function. Experiments have shown that this strategy can effectively block the neurovascular signaling pathway, inhibit abnormal angiogenesis, synchronously improve pain behavioral indicators, and promote the regeneration of cartilage bone interface structure (Figure 2).

　　The series of studies have deepened the understanding of the pathological mechanism of TMJ-OA from the perspective of neural regulation, and the proposed "neurogenic joint" theory provides a potential new target for simultaneously achieving TMJ-OA symptom intervention and lesion blockade.