Temporomandibular joint osteoarthritis is a common chronic degenerative disease,in which joint pain is the most signif-icant symptom,but its pathogenesis is still unclear.Significant subchondral bone lesions can occur in the early stage of osteoarthritis progression,and more and more experimental evidence shows that subchondral bone lesions play an important role in the pain caused by osteoarthritis.Osteoclasts,osteocytes,osteoblasts,endothelial cells,new generating nerves and blood vessels in the sub-chondral bone matrix microenvironment interact with each other and participate in the process of osteoarthritis pain.Therefore,regu-lating the subchondral bone matrix microenvironment is expected to become a new strategy to control joint pain.

Temporomandibular joint osteoarthritis (TMJ-OA) is a common disease often accompanied by pain, seriously affecting physical and mental health of patients. Abnormal innervation at the osteochondral junction has been considered as a predominant origin of arthralgia, while the specific mechanism mediating pain remains unclear. To investigate the underlying mechanism of TMJ-OA pain, an abnormal joint loading model was used to induce TMJ-OA pain. We found that during the development of TMJ-OA, the increased innervation of sympathetic nerve of subchondral bone precedes that of sensory nerves. Furthermore, these two types of nerves are spatially closely associated. Additionally, it was discovered that activation of sympathetic neural signals promotes osteoarthritic pain in mice, whereas blocking these signals effectively alleviates pain. In vitro experiments also confirmed that norepinephrine released by sympathetic neurons promotes the activation and axonal growth of sensory neurons. Moreover, we also discovered that through releasing norepinephrine, regional sympathetic nerves of subchondral bone were found to regulate growth and activation of local sensory nerves synergistically with other pain regulators. This study identified the role of regional sympathetic nerves in mediating pain in TMJ-OA. It sheds light on a new mechanism of abnormal innervation at the osteochondral junction and the regional crosstalk between peripheral nerves, providing a potential target for treating TMJ-OA pain.
Animals ; Osteoarthritis/physiopathology* ; Mice ; Sympathetic Nervous System/physiopathology* ; Temporomandibular Joint Disorders/physiopathology* ; Arthralgia ; Sensory Receptor Cells ; Disease Models, Animal ; Norepinephrine ; Male ; Temporomandibular Joint/physiopathology* ; Pain Measurement

Temporomandibular joint osteoarthritis(TMJ-OA)is a chronic disorder characterized by degeneration of articular cartilage,pain,and functional impairment,with pathological calcification serving as a central pathological hallmark closely associated with dis-ease progression.Recent studies have demonstrated that pathological calcification accelerates joint destruction by altering cartilage bio-mechanical properties,activating inflammatory responses,and promoting matrix degradation pathways.This review systematically re-views the critical role of pathological calcification in the pathogenesis of temporomandibular joint osteoarthritis(TMJ-OA),with a focus on molecular mechanisms including key signaling pathways,autophagy-derived calcifying vesicles,lysosomal destabilization and organ-elle crosstalk.It further summarizes novel intervention strategies such as pharmacological treatments,gene therapy,and nanotechnology-based approaches,thereby providing a theoretical foundation for the precise prevention and treatment of TMJ-OA.

Temporomandibular joint osteoarthritis is a common chronic degenerative disease,in which joint pain is the most signif-icant symptom,but its pathogenesis is still unclear.Significant subchondral bone lesions can occur in the early stage of osteoarthritis progression,and more and more experimental evidence shows that subchondral bone lesions play an important role in the pain caused by osteoarthritis.Osteoclasts,osteocytes,osteoblasts,endothelial cells,new generating nerves and blood vessels in the sub-chondral bone matrix microenvironment interact with each other and participate in the process of osteoarthritis pain.Therefore,regu-lating the subchondral bone matrix microenvironment is expected to become a new strategy to control joint pain.

Temporomandibular joint osteoarthritis(TMJ-OA)is a chronic disorder characterized by degeneration of articular cartilage,pain,and functional impairment,with pathological calcification serving as a central pathological hallmark closely associated with dis-ease progression.Recent studies have demonstrated that pathological calcification accelerates joint destruction by altering cartilage bio-mechanical properties,activating inflammatory responses,and promoting matrix degradation pathways.This review systematically re-views the critical role of pathological calcification in the pathogenesis of temporomandibular joint osteoarthritis(TMJ-OA),with a focus on molecular mechanisms including key signaling pathways,autophagy-derived calcifying vesicles,lysosomal destabilization and organ-elle crosstalk.It further summarizes novel intervention strategies such as pharmacological treatments,gene therapy,and nanotechnology-based approaches,thereby providing a theoretical foundation for the precise prevention and treatment of TMJ-OA.

BACKGROUND: Hemorrhage control has been an important issue in spine surgery. The widely used gelatin sponge is limited by its long-time bleeding control and poor hemorrhage control. Therefore, new techniques are needed to control bleeding in spine surgery. OBJRCTIVE: To compare the hemostatic effect of fluid gelatin Surgiflo™ with absorbable gelatin sponge in single level posterior lumbar fusion surgery. METHODS: Ninety-eight patients consisting of 52 males and 46 females, aged 54. 32 years who received treatment between September 2017 and December 2017 in Xijing Hospital of The Fourth Military Medical University were included in this study. All patients underwent single-level L4/5 lumbar fusion. Among them, 48 patients received intraoperative hemostasis with fluid gelatin SurgifloTM and 50 patients received intraoperative hemostasis with conventional gelatin sponge. Intraoperative bleeding volume, postoperative drainage volume, success rate of hemostasis in 3 minutes and changes of hemoglobin levels in perioperative period were compared between the two groups. RESULTS AND CONCLUSIONS: The operation time in the Surgiflo™group was significantly shorter than that in the gelatin sponge group [(105±26) vs. (118±32) min, P < 0. 05]. The amount of intraoperative blood loss and total amount of drainage were (156±57) mL and (106±42) mL in the Surgiflo™group which were significantly lower than those in the gelatin sponge group [(204±62) mL, (148±35) mL, P < 0. 05]. The success rate of hemostasis within 3 minutes in the Surgiflo™ group was significantly higher than that in the gelatin sponge group (94% vs. 80%, P < 0. 05). The change in hemoglobin level during the perioperative period relative to pre-surgery level was significantly higher in the Surgiflo™ group was significantly lower than that in the gelatin sponge group [(12. 3±3. 6) vs. (22. 8±4. 3) g/L, P < 0. 05]. No complications such as anaphylaxis, immune rejection, or delayed hematoma occurred in both groups. These results suggest that fluid gelatin Surgiflo™ can significantly reduce intraoperative blood loss and postoperative drainage volume in single-level lumbar fusion surgery and exhibit better hemostatic effects.