Journal of Oral Science Research ›› 2020, Vol. 36 ›› Issue (1): 28-32.DOI: 10.13701/j.cnki.kqyxyj.2020.01.008

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Effect of β2-adrenergic Signal Transduction on Subchondral Bone Loss of Rat Mandibular Condyles Induced by Abnormal Molar Occlusion.

LIU Geng*, LI Le, XING Lu, FAN Xiangfei   

  1. Department of Prosthodontics, Stomatology Hospital of Tianjin, Tianjin 300041, China
  • Received:2019-05-03 Online:2020-01-28 Published:2020-01-16

Abstract: Objective: To investigate the effects of β2-adrenergic signal transduction on the subchondral bone loss of rat mandibular condyles induced by abnormal molar occlusion. Methods: Abnormal molar occlusion (experimental group) and their sham control (control group) were established on rats by orthodontic methods. The experimental and control rats were intraperitoneally injected by normal saline (vehicle injection group) or β-adrenergic receptor blocker propranolol (propranolol injection group), respectively. Micro-CT was used to detect the changes of bone mineral density and microstructures of mandibular condylar subchondral bone in each group. The concentration of norepinephrine in subchondral bone was determined by enzyme-linked immunosorbent assay, while the gene expressions of adrenergic receptors were detected by real-time quantitative polymerase chain reaction and immunohistochemistry. Results: Bone mineral density (BMN), bone volume fraction (BVF), and trabecular thickness (Tb.Th) of the condylar subchondral bone decreased, while trabecular space (Tb.Sp) and norepinephrine content increased in 4- and 8-week experimental groups than those of the age-matched controls, respectively (P<0.05). The gene and protein expression of Adrb2 in the subchondral bone of the experimental group was significantly higher than those of the controls (P<0.05), while the gene expression of Adrb1 and Adrb3 were not significantly different between control and experimental groups (P>0.05). Propranolol injection significantly reversed the loss of condylar subchondral bone induced by abnormal occlusion, and the parameters of BMD and trabecular microstructures of condylar subchondral bone were significantly improved compared with the vehicle injection group (P<0.05). Conclusion: Activation of β2-adrenergic signal transduction promotes the subchondral bone loss of rat mandibular condyles induced by abnormal molar occlusion.

Key words: temporomandibular joint, mandibular condyle, subchondral bone, sympathetic nerve, β-adrenergic receptors