肾上腺素受体信号在磨牙异常咬合致大鼠髁突软骨下骨丢失中的作用

Effect ofβ2-adrenergic Signal Transduction on Subchondral Bone Loss of Rat Mandibular Condyles Induced by Abnormal Molar Occlusion

目的:探索肾上腺素受体信号在磨牙异常咬合致大鼠髁突软骨下骨丢失中的作用。方法:采用正畸分牙法建立磨牙异常咬合大鼠模型(实验组)及对照组,对照及实验组大鼠分别接受腹膜注射生理盐水(溶剂注射组)或β受体阻滞剂普萘洛尔(普萘洛尔注射组)。用Micro-CT检测各组大鼠髁突软骨下骨密度及骨小梁结构学参数变化,用酶联免疫吸附法测定各组软骨下骨去甲肾上腺素浓度,用实时定量聚合酶链反应及免疫组化检测各组软骨下骨肾上腺素受体表达。结果:4、8周实验组软骨下骨密度、骨体积分数及骨小梁厚度均较其对照组降低,但其骨小梁间隙及去甲肾上腺素含量则较对照组增高(P<0.05);实验组大鼠髁突软骨下骨中Adrb2基因及蛋白的表达较其对照组增高(P<0.05),但Adrb1及Adrb3基因的表达在两组间无显著差异(P>0.05);普萘洛尔注射可显著逆转实验组大鼠髁突软骨下骨丢失,其软骨下骨小梁密度、骨体积分数、骨小梁厚度及间隙等参数均较溶剂注射实验组显著改善(P<0.05)。结论:异常的咬合力可通过激活β2肾上腺素受体信号促进髁突软骨下骨骨丢失。

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 ofβ2-adrenergic signal transduction promotes the subchondral bone loss of rat mandibular condyles induced by abnormal molar occlusion.