实验性单侧前牙反牙合修复体对大鼠髁突软骨中甲状旁腺激素相关蛋白和PTH/PTHrP受体-1表达的影响

目的 探讨实验性单侧前牙反牙合修复体对大鼠髁突软骨中甲状旁腺激素相关蛋白（PTHrP）及PTH/PTHrP 受体-1（PTH1R）表达的影响。方法 在6周龄SD大鼠左侧上、下切牙粘接金属不良修复体，使其呈反牙合关系，2、 4、8周后取颞下颌关节（TMJ），苏木精-伊红（HE）染色观察组织形态学变化，免疫组织化学染色及实时定量聚合酶链反应检测PTHrP、PTH1R的表达情况。结果 8周时，实验组髁突软骨出现明显退行性变，PTHrP阳性细胞较对照组显著增多（P<0.01）， PTH1R阳性细胞明显减少（P<0.01）；实验组髁突软骨PTHrP mRNA的表达显著高于对照组（P<0.01），而PTH1R mRNA表达明显降低（P<0.01）。结论 髁突软骨PTHrP的高表达因PTH1R的低表达不能有效发 挥作用，可能是髁突软骨骨关节病样变的重要分子机制之一。

Effects of experimentally created unilateral anterior crossbite prosthesis on the expression of parathyroid hormone-related peptide and parathyroid hormone receptor-1 in mandibular condylar cartilage of rat

Objective  To study the effects of experimentally created unilateral anterior crossbite prosthesis on the expression of parathyroid hormone-related peptide(PTHrP) and parathyroid hormone receptor-1(PTH1R) in mandibular condylar cartilage of SD rat. Methods In experimental groups, the unilateral anterior crossbite metal prosthesis was cemented to the left incisors of the maxilla and mandible of 6-week-old SD rats, respectively. Animals were sacrificed at 2, 4, 8 weeks. Hematoxylin-eosin(HE) staining were carried out for studying the morphological changes of the condylar cartilage. Immunohistochemical staining and real-time polymerase chain reaction(PCR) analysis were performed to detect the levels of expression of PTHrP and PTH1R in the condylar cartilages. Results  The obvious degenerative changes were found in the condylar cartilages in experimental group at 8 weeks. Comparing to the control group, the expression of PTHrP mRNA(P<0.01) and protein (P<0.01) in the experimental group were increased， whereas PTH1R mRNA(P<0.01) and protein(P<0.01) levels were decreased. Conclusion  The expression of PTHrP was increased in the condylar cartilage of rat with unilateral anterior crossbite metal prosthesis but its effects might be limited because of decreased expression of PTH1R in the condylar cartilage. The low level expression of PTH1R should be a part of the constitution of the molecular pathomechanism of temporomandibular joint osteoarthritis(TMJOA)-like lesion.