■甲状旁腺激素相关蛋白(PTHrP)是生长的重要调节因子,骨或软骨的发育和重建,并通过其唯一的受体起作用,甲状旁腺激素受体-1(PTH1R)。本研究旨在研究PTHrP的表达变化,颞下颌关节骨关节炎(TMJOA)进展过程中髁突软骨中的PTH1R和其他相关因素。
■TMJOA的动物模型是通过“树脂改性方法”构建的,并在2周时对SD大鼠实施安乐死,4周,咬合后6周和8周抬高。X线观察髁突软骨的组织学变化,苏木精-伊红(HE)和藏红O-耐绿(SO-FG)染色。PTHrP的表达式,PTH1R,Ki67,II型胶原(II型),通过定量实时聚合酶链反应(qRT-PCR)和免疫组织化学(IHC)检测各组胶原X(ColX)和Caspase3。
■TMJOA进展是时间依赖性的。在实验组中,PTHrP表达是单峰的,在4周时达到峰值,但PTH1R表达呈下降趋势。实验组从2周到8周,ColX表达而不是Caspase3表达与PTHrP呈负相关,与Ki67或ColII没有正相关关系。这些结果证明异常咬合负荷可能是TMJOA的重要致病因素。
■由于PTH1R的低表达,PTHrP不能发挥有效作用可能是TMJOA进展的原因之一。PTHrP可能是调节软骨细胞肥大分化的直接因子,但它不直接调节软骨细胞的增殖和凋亡,两种调节作用的实现可能取决于对肥大分化的抑制。
UNASSIGNED: Parathyroid hormone-related protein (PTHrP) is an important regulatory factor in the growth, development and remodeling of bone or cartilage, and acts through its sole receptor, parathyroid hormone receptor-1 (
PTH1R). The present study aimed to research the expression changes of PTHrP,
PTH1R and other relevant factors in condylar cartilage during the progress of temporomandibular joint osteoarthritis (TMJOA).
UNASSIGNED: The animal model of TMJOA was constructed by the \"resin-modified method\", and Sprague Dawley (SD) rats were euthanized at 2 weeks, 4 weeks, 6 weeks and 8 weeks after occlusal elevation. The histological changes of condylar cartilage were observed by X-ray, hematoxylin-eosin (HE) and safranine O-fast green (SO-FG) staining. The expressions of PTHrP,
PTH1R, Ki67, Collagen II (Col II), Collagen X (Col X) and Caspase 3 in each group were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC).
UNASSIGNED: TMJOA progression was time-dependent. In the experimental group, PTHrP expression was unimodal with a peak at 4 weeks, but
PTH1R expression showed a decreasing trend. From 2 weeks to 8 weeks in the experimental group, Col X expression rather than Caspase 3 expression was negatively related to PTHrP\'s, which has no positive relation to Ki67 or Col II. These results demonstrated abnormal occlusal load may be an important pathogenic factor of TMJOA.
UNASSIGNED: It may be one of the reasons of TMJOA progression that PTHrP can\'t play an effective role due to the low expression of
PTH1R. PTHrP may be a direct factor regulating the hypertrophic differentiation of chondrocytes, but it does not directly regulate the proliferation and apoptosis of chondrocytes, and the realization of both regulatory effects may depend on the inhibition of hypertrophic differentiation.