The communication and interaction between osteoblast(OB) and osteoclast(OC) is the key factor for regional balance of bone remolding. OB and OC should be seen as “one unit” in the research of the mechanism of bone remolding. Previous studies for imbalance of periprosthetic bone remolding have paid little attention to the communication between OB and OC. They studied either OB or OC, evaluating the effect of particles on one kind of cells. Therefore, the results were being biased. The latest study has shown that the bidirectional ephrinB2/EphB4 signaling pathway is essential to the communication between OB and OC. It is proposed that this communication ought to be valued in the research of imbalance of bone remolding in the condition of co-culture of OB and OC. We hypothesize ephrinB2/EphB4 pathway as a key point in the imbalance bone remolding pathological event. The effect of particles on the interaction between OB and OC is observed through in vitro and in vivo procedures. The function and mechanism of ephrinB2/EphB4 pathway in this imbalance bone remolding pathological event will be evaluated. Through this research, the mechanism of imbalance of periprosthetic bone remolding may be explained more comprehensively from the new perspective of molecular communication. The research simulates real life condition, thus providing theoretical basis for normal procedure of bone remolding, and new idea and treatment methods for bone metabolic diseases and periodontal diseases.
成骨细胞和破骨细胞以接触通讯的方式共同调控骨重建平衡,这也决定了两者的不可分割性,因此在研究骨重建机制时,应将两者作为一个“单位”来探讨。既往对颗粒诱导骨重建失衡的实验忽视了成骨细胞和破骨细胞间的通讯联系,将两者分开研究,存在局限性。最新研究表明,具有双向信号传递特点的ephrinB2/EphB4在成骨细胞和破骨细胞间的通讯中起关键性作用。本项目提出对颗粒诱导骨重建失衡的研究,必须重视成骨细胞和破骨细胞间的通讯,将实验设置在两种细胞共存的条件下,以ephrinB2/EphB4通路作为切入点,观察颗粒对成骨细胞和破骨细胞间通讯的影响和相应骨重建的变化,在更接近实际病理状态的条件下,从细胞间分子通讯机制这一全新角度解释颗粒诱导骨重建失衡的原因,有望为阐明松动的发生机理提供科学依据,为防治提供有效靶点,还可为阐明骨重建的基本过程、为骨代谢性疾病和骨肿瘤等提供新思路。
成骨细胞和破骨细胞以直接接触通讯的方式共同调控骨重建平衡,这也决定了两者的不可分割性,因此在研究骨重建机制时,应将两者作为一个“单位”来探讨。既往对颗粒诱导骨重建失衡的实验忽视了成骨细胞和破骨细胞间的通讯联系,将两者分开研究,存在局限性。最新研究表明,具有双向信号传递特点的ephrinB2/EphB4在成骨细胞和破骨细胞间的通讯中起关键性作用。本项目提出对颗粒诱导骨重建失衡的研究,必须重视成骨细胞和破骨细胞间的通讯,将实验设置在两种细胞共存的条件下,以ephrinB2/EphB4通路作为切入点,观察颗粒对成骨细胞和破骨细胞间通讯的影响和相应骨重建的变化,在更接近实际病理状态的条件下,从细胞间分子通讯机制这一全新角度解释颗粒诱导骨重建失衡的原因,有望为阐明松动的发生机理提供科学依据,为防治提供有效靶点,还可为阐明骨重建的基本过程、为骨代谢性疾病和骨肿瘤等提供新思路。
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数据更新时间:2023-05-31
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