炎症反应作为骨性关节炎（osteoarthritis，OA）的重要组成部分已经被广泛接受，而趋化因子作为重要的炎症介质和趋化媒介在其中扮演着关键角色。我们前期研究发现血浆CCL3对膝关节退变人群具有较强的诊断作用，能较好的反映膝OA疾病负担。进一步我们通过临床标本检测观察到，膝OA患者体内存在血浆-关节液CCL3浓度梯度，并且滑膜中大量单核-巨噬细胞聚集。并且，体外实验也发现软骨细胞在OA过程中可大量合成CCL3，并通过CCL3-CCR1实现巨噬细胞定向趋化。基于前期工作我们提出：在骨性关节炎过程中病变软骨可能通过高表达的CCL3参与血液性单核-巨噬细胞定向趋化，进而影响OA疾病进程。本研究将从组织-细胞-分子的层次证明这一理论猜测，为骨性关节炎早期诊断以及DMOAD药物的研发提供新的思路。

Inflammation is now widely accepted to be an essential part of OA, chemokines as mediators of chemoattraction (chemotaxis) are known to play a vital role in this process. Our previous works have demonstrated that plasma CCL3 could be potential serum biomarker for knee OA with the capacity to detect pre-X-rays defined changes and stage the severity of damage in knee. We also have observed the CCL3 concentration gradient between plasma and synovial fluid and synovial tissue from patients with early knee OA is characterised by mononuclear macrophage cell infiltration. Our study as well suggested the greatly induction of CCL3 by OA chondrocyte can promote macrophage migration through CCR1. Therefore, we rise the hypothesis that CCL3 secreted by OA chondrocyte is responsible for monocyte directional migration and subsequently regulate OA progression. This program is designed to proved the hypothesis in tissue, cellular and molecular level, and offer a new visual for early OA diagnosis and DMOAD development.