骨性关节炎（OA）不仅仅是关节软骨的疾患，是软骨和软骨下骨功能体整体的疾患。OA发病过程中，伴随软骨下骨破骨细胞（Osteoclast）表达增加，破坏了原有TGF-β溶度梯度，从而最终导致骨髓间充质干细胞（MSCs）被诱导至骨髓腔形成异位“骨岛”而诱发OA。但是MSCs的来源仍不清楚。近期学者提出一种新型的可以偶联骨形成的H-type血管，即CD31hiEmcnhi血管。我们也在试验中进一步证实在骨皮质生长发育过程中破骨前体细胞（Pre-osteoclast）诱导了H-type 血管形成。但是在OA发病过程中，软骨下骨硬化是否伴有H-type 血管形成，以及该血管是否由软骨下骨Pre-osteoclast诱导产生目前仍不清楚。基于以上理论基础，我们将Pre-osteoclast诱导的血管-骨形成偶联机制引入到OA发病机制的探讨中，旨在为骨性关节炎的预防和临床治疗提供一个新的视点和理论基础。

Osteoarthritis (OA) is not just the disease of articular cartilage, but involving the function unit of cartilage and subchondral bone. During OA development, osteoclastic bone resorption in subchondral bone enhances, which leads to excessive activation and liberation of TGF-β and interrupts its original natural concentration gradient, finally, causing MSCs being recruited to bone marrow to form “osteoid islets”. However, the origin of MSCs for the formation of osteoid islets is still unclear until now. Recently, a new type of H-type vessels, also called CD31hiEmcnhi vessels, has been found with a function of coupling bone formation. We also found during the development of cortical bone, Pre-osteoclast induced the formation of H-type vessels to couple bone formation. However, during the onset of OA, it’s still unknown whether the subchondral bone sclerosis is accompanied with H-type vessels formation, and whether this type of vessels is induced by pre-osteoclast? Based on the theoretic basis above, we plan to introduce pre-osteoclast-regulated bone-vascular coupling mechanism into the OA development, to provide a new viewpoint for OA prevention and clinical treatment.