Osteoporosis is a common clinical bone disease caused by a variety of causes, it increases osteoclast production mainly by changing the inflammatory microenvironment of the body, the end result is increased bone resorption and decreased bone mass. Paradoxical bone formation is a process that regulates bone formation and increases bone mass, it can affect macrophage efferocytosis by regulating apoptosis in some osteoblasts, ultimately promoting osteoblast differentiation. Osteoblasts are mainly involved in bone formation, osteoclasts are involved in bone resorption, both of them mediate the regulation of bone homeostasis, and about 50% of the osteoblasts that underwent bone remodeling under normal homeostasis were apoptotic. When promoting the apoptosis of osteoblasts to paradoxical bone formation occurs, macrophages are recruited and perform efferocytosis, under the action of efferocytosis, macrophages were polarized into M2 macrophages, M2 macrophages regulate osteoblast differentiation, inhibit osteoclast generation, and inhibit bone resorption, at the same time, it enables the new osteoblasts to occupy the place of the original osteoblasts and continue to participate in bone formation. Because the amount of bone formation of the new osteoblasts is higher than that of the original osteoblasts, the final result is an increase in bone mass after apoptosis compared to before apoptosis. Promoting the apoptosis of some osteoblasts in the body with osteoporosis may reverse increase bone mass, paradoxical bone formation may be a new direction for the treatment of osteoporosis. Therefore, this paper proposes the treatment of osteoporosis by "paradoxical bone formation" and analyzes its related mechanism, in order to provide new ideas for the research and treatment of osteoporosis.

骨质疏松是一种临床常见的骨骼疾病，由多种因素引发，其主要机制是改变机体炎性微环境，促使破骨细胞生成增多，进而导致骨吸收增加、骨量减少。反常骨形成则是一种通过调控部分成骨细胞凋亡，进而影响巨噬细胞胞葬以促进成骨细胞分化，调节骨形成并增加骨量的过程。成骨细胞主要参与骨形成，破骨细胞参与骨吸收，二者共同介导骨稳态的调节。在正常稳态下，发生骨重塑的成骨细胞中约有50%会发生凋亡。当促成骨细胞部分凋亡引发反常骨形成时，巨噬细胞被募集并发挥胞葬作用。在胞葬作用下，巨噬细胞极化为M2型。M2巨噬细胞通过调节成骨细胞分化并抑制破骨细胞生成，在发挥骨吸收抑制作用的同时，使新鲜成骨细胞迅速占据原陈旧成骨细胞的位置继续参与骨形成。由于新鲜成骨细胞的骨形成量高于陈旧成骨细胞，所以会出现骨量较凋亡前显著增加。对出现骨质疏松的机体促进部分成骨细胞凋亡或许能够反向增加骨量，反常骨形成有望成为治疗骨质疏松的新方向。因此，本文提出通过"反常骨形成"治疗骨质疏松，并分析其相关机制，以期为骨质疏松相关研究及治疗提供新的思路。