Maintenance of optimal bone mass is controlled through the concerted functions of several cell types, including bone resorbing osteoclasts. Osteoclasts function to remove calcified tissue during developmental bone modeling, and degrade bone at sites of damage during bone remodeling. Changes to bone homeostasis can arise with alterations in osteoclastogenesis and/or catabolic activity that are not offset by anabolic activity; thus, factors that regulate osteoclastogenesis and bone resorption are of interest to further our understanding of basic bone biology, and as potential targets for therapeutic intervention. Several key cytokines, including Rankl and M-csf, as well as co-stimulatory factors elicit kinase signaling cascades that promote osteoclastogenesis. These kinase cascades are offset by the action of protein phosphatases, including members of the serine/threonine phosphatase family. Here we review the functions of serine/threonine phosphatases and their control of osteoclast differentiation and function, while highlighting deficiencies in our understanding of this understudied class of proteins within the field.

最佳骨量的维持是通过几种细胞类型的协同功能来控制的，包括骨吸收破骨细胞。破骨细胞的作用是在发育骨建模过程中去除钙化组织，并在骨重塑过程中降解损伤部位的骨。破骨细胞生成和/或分解代谢活动的变化可能会导致骨稳态的变化，而这些变化不会被合成代谢活动抵消；因此，调节破骨细胞生成和骨吸收的因素有助于我们进一步了解基础骨生物学，并作为治疗干预的潜在目标。几个关键的细胞因子，包括 Rank1 和 M-csf，以及共刺激因子引发促进破骨细胞生成的激酶信号级联。这些激酶级联反应被蛋白磷酸酶的作用所抵消，包括丝氨酸/苏氨酸磷酸酶家族的成员。在这里，我们回顾了丝氨酸/苏氨酸磷酸酶的功能及其对破骨细胞分化和功能的控制，同时强调了我们对该领域内这一未被充分研究的蛋白质类别的理解不足。