Bones undergo continuous cycles of bone remodelling that rely on the balance between bone formation and resorption. This balance allows the bone to adapt to changes in mechanical loads and repair microdamages. However, this balance is susceptible to upset in various conditions, leading to impaired bone remodelling and abnormal bones. This is usually indicated by abnormal bone mineral density (BMD), an indicator of bone strength. Despite this, patients with type 2 diabetes mellitus (T2DM) exhibit normal to high BMD, yet still suffer from an increased risk of fractures. The activity of the bone cells is also altered as indicated by the reduced levels of bone turnover markers in T2DM observed in the circulation. The underlying mechanisms behind these skeletal outcomes in patients with T2DM remain unclear. This review summarises recent findings regarding inflammatory cytokine factors associated with T2DM to understand the mechanisms involved and considers potential therapeutic interventions.

骨骼经历依赖于骨骼形成和吸收之间的平衡的骨骼重塑的连续循环。这种平衡使骨骼能够适应机械负荷的变化并修复微损伤。然而，这种平衡在各种情况下都容易受到破坏，导致骨骼重塑受损和骨骼异常。这通常由异常的骨矿物质密度 (BMD) 表示，这是骨强度的指标。尽管如此，2 型糖尿病 (T2DM) 患者表现出正常至高 BMD，但骨折风险仍然增加。正如在循环中观察到的 T2DM 中骨转换标志物水平降低所表明的那样，骨细胞的活性也发生了改变。T2DM 患者这些骨骼结局背后的潜在机制仍不清楚。