Figure 5

Activity of Osterix⁺ osteoprogenitors and Osteocalcin⁺ osteoblasts in subchondral bone from non-diabetic and diabetes patients. (a) The expression of Osterix⁺ osteoprogenitors and Osteocalcin⁺ osteoblasts was weaker in diabetes group than non-diabetic group on both lateral and medial sides. One-way ANOVA analysis showed that there were significant differences in the numbers of Osterix⁺ osteoprogenitors and Osteocalcin⁺ osteoblasts among groups. Of note, diabetes group had lower number of Osterix⁺ osteoprogenitors and Osteocalcin⁺ osteoblasts than non-diabetic group. ^#P<0.05 vs non-diabetic group and *P<0.05 vs control group on the same side according to Post-hoc tests. ^{^}P<0.05 between lateral and medial sides in non-diabetic group; ^&P<0.05 between lateral and medial sides in diabetic group. SB, subchondral bone. (b) Schematic figure of the potential mechanism of abnormal subchondral bone remodeling in pathogenesis of T2D-induced knee OA: the hyperglycemia and hyperinsulinemia and/or the subsequent response in T2D have adverse effects on osteoprogenitors/mesenchymal stromal cells in subchondral bone, leading to impaired osteogenesis; meanwhile, the osteoclasts are activated, further contributing to abnormal bone remodeling. These changes lead to impairments of subchondral bone microstructure and strength, adversely affecting the overlying cartilage, resulting in knee OA.