Abstract
Type 2 diabetes (T2D) is associated with systemic abnormal bone remodeling and bone loss. Meanwhile, abnormal subchondral bone remodeling induces cartilage degradation, resulting in osteoarthritis (OA). Accordingly, we investigated alterations in subchondral bone remodeling, microstructure and strength in knees from T2D patients and their association with cartilage degradation. Tibial plateaus were collected from knee OA patients undergoing total knee arthroplasty and divided into non-diabetic (n=70) and diabetes (n=51) groups. Tibial plateaus were also collected from cadaver donors (n=20) and used as controls. Subchondral bone microstructure was assessed using micro-computed tomography. Bone strength was evaluated by micro-finite-element analysis. Cartilage degradation was estimated using histology. The expression of tartrate-resistant acidic phosphatase (TRAP), osterix, and osteocalcin were calculated using immunohistochemistry. Osteoarthritis Research Society International (OARSI) scores of lateral tibial plateau did not differ between non-diabetic and diabetes groups, while higher OARSI scores on medial side were detected in diabetes group. Lower bone volume fraction and trabecular number and higher structure model index were found on both sides in diabetes group. These microstructural alterations translated into lower elastic modulus in diabetes group. Moreover, diabetes group had a larger number of TRAP+ osteoclasts and lower number of Osterix+ osteoprogenitors and Osteocalcin+ osteoblasts. T2D knees are characterized by abnormal subchondral bone remodeling and microstructural and mechanical impairments, which were associated with exacerbated cartilage degradation. In regions with intact cartilage the underlying bone still had abnormal remodeling in diabetes group, suggesting that abnormal bone remodeling may contribute to the early pathogenesis of T2D-associated knee OA.
Highlights
Type 2 diabetes (T2D) is an exceedingly common chronic metabolic disorder that affects over 387 million adults worldwide and is projected to reach 592 million by 2035.1 T2D affects a number of organs, including the skeleton
We found that T2D patients had abnormal bone remodeling and microstructural deterioration and decreased strength
The bony changes have occurred in regions with intact cartilage. These findings suggest that abnormal subchondral bone remodeling may account for the exacerbation of cartilage damage when T2D and knee OA co-exist simultaneously in the same individuals
Summary
Type 2 diabetes (T2D) is an exceedingly common chronic metabolic disorder that affects over 387 million adults worldwide and is projected to reach 592 million by 2035.1 T2D affects a number of organs, including the skeleton. T2D patients have increased fragility fracture (for example, at femoral neck, distal radius, and tibia) induced by bone loss and deficits of bony microarchitecture and strength.[2,3,4,5] It was evident that bone loss was attributable to increased bone resorption[6] and decreased osteoblastogenesis.[7] In addition, the disruption of bony microarchitecture partly accounts for strength deficits in T2D patients.[4]. It has been reported that T2D is associated with significantly increased prevalence of osteoarthritis (OA),[8] the most common degenerative joint disease and the major cause of physical disability in adults. T2D has been determined as an independent risk factor of knee OA,[9] and the concept diabetic OA
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