Diabetes Mellitus Accelerates Progression of Osteoarthritis in Streptozotocin-induced Diabetic Mice by Deteriorating Bone Microarchitecture, Bone Mineral Composition and Bone Strength of Subchondral Bone

Abstract

Background : The purpose of this study is to develop an optimal DM-OA mice model; to validate that diabetes aggravates OA; and to evaluate the microarchitecture, chemical composition and biomechanical properties of SB as a consequence of the damaged induced by diabetes OA. Methods: Mice were randomly divided into three groups: DM-OA group, OA group and Sham group. Blood glucose levels, body weight and food intake of all animals were recorded. A semi-quantitative grading system (OARSI) was used to evaluated cartilage and SB degeneration. Microspectroscopy, microindentations, micro‑CT imaging and fracture load of compression testing were also used to evaluated the properties of trabecular SB. Results: Glycemic monitoring and pancreas pathological results indicated stable high blood glucose and massive destruction of pancreas and islet cells in the DM-OA group. The mineral-to-collagen ratio, microindentation elastic modulus, hardness, micro-architectural parameters, bone mineral density and fracture load of SB trabecular bone of the DM-OA group joint was lower than other two groups. On the other hand, The OARSI score, trabecular spacing and structural model index of the DM-OA group joint was higher than the other two groups. Conclusions: The glycemic and pancreatic pathological results indicated the DM-OA model to be a simple and reliable model induced by STZ and surgery. The results showed the mechanisms in which diabetes accelerates OA by damaging and deteriorating the functions SB including microarchitecture, chemical composition and biomechanical properties.

Interactions Between Diabetes Mellitus and Osteoarthritis: From Animal Studies to Clinical Data

“…(28) STZ treated mice also showed enhanced cartilage damage and lower expression of collagen II when compared to the control mice. (18,29,30) Consistent with the T1D rat models, work from our group has recently shown a significant loss of proteoglycan content in an STZ-induced T1D C57BL/6 mouse model at 16 weeks of age. (31) C57BL/6 male mice on a high fat (HF) diet (as a model of T2D) had larger osteophytes and displayed more synovial hyperplasia than control mice on regular chow.…”

“…( 28 ) STZ treated mice also showed enhanced cartilage damage and lower expression of collagen II when compared to the control mice. ( 18,29,30 )…”