Biomechanical characteristics of bone in streptozotocin-induced diabetic rats: Anin-vivorandomized controlled experimental study

Abstract

AIM:To investigate the in vivo effects of type Ⅰ diabetes on the mechanical strength of tibial bone in a rodent model. METHODS:The biomechanical effect of diabetes on the structural integrity of the tibia in streptozotocin induced diabetic Wistar rats was analysed. Induction of diabetes was achieved by an intra-peritoneal injection and confirmed by measuring serial blood glucose levels (> 150 mg/dL). After 8 wk the tibiae were harvested and compared to a control group. Biomechanical analysis of harvested tibiae was performed using a threepoint bending technique on a servo hydraulic MTS 858 MiniBionix frame. Maximum force applied to failure (N), stiffness (N × mm) and energy absorbed (N/mm) were recorded and plotted on load displacement curves. A displacement control loading mode of 1 mm/min was selected to simulate quasi-static loading conditions. Measurements from load-displacement curves were directly compared between groups. RESULTS:Fourteen streptozotocin induced diabetic Wistar rats were compared against nineteen non-diabetic controls. An average increase of 155.2 g in body weight was observed in the control group compared with only 5 g in the diabetic group during the experimental study period. Levels of blood glucose increased to 440.25 mg/dL in the diabetic group compared to 116.62 mg/dL in the control group.The biomechanical results demonstrate a highly significant reduction in the maximum load to failure from 69.5 N to 58 N in diabetic group compared to control (P = 0.011). Energy absorption to fracture was reduced from 28.2 N in the control group to 23.5 N in the diabetic group (P = 0.082). No significant differences were observed between the groups for bending stiffness. CONCLUSION:Streptozotocin-induced diabetes in rodents reduces the maximum force and energy absorption to failure of bone, suggesting a predisposition for fracture risk.

Protection against T1DM-Induced Bone Loss by Zinc Supplementation: Biomechanical, Histomorphometric, and Molecular Analyses in STZ-Induced Diabetic Rats

“…Additionally, the reduction in biomechanical parameters in T1DM rats agrees with studies using similar tests at seven [ 11 ] and eight weeks after diabetes confirmation [ 10 , 12 ].…”

“…Biomechanical analysis was performed on the left tibias previously stored at −80°C using three-point bending mechanical tests according to the procedure described by Korres et al [ 12 ], with modifications. We used a servo hydraulic high-precision universal testing machine, model AG-X 10 kN (Shimadzu Corporation, Tokyo, Japan).…”

“…Diabetes-induced bone-loss mechanisms are not fully understood [ 4 – 7 ] although a variety of bone-related changes are known to be influenced by hyperglycemia such as bone mineral density, femoral neck geometry, microarchitecture (trabecular, cortical thickness, and bone area), and biomechanical markers of bone turnover (ultimate strain, strength and load, stiffness, and Young’s modulus) [ 3 , 8 – 11 ]. In addition, formation of the collagen network is affected by an increase in matrix metalloproteinase (MMP) expression in diabetic conditions, especially for MMP-9, which is considered a diabetogenic factor and is upregulated in T1DM, contributing to collagen degradation and resulting in low bone collagen content and poor bone biomechanical integrity [ 12 – 15 ]. One study showed a decrease in bone mineral content (BMC) associated with an increase in urinary calcium excretion in diabetic rats.…”

Sclerostin antibody prevented progressive bone loss in combined ovariectomized and concurrent functional disuse

“…Specimens were placed on the frame horizontally with mid-shaft of the diaphysis facing to the notch in the same position and orientation in order to minimize the variation. The rate of displacement was set to be 1mm/min with a preload of 1 N and the bending was imposed on specimen continuously until fracture occurred [36]. The maximal load and the curve of load-displacement were monitored.…”

High-Fat Diet/Low-Dose Streptozotocin-Induced Type 2 Diabetes in Rats Impacts Osteogenesis and Wnt Signaling in Bone Marrow Stromal Cells

“…Even with normal BMD, T2DM patients still face a high risk of bone fractures and impaired bone healing. Recent researches have shown that these disorders primarily result from impaired bone formation rather than from bone resorption [ 2 , 35 , 36 ]. Previous studies have concentrated on the abnormal osteogenesis of skeletal tissues in DM and on the depressed proliferation, osteogenic differentiation and new bone formation ability of osteoblast cells in T1DM [ 5 , 37 ], but not on osteoblast cells in T2DM.…”