Microcomputed tomography of the femur of diabetic rats: alterations of trabecular and cortical bone microarchitecture and vasculature—a feasibility study

Abstract

Background To better understand bone fragility in type 2 diabetes mellitus and define the contribution of microcomputed tomography (micro-CT) to the evaluation of bone microarchitecture and vascularisation, we conducted an in vitro preliminary study on the femur of Zucker diabetic fatty (ZDF) rats and Zucker lean (ZL) rats. We first analysed bone microarchitecture, then determined whether micro-CT allowed to explore bone vascularisation, and finally looked for a link between these parameters. Methods Eight ZDF and six ZL rats were examined for bone microarchitecture (group 1), and six ZDF and six ZL rats were studied for bone vascularisation after Microfil® perfusion which is a radiopaque casting agent (group 2). In group 1, we used micro-CT to examine the trabecular and cortical bone microarchitecture of the femoral head, neck, shaft, and distal metaphysis. In group 2, micro-CT was used to study the blood vessels in the head, neck, and distal metaphysis. Results Compared to ZL rats, the ZDF rats exhibited significantly lower trabecular bone volume and number and higher trabecular separation in the three locations ( p = 0.02, p = 0.02, p = 0.003). Cortical porosity was significantly higher in the ZDF rats at the neck and shaft ( p = 0.001 and p = 0.005). We observed a dramatically poorer bone vascularisation in the femur of ZDF rats, especially in distal metaphysis ( p < 0.047). Conclusions Micro-CT demonstrated not only significant alterations in the bone microarchitecture of the femurs of ZDF rats, but also significant alterations in bone vascularisation. Further studies are required to demonstrate the causal link between poor vascularisation and impaired bone architecture.

<p>High Glucose Downregulates Connexin 43 Expression and Its Gap Junction and Hemichannel Function in Osteocyte-like MLO-Y4 Cells Through Activation of the p38MAPK/ERK Signal Pathway</p>

“…28,29 Studies of mice models and patients with T2DM patients have shown that T2DM is associated with a high rate of small core and microcracks in cortical bone, altering stiffness. 6,7,[30][31][32] These results suggest that cortical bone structure damage may play a crucial role in T2DM-related osteoporosis fractures.…”

“…1,2 Recent studies focused on bone structure quality have shown that trabecular and cortical bone microstructure are more fragile in patients with T2DM. [3][4][5][6] These findings have led to increased interest in the mechanisms of T2DM-induced bone microstructure damage, with the goal of developing new treatments for T2DM-induced osteoporosis.…”

“…7 Increased cortical porosity and cracking have been observed in patients with T2DM and in mouse models of the disease. 6,8,9 Osteocytes are the most abundant cells in cortical bone. Historically, osteocytes were considered inactive with no apparent function.…”

The Hyperglycemia and Hyperketonemia Impaired Bone Microstructures: A Pilot Study in Rats

“…Hyperglycemia increases the osteocyte lacunar density by decreasing osteocytic territorial matrix volume, thus increasing cellularity of cortical bone as well as affecting the bone length (27). The STZ-rats displayed an apparently smaller cortical area and a higher cortical porosity (28). The micro-CT data showed that the bone area, the total area and cortical thickness of the mid-shaft of femur were significantly decreased in the DM rats than those in the sham rats.…”

Cornelian Cherry Pulp Has Beneficial Impact on Dyslipidemia and Reduced Bone Quality in Zucker Diabetic Fatty Rats

“…This mutation causes obesity, glucose intolerance, hyperglycemia, hyperlipidemia and hyperinsulinemia [ 17 , 18 ]. ZDF rats show lower trabecular bone volume and trabecular number, higher trabecular separation and cortical porosity, improper vascularization [ 19 ], and decreased osteoblast differentiation and mineral capacity [ 15 ].…”