Effects of Diabetes Mellitus on Reparative Osteogenesis

Abstract

Introduction: Chronic hyperglycemia as the main link in DM pathogenesis leads to systemic vessels and nerves lesion with chronic bone complications development consequently. The aim: To evaluate influence of hyperglycemia on reparative osteogenesis after perforated tibial fracture in rats. Materials and methods: A total of 30 white adult rats were subdivided into two groups: 15 healthy rats in Group 1 (control) and 15 rats with alloxan induced hyperglycemia in Group 2 (investigated) and were carried out of experiment on the 10th, 20th and 30th day after the fracture. Hyperglycemia in rats was verificated as the postprandial glycemic rate ≥ 8,0 mmol/l. Tibia diaphysis fracture was modeled by a cylindrical defect with a diameter of 2 mm with portable frezer. Morphological evaluation. A complex morphological studies included histological, morphometric and immunohistochemical examination. Results: This is confirmed by an increase in MMP-9 expression in connective tissue, a decrease in TGF-β expression in all phases, an increase in the expression of CD3 and CD20 and a marked decrease in the expression of all vascular markers. During hyperglycemia, incomplete blood supply to the tissues occurs, necrosis of bone and soft tissues develop in the area of the fracture, the reparative reaction slows down considerably and manifests itself in the development of fibrous and, less commonly, cartilage tissue. Conclusions: In hyperglycemia rats, there was a delay in the callus formation, a decrease in proliferation and ossification, and a slowdown in the processes of angiogenesis.

Melatonin inhibits osteoclastogenesis via RANKL/OPG suppression mediated by Rev‐Erbα in osteoblasts

“…Diabetes can lead to osteoporosis due to the high glucose environment inhibiting osteogenesis. [47][48][49] Moreover, diabetes can promote osteoclastogenesis. [50][51][52] These processes are closely associated with regulating RANKL/OPG expression and secretion under high F I G U R E 8 Inhibition of mir-882 inhibits expression and secretion of RANKL/OPG.…”

“…Diabetes can lead to osteoporosis due to the high glucose environment inhibiting osteogenesis 47–49 . Moreover, diabetes can promote osteoclastogenesis 50–52 .…”