Abstract

There is controversy concerning the diabetes impact on bone quality, notorious in type 2 diabetic postmenopausal women. One pointed cause might be uncontrolled glycemia. In this study, the effect of chronic hyperglycemia in bone turnover, morphology, and biomechanics was evaluated in female Wistar rats in the presence/absence of estrogens (ovariectomy). Animals (n = 28) were divided into sham, ovariectomized (OVX), hyperglycemic (streptozotocin 40 mg/kg, single-dose i.p.-STZ), and hyperglycemic-ovariectomized (STZ + OVX) animals. Blood biomarkers were estimated 60 days postovariectomy. Body weight, vertebral microarchitecture (L4-histomorphometry), femur biomechanical properties (bending tests), tibia ultrastructure (scanning electron microscopy), and femur and urinary calcium (atomic absorption) were also evaluated. The increased PINP/CTX ratio of hyperglycemic animals and the similar ratio between STZ + OVX and healthy animals contrasting with the lower ratio of OVX (in line with its histomorphometric data) suggest a tendency for improved bone formation in hyperglycemic-ovariectomized animals. The increased tibia medullar canal, which contrasts with the unaffected cortical thickness of both hyperglycemic groups while that of OVX decreased, was associated to the increased stiffness and strength of STZ + OVX bones compared to those of OVX, in line with the observed ultrastructure. Concluding, chronic hyperglycemia in ovariectomized female rats causes bone morphological changes that translate positively in the ultrastructure and mechanical properties of cortical bones.

Highlights

  • The bone structure needs to be stiff, flexible, and light in order to resist biomechanical loading and torsion while allowing movement

  • The monitorization of blood glucose levels along the study confirmed the maintenance of the hyperglycemic status of STZ-treated animals (Figure 1) in line with serum glucose levels measured at sacrifice (Table 1)

  • Several studies have investigated the association between diabetes and osteoporosis [18,19,20] and different theories have been proposed [8, 9, 11], the mechanism by which diabetes increases the risk of fractures, independent of bone mineral density (BMD), has not been properly identified

Read more

Summary

Introduction

The bone structure needs to be stiff, flexible, and light in order to resist biomechanical loading and torsion while allowing movement. These properties are determined by a complex set of interdependent factors, including bone mass, geometrical structure, and tissue composition, which define bone quality and maintain its structural integrity and strength. This overall bone structure is influenced by both the bone ultrastructural properties and bone turnover. Bone cells (osteoclasts and osteoblasts) play an important role in this recycling process by performing bone resortion and formation continuously, whose equilibrium depends on local and endocrinal signals [1]

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call