Background
Obesity affects bone health to varying degrees, depending on the skeletal site (weight-bearing or non-weight-bearing) and compartment (cortical or trabecular), and is a risk factor for orthopedic disorders, including bone fractures. However, the effect and mechanisms of obesity on healing of bone fracture is little understood.
Conclusion
Bone fracture healing was significantly slower in the obese mice, relative to that of normal mice. The lower levels of CGRP, FGF, and TGF-β, and higher level of TNF-α, observed in obese mice may contribute to this observed delay in fracture healing.
Methods
The healing bone fractures of the tibia in genetically obese mice was evaluated relative to normal mice at weekly intervals for 28 days using X-ray scans, hematoxylin and eosin (H&E) stain, and alcian blue (AB) stain. Plasma concentrations of relevant proteins were also compared via enzyme-linked immunosorbent assay (ELISA). These included calcitonin gene-related peptide (CGRP), fibroblast growth factor (FGF), transforming growth factor beta 1 (TGF-β1), and tumor necrosis factor-α (TNF-α).
Results
Bone fracture healing was delayed in the obese mice compared with the control group of normal mice, based on X-ray, H&E stain, and AB stain analysis. This was accompanied with significantly low plasma CGRP, FGF, and TGF-β1 (ELISA). However, TNF-α was significantly higher in obese mice compared with the control.