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.
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.
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.
Keywords: Bone healing; CGRP; FGF; Obesity; TGF-β1; TNF-α.