Simulation of the nutrient supply in fracture healing.
The healing process for bone fractures is sensitive to mechanical stability and blood supply at the fracture site. Most currently available mechanobiological algorithms of bone healing are based solely on mechanical stimuli, while the explicit analysis of revascularization and its influences on the healing process have not been thoroughly investigated in the literature. In this paper, revascularization was described by two separate processes: angiogenesis and nutrition supply. The mathematical models for angiogenesis and nutrition supply have been proposed and integrated into an existing fuzzy algorithm of fracture healing. The computational algorithm of fracture healing, consisting of stress analysis, analyses of angiogenesis and nutrient supply, and tissue differentiation, has been tested on and compared with animal experimental results published previously. The simulation results showed that, for a small and medium-sized fracture gap, the nutrient supply is sufficient for bone healing, for a large fracture gap, non-union may be induced either by deficient nutrient supply or inadequate mechanical conditions. The comparisons with experimental results demonstrated that the improved computational algorithm is able to simulate a broad spectrum of fracture healing cases and to predict and explain delayed unions and non-union induced by large gap sizes and different mechanical conditions. The new algorithm will allow the simulation of more realistic clinical fracture healing cases with various fracture gaps and geometries and may be helpful to optimise implants and methods for fracture fixation.
Chen
G
G
Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, QLD 4059, Australia. g3.chen@qut.edu.au
Niemeyer
F
F
Wehner
T
T
Simon
U
U
Schuetz
M A
MA
Pearcy
M J
MJ
Claes
L E
LE
D000818:Animals; D001842:Bone and Bones / Q000293:injuries* / Q000503:physiopathology*; D003198:Computer Simulation; D017102:Fracture Healing / Q000502:physiology*; D050723:Fractures, Bone / Q000503:physiopathology*; D006801:Humans; D008954:Models, Biological; D018919:Neovascularization, Physiologic / Q000502:physiology*