Abstract

Sufficient vascularization of the fracture-healing zone is a prerequisite for undisturbed bone healing. One important factor affecting the vascularization is the interfragmentary movement in the fracture-healing zone. Many studies have demonstrated that stable fixation with predominatly moderate interfragmentary compression movement can stimulate vascularization and the healing process whereas unstable fracture fixation delays the vascularization and bone healing process. Instability of fracture fixation, in particular large shearing interfragmentary movement, can cause delayed healing or non-unions.We hypothesize that the direction of interfragmentary movement affects vascularization in the fracture-healing zone. Cyclic compressive strain stimulates greater vessel formation than tensile or shearing strain. This is due to differences in the local mechanical environment which are not delineated by the direction-independent characterization of interfragmentary movement typically reported. We propose that new vessel formations buckle under compressive loading without significant load transfer across endothelial cell junctions while both tensile and shearing deformations result in disruptive loads despite a biochemically angiogenic environment.From a clinical perspective, this means that the optimal conditions for rapid vascularization result from fracture fixation that minimizes cyclic tensile and shearing movements in the healing zone while allowing moderate compressive movements

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