The benefits of locked-plate fixation, which include improved fixation strength in osteoporotic bone1-3 and the ability to provide a more biologically friendly fixation construct4,5, have led to the rapid adoption of this technology. Biological fixation of comminuted fractures with locking plates relies on secondary fracture-healing by callus formation6,7, which is stimulated by interfragmentary motion in the millimeter range8,9. Secondary bone-healing can be enhanced by active or passive dynamization10,11. Conversely, bone-healing can be suppressed by rigid fracture fixation aimed at preventing interfragmentary motion12.

Biomechanical studies have suggested that locked-plate constructs are stiff and suppress interfragmentary motion to a level that may be insufficient to reliably promote secondary fracture-healing1,13-15. Recent clinical studies substantiate the concern that the inherently high stiffness of locked-plate constructs suppresses callus formation, contributing to a nonunion rate of up to 19% seen with periarticular locking plates16,17. Deficient healing may also contribute to late hardware failures seen with locking plates18-20 since, in the absence of osseous union, constructs remain load-bearing and eventually fail by hardware fatigue or loss of fixation.

This paper summarizes a line of research that addresses two questions of critical importance when using locked-plate constructs:

Does the high stiffness of locked-plate constructs suppress callus formation and fracture-healing?

Can a stiffness-reduced locked-plate technique, termed far cortical locking, improve fracture-healing, compared with standard locked plating, by providing flexible fixation and parallel interfragmentary motion?



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