Tornetta Rockwood Adults 9781975137298 FINAL VERSION

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SECTION ONE • General Principles

A, B, C

D, E Figure 1-27.  Locked plating of diaphyseal fractures ( A, B, C ) and metaphyseal osteotomies ( D, E ). A: Load- ing of locked plate constructs with a remaining fracture gap leads to an asymmetric strain distribution ( blue area ) with some interfragmentary strain opposite the plate but minimal strain directly beneath the plate. B: Reducing the stiffness of plate fixation by using a longer bridge span increases strain opposite the plate but not beneath the plate. C: From a mechanobiologic point of view, a uniform strain distribution across the fracture gap is desirable for stimulation of circumferential bone healing. An open-wedge osteotomy of the proximal tibia stabilized by a stiff plate ( D ) leads to minimal interfragmentary motion (IFM) beneath the plate and suppresses bone formation even 18 months after operation ( E ). ( D, E ) (Reprinted from Roderer G, Gebhard F, Duerselen L, et al. Delayed bone healing following high tibial osteotomy related to increased implant stiffness in locked plating. Injury . 2014;45(10):1648–1652. Copyright © 2014 Elsevier. With permission.)

of the leg and a clinically relevant fracture gap of 2.5 mm, the interfragmentary motion opposite the plate causes a tissue strain of approximately 30%. Such an interfragmentary tissue strain is known to stimulate callus formation. 54 Should plate fixation lead to contact between the bony fragments opposite of the plate, the entire construct becomes very stiff, with virtually no interfrag- mentary motion or tissue strain beneath the plate (Fig. 1-27D). For example, after stabilizing an open-wedge osteotomy of the proximal tibial with a plate applied to bridge the open wedge, a 500 N axial load induced only 0.05 mm of axial motion adja- cent to the plate, corresponding to a stiffness of 10,000 N/mm. 180 Accordingly, a clinical study on plating of high tibial osteotomies reported that no bone healing was observed in 66% of all patients directly beneath the plate (Fig. 1-27E). 180 CONSTRUCT STIFFNESS AND FRACTURE HEALING How can the stiffness information for different fixation con- structs be used to target a specific mode of bone healing in order to improve patient outcomes? Unfortunately, the lack of clinical evidence prevents drawing conclusive correlations between the stiffness of fixation constructs and healing outcomes for two reasons. First, clinical assessment of construct stiffness has only been performed in a few studies, and secondly there are no prospective randomized clinical studies that quantitatively cor- relate the healing outcome to the construct stiffness. Consequently, animal experiments provide the best method to investigate the effect of fracture fixation stiffness on bone

healing. In standardized large animal experiments, construct stiffness can be controlled and the healing outcome can be quantified and correlated. Sheep studies have shown that both axial and shear stiffness must be controlled to achieve the most favorable healing outcome. 202 Steiner numerically simulated the fracture-healing outcome for 96 different combinations of shear and axial stiffness values and plotted the results in a bone healing map (Fig. 1-28). 202 The results were corroborated by comparison with 14 animal studies that documented construct stiffness and healing outcome. 202 The bone healing map shows that optimal healing can be expected with a construct that pro- vides shear stiffness > 300 N/mm and an axial stiffness in the range of 1,000 to 2,500 N/mm. This conclusion was limited to a 3-mm fracture gap, and other gap sizes may lead to different stiffness requirements. 55,202 Recent studies have shown that plat- ing constructs with an axial stiffness of approximately 600 N/ mm significantly improved fracture healing compared to more rigid fixation, both in the presence of a 3-mm fracture gap and for well-reduced fractures. 39 The bone healing map does not account for these most recent data; inclusion of which may shift the lower boundary of the optimal healing region. Insufficient axial stiffness can delay healing because of instability of the fix- ation, while excessive axial stiffness reduces the stimulus for bone formation due to deficient interfragmentary tissue strain. Shear stiffness < 300 N/mm generally delays the healing process. When the published stiffness data of clinical fracture fixation constructs are plotted on the bone healing map, 59 it becomes evident that the axial stiffness of external fixators is low and

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