ESB Research Award 1992. The mechanism of bone remodeling and resorption around press-fitted THA stems.
ESB Research Award 1992. The mechanism of bone remodeling and resorption around press-fitted THA stems.
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DOI：
10.1016/0021-9290(93)90001-u
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发表时间：
1993-04
影响因子：
2.4
通讯作者：
B. Rietbergen;R. Huiskes;H. Weinans;D. Sumner;T. Turner;J. Galante
中科院分区：
文献类型：
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作者：
B. Rietbergen;R. Huiskes;H. Weinans;D. Sumner;T. Turner;J. Galante
威胁全髋关节置换术长期完整性的一个主要问题是，从长期来看，非骨水泥假体周围的近端骨丢失。人们普遍认为“应力屏蔽”是导致这一问题的原因：假体植入后，周围的骨骼部分被“屏蔽”，不受负荷的影响，开始吸收。对这个问题提出的解决方案之一是应用压装阀杆。这些表面光滑的植入物被认为会引起更高的近端骨负荷，因此，与粘结植入物相比，应力屏蔽更少，因为每次加载时，它们都会嵌进股骨。然而，在一项为期两年的狗实验中，在压合和粘结的植入物周围发现了类似数量的近端皮质吸收。问题是如何在完全不同的应力条件下形成类似的吸收模式，以及这种现象是否可以用基于Wolff定律的自适应骨重塑理论来解释。采用一种先进的迭代计算机模拟模型对动物实验中的重塑过程进行分析。根据动物实验构型建立三维有限元模型，在该构型中，将光滑的、压紧的支架单侧施加于犬体内。有限元模型与迭代重塑程序相结合，在早期的研究中得到了验证。在该模型中，实现了松动的骨-种植体界面的适当的非线性表示，也能够模拟未涂覆的种植体周围的近端界面间隙。模拟模型预测的近端骨丢失和远端骨密度与动物模型中发现的相似。因此，皮质骨丢失确实可以用应变适应性骨重建理论来预测。通过解开模拟过程，上述问题就可以得到解答。在最初的重建过程中，远端骨床的致密化导致轴向干位移(弹性下沉)减少，减少了干的楔入效应，从而降低了近端骨的负荷，导致近端骨丢失。因此，在粘合的茎的情况下，近端的吸收过程单调地发展到一个新的平衡，而围绕光滑的、压紧的茎的过程发展是非单调的。这主要是由于未结合的界面条件和近端纤维膜的发展所致。重塑过程逐渐导致干卡在远端的骨干(近端的‘应力旁路’)。
A major problem threatening the long-term integrity of total hip replacement is the loss of proximal bone often found around noncemented stems in the long term. It is generally accepted that ‘stress shielding’ is the cause for this problem: after implantation of the prosthesis the surrounding bone is partially ‘shielded’ from load carrying and starts to resorb. One of the proposed answers to this problem is the application of press-fitted stems. These smooth-surfaced implants are thought to provoke higher proximal bone loading, and, hence, less stress shielding than bonded implants, because they are wedged into the femur every time when loaded. However, in a two-year experiment in dogs, similar amounts of resorption of the proximal cortex were found around press-fitted and bonded implants. The question arises how similar resorption patterns can develop under completely different stress conditions, and whether this phenomenon can be explained by adaptive bone remodeling theories based on Wolff's law.In the present study an answer was sought for this question. An advanced iterative computer simulation model was used to analyze the remodeling process in the animal experiment. Three-dimensional finite element models were constructed from the animal experimental configuration, in which smooth, press-fitted stems were applied unilaterally in the canine. The FE model was integrated with iterative remodeling procedures, validated in earlier studies. In the model an appropriate non-linear representation of the loose bone-implant interface was realized, also capable of simulating the proximal interface gap that was found around the uncoated implants. The simulation models predicted similar amounts of proximal bone loss and distal bone densification as found in the animal model. Hence, the cortical bone loss could indeed be predicted by the strain-adaptive bone remodeling theory. By unraveling the simulation process, the question stated above could be answered. Densification of the distal bone bed during the initial remodeling process was found to cause reduced axial stem displacement (elastic subsidence), decreasing the wedging effect of the stem and, hence, decreasing the loading of the proximal bone, resulting in proximal bone loss. Hence, whereas in the case of bonded stems the proximal resorption process develops monotonously to a new equilibrium, the process around smooth, press-fitted stems develops nonmonotonously. This is due primarily to the unbonded interface conditions and the development of a proximal fibrous membrane. The remodeling process the gradually causes the stem to be jammed in the distal diaphyses (proximal ‘stress bypass’).