踝关节内翻性骨关节炎的生物力学研究

The hindfoot is stabilized by bone structure, ligaments and muscles. Approximately 70% of ankle osteoarthritis concomitant with varus deformity, and its etioloty、development and treatment options still remain controversial. Nevertherless, joint preserving surgery is acknowledged. Chronic lateral ankle intability can result in ankle varus and internal ratation of the talus. Valgus inclination of the subtalar joint may compensate for mild varus ankle inclination; however, varus inclination of the subtalar joint may occur for sever varus ankle deformity. Asymmentrical ankle arthritis may be the result of stress consentration on the medial side of the ankle joint,thus varus ankle deformity can be the etiology of the ankle osteoarthritis and also the result of this process.Coronal deformity can be corrected by supramalleolar osteotomy, but not for rotational deformity. Could that explain why some of the patients do not benefit from the surgery? To confirm our hypothesis, cadaveric specimens are used in our biomechanical tests. Varus ankle deformity, lateral ligaments insufficiency, calcaneal or supramalleolar osteotomy models are created. The subtalar joint compensatory behavior and the efficacy of calcaneal or supramalleolar osteotomy are explored further. By adding the kinetic study of the patients and normal people, we are trying to elaborate the relationship of hindfoot joints and lateral soft tissue structure in varus ankle deformity, and to provide the theoretical basis for the treatment strategy of varus ankle osteoarthritis with chronic ankle instability.

踝后足稳定性主要由骨性结构、韧带及周围肌力平衡提供。近70%踝关节骨关节炎伴内翻畸形，其发生、发展及临床干预仍有很多疑问。但无论怎样，尽量延缓骨关节炎的发展是业界公认的。因为终末期骨关节炎治疗，如关节置换和融合，仅适用于老年病人，所以保留关节的踝关节周围截骨术显得尤为重要。外侧不稳可致踝关节内翻和距骨内旋，轻度内翻时距下关节将外翻代偿；严重内翻时距下关节将内翻。可能内翻致应力集中产生骨关节炎；内翻既是诱因又是发展结果。我们拟采用生物力学实验，建立踝关节内翻、外侧韧带损伤模型，通过检测踝关节、距下关节压力分布与骨性位移，研究踝上截骨、跟骨截骨对关节内压力分布影响，以及距下关节在踝关节内翻时的代偿机制。同时结合运动机能检测，从骨性、韧带、肌肉三方面综合分析，寻找踝关节内翻时踝关节、距下关节及周围软组织结构之间相互联系，为临床踝关节慢性不稳定、踝关节内翻性骨关节炎治疗时机、方案提供理论依据。

距下关节与踝关节外侧韧带在踝关节内翻性骨关节炎发生、发展过程中起重要作用。但距下关节的具体代偿机制及代偿能力不清。我们一方面通过生物力学实验，测定踝关节不同内翻角度下踝关节内压力分布情况，另一方面通过模拟负重位下CT，测量距下关节随踝关节内翻角度改变时的变化情况。发现距下关节在踝关节内翻畸形时总是外翻代偿，即使严重内翻也未发现距下关节内翻失代偿现象。踝关节从0度到10度内翻过程中，距下关节逐渐外翻代偿，踝关节内侧压力并未增高，相反因距下关节外翻代偿作用，踝关节外侧区域压力相对集中，最高达2295.3kPa。踝关节外侧压力中心外移，最大达2.11mm；而随着内翻角度的逐渐增加从10度到20度过程中，踝关节内压力中心向内侧移动，最大内移4.22mm。胫骨从0度到20度逐渐内翻过程中，距下关节总是外翻代偿的。胫骨内翻从0度到10度过程中，距下关节外翻代偿达到极限，胫骨-跟骨角度从18.1度增加到26.1度，且维持最大代偿位置，出现平台期。. 另外，通过临床随访研究发现，对于Takakura 3B期踝关节内翻性骨关节炎患者，踝上截骨与踝关节外侧韧带重建手术可有效纠正胫骨远端关节面角（TAS角）、距骨倾斜角（TT角），TT角可从术前约15度改善到术后约4度，术后踝关节Takakura分期明显改善。通过截骨纠正了踝关节力线平衡关节内压力、通过外侧韧带重建踝关节稳定性，很大程度上延缓了踝关节骨关节炎进展，为保留踝关节提供了可能。

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