The unstable TKA may result from a variety of distinct etiologies,1 and the identification and treatment of these etiologies at the time of revision is crucial in order to restore stability. The causes of instability that have been described include, flexion/extension gap mismatch, component malposition, isolated ligament insufficiency, extensor mechanism insufficiency, component loosening, and global instability.¹ Calliess et al. in a survey of 1449 TK revisions remarks the evolving etiology of TKA failure.² Low‐grade infection and instability are two major causes that have increased over the years. To our knowledge, this study represents the largest published series evaluating the specific failure mechanisms in revision TKA.

Surgical treatment for instability may encompass a variety of procedures, especially when the instability results from more than one etiological factor. Technical errors such as flexion/extension gap mismatch and component malpositioning tend to present early. Other causes tend to present late and result in attenuation of the soft tissue around the knee.¹ Isolated ligament insufficiency may be persistent or iatrogenic. Extensor mechanism insufficiency causing TKA instability may be categorized into patellar component problems, tendinous and patellar bone integrity problems, and soft tissue imbalance or instability of the patellofemoral joint.³ Component loosening is often identified preoperatively and confirmed at the time of revision surgery. Knees with component loosening may progress to multidirectional instability.⁴ Global instability has been subcategorized into soft tissue attenuation (due to chronic synovitis, recurrent hemarthrosis, or undersizing of the polyethylene [PE] insert), direct negative effects of the PE insert (post fracture or wear) and knee dislocation.¹ Knee dislocation after TKA has been attributed to severe flexion/extension gap mismatch and extensor mechanism insufficiency.¹