Due to the success, quantified by both clinical improvement and durability, the number of TKA procedures performed annually has steadily increased since its introduction and it is predicted that approximately 3 million knee arthroplasties will be performed in 2030. Part of this exponential growth is due to indication expansion and TKA is now often performed for younger, more active and heavier patients that historically would have been denied the procedure. Combined with an aging population, often afflicted with comorbidities, it is not surprising that the number of TKA revisions performed annually is also increasing. TKA failure, with subsequent revision surgery, is a costly problem often associated with substantial morbidity. In order to reduce the incidence of TKA failure, it is critical that we expand our knowledge of the issue by asking the question, why are TKAs failing today? Due to a demographically evolving arthroplasty population, the introduction of the new surgical techniques and the routine addition to the market of next generation implants, it is likely that the mechanisms for TKA failure will change over time. It is also possible that there may be regional and even institutional variance when the reasons for TKA failure are investigated. Therefore, it is critical that this question concerning failure mechanisms be repeatedly studied and examined by various study designs in multiple clinical settings.

This lecture will focus on several key aspects of TKA failure: Early (less than 2 to 5 years) vs. late failure; Historically, why did TKAs fail and what has been done to decrease certain failure modes; Why are TKAs failing today?

Only with a comprehensive understanding of TKA failure mechanisms will we be able to properly address this problem and focus our efforts and resources on meaningful solutions. Even incremental improvements that only modestly decrease TKA failure incidence should provide our healthcare system with enormous savings and more importantly, greatly decrease patient morbidity.

Bone marrow lesions (BMLs), identified by MRI, are defined as a region of cancellous bone with high T2 and low T1 signal intensity. They are associated with various knee pathologies including spontaneous osteonecrosis of the knee (SPONK), AVN, trauma (fracture and bone contusion), following arthroscopy and secondary to overuse (i.e., after completing a marathon). They also are commonly recognised in patients with knee OA (referred to as OA-BMLs) and their substantial importance in knee OA pathogenesis has been recently identified. Depending upon the etiology (i.e., bone contusion, overuse, etc.) of the BML, these lesions can be “acute” in nature and spontaneously resolve over time. However, OA-BMLs generally are considered to be a “chronic” condition and overtime they have been shown to often persist and increase in size. Retrieval studies following THA and TKA, in patients with a preoperatively identified BML, have greatly expanded our understanding of OA – BMLs and these investigations consistently identify the critical role subchondral bone plays in OA disease progression. Histologic, histochemical and mechanical studies of OA-BMLs demonstrate significant alternations from healthy subchondral bone. The effected bone contains regions where fibrous tissue has replaced cancellous bone, microfractures are present and vascularity is increased. There is an increased concentration of inflammatory mediators and the bone structural integrity is compromised.

Standard radiographs of the knee correlate only modestly with patient symptoms, but conversely, the presence of an OA-BML is an extremely strong predictor of pain and knee joint dysfunction. Felson et al. reported this relationship. In a large group of patients with painful knee OA, 77.5% of these patients had a BML. Both the presence and size of the BML, following multiregression analysis, were significant predictors of knee pain severity.

Additionally, likely secondary to inadequate subchondral bone plate support, the presence of an OA-BML is associated with subchondral bone attrition (SBA). SBA leads to collapse of the subchondral bone plate and progressive joint deformity.

Based on the association of an OA-BML with pain, joint dysfunction and deformity, it is not surprising that these lesions are prognostic for patients seeking knee arthroplasty. Several studies have demonstrated that the odds of knee arthroplasty performance are substantially higher in patents with an OA-BML.

This enhanced understanding of knee OA pathogenesis and the critical role of subchondral bone in this process creates an opportunity for development of novel prevention and treatment strategies. Prevention of OA-BML formation has been considered and pharmacologic interventions proposed. Recent studies have reported positive results for treatment with bisphosphonates in patients with knee OA. One study reported significant pain and OA-BML size reduction in patients receiving a bisphosphonate for 4 months.

A strategy aimed at repairing and/or enhancing subchondral bone compromised by an OA-BML has also been proposed. Early results reported with this intervention are encouraging, but preliminary.

Introduction

Various 2D and 3D surfaces are available for cementless fixation of acetabular cups. The goal of these surface modifications is to improve fixation between the metallic cups and surrounding bone. Radiographs have historically been used to evaluate the implant-to-bone fixation around the acetabular cups. In general, a well fixed cup shows no gaps or radiolucency around the cup's outer diameter. In post-operative radiographs, the presence of progressive radiolucent zones of 2mm or more around the implant in the three radiographic zones is indicative of aseptic loosening, as described by DeLee and Charnley [1]. In this cadaveric study, we investigated the X-ray image characteristics of two different types of acetabular shell surfaces (2D and 3D) to evaluate the implant-to-bone interface in the two designs.