Medial patellar subluxation (MPS) is a disabling condition caused by an imbalance in the medial and lateral forces in the normal knee, allowing the patella to displace medially. Normally, the patella glides appropriately in the femoral trochlea, but alteration in this medial–lateral equilibrium can lead to pain and instability.1 MPS was first described in 1987 by Betz and colleagues2 as a complication of lateral retinacular release. Since then, multiple cases of iatrogenic, traumatic, and isolated medial subluxation have been reported.3–15 However, MPS after lateral release is the most common cause, accounting for the majority of published cases, whereas only 8 cases of isolated MPS have been reported to date.
Optimal treatment for MPS is not well understood. To better comprehend and manage MPS, we must fully appreciate the pathoanatomy, biomechanics, and current research. In this review, we focus on the anatomy of the lateral retinaculum, diagnosis and treatment of MPS, and outcomes of current treatment techniques.
Anatomy
In 1980, Fulkerson and Gossling16 delineated the anatomy of the knee joint lateral retinaculum. They described a 2-layered system with separate distinct anatomical structures. The lateral retinaculum is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserting into the lateral margin of the patella and the patella tendon. The deep layer of the retinaculum consists of several structures, including the deep transverse retinaculum, lateral patellofemoral ligament (LPFL), and the patellotibial band.
Over the years, several studies have described the importance of the lateral retinaculum and, in particular, the LPFL. Examining the functional anatomy of the knee in 1962, Kaplan17 first described the lateral epicondylopatellar ligament as a palpable thickening of the joint capsule. Reider and colleagues18 later named this structure the lateral patellofemoral ligament in their anatomical study of 21 fresh cadaver knees. They described its width as ranging from 3 to 10 mm. In a comprehensive cadaveric study of the LPFL, Navarro and colleagues19,20 found it to be a distinct structure present in all 20 of their dissected specimens. They found its femoral insertion at the lateral epicondyle with a fanlike expansion of the fibers predominantly in the posterior region proximal to the lateral epicondyle. The patellar insertion was found in the posterior half and upper lateral aspect, also with expanded fibers. Mean length of the LPFL is 42.1 mm, and mean width is 16.1 mm.
Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this medial–lateral equilibrium can lead to pain and instability.1 Normally, the patella lies laterally with the knee extended, but in early flexion the patella moves medially as it engages in the trochlea. As the knee continues to flex, the patella flexes and translates distally.21 By 45°, the patella is fully engaged in the trochlear groove throughout the remainder of the knee’s range of motion (ROM).
Lateral release procedures, as described in the literature, result in sectioning of both layers of the lateral retinaculum. In a biomechanical study, Merican and colleagues22 found that staged release of the lateral retinaculum reduced the medial stability of the patellofemoral joint progressively, making it easier to push the patella medially. At 30° of flexion, the transverse fibers of the midsection of the lateral retinaculum were found to be the main contributor to the lateral restraint of the patella. When the release extends too far proximally, the transverse fibers that anchor the lateral patella and the vastus lateralis oblique tendon to the iliotibial band are disrupted. Subsequent loss of a dynamic muscular pull in the orientation of the lateral stabilizing structures results in medial subluxation in a range from full knee extension to about 30° of flexion.
Furthermore, the attachments of the LPFL and the orientation of its fibers suggest that the LPFL may have a significant role in limiting medial excursion of the patella. Vieira and colleagues23 resected the LPFL in 10 fresh cadaver knees. They noticed that, after resection, the patella spontaneously traveled medially, demonstrating the importance of this ligament in patellar stability. In cases of isolated MPS, there have been no reports of associated pathology, such as muscular imbalance or coronal/rotational malalignment of the lower extremity. With an intact lateral retinaculum, medial subluxation is likely caused by pathology in the normal histologic structure of the LPFL and lateral retinaculum. However, the histologic structure of the LPFL and its contribution to the understanding of the pathoetiology of MPS have not been documented.