Patellofemoral instability (PFI) is a relatively common condition in children and adolescents with an incidence estimated to be approximately 43 per 100,000.¹ In a recent study by Abbasi et al.,² 31% of 131 adolescent patients presenting with an acute traumatic knee effusion who underwent magnetic resonance imaging (MRI) were diagnosed with a patellofemoral dislocation. Patellofemoral dislocation was more commonly the causative factor for the knee effusion in children aged 10 to 14 years, compared to anterior cruciate ligament (ACL) disruption for those aged 15 to 18 years.²

Surgical treatment for PFI with anatomic medial patellofemoral ligament (MPFL) reconstruction has risen dramatically in the last decade.³ However, the pathomechanics that contribute to PFI are multifactorial. Therefore, a combination of options exists for surgically treating PFI. This chapter helps to provide an understanding of the relevant risk factors for recurrent PFI and reviews the clinical and radiographic tests that are necessary to determine optimal surgical or nonsurgical treatment of patients presenting with PFI.

Consider reviewing the pediatric patellar dislocation classification described by Weeks et al.^3a in the 2013 review article in Sports Medicine and Arthroscopy Review (SMAR).

The stability of the patellofemoral joint relies on the integration of static (bony configuration), passive (capsule/ligament), and dynamic (muscle) stabilizers.⁴ Pathology in any of the stabilizers can quickly disrupt the balance and lead to PFI.

In full knee extension, the patella is located slightly superior and lateral to the trochlear groove. Between 10 and 30 degrees of knee flexion, the patella starts to make contact with the trochlea and slides into the sulcus.⁵ The MPFL is a portion of the medial soft tissue complex of the knee and is the main stabilizer of the patellofemoral joint in extension and lower degrees of knee flexion (0 to 3 degrees). Warren and Marshall⁶ described a three-layered structure of the medial soft tissue complex of the knee joint. The MPFL is in the second layer and has a “sail-like” appearance with two functional portions: (1) inferior straight bundle and (2) superior oblique bundle (SOB).⁷ The MPFL originates from the medial femoral condyle just proximal to the femoral attachment of the medial collateral ligament and distal to the adductor tubercle. It inserts on the superomedial border of the patella.⁸ In children and adolescents with open physes, the femoral insertion is located slightly distal (4 to 5 mm) to the medial femoral physis.⁹,¹⁰ During 0 to 30 degrees of knee flexion, the MPFL contributes more than 60% of the medial stability of the patella and isolated insufficiency leads to increased lateralization or dislocation.¹¹

As the knee continues past 30 degrees of flexion, the depth of the trochlea increases and the bony anatomy becomes the major stabilizer of the patellofemoral joint.¹² Past 90 degrees of knee flexion, the patella is located in the notch. The vastus medialis obliquus (VMO) is the most important dynamic stabilizer. However, it only affects patellofemoral stability in flexion greater than 60 degrees, when the fibers run perpendicularly to the patellar motion, and an intact connection exists between the SOB of the MPFL and the quadriceps tendon.⁴

In extended positions, when the patella is not engaged in the trochlea, the MPFL is the only structure that resists lateralizing forces. Therefore, a functionally deficient MPFL contributes greatly to the pathomechanics of PFI. Recently, two studies have shown MRI evidence of pathologic alteration of the MPFL in the majority (78% to 94%) of children and adolescents who had sustained a recent patellofemoral dislocation.¹⁰,¹³

One may question: How does a patella dislocate without an MRI demonstrating evidence of MPFL injury? In a recent article,⁴ senior author Schoettle describes a condition that he termed early and chronic PFI. I prefer the term early-onset PFI.

Early-onset PFI occurs when the MPFL becomes chronically insufficient due to underlying bony malalignment. The bony malalignment is often related to trochlear dysplasia, patella alta, valgus mechanical axis, excessive internal femoral rotation (excessive
anteversion), and/or excessive external tibial torsion. The combination of excessive anteversion and external tibial torsion is called miserable malalignment.¹⁴ These congenital bony pathologies combine and lead to lateral shift and tilt of the patella. This places persistent traction on the MPFL, which then results in a stretched and nonfunctional passive stabilizer. A “normal” MPFL does not develop due to the persistent traction, and the major restraint to PFI in low knee flexion angles is (functionally) absent.⁴

Early-onset PFI can also occur in patients with hyperlaxity syndromes (Ehlers-Danlos syndrome). The genetic alterations in the tissue that form the MPFL lead to stretching and insufficiency with the forces of daily activity. Even without the underlying bony pathology, these hyperlaxity in patients have a “functionally absent” MPFL leading to PFI at low flexion angles.

PFI is a common but complex condition. It can occur as an isolated event (acute, first-time dislocation) or it can be chronic condition. The instability can also occur as a traumatic or nontraumatic injury. Most traumatic PFI occurs in sports that involve cutting and pivoting, such as soccer, football, or basketball. The involved limb often is in a position of significant internal rotation and valgus stress.⁴ Nontraumatic dislocations occur with minimal force during activities of daily living and often reduce spontaneously. Patients with nontraumatic recurrent instability will often subluxate their patella on multiple occasions between dislocation events.

It is important to take a detailed history to help distinguish between acute traumatic PFI and chronic nontraumatic PFI because the risks for recurrent PFI differ when the two groups are compared.

Two studies have recently been published that investigate pediatric/adolescent (18 years old or younger) patients presenting with an acute, first-time patellofemoral dislocation.¹,¹³ The rate of recurrent PFI ranges between 30% and 38%. In other words, during the study periods, 62% to 70% of patients successfully completed nonoperative treatment and did not experience a subsequent episode of PFI.

However, a similar and important conclusion arose from both studies. Younger patients between the ages of 11 and 13 years with immature growth plates had a statistically significant higher rate of recurrent PFI.

In the study by Seeley et al.,¹³ the overall rate of recurrent PFI was 30.6%, with the highest rate (43%) occurring in patients between the ages of 11 and 13 years. Lewallen et al.¹ concluded that the rate of recurrent PFI was 38% for the group as a whole. However, skeletally immature patients with open growth plates and trochlear dysplasia had a recurrence rate of 69%.¹ Trochlear dysplasia increased the risk of recurrent PFI by a factor of 2.2, and combining trochlear dysplasia with immature physes increased that risk by a factor of 3.3 (Table 15.1).