BIOMECHANICS OF PATELLOFEMORAL INSTABILITY

C. C U R T I S ELLIOTT, M D , a n d D A V I D R. D I D U C H , MS, MD

The patellofemoral joint functions as a complex extensor apparatus with important biomechanical contributions provided by both articular contact and the surrounding soft tissues. The patella must remain relatively stable while tracking along the anterior and distal surfaces of the femur. If there is instability in the coronal plane (subluxation or dislocation) or around the caudocranial axis (tilt), then pain may result. Stability is maintained through the precise interaction of the patellofemoral articulating surfaces, passive and active soft-tissue restraints, and the alignment of the lower extremity. The purpose of this article is to review these biomechanical variables and how they relate to the treatment of patellofemoral instability.

KEY WORDS: biomechanics, patellofemoral, instability, subluxation, dislocation

Copyright 2001 by W.B. Saunders Company

The articular surface of the patella is divided into medial and lateral facets by a central ridge. A second vertical ridge near the medial border isolates a narrow articulating strip known as the odd facet. Wiberg 1 classified patellae into 3 types based on the position of the major vertical ridge. Baumgartl 2 added a fourth type. When progressing from a type I to a type IV, there is a gradual increase in the size of the lateral facet. Reider et al 3 found a high correlation between the Wiberg type and the width of the lateral patellofemoral ligament. The larger the lateral facet, or greater the Wiberg type, the broader its lateral patellofemoral ligament tended to be. This does not suggest that a thick, broad lateral patellofemoral ligament causes lateral patellar tracking, but it appears to be associated with it. The medial and lateral facets of the femoral trochlea are asymmetrical. In a normal knee, the patella enters the trochlear sulcus from the lateral side, causing the lateral facet to extend proximally more than the medial. The lateral facet is also a few millimeters more prominent than the medial. The greater height or thickness of the lateral trochlear facet contributes to the osseous stability of the joint. The trochlear sulcus averages 7.8 mm in depth. 4 A shallow trochlea may be insufficient to prevent the patella from dislocating laterally even if it engages properly at the beginning of flexion, s A shallow trochlear sulcus is common in knees with lateral patellar instability. 6 Although orthopedists traditionally rely on axial radiographs of the knee to evaluate the patellofemoral articulation, magnetic resonance arthrotomography has now proven that there are substantial differences in the geom-

etry and anatomy of the surface of the articular cartilage and the corresponding subchondral osseous contours of the patellofemoral joint 7 (Fig 1). Before decisions are made concerning the diagnosis and management of patellar a n d / o r trochlear dysplasias, the geometry of the opposing articular surfaces may need to be considered b y w a y of magnetic resonance arthrogram.

THE PATELLOFEMORAL PASSIVE SOFT-TISSUE RESTRAINTS

During knee flexion and extension, the patella is guided by both passive and active soft-tissue restraints. These structures anchor the patella by forming a cruciform arrangement 6 (Fig 2). The passive restraints consist of the patella tendon, the quadriceps tendon, and those structures combining to form the medial and lateral retinaculum. The average length of the patellar tendon 3 is 4.6 cm. It runs from the inferior margin of the patella to the tibial tubercle in an oblique, lateral direction. This contributes to the normal valgus alignment of the extensor apparatus, which adds to the tendency toward lateral displacement of the patella. 6 There is a negative correlation between the length of the patellar tendon and the width of the medial patellofemoral ligament (MPFL). 3 Longer patellar tendons (patella alta) are associated with smaller or absent MPFL 3 as well as lateral instability of the patella. 8 Regarding the medial retinaculum, anatomic studies have identified at least 4 distinct soft-tissue structures along the medial side of the knee that may play a role in maintaining patellar stability 9 (Fig 3). (1) The MPFL runs from the adductor tubercle to the proximal two thirds of the medial border of the patella. 1 It also has insertions on the deep surface of the vastus medialis and the vastus intermedius. (2) The medial parapatellar retinaculum is formed from a condensation of 2 fascial planes on the medial aspect of the knee and has a broad insertion on the medial patella. 1 (3) The medial patellomeniscal ligament originates from the anterior portion of the medial meniscus and inserts onto the inferior one third of the patella. 1~

From the Department of Orthopaedic Surgery, University of Virginia, Charlottesville, VA. Address reprint requests to David R. Diduch, MD, UVA Department of Orthopaedics, Universityof Virginia, PO Box 800159, Charlottesville, VA 229O8-0159. Copyright 2001 by W.B. Saunders Company 1060-1872/01/0903-0001 $35.00/0

doi:10.1053/otsm.2001.25157

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Operative Techniques in Sports Medicine, Vol 9, No 3 (July), 2001: pp 112-121

Fig 1. Imaging modalities and diagrams of the same right knee in extension, axial plane. Note the error in the radiologic appearance of the osseous contours (A and C) and the perfect matching of articular cartilage surfaces in the axial plane of the same right knee on double-contrast magnetic resonance arthrotomography (B and D). (Reprinted with permissionF)

and patellotibial ligaments were shown to be important secondary stabilizers. Additional release of these ligaments after release of the MPFL resulted in considerably greater lateral patellar displacement. In addition, repair of these 2 ligaments restored medial-lateral balance to near normal levels. The medial retinaculum, as shown by other investigators played only a minor role in providing medial stability. In a cadaver study by Reider et al, 18 a medial parapatellar soft-tissue release resulted in decreased medial patellar shift and a switch to lateral tilting in a significant portion of the specimens. They concluded that weakening or disruption of these static medial soft-tissue restraints leads to abnormal tracking. A finding in their study was that the MPFL was present in only 7 of 20 (31%) knees that they dissected. When present, the breadth of the ligament ranged from 5 to 12 mm. The lack of a clearly identifiable MPFL in 69% of their specimens, as opposed to others in which it was present in 90% to 100% of dissected knees, 9,11 suggests that this structure may not be a constant entity in normal knees. This is an important issue because several new surgical strategies aimed at patellar instability (especially acute dislocations) are based on repairing or augmenting this structure. The third passive, or static, soft-tissue restraint is provided by the lateral retinaculum. Fulkerson and Grossling ~4 described the anatomic details of the lateral retinaculum in 24 dissected knees (Fig 4). The most super-

(4) The medial patellotibial ligament is a thickening of the anterior capsule and runs from the anteromedial aspect of the tibia to the inferior aspect of the patella. 12 There have been several investigations to evaluate the relative contributions of the various medial structures that act to resist a laterally directed force. By sectioning different structures along the medial aspect of knee specimens, Conlan et a111 found that the MPFL is the major soft-tissue static restraint that resists lateral patellar displacement, contributing an average of 53% of the total medial, static restraining force. The medial patellomeniscal ligament was also found to be a significant medial stabilizer, contributing 22% of this total force. The medial retinaculum and the patellotibial ligaments made minimum contributions of 11% and 5%, respectively. Desio et a113 also studied the medial soft-tissue structures in 9 fresh-frozen cadaveric knees. They found the MPFL to be the primary static restraint to lateral patellar translation at 20 of flexion, contributing 60% of the total restraining force. The medial patellomeniscal ligament contributed 13% of the restraining force. The medial retinaculum and the medial patellotibial ligament were not found to be functionally important. Hautamaa et al 9 studied 17 fresh-frozen anatomic knee specimens. They also sequentially sectioned different parts of the medial soft-tissue stabilizers. The MPFL, which they identified in every specimen, was found to be the major static restraint. Isolated release resulted in a 50% increase in lateral patellar displacement, and isolated repair restored balance to the patella. The medial patellomeniscal
BIOMECHANICS OF PATELLOFEMORAL INSTABILITY

lateral r vastus If iliotibiat

,,dial retinaculum d vastus medialis

Fig 2. The patella is anchored and stabilized to the knee by 4 structures in a cruciform fashion: the patellar tendon inferiorly, the quadriceps tendon superiorly, and the retinacula medially and laterally. (Reprinted with permission. 6)

113

~ductor agnus ~don

:Ulum
aiscal

angle

Fig 3. Anatomy of the medial patellofemoral passive softtissue restraints. Fig 6. The Q angle.

Vastus medialis Iongus

Vastus medialis obliquus

Fig 5. The vastus medialis complex is composed of the vastus medialis Iongus and VMO muscles.

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,Vastus.

THE PATELLOFEMORAL ACTIVE SOFT-TISSUE RESTRAINTS The active restraints on medial-lateral patellar motion consist mainly of the quadriceps apparatus. Because of their obliquity in relation to the long axis of the femur, the vastus medialis and the vastus lateralis are the most important contributors in preventing and causing instability, respectively. In 1968, Lieb and Perry 19 described the anatomy and function of the quadriceps mechanism. After dissecting 6 cadaver specimens, they considered the vastus medialis to be composed of 2 parts because of the marked and abrupt change in fiber alignment between its proximal and distal portions. The upper fibers, which they named the vastus medialis longus, angled 15 to 18 medially in relation to the long axis of the femur. The lower fibers, they called the vastus medialis obliquus (VMO), angled 50 to 55 medially, and their insertion is close to the superomedial margin of the patella (Fig 5). The VMO has been found to contribute approximately 30% of the physiologic cross-sectional area of the vastus medialis complex. Lieb and Perry 19examined the function of the separate heads of the quadriceps in an additional 22 specimens. By altering the applied forces of cables connected with the different muscles, they concluded that the only selective function attributable to the VMO is patellar alignment. Goh et al 2 examined the function of the VMO in 6 normal cadaver limbs. They found that absent VMO tension caused the patella to displace laterally and increased the load on the lateral patellar facet throughout the range of knee motion. A 40% reduction of the lateral vector was required to counterbalance the lateral displacement of the patella caused by the absent VMO. The VMO is thought to be the main active medial patellar stabilizer. In a study by Henry and Craven, 2I 91% of 557 knees with patellar subluxation showed signs of a dysplastic VMO. Dysplasia of the VMO has been defined clinically as a large concavity medial to the patella that correlates with muscle atrophy. 22 Other investigators believe that VMO dysplasia refers to an insertion angle less oblique than normal, decreasing its mechanical advantage and its ability to act as a medial stabilizer. 23 There is a notable relationship between the static restraint mechanism, the MPFL, and the active restraint mechanism, the VMO. Conlan et a111 performed an anatomic dissection of the medial soft tissues in 25 freshfrozen knee specimens. They noted that the MPFL, present in more than 90% of dissected knees, had insertions on the deep surface of the distal aspect of the VMO and vastus intermedius, as well as on the superomedial aspect of the patella. By originating from the adductor tubercle and having insertions on the deep surface of the distal anterior fibers of the VMO, it acts as a checkrein, preventing excessive elongation of the fibers of the VMO and lateral subluxation of the anterior portion of the VMO over the medial femoral condyle. They believed that disruption of the MPFL origin from the femur might have led other investigators to conclude that the VMO had avulsed from the adductor tubercle. 24 Conlan et al ~ found that the origin of the VMO was actually 0.5 to 6.0 cm (average of 3.3 cm) proximal to the adductor tubercle, at the medial

ylopatellar Suoerfic oblique

(reflecte lnsverse rum ~ial band

Fig 4. Anatomy of the lateral patellofemoral passive softtissue restraints. (Reprinted with permission, s)

ficial layer, the superficial oblique retinaculum, is composed of fibers running distally and anteriorly from the anterior border of the iliotibial band to the lateral margin of the patella and patellar tendon. They described a deep layer consisting of 3 bands including an epicondylopatellar band, a transverse band from the deep surface of the iliotibial band to the lateral border of the patella, and a patellotibial band. Kaplan 15 also described the lateral epicondylopatellar ligament, which is the most proximal of these 3 condensations. However, Reider et al 3 was only able to find the epicondylopatellar ligament, which they called the lateral patellofemoraI ligament, in 13 of 20 (65%) fresh knee specimens. Luo et al ~6 examined 7 cadaveric specimens and found that the tensile stress in the lateral patellofemoral ligament increased significantly around 30 of knee flexion. They believed that this increase in the lateral restraining force contributed to the lateral subluxation that occurs at 20 to 30 of knee flexion in a patient who has patellar instability. It has also been postulated that the portion of the lateral retinaculum connecting the patella to the iliotibial band may cause a laterally directed force with knee flexion. 6 However, other investigators have shown that the lateral retinaculum plays only a passive role; in other words, there is no active pull on the patella. Heegaard et a117 found that the lateral retinaculum contributed very little to patellar tracking in knee specimens which were examined before and after a dissection which left only the bony elements, the cruciate and collateral ligaments, the patella tendon, and the rectus femoris tendon. In another cadaver study, Reider et a118 illustrated that release of the lateral retinaculum had no effect on the tracking of most of the 20 specimens they examined. They concluded that the indiscriminate use of isolated lateral release would not be beneficial in knees in which the lateral retinaculum is normal.
BIOMECHANICS OF PATELLOFEMORAL INSTABILITY

1 15

intermuscular septum and the adductor magnus tendon. Bose et a125 also showed that the VMO arises primarily from the adductor magnus tendon, not from the adductor tubercle. In their study, the origin of the VMO ranged from 1.5 to 7.5 cm (average 3.5 cm) proximal to the adductor tubercle. It was believed that injury to the VMO origin and its checkrein, the MPFL, changed its normal oblique orientation to a more vertical orientation, impairing the ability to offer medial stability to the patella. The muscle fibers of the vastus lateralis approach the patella at an angle to the rectus tendon averaging 31 . The fibers terminate more proximally than those of the VMO (average of 2.8 cm from the superolateral corner of the patella). 3 Similar to the VMO configuration, the most distal part of the muscle has been shown to be anatomically distinct and was named the vastus lateralis obliquus. 26 These fibers originate from the lateral intermuscular septum and appear to function as a lateral displacing force on the patella.

F[.* FR"*#M
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BIOMECHANICAL INFLUENCES ON PATELLAR TRACKING

In full extension, the screw-home mechanism of the tibia, rotating externally in the terminal 30 of extension, displaces the tibial tubercle laterally. 27 The angle formed between the direction of the quadriceps force and the direction of the patellar tendon is called the Q angle (Fig 6). It is measured clinically b y the intersection of the line connecting the anterior superior iliac spine to the center of the patella (rectus femoris vector), and the line between the center of the patella and the tibial tubercle. Aglietti et a128 reported a normal Q angle of 14 in males and 17 in females, with both genders having a standard deviation of 3 . Post and Fulkerson 29 noted that an angle of greater than 10 in males and 15 in females is considered potentially abnormal. The Q angle is a useful dynamic concept, but can be an unreliable measurement, because an unstable patella lies more lateral than normal in full extension, decreasing the angle. This may produce a "J sign," which can be appreciated when observing active patellar tracking through a range of motion, indicating subluxation in full extension. In this case, slight flexion of the knee to about 15 will engage the patella within the trochlear groove to allow a more accurate measurement of the Q angle. Tension on the quadriceps, specifically the rectus femoris and the vastus lateralis, tends to produce a lateral displacement vector on the patella. As noted, this lateral or "valgus vector" is resisted by the distal muscle fibers of the VMO. By evaluating the normal torque equilibrium about the knee, 3 one can see the importance of the VMO's action (]qM)" The sum of the forces of the rectus femoris (FM), vastus lateralis (FL), and the patella tendon (};T1) is equal to the resultant lateral force created by the Q angle (RL). The sum of the normal quadriceps mechanism (FM + F R + FL) is equal to the counterforce at the tibia (FT2). Therefore, the potential lateral vector (RL) is equal to zero when the quadriceps, including the VMO, is functioning normally (Fig 7). The static medial soft-tissue restraints (MPFL) and the prominent lateral trochlear facet also help resist this laterally directed force. 27

\
, ~\ \
\

FT1

FT2
Fig 7. Vector diagram of the quadriceps muscle. FL, force exerted by the vastus iateralis; FR, force exerted by the rectus femoris; FM, force exerted by the vastus medialis; RL, resulting lateral force as the sum of FL + FR -I- FT1 , FT1 = force at the tibia = the counter act force of F L -F FR, FT2 = force at the tibia = the counter act force of F L + F R 4- F M. (Reprinted with permission. 3o)

With the knee in full extension and the quadriceps contracted, the patella lies proximal to the trochlea, resting against the supratrochlear fat pad. Heegaard et a117 showed that the tibia internally rotates during the first 15 of flexion. This derotation decreases the Q angle, decreasing the lateral vector. As flexion proceeds, the patella is drawn into the entrance of the trochlea. Because of the Q angle, the patella enters the troclea from the lateral side. 27 The degree of knee flexion required for the patella to reach the trochlea depends on the patellar tendon l e n g t h y When a long patella tendon is present, a high patella, or patella alta, is the result. Normally, patellofemoral contact is made between 10 to 20 of flexion along the inferior margin of the patella in a broad, continuous band across both medial and lateral facets. With patella alta, the patella will not engage the trochlea until the knee is flexed more, so there is a greater range in which instability may occur. As flexion proceeds, the contact area moves proximally on the patella, extending from the ridge separating the medial from the odd facet to the lateral border of the lateral facet. 27 As flexion continues, patellar contact shifts proximally. The odd facet does not come into contact with the

116

ELLIOTT AND DIDUCH

femur until significant flexion is obtained and the patella sinks into the intercondylar notch. Before about 30 of flexion, the soft-tissue restraints, both active and static, are the most important factors in preventing patellar tilt a n d subluxation. 17 After firm patella-trochlea contact is made, the resultant flexion compresses the patella against the femur. The congruence of the patellofemoral joint and this force provide considerable stability irrespective of the restraining soft tissuesY ,27

iliotibial band, the quadriceps, the hip rotators, and the Achilles tendon. 5

BIOMECHANICAL CONSIDERATIONS IN THE TREATMENT OF PATELLOFEMORAL INSTABILITY

Nonoperative Treatment

PREDISPOSING RISK FACTORS FOR PATELLOFEMORAL INSTABILITY

Before beginning a course of treatment, the surgeon should pay careful attention to all potential contributions to patellar instability. Failure to correct an anatomic contributor such as a high Q angle may predispose to treatment failure. The biomechanical factors described that influence patellar tracking are affected by the anatomy a n d c a n be seen on physical examination (Table 1). Normal overall alignment of the lower extremity is important for a proper functioning patellofemoral joint. Limb alignment that includes increased anteversion of the femoral neck, internal femoral rotation, external tibial rotation, genu valgum, and lateral insertion of the patellar tendon c a n singly or collectively increase the Q angle, assuming that the patella remains in the femoral sulcus. 31 Larson has shown that the effects of limb alignment on patellar tracking may be exaggerated during functional activities. 32 Genu recurvatum is also a potential contributor to lateral patellar instability. 33 The position of the foot may be important as well, because excessive pronation at the subtalar joint is accompanied by external tibial torsion and compensatory valgus positioning of the knee, which can increase the Q angle. 6 Abnormalities of the patellofemoral articulation may affect tracking, is The patella may fail to engage and remain in the trochlea if there is patella alta, 34-36 patellar dysplasia, 37-42 or a poorly developed trochlea. 5,24,33,34,37-49 The importance of the supporting soft-tissue structures in maintaining medial and lateral stability has been discussed. Abnormalities of these structures include VMO dysplasia, laxity of the medial static restraints (MPFL, patellomeniscal ligament, patellotibial ligament) 9,11,1s either secondary to injury or as a part of a generalized joint laxity, and tightness of the lateral restraints, including the vastus lateralis, lateral retinaculum, and lateral patellofemoral ligamentY s,31 Other soft tissues that may be tight with patellar malalignment are the hamstrings, the

Historically, nonoperative treatment has been the hallmark of therapy for all patellofemoral instability. Patients with patellar malalignment and pain should receive a well-structured program of rehabilitation that consists of stretching the tight soft tissues which affect patellar tracking, strengthening exercises for the quadriceps (especially the VMO), and modification of activity. 5,5~ Strengthening of the quadriceps is usually beneficial as long as it does n o t cause pain. 5 Coordination of VMO and vastus lateralis muscle activity is as important as strength training. Biofeedback from surface electrodes has been used to help facilitate this therapy. 52,53 Simple bracing with an elastic patellar cutout brace may be helpful to some patients. 54 Their mode of action is speculative, but it is felt that the brace provides relief by stabilizing the patella during early flexion. This may help to overcome lateral forces, which cause subluxation or dislocation. McConnel155 recommended a patellar taping method that helps to pull the patella medially, controlling tilt and subluxation. Going back to the torque equilibrium, it is believed that the taping contributes to the medial stabilizing vector. This may be especially beneficial in a patient who has VMO weakness or dysplasia. Initial results of a rehabilitation program using McConnell's patellar taping protocol had a success rate of 92%. However, in a prospective, randomized study, Kowall et a156suggested that there was no benefit of adding a patellar taping program to a standard physical therapy protocol. Finally, orthotic devices may help alleviate lower extremity malalignment caused by excessive foot pronation. 57,58
Operative Treatment

T A B L E 1. Anatomic Contributors to Increased Lateral Displacement Forces on the Patella and Patellar Instability increased Q angle Femoral anteversion
Tibial torsion Soft-Tissue Contributors Bony Contributors

Dysplasic VMO Tight lateral retinaculum

Patellar dysplasia Trochlear dysplasia

Valgus knee alignment Patella alta Generalized ligamentous Excessive foot laxity pronation Wide pelvis (females) Torn or attenuated MPFL
BIOMECHANICS OF PATELLOFEMORAL INSTABILITY

Surgical intervention is usually considered when symptoms from patetlar instability persist for longer than 6 months despite undergoing an individualized therapy program. If an episode of subluxation or dislocation occurred primarily because of a direct traumatic force, the patient is more likely to respond to conservative management. The indirect mechanism is more common, and involves the combination of a strong quadriceps contraction, a slightly flexed and valgus knee position, and an internally rotated femur on an externally rotated tibia. 59 Patients with an indirect mechanism typically have predisposing risk factors, such as malalignment. When there is significant malalignment, there is a greater tendency for dislocation to recur. 6 Younger patients with partially developed quadriceps musculature are also more prone to have problems with recurrent patellofemoral instability. 61 There has been an abundant number of surgical procedures put forth to address patellofemoral instability. Although the list seems endless, the procedures can be grouped into 2 main types based on how the biomechanics
1 17

of the patellofemoral joint are affected. The first type, proximal realignment, includes procedures that release tight lateral structures a n d / o r repair, reinforce, or transfer medial stabilizing structures. This category includes lateral retinacular release, 47,62-66 medial plication, 67-69 VMO advancement, 7 and MPFL repair or reconstruction. 9,71-77 By enhancing the action of the VMO, the active, medial stabilizing force is increased. The balance between the static restraints may be shifted medially b y restoring the MPFL a n d / o r releasing a tight lateral retinaculum. Most of these procedures not only stabilize the patella, but also medialize it. This fact must be appreciated because the Q angle can actually increase after performing a proximal realignment procedure. The next category, distal realignment, improves the Q angle by reorienting the insertion of the patellar tendon. 7s This effectively decreases the lateral vector acting on the patella. These include medial transfer of the patellar tendon, 79 medial transfer of the lateral portion of the patellar tendon, s medial displacement of the tibial tubercle, s1 anteromedial displacement of the tibial tubercle, s2-s4 and distal and medial transfer of the tibial tubercle. 44 A lateral release is usually added to the distal realignment procedures to remove the tethering effect of the static lateral restraints. 29 An operation that has fallen out of favor is the Hauser procedure, in which the tibial tubercle is transferred distally and medially. 44 The distal advancement is beneficial when the patient has instability resulting from patella alta. The medial displacement improves the Q angle. However, the d o w n w a r d slope of the medial, proximal tibia causes a posterior displacement of the tibial tubercle. This has been associated with a high rate of patellofemoral arthritis, presumably because of its tightening effect on the extensor mechanism and the resultant increase in joint reactive force. 85 The Roux-Emslie-Trillat procedure is usually the preferred technique for a direct medial transfer of the tibial tubercle, s~ This osteotomy is made in the true coronal plane of the body, therefore there is no posterior displacement along the slope of the proximal tibia. A lateral release and medial capsular reefing are usually performed in addition to the osteotomy. When there are articular cartilage lesions at the distal, lateral aspects of the patella in addition to a laterally positioned tibial tubercle, a Fulkerson osteotomy is the more likely successful procedure. 29,54,s3 An anteromedial tibial tubercle transfer is created by an oblique osteotomy. Depending on the obliquity of the osteotomy, the amount of anterior or medial displacement can be varied. A steeper cut allows more anterior displacement of the tubercle, which increases the moment arm of the patella tendon. Patellofemoral joint reactive forces are transferred from the distal, lateral patella to the articular surface at the proximal, medial patella. This procedure will not be beneficial to a patient who also has chondral defects on the proximal, medial patella. When malalignment from an increased Q angle is more of a concern, the obliquity of the osteotomy is decreased, resulting in more medial displacement of the tibial tubercle. When treating patellofemoral instability, a lateral retinacular release is used as an adjunct to a proximal a n d / o r
118

distal realignment. When used alone to treat lateral patellar instability, lateral retinacular release will give poor results. 86 Huberti and Hayes s7 showed that there is little redistribution of stress after lateral release of a normally aligned patella. Release of this static restraint does not significantly reduce the active lateral vector, s6 It also does not affect predisposing factors for instability, such as an increased Q angle. However, patients who have excessive tilt to their patella radiographically, and on physical examination display painful signs resulting from lateral patellar compression syndrome, may do well with an isolated lateral retinacular release, s6 Before selecting a procedure to treat patellofemoral instability, the orthopaedist must identify any pathologic anatomy the patient may have. Injured soft-tissue structures that stabilize the patella, such as the MPFL, may need to be addressed. The surgeon must also consider the patient's age, level of activity, causative factors, and the condition of the articular surfaces, ss By customizing the treatment to each individual patient, optimum results will be obtained.

Treatment of Acute Patellofemoral Dislocations

The treatment of acute, primary patellar dislocations has recently become somewhat controversial. Natural history studies of the nonoperative management of these injuries have shown mixed and poor results. Cofield and Bryan 1 noted a 44% redislocation rate in 48 patients with conservatively treated patellar dislocations. Hawkins et al, 6 reported a 15% redislocation rate in patients who were immobilized for 3 weeks after the injury. Hughston and Deese s9 had a 20% to 43% redislocation rate in their patients. Maenpaa and Lehto 90 reported on 100 patients treated nonoperatively for first-time dislocators. They reported a 44% redislocation rate and an additional 19% of patients had patellofemoral pain or subluxation. Cash and Hughston 61 noted a 43% redislocation rate in a group of 69 patients with acute patellar dislocation and prior evidence of extensor mechanism abnormalities. In a second group of patients with acute dislocations, without predisposing patellofemoral problems, the redislocation rate was only 20%. Many orthopedists are rethinking the traditional treatment for these patients. An emerging trend, similar to one used in those treating patients with first-time shoulder dislocations, is the decision to operatively stabilize acute, primary patellar dislocations. The recent biomechanical studies that highlighted the importance of the medial stabilizers, especially the MPFL, have directed attention to the repair of this structure. In a study by Sanders et al, 91 which examined 14 patients with transient acute patellar dislocations, findings at surgery showed disruption of the MPFL in 7 of 14 patients (50%), with stretching or partial tearing of the MPFL in the remaining 50%. Sargent and Teipner 73 reported no redislocations in 11 patients with acute first-time dislocation who underwent primary repair of the medial patellar retinaculum to the medial margin of the patella. Boring and O'Donoghue 92 treated a similar pool of 17 patients with acute dislocation. No redislocations occurred after immediate medial retinacular reefing in 8 patients or after a
ELLIOTT AND DIDUCH

,a

jY

~7~--

Medial

Fig 8. (A) The VMO muscle places a medially directed force on the patella because of its attachment location. (B) When the muscle is torn, its medial stabilizing force on the patella is disrupted.

distal realignment in 9 patients. These investigators believed that a distal realignment procedure was more appropriate if the patient had an increased Q angle, patella alta, a shallow trochlear groove, or a history of patellar subluxation. Avikainen et al TM reported on 14 patients, 10 with primary dislocation and 4 with recurrent instability who underwent repair of the MPFL and augmentation with the adductor magnus tendon. A constant surgical finding in the patients with acute dislocation was detachment of the MPFL from the medial femoral epicondyle. Postoperatively, 12 of the 14 patients regarded their knees as good and 2 as fair. Sallay et a175 noted that 15 of 16 patients (94%) had tears of the MPFL off of the femur at surgical exploration after acute dislocation. After repair of the MPFL, none of the patients experienced redislocation. Ahmad et a176 reviewed 8 cases of acute patellofemoral dislocation treated surgically. All patients were noted to have a tear of the MPFL off the adductor tubercle as well as injury to the VMO origin from the adductor magnus tendon. The VMO muscle was retracted in an anterior and superior direction (Fig 8). All patients underwent arthroscopic lateral release, then repair of the torn MPFL to the adductor tubercle and the VMO to the adductor magnus tendon. They addressed injuries to both the static (MPFL) and dyanamic (VMO) medial restraints. No patients experienced a recurrent dislocation and the average patient satisfaction with the operation was 97%. Nikku et a193 found less satisfying results with primary operative treatment. They performed a prospective, randomized study on 125 patients with primary patellofemoral dislocation. Fifty-five patients had closed treatment and 70 patients underwent surgery. Sixty-three of the patients had repair of the medial retinaculum, by suturing in 39 patients, by duplication in 18 patients and by additional augmentation of the MPFL with the adductor magnus tendon in 6 patients. Of these 63 patients, 54 had a lateral release. Seven patients were treated only with lateral release. After a 2-year follow-up, the subjective results and function were better in the nonoperative group. ReBIOMECHANICS OF PATELLOFEMORAL INSTABILITY

current instability occurred in 20 patients treated nonoperatively and in 18 treated operatively. The various patient profiles and techniques in these studies make a direct comparison between them difficult. In a patient who sustains an acute, first-time patellofemoral dislocation, treatment of the injured static (MPFL), and possibly dynamic (VMO) restraints appears promising. If predisposing patellofemoral risk factors are present, these need to be addressed as well to optimize the surgical results.
CONCLUSION

There is no consensus as to the best method to treat the spectrum of patellofemoral instability. As a result, the literature is full of various nonoperative protocols and surgical procedures. It appears that most of these treatment methods are anecdotal, usually based on surgeon preference. Surgeons are n o w discovering more information about the pathoanatomy of patellofemoral instability. Injury to the medial static restraints, specifically the MPFL, may prove to be the "essential lesion" leading to recurrent patellofemoral instability, similar to the Bankart lesion seen in anterior shoulder instability. 94 As in the shoulder, other anatomic predisposing factors must be considered. By understanding the biomechanics of patellofemoral instability, the treating physician can develop a more scientific-based treatment algorithm that is specifically targeted to correct a patient's anatomy, including traumatic injury and predisposing malalignment.
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