Patellar Luxation in Dogs

Patellar luxation, defined as the displacement of the patella out of the trochlear groove of the femur, is a common problem in both small and large dogs. The condition may be congenital, developmental, traumatic, or iatrogenic in origin. The pathology can vary from mild instability of the patella within the trochlear groove to severe permanent luxation of the patella, either medially or laterally, with skeletal deformities. Medial patellar luxation (MPL) is more common in all sizes and breeds of dogs. Anatomic deviation of the patella interferes with its normal function, resulting in skeletal deformities of the pelvic limb, contracture of pelvic muscles, loss of normal mechanics of the stifle, degenerative changes of the joints, and impairment of limb function. Clinical signs vary with many factors, including degree of luxation, age of patient, degree of musculoskeletal abnormalities, and degree of degenerative joint disease. The majority of patellar luxations likely have a hereditary basis and genetic predisposition; however, the exact disease mechanisms have not been defined.

Anatomy

The patella is an ossification in the tendon of insertion of the quadriceps muscle group and the largest sesamoid bone in the body [1]. The patella is ovate: the proximal blunt surface is the base and may extend beyond the articular surface, whereas the distal pointed end, the apex, does not (Fig. 106-1). The articular surface of the patella is smooth and convex in all directions, and articulates with a wide concave articular groove on the cranial surface of the distal femur called the femoral trochlea. The medial and lateral trochlear ridges, with the medial ridge usually being thicker than the lateral, bound the femoral trochlea.

Figure 106-1. Normal anatomy of the articular aspect of canine patella. a: vastus medialis, b: rectus femoris, c: vastus lateralis, d: medial parapatellar fibrocartilage, e: lateral parapatellar fibrocartilage, f: medial retinaculum, joint capsule, femoropatellar ligament, and femoral fascia, g: lateral retinaculum, joint capsule, femoropatellar ligament, and femoral fascia, h: infrapatellar fat pad, i: patellar ligament.

The patella is held in the trochlea of the femur primarily by the joint capsule, thick lateral femoral fascia (fascia lata), and thinner medial femoral fascia (Fig. 106-1). The cranial part of the sartorius and biceps femoris blend into the femoral fascia at the stifle and may contribute to the medial and lateral stability of the patella. The medial and lateral femoropatellar ligaments also aid in stability of the patella within the trochlea. The lateral femoropatellar ligament can be traced from the lateral side of the patella to the lateral fabella. The medial ligament is weaker than the lateral and blends with the periosteum of the medial epicondyle of the femur. The edges of the patella are connected to the femoral fascia via the medial and lateral parapatellar fibrocartilages (Fig. 106-1). The parapatellar fibrocartilages ride on the ridges of the femoral trochlea and aid in patellar stability through contact with the ridges of the femoral trochlea. The vastus medialis muscle and vastus lateralis muscle of the quadriceps muscle group are fixed to the patella by the medial and lateral parapatellar fibrocartilages, respectively. A suprapatellar fibrocartilage may also be present in the tendon of the rectus femoris.

The quadriceps muscle group is formed by the rectus femoris, vastus lateralis, vastus intermedius, and vastus medialis. The rectus femoris arises from the ilium cranial to the acetabulum, the vastus lateralis and intermedius arise from the proximal part of the lateral lip of the caudal rough surface of the femur, and the vastus medialis arises from the medial side of the proximal femur. This muscle group converges on the patella and continues as the patellar ligament to insert on the tibial tuberosity distally.

Function

The extensor mechanism is composed of the quadriceps muscle group, patella, trochlear groove, patellar ligament, and tibial tuberosity. Physiologic (near straight) alignment of these structures, together with normal gliding articulation of the patella and trochlea, are essential for smooth and efficient movement of the stifle during its extension [2]. Muscular forces of the vastus medialis and vastus lateralis control medial and lateral movement and stability of the patella. The patella is an essential component of the extensor mechanism, serving to alter the direction of the pull of the quadriceps mechanism, preserving even tension of the extensor mechanism during stifle extension, and acting as a lever arm, increasing the mechanical advantage of the quadriceps muscle group. The patella also protects the tendon of the quadriceps muscle group during movement, provides a greater surface area for the tendon to engage the trochlea of the femur, and provides cranial and rotary stability to the stifle joint in the extensor mechanism. The location and prominence of the tibial tuberosity are important for the mechanical advantage of the extensor mechanism.

Epidemiology

Patellar luxation can be congenital, developmental, iatrogenic, or traumatic, although the majority of luxations are congenital and are often related to other musculoskeletal abnormalities [3,4]. It is a common problem of both small and large dogs and is the most common congenital abnormality in dogs [5]. In a study that examined 1679 pet store puppies, 253 had at least one congenital effect (15%) among which 121 were patellar luxation (7.2%) [6]. These puppies were mostly small breeds: 48.8% would likely weigh less than 7 kg when mature. Patellar luxation is diagnosed most commonly in small breed dogs as a congenital or developmental problem within 6 months of age. However, as many as 32 breeds, including large breeds such as Akita, Great Pyrenees, and Labradors have been identified as at increased risk for patellar luxation [7]. Toy and miniature breeds are affected approximately 12 times more frequently than are large breed dogs, with toy poodles, Yorkshire terriers, Pomeranians, Pekingese, Chihuahuas, and Boston terriers being at increased risk for medial luxation [4].

Medial Patellar Luxation

Medial patellar luxation is more common in all sizes and breeds of dogs than is lateral patellar luxation (LPL). In a study of 124 dogs that were referred for patellar luxation, the majority of dogs had a congenital form (82%), as opposed to acquired patellar luxation (15%), and the majority (89%) had MPL, as opposed to lateral luxation [3]. MPL accounted for 98% in small breeds (<9.1 kg), 81% in medium breeds (9.1-18.2 kg), 83% in large breeds (18.2-36.4 kg), and 67% in giant breeds (>36.4 kg). In one study of 70 referred large breed dogs, MPL accounted for 97% and LPL accounted for 2.8% [8]. That study also suggested that in large breed dogs MPL occurs more frequently in males (male:female sex ratio of 1.8:1). In contrast, other studies have shown that in small breed dogs females are more frequently affected (male:female sex ratio of 1:1.5) [4]. Although females are more likely to be affected than males, prevalence is similar among spayed females, neutered males, and intact females, with intact males being at a lower risk. Bilateral luxations are significantly more common (65%) than unilateral luxations (35%) [3,8].

Three groups of patients were identified based on clinical pattern by Brinker, Piermattei, and Flo: 1) neonates and older puppies with abnormal hind-leg carriage and function from the time of ambulation; 2) young to mature dogs with intermittent and/or progressively abnormal gait; and 3) older dogs with an acute onset of lameness associated with degenerative changes and cranial cruciate ligament rupture [9].

Lateral Patellar Luxation

Lateral patellar luxation occurs infrequently in dogs. Although LPL can occur in any size breed, it is proportionally seen more frequently in large breed dogs. The reported incidence of LPL varies widely between studies from 3% [8] to 8.9% of patellar luxations in large breed dogs [4] to 38.7% of patellar luxations when all small and large dogs are included [3]. The male to female ratio of patellar luxation is 1.5:1, with intact males being at lowest risk [3,4].

Pathophysiology

Medial Patellar Luxation

The cause of MPL remains unclear. Because toy and miniature breeds are affected with MPL approximately 12 times more than large breeds, a hereditary basis and genetic predisposition of this condition is likely. In addition, because many affected dogs are presented at 3 to 6 months of age, in absence of trauma, often with a bilateral condition, a congenital or developmental disorder rather than an acquired disorder is likely. It is also possible that congenital patellar instability predisposes an animal to traumatic luxation.

It is generally accepted that MPL is a multifactorial anatomic anomaly, not only of the stifle but of the entire pelvic limb. Although the sequence of structural remodeling and variety of deformities of the pelvic limb have been well described, information regarding cause and effect relationships in MPL is limited in the veterinary literature. Specific musculoskeletal abnormalities such as coxofemoral anomalies, malalignment of the extensor mechanism, muscular pathology in the quadriceps, and shallow trochlear groove have been proposed as underlying causes of MPL.

Coxofemoral abnormality may cause MPL and related limb deformities, however no correlation has been found between hip dysplasia and MPL. Based on Putnam’s hypothesis, it has been proposed that primary changes in the coxofemoral joint and resultant postural abnormalities lead to compensatory mechanisms more distally, resulting in the eventual malformation in the distal part of the limb and patellar luxation [10]. Development of MPL has been linked to the radiographic appearance of coxa vara (decreased angle of inclination of the femoral neck) and decrease in femoral anteversion (relative retroversion), which in turn leads to genu varum, medial displacement of the extensor mechanism, and further anatomic changes during growth by abnormal medial tension of the extensor mechanism (Fig. 106-2). In a theory extrapolated from human literature, it was hypothesized that the reduced anteversion causes external rotation of the coxofemoral joint, which requires compensatory internal rotation of the distal limb to place the foot properly. As a result, the lateral soft tissues supporting the stifle joint are stretched and a lateral torsion force is exerted on the distal femoral growth plate, causing lateral torsion of the distal femur. This lateral rotation of the distal femur displaces the femoral trochlea lateral to the line of contraction of the quadriceps. The compensatory internal rotation of the limb simultaneously causes displacement of the quadriceps muscle group medially, which in turn results in a medial displacement of the patella.

Figure 106-2. Radiographic appearance of grade 4 medial (a) and lateral (b) patellar luxation. Note the extreme internal (a) and external (b) rotation of the tibia as well as the ectopic position of the patella. Clinical signs associated with bilateral grade 4 LPL (c). In such an advanced case, stifle extension is prevented in part because of periarticular adhesions and fibrosis of the periarticular tissues. Permanent stifle flexion may be seen with severe grade 4 LPL and MPL. Intraoperative skyline views of a normally shaped trochlea (d) and a shallow trochlea (e) secondary to juvenile grade 4 patellar luxation.

Contrary to this hypothesis, a study of anteversion angle of the femoral neck using magnetic resonance image (MRI) did not reveal any correlation between patellar luxation and anteversion angle [11]. This study also demonstrated that anteversion angle measurement based on radiographs is not reliable. In another radiographic study of 100 papillons, there were no significant differences in angle of anteversion and inclination of the femoral neck between those with patellar luxation and normal dogs [12]. Interestingly, there were significant differences in weight and size between these groups: dogs with patellar luxation were significantly smaller and lighter. In addition, morphologic analysis of the pelvis showed that the origin of the cranial part of the sartorius muscle lies significantly more medially in dogs with MPL than in normal dogs. Such conformational variation may lead to increased medial traction on the patella and medial displacement of the patella. Various deformities of the pelvic limb can cause deviated direction of force of the quadriceps group. The deviation between the direction of force of the quadriceps group (from origin of the quadriceps to the center of the trochlea or patella) and the patellar ligament is referred to as the quadriceps angle or Q-angle (Fig. 106-3) [11]. The Q-angle has been measured using MRI in dogs with varying degrees of MPL, and dogs with MPL have significantly greater Q-angle, although the cause and effect relationships have not been established.

Figure 106-3. In humans, the quadriceps angle (Q-angle) is defined as the angle between the line of action of the quadriceps and the line formed by the patellar ligament and patella in normal limbs. Similarly, the Q-angle in dogs with PL has been defined as the line from the origin of the rectus femoris muscle to the center of the trochlea and the line between the center of the trochlea and the tibial tuberosity. Deviation of the course of the patellar ligament in one direction generates a resultant force (arrow) that pulls the patella in the same direction, resulting in patellar luxation (the greater the Q-angle, the greater the risk of luxation). The average Q-angle increases with the severity of the luxation from ~11° (normal dogs) to ~12° (grade I), ~24° (grade II) and ~37° (grade III). (Adapted from: Kaiser S, Cornely D, Golder W, et al. Magnetic resonance measurements of the deviation of the angle of force generated by contraction of the quadriceps muscle in dogs with congenital patellar luxation. Vet Surg 30(6):552-558, 2001. ).

Malalignment of one or more structures in the extensor mechanism of the stifle may cause MPL. As indicated above, the location and stability of the patella during range of motion are governed by regional anatomic structures about the patella. Quadriceps muscles and other structures in the extensor mechanism, soft-tissue constraints of the patella, and conformation of femoropatellar articulation dictate patellar tracking on the stifle, which is influenced by anatomic relationships among the pelvis, hip joint, femur, tibia, and tarsal joint. Proper anatomic alignment of the extensor mechanism with the underlying skeleton is the primary component of patellar stability [2]. During stifle extension, strong tensile forces within the quadriceps seek to align the patella between the muscular origin and insertion. If the long axis of the quadriceps muscle is not centered over the trochlea, there is an imbalance in muscular force favoring patellar luxation.

Muscular imbalance among the quadriceps may be a primary cause of malalignment of the extensor mechanism and MPL. A clinical study reported grossly evident atrophy and fibrosis of vastus medialis (tight band-like appearance) in puppies with severe MPL [13]. As puppies grow, medial displacement of the patella and the quadriceps muscle group, and underdevelopment of the patella and trochlear groove occur. Abnormal tension from the pathologic vastus medialis and medially displaced extensor mechanism may produce a "bowstring effect", causing lateral bowing of femur and internal rotation of tibia. Clinical observation that skeletal deformities can be completely reversed in young puppies (less than 2 months of age) by the release of tight vastus medialis suggests that muscular pathology is the primary cause of MPL and related deformities of the pelvic limb.

Regardless of primary etiology, medial displacement of the extensor mechanism causes increased pressure on the medial femoral cortex, and thus unequal growth between the medial and lateral aspects of the distal femoral growth plate. Subsequent to this asymmetrical stress distribution, the growth rate on the lateral side of the distal femoral physis is relatively greater than on its medial side. This results in more growth on the lateral side of the bone, and thus lateral bowing of the distal femur (bowstring). Similarly, this increased pressure on the medial part of the distal femur slows the growth of the medial femoral condyle, causing dysplasia of the femoral epiphysis. The proximal tibia compensates with greater bone growth medially, which causes medial bowing of the proximal tibia.

Formation of a shallow femoral trochlea has also been proposed as a primary cause for subsequent dislocation of the patella and extensor mechanism. However, because the femoral trochlea does not develop normally in the absence of normal patellofemoral compression, underdevelopment of the trochlear groove is believed to be a secondary deformity.

The degree of musculoskeletal pathology depends on age and the degree and duration of patellar luxation. Medial patellar luxation often causes progressive deformation of both bony and soft tissues (Table 106-1). Skeletally immature animals develop angular and torsional deformity secondary to abnormal forces directed against open physes, and older animals with MPL may develop degenerative joint disease. Both hip and tarsal joints are also affected. Dogs may show bowlegged appearance with the feet turned inward, with severely decreased range of motion of the stifle and extended tarsal joints (Fig. 106-2). Increased rotational laxity of the stifle joint, bidirectional (medial and lateral) instability of the patella, and extensive cartilaginous erosion on the medial trochlear ridge may also be present. In addition to these abnormalities, the stifle joint may have concurrent problems of instability such as rupture of the cranial cruciate ligament. Because one of the functions of the cranial cruciate ligament is to limit tibial internal rotation during flexion, it has been suggested that MPL and subsequent increased tibial internal rotation amplify the stress on the cranial cruciate ligament, predisposing to stretching and rupture. In addition, one can speculate that the loss of the quadriceps support cranially (a secondary constraint against tibial cranial translation) further increases cranial cruciate ligament stresses. The association between MPL and cranial cruciate ligament rupture remains uncertain. Although some studies have reported concomitant cruciate ligament rupture in up to 20% of MLP cases, others found that the prevalence of cranial cruciate ligament injury in dogs with patellar luxation was similar to that of dogs with other orthopedic conditions [14].

Lateral Patellar Luxation

Owing to the paucity of scientific and clinical studies of LPL in veterinary orthopedics, the proposed pathophysiology of LPL in dogs has often been extrapolated from the human literature where LPL is the most frequent form of patellar luxation. Although several pathologic factors have been associated with LPL, whether these are causative or result from the luxation remains unclear (Table 106-2). Although in rare cases, no apparent factor other than LPL is identified, in most instances (95%) LPL is associated with one or more structural defects [1,15,16].

As seen with MPL, the normal development of the femoral condyles and trochlear groove depends on the balance between gravity and muscle forces during normal weight bearing. Anatomic alterations such as angular and torsional malalignment of the femur and tibia may result from an abnormal distribution of growth-plate stresses during growth. Similarly, alteration of the normal anatomy such as coxa valga and excessive anteversion of the femoral neck may induce relative medialization and internal torsion of the distal femur, respectively. An increased anteversion angle either can be compensatory as the dog adjusts the position of the hip, or fixed because of a femoral deformity. Both neck anteversion and coxa valga may contribute to medialization of the trochlea with regard to the line of action of the quadriceps (lateral Q-angle) and, therefore, to lateral luxation of the patella (Fig. 106-3). Subsequently, the lateral aspect of the distal femoral growth plate may become overloaded, thus contributing to a slower rate of growth of the lateral femoral cortex compared with the medial one and, over time, to lateral bowing of the distal third of the femur. The lateralization of the compressive loads across the joint may also constrain the development of the tibia, leading to a lateral deviation of the limb at the stifle, a condition known as genu valgum. With genu valgum, although the medial condyles and tibial plateau develop normally, increased forces through the lateral aspect of the distal femoral physis can lead to lateral condylar dysplasia and luxation of the patella. In turn, the absence of patellar pressure during growth interferes with the development of the trochlea, which becomes shallow. Under contraction of the quadriceps, the unconstrained patella is able to move laterally, leading to wear and erosion of the lateral trochanteric ridge, thus exacerbating the problem.

It has been theorized that, in humans, LPL may be initiated by hypoplasia of the vastus medialis muscle [17]. As the vastus medialis becomes hypoplastic, it cannot counteract the antagonist vastus lateralis, resulting in lateral patellar luxation. Phylogenetically, the vastus medialis is the last muscle to develop in humans [18]. It is also the first to undergo atrophy if it is injured or immobilized, and the last to respond to rehabilitation. Although hypoplasia of the vastus medialis may be present in dogs with LPL, this theory is currently unproven.

As with any developmental condition, the anatomic malformations will be more severe if initiated in a younger animal. It has been shown experimentally that alterations in the lines of force produced by soft-tissue restraints in young animals can lead to permanent recognizable bone deformities within 2 weeks [19]. These conformational alterations, including lateral displacement of the tibial tuberosity, are fixed after 4 weeks in 6- to 8-week-old puppies [19]. The permanent lateralization of the quadriceps results in unbalanced strain on the lateral condyle, medial retinaculum, and joint capsule. The lateral retinaculum tightens, and the medial retinaculum stretches further, exacerbating lateral patellar luxation [19].

Three cases of pes varus resulting in LPL and lameness in miniature dachshunds have been reported [20,21]. Pes varus describes the inward rotation of the distal tibia secondary to the asymmetrical premature closure of the medial aspect of the distal tibial growth plate [21]. As pes varus progresses, compensatory righting of the tarsus and paw placement lead to lateralization of the limb, laxity of the stifle, and eventually, LPL. In two cases, pes varus was thought to be the result of autosomal recessive inheritance [21]; in the third case, it was thought to result from an injury to a distal tibial growth plate [20]. Although the distal tibial physis is affected in 3% of all traumatic physeal injuries [22], resultant pes varus does not occur in all cases.

Clinical Signs

Clinical signs associated with MPL vary with degree of the pathology of the pelvic limb. A classification of MPL was designed by Putnam and adapted by Singleton [10,16]. Grades l and 2 represent reducible luxations, whereas grades 3 and 4 represent the permanent luxations.

Grade l: Patella can be manually luxated on full extension, with spontaneous reduction on release. Minimal skeletal deformity.

Grade 2: Patella luxates on stifle flexion or manual manipulation, and remains luxated until stifle extension or manual reduction. As much as 30° of medial tibial rotation.

Grade 3: Patella remains luxated continuously but can be reduced manually; 30° to 60° of medial tibial rotation.

Grade 4: Patella luxated permanently and cannot be reduced; 60° to 90° of medial tibial rotation.

Conclusion

The patella/trochlea arrangement acts as a pulley system that optimizes the function of the quadriceps during stifle extension. By moving the patella away from the axis of flexion/extension of the stifle, the trochlea provides a lever arm to the quadriceps muscle, thus minimizing muscle contraction during extension. Any reduction of the trochlear leverage owing to patellar luxation results in a relative increase in the magnitude of the contractile force necessary to produce stifle extension. In extreme cases, such as severe grade IV MLP or LPL, the line of action of the quadriceps may become caudal to the stifle axis of flexion/extension. The net result is flexion rather than extension of the stifle during quadriceps contraction (Fig. 106-4). This severe alteration of the stifle biomechanics along with the development of fibrous adhesions between the patella and the retinaculum precludes stifle extension and clinically results in dogs walking in a permanently crouched position (Fig. 106-2).

Figure 106-4. The patella and trochlea form a pulley system that optimizes the function of the extensor mechanism by providing a lever arm to the quadriceps muscle (Qm). Patellar luxation reduces the trochlear leverage (L), which in turn induces a relative increase in the quadriceps muscle force needed to achieve stifle extension. Similarly, the quadriceps muscle force has been shown to increase by 15% to 30% following patellectomy in people. In extreme cases, such as severe grade IV luxations, the quadriceps line of action moves caudally to the stifle axis of flexion/extension, thus transforming the quadriceps into a flexor muscle.

Various surgical procedures have been proposed to treat patellar luxations with the common objective of restoring the alignment of the extensor mechanism through a combination of corrective osteotomies and soft-tissue procedures. Until the pathophysiology of patellar luxation is more completely understood, surgeons must be content to repair the apparent structural abnormalities of their patients.