Idiopathic patellofemoral pain is a significant problem that affects as many as 1 in every 10 active, adolescent females.1 Despite persistent research effort, the etiology of this common problem remains a misunderstood and controversial topic. Vastus medialis obliquus insufficiency and abnormal pronation have been frequently associated with patellofemoral pain. However, interventions targeting these clinical findings have not demonstrated consistent, successful outcomes.2 The importance of these 2 etiologies in patellofemoral pain is now being challenged by more recent evidence that patellofemoral pain may be directly related to hip weakness and poor functional control of the femur during weight-bearing tasks.3 With special emphasis on adolescent females, this article reviews past and current perspectives on the etiology and conservative management of patellofemoral pain.
The characteristic complaint among patients with patellofemoral pain is the insidious onset of pain while running, walking, climbing stairs, or otherwise engaging in activities that involve prolonged and/or repetitive weight bearing over a flexed knee.1,3-7 The symptoms of patellofemoral pain are often debilitating enough to limit participation in competitive sports and daily activities and reduce overall quality of life.1,8,9
Clinically, patellofemoral pain is commonly depicted as being nondescriptly centralized to the anterior or retropatellar aspect of the knee.4,5,10,11 Differential diagnoses include: bursitis around the patella, history of acute trauma to the knee joint, iliotibial band syndrome, intracapsular pathology, ligamentous instability, meniscal lesions, osteoarthritis, patellar tendonitis, plica syndrome, referred pain from hip or spine, and/or traction apophysitis.6,9,11-13
Biomechanical Mechanisms of Symptom Onset
Significant research effort has been devoted to understanding the etiology of patellofemoral pain and consequently, the literature contains an exhaustive list of both intrinsic and extrinsic causative factors such as, over activity,14,15 decreased hamstring flexibility,16 decreased explosive strength,1 inadequate equipment,15 decreased trochlear groove depth,17 decreased gastrocnemius flexibility,1 decreased quadriceps flexibility,1,12 increased medial patellar mobility,1 increased Q angle,15,18,19 patella alta,20 decreased iliotibial band flexibility,21 and an increased medial tibial intercondylar distance.22 Most physicians will agree, however, that patellofemoral pain is related to abnormal lower extremity mechanics.3-5,7,10-13,18,23-33 This review article focuses on 3 key biomechanisms of lower extremity dysfunction associated with patellofemoral pain onset addressed in the literature: vastus medialis obliquus insufficiency/dysfunction; excessive foot pronation; and, most recent, faulty femoral mechanics related to proximal core and hip musculature weakness.
Vastus Medialis Obliquus Dysfunction Mechanism of Symptom Onset
Altered vastus medialis obliquus strength and/or recruitment have long been implicated as key factors in the onset of patellofemoral pain.3,13,34 The primary forces acting on the patella (Figure 1), the quadriceps (sum of all 4 quadriceps muscles), and tibial ligament forces are offset into valgus (Q angle) such that there is an inherent tendency of the patella to track laterally.31
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Figure 1: Generalized diagram depicting the orientation of the forces and constraints about the knee joint. It has been hypothesized that due to the valgus orientation of these forces, decreased force production from the vastus medialis obliquus may result in excessive lateral patellar tracking and thus, knee pain. Abbreviations; LR, lateral retinaculum; MR, medial retinaculum; P, patella; RF, rectus femoris; T, tibia; TT, tibial tubercle; VI, vastus intermedius; VLL, vastus lateralis longus; VLO, vastus lateralis obliquus; VML, vastus medialis longus; VMO, vastus medialis obliquus. (Reprinted from Waryasz GR, McDermott AY. Patellofemoral pain syndrome [PFPS]: A systematic review of anatomy and potential risk factors. Dyn Med. 2008;:9).
Due to the orientation of its fibers medial to the patella, it has been theorized that the vastus medialis obliquus may function to oppose lateral patellar movement.31,35,36 In theory, if the vastus medialis obliquus is atrophied31 or not appropriately recruited10 the lateral forces acting on the patella would be unopposed, the lateral tracking of patella would become excessive, and thus, patellofemoral pain symptoms may follow.10,20,31,35
The role of altered vastus medialis obliquus function as a causative factor in patellofemoral pain onset is supported by observed differences in vastus medialis obliquus morphological characteristics and recruitment patterns between affected individuals and asymptomatic controls. The sonographic study of 54 patients affected by patellofemoral pain and 54 matched controls revealed significantly higher insertion of vastus medialis obliquus on the patella, decreased vastus medialis obliquus fiber angle (relative to the rectus femoris) and decreased vastus medialis obliquus volume among the patellofemoral pain patients.37 Differences in the activation of the vastus medialis obliquus, compared to the vastus lateralis, have been observed among affected patients during the following dynamic activities such as stair climbing.10,38 In a systematic review of electromyographic (EMG) data pooled from studies investigating vastus medialis/vastus medialis obliquus reflex response times and activation patterns during static, and dynamic tasks, Chester et al39 identified a trend towards a delay in the onset of the vastus medialis obliquus relative to the vastus lateralis among symptomatic patients.
Despite the widespread acceptance of the above biomechanism, the role of vastus medialis obliquus dysfunction in patellofemoral pain onset remains debatable as several studies have observed no difference in vastus medialis obliquus recruitment between patellofemoral pain and control subjects during functional tasks.34,40-42 For example, when comparing EMG data of the vastus medialis obliquus relative to the vastus lateralis in healthy and symptomatic patients, several studies have reported no difference in onset of timing34,40,43 or activation magnitude ratios during stair descent or ascent.
Wong44 recently reviewed studies comparing EMG data from symptomatic and control patients and reported that only half of the 12 studies included in the review supported the hypothetical role of altered vastus medialis obliquus activation in patellofemoral pain. Chester et al39 identified a trend towards a delay in onset of the vastus medialis obliquus relative the vastus lateralis in a meta-analysis of EMG data, however, there was a significant degree of heterogeneity across the pooled studies (I2=69.9-93.4; P>.01). The possibility that differences in both morphological characteristics and activation patterns may be secondary to symptom onset among affected patients has yet to be excluded37 thus, the role of the vastus medialis obliquus in etiology of patellofemoral pain remains an area of continued research interest.
The Excessive Pronation Mechanism of Symptom Onset
Abnormal ankle joint biomechanics have also been implicated in patellofemoral joint dysfunction. Based on normal hindfoot function, retrospective evidence of excessive pronation among runners with knee injuries and reports of symptomatic improvement following orthotic use, a cause and effect relationship between excessive pronation and patellofemoral pain was theorized.23,24,32
Typical foot pronation (Figure 2) during the heel contact/weight acceptance phase of gait, is characterized by eversion of the calcaneus. This motion causes the talus to both plantar flex and rotate inwardly, taking the tibia with it.45 During supination, which occurs after shock absorption/loading response, these trends reverse as body weight shifts over the foot, and the knee becomes terminally extended (screw-home mechanism).45
Figure 2: Normal biomechanics of the foot during the loading response phase of the gait cycle: Eversion of calcaneus and inward rotation of the talus (left); medial rotation of ankle joint axis (middle); subsequent internal rotation of the tibia (right). It has been hypothesized that excessive pronation may negatively affect patellofemoral mechanics by increasing the internal rotation of tibia. (Modified with permission from Perry J. Ankle Foot Complex in Gait Analysis: Normal and Pathological Function. Thorofare, NJ: Slack; 1992:76. Copyright © 1992, Slack.)
It is hypothesized that excessive pronation would cause increased calcaneal eversion and as a result, exaggerated internal rotation of the talus and tibia. In this scenario, as the foot attempts to supinate, the excessive rotation of tibia/talus would delay the external tibial rotation needed to facilitate knee extension. Consequently, to achieve full knee extension, the femur would have to compensate by internally rotating more than normal,24,32 the lateral tracking of patella would increase, patellofemoral contact force would be exaggerated, and knee pain would follow.24,32
Support for the role of altered ankle joint biomechanics in patellofemoral pain symptom onset is based on reported differences in measures of pronation/eversion between symptomatic and asymptomatic patients. Three dimensional kinematic and kinetic analysis of hindfoot motion has revealed the following significant differences among symptomatic subjects: delayed peak hindfoot eversion (P=.02),46 greater frontal plane hindfoot eversion angle at heel contact (P=.001),47 decreased peak medial ground reaction force (P=.03),46 and delayed heel strike transient (P=.04)47 (the characteristic peak in vertical ground reaction force after heel strike that precedes a brief reversal in direction of ground reaction force during stance).48
Two dimensional kinematic and kinetic measurement of hindfoot motion has also revealed significant differences in the time to reach maximum eversion (P<.05),49 increased time to achieve maximum lateral force (P<.05),49 and increased lateral ground reaction force (P<.01)49 among symptomatic patients. Differences in kinetics in combination with alterations in timing of pronation, have led authors to suggest that these differences could affect the transfer of loading forces to the knee46 and the onset of patellofemoral pain.
The hypothesis that altered pronation is related to patellofemoral pain onset is challenged by the lack of evidence supporting the existence of a significant, predictive, and/or direct relationship between patellofemoral pain and measures of pronation.28,46,49-51 Kinematic measures of hindfoot motion have consistently revealed that no difference exists in either peak pronation/eversion or the range of eversion46,49/foot pronation28 between symptomatic and asymptomatic patients. The prospective study of incoming military recruits has also demonstrated that baseline measures of static and dynamic pronation are not predictive of symptom onset during basic training.51
Most importantly, central to the hypothetical role of altered pronation in patellofemoral pain is the assumption that, due to the transverse rigidity of the ankle mortise joint, the rotational movement of the subtalar joint during pronation is directly translated into tibial rotation.24,32,45 However, pronation has not been shown to be predictive of tibial rotation nor has tibial rotation been shown to be predictive of pronation.28,46,50 For example, based on kinetic data obtained during end-of-stance period among patients walking at self-selected speeds, Bellchamber and van den Bogert50 suggested that a proximal power source drives tibial rotation during weight-bearing activities rather than a distal power source, as was previously assumed.23,24,32 Therefore, despite evidence of abnormalities in the timing of hindfoot motion among patellofemoral pain patients, the role of ankle joint biomechanics in the pathophysiology of patellofemoral pain remains debatable.
The Medial Collapse Mechanism: Role of Decreased Hip Strength & Faulty Lower Extremity Kinematics
Within the past decade, abnormal hip joint biomechanics have been implicated in the pathogenesis of patellofemoral pain. This shift in thought is due to evidence of a theoretical association between patellofemoral pain, patellofemoral joint stress, femoral kinematics, and hip strength. Elevated patellofemoral joint stress (patellofemoral joint reaction force/contact area) has been frequently cited in relation to patellofemoral pain symptom onset,30,52 but, has often lacked sufficient explanation. Recently, however, advanced in vitro stress modeling comparisons of symptomatic patients and asymptomatic controls enabled Heino Brechter and Powers52 to document elevated levels of patellofemoral joint stress among symptomatic patients during walking (2.5-fold increase, P=.08) and fast walking (2.1-fold increase, P=.02) conditions. Based on equivalent patellofemoral joint reaction forces observed in the 2 groups, the investigators concluded that increased patellofemoral joint stress among the symptomatic patients was caused by a decrease in contact area between the patella and femur.52
Using dynamic magnetic resonance imaging, Powers29 provided further explanation by observing that changes in patellofemoral articulation among symptomatic patients during weight-bearing conditions may be directly related to abnormal femoral kinematics. In contrast to the traditional assumption that patellofemoral pain is associated with maltracking of the patella “over” the femur, this new evidence suggests that, decreased patellofemoral contact area and subsequently, elevated patellofemoral joint stress, are related to abnormal movement of the femur “under” the patella (Figure 3).3 Due to the role of hip strength in dynamic hip joint stability, it is theorized that the pathogenesis of patellofemoral pain is the result of hip strength-related abnormalities in femur kinematics,3 a notion supported by evidence of significant hip external rotator, abductor, and extensor weakness among symptomatic females (Table 1).4,5,7,13,25,53-55
Figure 3: Kinematic magnetic resonance image that depicts the femur rotating underneath the patella during a single-limb, weight bearing task. Note how the patella maintains a relatively horizontal position while the femur inwardly rotates. (Adapted with permission from Powers CM, Ward SR, Fredericson M, Guillet M, Shellock FG. Patellofemoral kinematics during weight-bearing and non-weight-bearing knee extension in persons with lateral subluxation of the patella: a preliminary study. J Orthop Sports Phys Ther. 2003; :677-685. Copyright © 2003, American Physical Therapy Association.)
Collectively, evidence of hip weakness, abnormal femoral kinematics, and elevated stress among symptomatic patients has led to the emergence of the “medial collapse” mechanism of symptom onset.3,30 This theory attributes patellofemoral pain to the inability of weak hip muscles to control hip kinematics during dynamic, closed chain tasks (Figure 4). Consequently, the lower extremity falls into a faulty movement pattern characterized by increased hip adduction, internal femoral rotation and/or knee valgus. In theory, this movement pattern may change the relationship between the patella and femur, decrease patellofemoral joint contact area, elevate patellofemoral joint stress and thus, lead to symptom onset.3 Cadaveric studies have provided evidence to support this theory as alterations in frontal and transverse plane alignment of the lower extremity have been shown to be directly related to increased patellofemoral joint stress.18,26,27
Figure 4: Computer generated skeletal model of an adult female with hip weakness completing a single limb squat task. Beginning of maneuver (left), approximately one half of maximum knee flexion (middle), and maximum knee flexion (right). Note the changes in lower extremity alignment between the femur and pelvis as the female patient falls into progressively greater internal femoral rotation, hip adduction, and contralateral pelvic drop.
Evidence for the medial collapse mechanism of patellofemoral pain onset is emerging. Mascal et al13 observed favorable intra-subject kinematic changes following a 14-week core and hip strengthening program. In addition to substantial improvements in hip strength and decreased symptom severity, a 20-year-old female patient demonstrated decreased hip adduction, reduced contralateral pelvic drop and most notably, decreased internal rotation during the 3-D kinematic analysis of a single-leg step down task. By averaging the hip rotation kinematics of 21 asymptomatic and 20 symptomatic adult females across running, drop jump, and single limb step down tasks, Souza and Powers55 reported significantly (P<.05) greater peak hip internal rotations in the symptomatic group, 7.6° , compared to the control group 1.2°.55 Among the symptomatic patients, significant deficits in hip extensor (P=.005) and hip abductor (P=.02) torque were also reported.
Role of Hip External Rotation in the Medial Collapse Mechanism
Much of the current theoretical support for medial collapse mechanism of patellofemoral pain has centered around the deleterious effect that increased internal femoral rotations (or hip/thigh rotations)18,26,27,30 may have on patellofemoral force distribution. However, findings in the literature do not consistently support this hypothesized role of increased internal femoral rotation in symptom onset (Table 2). Specifically, in contrast to the evidence reported by Mascal et al13 and Souza and Powers,55 increased external hip rotations or decreased internal hip rotations were identified in symptomatic populations by 3-D kinematic analysis of: level ground walking,28 single leg hop,7,33 single limb squat,33 running,33 and fatigued25 conditions (Table 2). Interestingly, external rotation and contralateral hip external rotator weakness have been reported concomitantly.4,7,25 It has been speculated that these inconsistencies may be secondary to the use of nondemanding tasks,4 or the result patients adopting compensatory strategies,3,4,28 to reduce the Q angle and decrease patellofemoral joint stress.4,33
In an effort to determine if lower-extremity kinematics change during conditions when patients would be less able to maintain compensatory strategies, Wilson et al7 and Dierks et al25 respectively evaluated the effects of exertion on symptomatic and asymptomatic patients during repeated single limb hops and a prolonged run to fatigue. The role of external rotation as a compensatory strategy was not well supported as the authors from both studies concluded that asymptomatic patients tended to demonstrate comparable changes in lower-extremity kinematics when fatigued.7,25
Due to the fact that increased external femoral rotation has also been associated with increased patellofemoral contact pressure,27 the alternative hypothesis, in which external rotation is a contributing factor to patellofemoral pain, must also be considered. Cibulka and Threlkeld-Watkins56 provide some support for this notion in a case study of a symptomatic adolescent female. Following therapy, dramatic symptomatic improvement was reported in conjunction with normalization in hip range of motion, increased hip strength, and decreased external hip/thigh rotation during observational gait analysis.56
Based on the above evidence, trends of increased external rotation among symptomatic patients seem to warrant further investigation to elucidate the seemingly contradictory relationship between external hip/thigh rotation, hip muscle weakness and patellofemoral pain symptom onset. This is no easy task and investigators must be forewarned that the measurement of lower extremity transverse plane rotations may be complicated by, among many confounding factors, the underestimation of true rotations.57
Considerable research effort has been devoted to the study of conservative interventions for patellofemoral pain. This has proven to be a difficult task due to the benign course of the disease in this population. For example, Nimon et al9 and Sandow and Goodfellow58 followed a series of symptomatic adolescent girls who were assured by the clinician that their “condition was benign.” Within 3.8 and 16 years respectively, the pathology was absent in nearly 50% and 73% of the “untreated patients.”9,58 Although the natural course of disease may be benign for most, >1 in 4 (27%) of the patients in this population continued to report significant symptoms for nearly 20 years.9 Due to the fact that the clinical presentation of patients who develop persistent and debilitating symptoms is indistinguishable from those patients whose symptoms resolve spontaneously, more effective intervention strategies are warranted to prevent the development of chronic symptoms.
Among most clinicians, conservative therapeutic approaches are regarded as the gold standard.9,11,58 Common conservative interventions include stretching, strengthening, taping, bracing, activity modification, the use of modalities, cast immobilization, and nonsteroidal anti-inflammatory drugs for pain management.2,3,11,12,20 In general, the mode of conservative treatment used by the clinician is related to the assumed underlying mechanism of symptom onset. In the case of assumed vastus medialis obliquus insufficiency/dysfunction, treatment is aimed at improving patellar tracking through soft tissue mobilization and selective vastus medialis obliquus activation/strengthening.2,6,20
Although successful treatment outcomes have been reported,20 in a review of 20 articles (387 patients), Smith et al59 concluded that there was insufficient evidence to support the notion that any 1 or combination of the following factors are capable of increasing activation of vastus medialis obliquus compared to the vastus lateralis: altered foot positioning, modifications in lower extremity joint orientation or co-contraction of lower extremity musculature. Thus, the efficacy of vastus medialis obliquus strengthening remains debatable.2,6 When excessive pronation is assumed, patellofemoral pain treatment is centered on the use of orthotics to limit hindfoot motion. Favorable treatment outcomes and improvements in quality of life8 have been observed, but no sufficient evidence exists to support use of foot orthoses in all patients with patellofemoral pain.2,3,6
More recently, the documentation of significant hip weakness linked to the medial collapse mechanism among symptomatic study populations4,5,7,13,25,53-55 has led many clinicians to favor hip strengthening and neuromuscular retraining interventions. Little has been reported on the direct efficacy of hip/core strengthening but, preliminary evidence has been promising.
In a randomized, double-blinded, placebo controlled trial, Crossley et al11 reported that compared to a placebo group, the intervention group self-reported significantly (P<.05) reduced scores of disability and knee pain following a physical therapy protocol that emphasized hip strengthening. Vastus medialis obliquus strengthening exercises and stretching were used concomitantly and thus, caution needs to be exercised when interpreting the results of this adult study.
Tyler et al12 reported significantly increased (P<.05) hip strength and significantly decreased (P<.001) scores of pain and discomfort during activities of daily living and exercise in symptomatic patients following the completion of a 6-week hip strengthening and stretching protocol. Stretching was emphasized, and as improvements in iliotibial band and hip flexor flexibility were achieved, it is difficult to directly attribute the results of this study to general hip strengthening alone. Of greatest interest, Mascal et al13 reported substantial reduction in knee pain among 2 adult females completing a comprehensive 14-week hip and core strengthening program. Outcomes of hip strengthening interventions have been promising but, due to the inclusion of multiple therapeutic strategies or use of small patient populations, it is difficult to draw definitive conclusions about the effectiveness of this new intervention approach.
Considerations and Future Directions
A review of the literature revealed no single or combination of conservative interventions for patellofemoral pain have, to date, been proven to be superior.2,6 Based on this lack of evidence and the observation that the majority of patients affected by patellofemoral pain seem to get better with time, clinicians are often left to assume the etiology of patellofemoral pain is multifactorial and thus, that treatment should be nonspecific. This default approach is not only inefficient but more importantly, as patellofemoral pain can rapidly develop into a chronic and debilitating condition, this method is less than optimal.
The lack of treatment success among those affected by long-term symptoms is likely related to the absence of an evidence-based mechanism for symptom onset that may be used by the clinician to guide intervention towards addressing the underlying cause of the patient’s symptoms. In light of these past shortcomings, the medial collapse mechanism and related treatment methodologies are an intriguing development because, in this model, intervention is directed towards a specific underlying abnormality that is supported in the literature, hip musculature weakness. Clinically, the medial collapse theory is appealing because patellofemoral pain patients with hip weakness may be easily identified by in-office hip strength screening and clinical functional task assessment.
Despite the promise of this new theory, it is important to note that knee surgery has been shown to cause a loss of proximal muscle (hip) strength in the operated, relative to the unoperated leg.60 Therefore, the possibility that hip weakness may be secondary to the onset of patellofemoral pain remains a scenario yet to be completely excluded. In order to refute this alternative hypothesis and substantiate this new clinical model, future research should focus on 3 key areas: (1) Establishing a direct, cause and effect relationship between patellofemoral pain onset and abnormal hip mechanics. Evidence of hip weakness among symptomatic patients is supported in the literature. However, inconsistencies in kinematic data have complicated the conclusion that there exists a direct causal relationship. Specifically, explanations for the inconsistencies in the measurements of hip/thigh rotations must be explored. (2) Establishing the efficacy of hip strengthening interventions. Confounding factors in clinical trials have clouded the evidence, making strong conclusions difficult to support.2 Thus, a need exists for the orthopedic community to critically evaluate the efficacy of hip and core strengthening interventions in randomized controlled trials with well defined patient populations. (3) Validating a clinical screening test of hip strength for the identification of patients likely to benefit from hip core strengthening interventions. Manual muscle testing and hand held dynamometry are common methods for assessing hip strength but, are subjective and time intensive respectively. More importantly, these static measurements do not assess lower extremity movement or neuromuscular control. By placing a dynamic load on the hip,61 the single leg squat task (Figure 5) is a simple and appealing assessment of lower extremity kinematics, hip strength, and injury risk.61,62 This screening assessment has not yet been standardized and thus, future research could be directed towards establishing objective measurements of lower extremity strength and kinematics during a standardized version of this test.
Figure 5: Biomechanical evaluation of a single limb squat task.
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Mr Carry and Dr Miller are from the Musculoskeletal Research Center (MRC), Department of Orthopedic Surgery, and Ms Kanai is from the Center for Gait and Movement Analysis (CGMA), The Children’s Hospital, Aurora, and Dr Miller is also from the Department of Orthopedic Surgery, University of Colorado, Denver, and Dr Polousky is from the Youth Sports Medicine Institute, Rocky Mountain Hospital for Children, Denver, Colorado.
The material presented in any Vindico Medical Education continuing education activity does not necessarily reflect the views and opinions of Orthopedics or Vindico Medical Education. Neither Orthopedics nor Vindico Medical Education nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.
Correspondence should be addressed to: John D. Polousky, MD, Youth Sports Medicine Institute, 14100 E Arapahoe Rd, #210, Centennial, CO 80112 (firstname.lastname@example.org).