Patellofemoral pain is characterized by insidious onset anterior knee pain that is exaggerated under conditions of increased patellofemoral joint stress. A variety of risk factors may contribute to the development of patellofemoral pain. It is critical that the history and physical examination elucidate those risk factors specific to an individual in order to prescribe an appropriate and customized treatment plan. This article aims to review the epidemiology, risk factors, diagnosis, and management of patellofemoral pain.
Key points
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Patellofemoral pain (PFP) is a common condition, especially among runners.
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A variety of risk factors for PFP have been identified and may be loosely categorized by local joint abnormalities, aberrations in lower extremity biomechanics, and training errors.
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Proper diagnosis and management of PFP mandate close inspection and targeted intervention according to the individual’s risk factor profile.
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Management strategies for PFP include quadriceps strengthening, stretching key muscle groups (quadriceps, hamstrings, and gastrocnemius), patellar taping, patellar bracing, hip strengthening, foot orthoses, gait re-education, and training modification.
Introduction
Patellofemoral pain (PFP) is characterized by anterior knee pain of insidious onset that is exacerbated under conditions of increased patellofemoral joint stress. It is commonly observed in runners and may arise in the setting of a variety of risk factors. PFP does not seem to be self-limited but rather can persist chronically if those factors contributing to its development are not properly recognized and addressed. Here, the epidemiology, risk factors, diagnosis, and management of PFP are reviewed.
Introduction
Patellofemoral pain (PFP) is characterized by anterior knee pain of insidious onset that is exacerbated under conditions of increased patellofemoral joint stress. It is commonly observed in runners and may arise in the setting of a variety of risk factors. PFP does not seem to be self-limited but rather can persist chronically if those factors contributing to its development are not properly recognized and addressed. Here, the epidemiology, risk factors, diagnosis, and management of PFP are reviewed.
Discussion
Epidemiology
PFP accounts for up to 25% of knee injuries that present to sports medicine clinics. PFP seems to be particularly common among runners, representing one of, if not the most, common running-related musculoskeletal injury, particularly among longer-distance runners.
PFP demonstrates a clear predilection for women with prevalence and incidence rates that are 2 to 3 times greater for women than men. This prevalence and incidence rate are thought to reflect specific anatomic and biomechanical variations in women that predispose to PFP. Women, for example, exhibit lower cartilage thickness and greater peak cartilage stress during stair-walking. Disparities in lower extremity strength as well as both static and dynamic alignment have also been purported as contributing factors. Comparative studies of lower extremity strength demonstrate greater hip abduction and external rotation strength in men when compared with women. Meanwhile, increased Q-angle, as well as dynamic knee valgus angle and hip internal rotation angle, has also been reported in women compared with men. Each of these variables has been independently implicated as risk factors for PFP and are discussed in greater detail in subsequent sections.
Traditionally, PFP has been considered an affliction of younger patients. Interestingly, a recent investigation of injury patterns in masters runners demonstrated similar rates of PFP between those older and younger than 40 years of age. This trend may reflect greater involvement of older athletes in sport, and the increasingly recognized chronic nature of PFP. Certainly more current studies evaluating the incidence and prevalence of PFP across a wide age range are warranted.
Cause of Patellofemoral Pain
The precise pathogenesis of PFP remains poorly understood; however, the pain of PFP seems to represent the end result of increased stress at the patellofemoral joint. The cause of exaggerated joint strain is a point of particular contention. Classically, aberrant patellar alignment and tracking were thought to signify the primary precipitant of patellofemoral stress and PFP. Nevertheless, it has become increasingly clear that patellofemoral malalignment, while representing one risk factor, cannot solely account for the development of PFP. Indeed, clinical and radiographic malalignment is observed in a mere subset of individuals presenting with PFP. Contrariwise, many with evidence of abnormalities in patellar position never develop symptoms of PFP.
Remedying this incongruity, Dye proposed his “theory of tissue homeostasis.” He suggested that alterations in tissue homeostasis may occur under any circumstance that supersedes the so-called envelope of function or load acceptance capacity of the joint. According to his model, gross structural abnormalities and repetitive overload alike may challenge the envelope of function, exceeding the force across the joint that can be safely tolerated and ultimately result in disruption to the osseous and periosseous tissues. Among the tissues thought to cause pain in PFP are the subchondral bone (by way of disrupted articular cartilage), medial and lateral retinacula, and infrapatellar fat pad.
Risk Factors
PFP is thought to be multifactorial, with a variety of risk factors that may contribute to its inception. Although the significance of these risk factors in isolation is debatable, it is more likely the culmination of multiple predisposing conditions that challenges the load-bearing tolerance of the joint and results in symptoms. In order to develop a framework for the diagnosis of PFP, then, it is critical to first understand these underlying risk factors, which may be categorized broadly as local joint impairments, deficits in lower extremity biomechanics, and training errors ( Table 1 ). Moreover, recognition of these factors allows for a more targeted approach to treatment and may help prevent recurrence.
| Local Joint Factors | Lower Extremity Biomechanics | Training Considerations |
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Local joint impairments
To begin, it is important to consider the stabilizing structures of the knee joint itself, because these local structures have a direct effect on patellofemoral function, including patellar position and tracking.
Quadriceps muscle weakness
The quadriceps muscle complex represents one such structure that influences the patellofemoral joint. Quadriceps muscle weakness has long been implicated in PFP. Observational studies have reported an association between reduced quadriceps torque and volume in patients with PFP. A recent meta-analysis further established a significant correlation between quadriceps atrophy and PFP, both when compared with the asymptomatic limb and when compared with a distinct control group. More directed attention has been given to vastus medialis oblique (VMO) strength in particular, as VMO fibers insert more distally and horizontally on the patella and are thought to impart dynamic medial patellar stability. Accordingly, studies have also found an association between reduced VMO volume and PFP.
However, such studies fail to define the presence of quadriceps weakness in PFP as causal or secondary. Two prospective studies have attempted to clarify the relationship between quadriceps strength and PFP with varying results. When normalized for body weight, Milgrom and colleagues reported no relationship between knee extension strength and the development of PFP, whereas Boling and colleagues found that individuals with reduced quadriceps strength had an apparent predisposition to PFP. Pooled analysis of the 2 studies demonstrated a significant ( P <.01) association between decreased knee extension strength and the development of PFP, suggesting that quadriceps weakness may play a causal role in PFP, although more prospective studies are needed to confirm this notion.
Delayed vastus medialis activation
In addition to quadriceps strength, vastus medialis (VM) and vastus lateralis (VL) activation seems closely entwined with PFP. Delayed VM activation relative to that of VL has been implicated in multiple studies of PFP. It has been postulated that the role of vasti muscle activation is especially relevant among a subset of individuals with PFP who demonstrate evidence of lateral patellar maltracking. Pal and colleagues identified patellar maltrackers based on the presence of patellar tilt and bisect offset as measured from weight-bearing MRI and found that, within this group specifically, the degree of maltracking was closely correlated with delay in VM activation. As with quadriceps strength, additional prospective evidence is necessary to more clearly define the cause-and-effect relationship between vasti muscle activation and PFP.
Soft tissue inflexibility
Inflexibility of the soft tissues surrounding the knee joint seems to represent another risk factor for PFP. Excessive tension involving the lateral restraints of the knee, and especially the lateral retinaculum, has been heavily implicated for its role in patellar maltracking. The midportion of the lateral retinaculum represents the strongest and most substantial layer and derives its fibers from the iliotibial band. The transverse orientation of these fibers resists medial displacement of the patella and when excessively taught may result in disproportionate lateral translation. It follows that dysfunction of the iliotibial band could result in aberrant patellar tracking and increased contact forces across the patellofemoral joint, and in turn contribute to the development of PFP. In support of this, several cross-sectional studies have observed a relationship between iliotibial band tightness and the presence of PFP. It has been reported that among runners with PFP specifically, a high proportion (67%) have tightness of the iliotibial band.
Inflexibility of the quadriceps, gastrocnemius, and hamstring muscles likewise seems to correlate with PFP. Tightness of the quadriceps femoris seems to represent a risk factor for the development of PFP. Mechanistically, quadriceps tightness is theorized to increase the posterior force of the patella against the femoral trochlea, in turn elevating patellofemoral joint stress, especially with activity. Hamstring inflexibility has also been linked to PFP. Several case-controlled studies have reported a significant difference in hamstring flexibility between PFP and control groups. It has been theorized that tightness of the hamstring exerts a constant flexion moment to the patella, thereby requiring greater quadriceps power to extend the knee, and increasing patellofemoral joint reaction forces ; however, such a causal relationship has yet to be confirmed. Finally, inflexibility of the gastrocnemius has been prospectively associated with the development of PFP. The precise role of gastrocnemius tightness in the pathophysiology of PFP remains unclear, although alterations in foot position and excessive subtalar joint pronation have been proposed.
Deficits in lower extremity biomechanics
By way of a closed kinetic chain, function of the entire lower extremity can alter movement and stress patterns at the patellofemoral joint. Thus, lower extremity biomechanics, including those involving the hip, trunk, foot, and ankle, are important to consider in the pathogenesis and treatment of PFP. Excessive internal rotation of the femur, in particular, can increase patellofemoral stress and in turn predispose to PFP. Internal rotation of the femur under a fairly fixed patella generates a relative lateral displacement of the patella with respect to the femur. Dynamic MRI studies have helped define the influence of femoral internal rotation in PFP, demonstrating increased femoral rotation and consequent lateral patellar displacement and tilt across degrees of knee flexion during weight-bearing in women with PFP.
Hip weakness
Weakness involving the external rotators and abductors of the hip can contribute to excessive internal rotation of the femur and, in turn, has been implicated in the development of PFP. A correlation between isometric hip abductor and external rotator weakness to PFP is supported by several studies. Further corroborating the role of hip strength in PFP are numerous randomized controlled trials, which upheld hip abductor strengthening in the treatment of PFP to improve both symptoms and function. However, such studies fail to define hip weakness as causative of PFP. It is worth noting that more recent prospective investigations found no association between hip abductor or external rotator strength to the eventual development of PFP. Separately, a meta-analysis likewise failed to identify a causal relationship of hip weakness to PFP. It may be that hip weakness is consequential rather than contributory to PFP. In support of this, Finnoff and colleagues discovered a significant decrement over time in hip abductor and external rotator strength among individuals who developed PFP. These findings may reflect a greater role for hip muscle performance rather than static strength in the dynamic control of femoral internal rotation. Indeed, as is later discussed, hip muscle performance during dynamic tasks seems to represent a distinct risk factor for PFP, independent of hip strength.
Foot pronation
Foot pronation is important for force absorption during walking and running. However, excessive pronation is thought to predispose to increased patellofemoral stress and PFP. The precise mechanism by which this occurs is unproven, although compensatory internal rotation of the femur has been conjectured. In normal gait, the foot pronates and the tibia internally rotates during early contact. Once the foot reaches midstance and the foot is in full contact with the ground, the subtalar joint supinates and the tibia follows, externally rotating, in order to move the knee into extension. In situations of excessive pronation, the subtalar joint remains in a pronated position at midstance, preventing the tibia from externally rotating. Tiberio has theorized that to compensate and promote knee extension, the femur internally rotates on the tibia. As was previously discussed, increased internal rotation of the femur beneath the patella yields lateral displacement of the patella and increased patellofemoral joint strain. Most prospective studies to date have suggested a predisposition to PFP under conditions of overpronation. Furthermore, a recent meta-analysis for the role of foot posture in overuse injuries concluded that evidence, albeit limited, maintains overpronation of the foot as a risk factor for PFP. It seems, however, that the changes in foot position necessary to increase one’s risk of PFP are quite subtle with differences in navicular drop or hindfoot motion of 1 mm and 1° to 2°, respectively.
Gait aberrations
By definition, running-related injuries are the consequence of circumstances related to the act of running, including dynamic biomechanics and training habits. Thus, such factors must be considered potential contributors, especially in runners presenting with PFP. Excessive hip adduction and internal rotation during dynamic activities, for example, have been strongly implicated in PFP. Studies have shown greater hip internal rotation during single leg squat, jump landing tasks, and running in women with PFP. It is interesting that targeted hip-strengthening regimens, while improving strength, may not affect these associated gait impairments. It seems that muscle performance including endurance and neuromuscular coordination likely also play a role in the dynamic control of femoral internal rotation. Souza and Powers reported an association between greater hip internal rotation during running and diminished hip extension endurance. As well, altered neuromuscular activity of the gluteus medius and maximus muscles has been associated with PFP.
Other gait deviations that have been implicated in PFP include accelerated foot pronation, increased peak ground reaction force, reduced step rate, and decreased knee flexion angle at initial contact. However, such findings to date are observational, and further research is needed to confirm their association and any causal relationship to PFP.
Training errors
A proportion of running-related injuries, inclusive of PFP, are undoubtedly related to errors in training. Training errors, including improper or overly worn footwear, hard or irregular training surfaces, abrupt escalation in exercise including rapid increases in duration, frequency, speed, intensity, or hill work, and inadequate time for recovery, represent mechanisms by which the athlete may exceed Dye’s proposed envelope of function or load acceptance capacity of the joint. Although not enough to produce an immediate structural damage, these repetitive stresses result in loss of tissue homeostasis over time and consequent injury. Athletes who are new to running may be at particularly high risk. A recent analysis of 874 novice runners demonstrated that those who increased their weekly distances by more than 30% over a 2-week period were more likely to develop running-related injuries, including PFP. In addition, high weekly mileage has been associated with a greater risk of running-related injuries, with 20 to 40 miles per week representing a critical threshold beyond which injury becomes significantly more likely.
Other considerations: generalized laxity
Generalized ligamentous laxity has been implicated in PFP. It is rational to assume that diffuse laxity would not spare the knee, but rather predispose to increased patellar mobility and patellar maltracking. Although logical, few studies have investigated the relationship between generalized ligamentous laxity and PFP. al-Rawi and Nessan observed greater joint laxity in patients with chondromalacia patellae, noting a higher proportion of patients with hypermobile joints when compared with controls, as well as greater total mobility scores within the patient group. Witvrouw and colleagues prospectively evaluated the role of generalized ligamentous laxity in PFP and found that, among various measures of joint laxity, only thumb-to-forearm mobility correlated with development of PFP.
Diagnosis
History
An important first step in the diagnosis of PFP is a thorough history. The history should emphasize symptom onset, location, and aggravating factors, as well as an investigation to underlying risk factors for the development of PFP.
The pain of PFP is typically described as spontaneous and insidious, without any clear precipitating event. Patients tend to describe a vague ache localized diffusely to the anterior knee. Pain will typically be exacerbated by activities that increase stress to the patellofemoral joint, including prolonged knee flexion (the so-called positive theater sign), as well as walking down stairs, running, jumping, or squatting. Patients may relate associated symptoms of knee catching or buckling while walking. They may also endorse subjective sensations of stiffness or swelling; however, significant swelling of the knee joint is not a prominent feature of PFP in isolation and should evoke consideration for alternative pathologic abnormalities.
In addition to a complete symptom inventory, it is critical to elicit a history of risk factors for PFP. In particular, the practitioner should evaluate for training habits resulting in repetitive overload to the patellofemoral joint (see Table 1 , column 3, Training Considerations). The provider should inquire regarding the initiation of any new activities. In the running population specifically, it is important to consider any abrupt escalation in training, including sudden increases in duration, frequency, or intensity of workouts. In addition, it is important to consider the presence of excessive hill training, and in particular, running steep descents, because this may increase stress about the knee joint by up to 6 times body weight.
Physical examination
PFP is a clinical diagnosis and should be based on the amalgamation of historical features and examination findings ( Table 2 ). The physical examination serves to more precisely localize the patient’s pain, exclude alternative diagnoses ( Box 1 ), and also identify any underlying factors predisposing to the development of PFP. The recognition of risk factors not only further supports the diagnosis but also represents a critical first step in designing an appropriate and targeted rehabilitation protocol.
Patellar tendinopathy
Prepatellar or infrapatellar bursitis
Infrapatellar fat pad syndrome
Plica syndrome
Chondromalacia patellae
Patellofemoral osteoarthritis
Osteochondritis dissecans
Patellar stress fracture
Patellar instability
Osgood-Schlatter disease a
Sinding-Larsen-Johansson disease a
A variety of conditions may cause anterior knee pain. These should be considered and excluded when evaluating a patient with suspected PFP.
a Indicates pediatric-specific conditions.
Beginning with the patient standing, lower extremity alignment should first be observed statically. The examiner may assess the presence of either genu valgum or genu varum deformities of the knee. In addition to genu valgum, it is important to make note of any excessive internal rotation of the femur, which is indicated by an inward-pointing patella (or so-called squinting patella), external rotation of the tibia, and hindfoot valgus. The finding of a femoral internal rotation is common in PFP and is often associated with a tight iliotibial band or weak hip abductors and external rotators. Moving distally, one may also ascertain foot position, and in particular, the presence of excessive foot pronation.
An assessment for generalized ligamentous laxity should also be undertaken. Joint laxity may be ascertained based on the criteria defined by Beighton and Horan. This criteria include the presence of hyperextension of the elbows and knees beyond 10°, passive dorsiflexion of the fifth digit metacarpophalangeal joints beyond 90°, passive thumb-to-forearm apposition, and forward flexion of the trunk with the knees held straight such that the hands rest on the floor with palms flat. Three of 5 positive tests indicate generalized laxity. In instances of suspected generalized laxity, it is important to look for other phenotypic features that may suggest an underlying syndrome, such as Ehler-Danlos or Marfan, that would warrant further evaluation for systemic manifestations and consultation to appropriate specialists for management.
With the patient still standing, an evaluation of dynamic lower extremity biomechanics is critical, particularly for the athlete presenting with suspected PFP. A single leg squat is useful to identify hip abductor weakness. The patient is asked to stand with full weight on the affected limb and slowly squat with the knee flexed to 45° to 60°. The examiner should observe for exaggerated knee valgum or femoral internal rotation as the patient descends. The squat should also be evaluated for proper form, ensuring that the knee does not extend beyond the toes. Alternatively, a unilateral or bilateral landing task may be similarly used to assess for the presence of dynamic knee valgum.
For runners in particular, a running gait analysis may provide additional information. It is important to scrutinize the position of the hip, knee, and foot, taking note of excessive hip internal rotation or adduction, increased dynamic knee valgum, and excessive foot pronation. Other factors that are worth considering, although their precise clinical significance requires further investigation, include ground reaction force, step rate, running speed, and body orientation at initial contact.
Moving next to a seated position, it is possible to evaluate dynamic patellar tracking. The J-sign is used to describe pathologic tracking and may be observed by having the patient actively extend the knee from 90° of flexion to full extension. Normal patellar motion is characterized by nearly straight movement of the patella proximally with only slight lateral shift near terminal extension. Improper patellar tracking is demonstrated when the patella frankly deviates laterally with extension, creating an inverted “J” shape and thus representing a positive J-sign.
With the patient supine, gross static inspection of the knee joint is typically relatively unremarkable. Findings of marked swelling, erythema, or warmth should prompt investigation to alternative causes for pain. Astute inspection may reveal atrophy of the VM or the quadriceps complex more generally. This finding may be accentuated when the patient is asked to contract the muscle. With this, the examiner might also make note of the timing of VM, and in particular, VMO contraction relative to VL, looking for any delay in onset between VMO and VL.
The quadriceps angle, or Q-angle, is designed to quantify risk for lateral patellar displacement and patellar maltracking. It is measured as the angle formed by the intersection of 2 lines: the line formed between the anterosuperior iliac spine to the center of the patella, and the line generated from the center of the patella to the middle of the anterior tibial tuberosity. The significance of the Q-angle in the diagnosis of PFP has been widely debated. The variable association of Q-angle with PFP is likely in part related to inconsistency in measurement technique and poor interobserver as well as interrater reliability. Indeed, a properly gauged clinical Q-angle has demonstrated moderate correlation with MRI-derived Q-angles. Accurate measurement mandates a neutral position of the leg. Any outward rotation of the foot will superficially increase the Q-angle, while internal rotation of the thigh will spuriously reduce the Q-angle. In addition, a modified, long-arm goniometer may enhance the reliability of Q-angle assessment. Q-angles exceeding 15° to 20° denote increased lateral pull about the patella and greater propensity for patellar malalignment.
Next, gentle palpation over the anterior knee while passively flexing the joint may yield crepitus, although this finding is poorly specific for PFP and has limited diagnostic bearing. More directed palpation should include, in particular, the medial and lateral retinacula. With the knee extended, the examiner may begin with palpation over portions of the retinacula. If tolerated, the patella may be gently displaced both medially and laterally, which not only further stresses each retinacula but also permits more direct palpation of the retinacular fibers.
From this position, the examiner may also evaluate patellar position and mobility by way of the mediolateral glide, patellar tilt, and patellar mobility tests, which when positive suggest deficits or tightness of the medial or lateral soft tissue restraints. Mediolateral glide represents the position of the patella relative to the trochlea in the coronal plane. It is assessed with the knee flexed to 20°, and by comparing the distance from the midpatella to the lateral femoral condyle and to the medial femoral condyle. Under normal conditions, the patella should rest equidistant from each epicondyle. Instances whereby the distance to the medial femoral epicondyle exceeds the distance to the lateral femoral epicondyle (ie, lateral displacement) by greater than 0.5 cm indicate a positive test and suggest excessive tightness of the lateral restraints and reduced VMO tension. Patellar tilt describes the inclination of the patella in the transverse plane. With the knee extended, the examiner palpates the height of the medial and lateral patellar borders. The 2 heights should be equal. Increased height of the medial patellar border implies that the patella is tilted laterally, while reciprocally, increased height of the lateral patellar border indicates medial patellar tilt. Use of a pluri-cal caliber applied to the medial and lateral aspects of the patella to measure the respective tilt angles has also been described and may enhance intrarater and interrater reliability of the test. Finally, the patellar mobility test quantifies the mediolateral range of motion of the patella. The knee is placed in 20° of flexion, and the patella is divided into 4 longitudinal quadrants. With the quadriceps fully relaxed, the examiner translates the patella medially and laterally. Medial glide to a distance less than that of one quadrant is consistent with tightness of the lateral restraints. Conversely, motion in the medial or lateral direction exceeding the distance of 3 quadrants suggests hypermobility of the patella.
Another important risk factor for PFP that should be assessed in the course of examination is soft tissue flexibility. With the patient remaining supine, hamstring and gastroc soleus flexibility may be approximated by measurement of the popliteal angle, and passive ankle dorsiflexion with the knee in extension, respectively. Next, with the patient side-lying, iliotibial band tightness may be assessed via Ober test. Last, quadriceps flexibility is ascertained with the patient prone via Ely test. The examiner should stabilize the pelvis while flexing the knee and bringing the heel toward the buttock until reaching a point of firm resistance. The distance between the heel and buttock is measured, most conveniently by way of finger breadths and compared side to side.
Imaging
Because PFP is a clinical diagnosis, there is limited utility for imaging in the diagnosis of PFP. Imaging plays the greatest role in excluding alternative diagnoses. Nevertheless, plain radiographs of the knee are often a reasonable first-line study in the evaluation of knee pain, and specific risk factors for PFP (especially patellar position) can be inferred from such images. An axial radiograph taken at 30° to 45° of knee flexion, or Merchant view, is ideal for interpreting the position of the patella within the trochlear groove and thus establishing the presence of lateral displacement or tilt. Measures that may be obtained from the axial view include the sulcus angle, congruence angle, lateral displacement, and lateral patellofemoral angle ( Fig. 1 A–D). The lateral view may be useful to assess the superior-inferior relation of the patella. Pal and colleagues found that a high-riding patella (patella alta) predisposed to PFP, possibly due to reduced osseous contact and subsequent instability of a patella that articulates superior to the trochlea. Measures of vertical patellar position include the Insall-Salvati and Blackburne-Peel indices (see Fig. 1 E–F).
