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Knee Pain: Patellofemoral Pain Syndrome (What do we know)

Knee Pain: Patellofemoral Pain Syndrome (What do we know)

Patellofemoral Pain Syndrome

The source of patellofemoral pain (PFP) is believed to be multifactorial. The obvious factors are those that can be defined as having a direct pathway to pain (eg, ligament tears, arthritis, acute trauma, bone bruise, stress fractures, patellar replacement, or total knee replacement). Once the standard sources of pain are ruled out, a large percentage of patients remain with what can only be termed as having “chronic idiopathic PFP.” Due to the high prevalence of idiopathic PFP,7,27,56 much research has been focused on trying to identify the true sources of this pain. At the current time, the primary theory is that patellofemoral malalignment and maltracking (pathomechanics) result in PFP. One potential pathway to pain is that patella malalignment/maltracking overloads the subchondral bone, resulting in pain. This theory has been substantiated by a recent study that demonstrated a direct correlation between the level of pain and patellofemoral kinematics.53 Another potential pathway to PFP is that patella malalignment/maltracking leads to a shortened lateral retinaculum and/or ischemia, with eventual secondary nerve changes resulting in pain.46 An alternative theory, the tissue homeostasis model, has been proposed by Dye.17 This theory states that a loss of tissue homeostasis at the patellofemoral joint, resulting from pathophysiological processes (eg, an inflamed synovial lining and fat pad tissues, retinacular neuromas, increased intraosseous pressure, and increased osseous metabolic activity), accounts for idiopathic PFP. Although this theory has been presented as exclusive to potential patellofemoral pathomechanics, it remains an expert opinion (level of evidence, 5), and it is highly likely that patella malalignment/maltracking underlies the loss of tissue homeostasis leading to PFP.
What Have We Learned?

1. The patella acts as a dynamic lever65 for the quadriceps musculature and experiences some of the highest loads of any structure in the human body (0.5 times body weight for walking34,43 to over 7 times body weight for squatting33). Because this lever’s fulcrum (center of patellofemoral contact)50 changes with knee angle and activity, the relationship between the quadriceps forces and the torque it produces likewise changes with knee angle and activity.

2. PFP can arise from any innervated patellofemoral joint structure18 and a combination of innervated tissues may be involved concurrently.6,22,31 These structures include subchondral bone, infrapatellar fat pad, quadriceps tendon, patellar tendon, synovium, the medial and lateral retinaculum,23,45 and patellar (medial and lateral) ligaments. Although cartilage is aneural, the forces applied are passed to the innervated subchondral bone.

3. Pain is subjective, thus the importance of psychological state cannot be overstated.13,26,40

4. Proprioception appears to play an important role in the dynamic stability of the patellofemoral and tibiofemoral joints,11 and a decrease in proprioception has been noted in patients with posttraumatic patellar dislocation.29

5. Although there are competing theories as to the source of idiopathic PFP, few variables have been directly correlated with pain. A recent study demonstrated a correlation between patellofemoral kinematics (change in varus rotation during extension) and pain intensity on an average day (r = 0.56).53 Another study documented a correlation between a measure of bone metabolic activity and the highest level of pain experienced in the previous year (r = 0.55).15 The latter study excluded patients with pain who demonstrated no bone metabolic activity, thus the strength of the correlation is suspect. Last, 1 study documented a significant (P = .04) correlation between pain and mean innervated area in the lateral retinaculum.44 The study size was small (n = 13) and a correlation coefficient was not provided, but with a P value close to .05, it is most likely that the correlation was weak.

6. Patellar and femoral bone shape and the amount of patellar engagement in the femoral trochlea sulcus influence patellofemoral kinematics. Specifically, a low lateral trochlea inclination angle has been associated with excessive lateral shift and patellar dislocation,2 whereas a high lateral trochlea inclination angle has been correlated to medial patellofemoral shift and tilt in patients with PFP (r = 0.48 and 0.57, respectively) and controls (r = 0.35 and 0.61, respectively).24 When the percentage of patellar to trochlear cartilage overlap is less than 30%, the patella tends to sublux.36

7. Increased subchondral bone metabolic activity has been demonstrated in individuals with idiopathic PFP.15,37 The study with the largest population37 found that 44% (48/109) of the knees experiencing patellofemoral pain had increased metabolic activity.

8. The medial patellofemoral ligament has been identified as the strongest static patellofemoral joint stabilizer in early knee flexion (0°–30°), contributing 50% to 60% of the passive resistance to lateral patellar motion in this range.38

Maltracking

9. Maltracking occurs in a subset of patients with PFP and potentially progresses toward patellofemoral osteoarthritis.58 In certain patients, maltracking is likely the primary impairment leading to repetitive patellofemoral joint cartilage overload from the continuous impact load as the patella re-engages with the femur.53 This, in turn, overloads the underlying subchondral bone, resulting in pain. Alternatively, maltracking can damage the ligaments of the patellofemoral joint, potentially leading to increased innervation and pain.45

10. There is a large amount of intersubject variability in patellofemoral joint kinematics. However, based on recent 3-dimensional studies, there is general agreement that the patella extends and moves proximally as the tibiofemoral joint extends.4,32,48,61 One potential source for this intersubject variability is the likely presence of subgroups47,53 within the general population of individuals experiencing maltracking. In addition, variability in the anatomical references used to define the kinematics can result in large inconsistencies (eg, measuring the patellar tilt angle in an axial image 10 mm above versus 10 mm below the patellar center results in a 27° change in this angle).54

11. The specific type of maltracking pattern likely alters the pathway to pain and can influence the effectiveness of interventions.14

12. Recent 3-dimensional patellofemoral kinematic studies53,61 have documented that maltracking exists outside the axial plane (eg, patella alta, flexion, and varus rotation).

Loading of the Lower Limb

13. The manner in which the lower limb is loaded affects patellofemoral kinematics.35 For example, there is evidence to suggest that in weight bearing, patellofemoral malalignment and/or maltracking may be the result of internal rotation of the femur as opposed to lateral tilt/displacement of the patella.42,55 Conversely, patellofemoral malalignment/maltracking in non-weight bearing is the result of the patella moving on a relatively stable femur.42,55

14. Increased quadriceps force tends to exacerbate pathological patellofemoral kinematics.9,28,42 For this reason, it has been stated that “radiographic examination under static conditions can be misleading.”47

15. During weight-bearing exercises, the quadriceps force decreases as the knee extends into terminal extension, whereas the opposite occurs for non-weight-bearing exercises.25 Specifically, when standing with the knee fully extended, there is minimal required active quadriceps force, and this force requirement increases with increasing flexion. In sitting, with the knee at 90° of flexion, there is no required active quadriceps force and this force requirement increases as the knee extends.25 Thus, in weight-bearing terminal knee extension, there are minimal loads on the patella and patellar maltracking is often not observed.42,61 Yet, in deep knee flexion (greater than 60°) during weight bearing, maltracking has been observed in individuals with chronic patellofemoral pain.61 This is due to the distal widening of the femoral groove and the high quadriceps forces on the patella in this range of motion.

16. As the axial plane kinematics tend to “normalize” once the patella engages with the femoral sulcus,53,61 documented patellar maltracking in full knee extension during non-weight-bearing exercises may serve as a marker of altered patellofemoral joint contact stress in deeper flexion.

Patellofemoral Cartilage Contact

17. Patellofemoral joint pressure distribution has been studied using pressure-sensor films in vitro, and it has been reported that patellofemoral contact force, contact area, and maximum peak pressure rise with increasing flexion angles in cadaveric specimens with loaded quadriceps.64

18. Peak cartilage thickness in healthy adults has been reported to range from 4.5 to 5.5 mm for the patella and 3.5 to 4.0 mm for the femur,16,19 indicating that submillimeter accuracies are necessary to keep the errors in estimating patellofemoral contact kinematics within acceptable limits. Few techniques that can noninvasively quantify in vivo patellofemoral kinematics/alignment have reported accuracies to such a level.3,5,21

19. Based on modeling studies, patellofemoral joint and cartilage stress is significantly greater in individuals with PFP compared to controls.20

Bracing and Taping

20. Patellar taping has been shown to reduce pain60 and alter patellofemoral kinematics.14

21. Taping has been shown to improve knee joint proprioception in individuals experiencing PFP who were rated as having poor proprioception,11 whereas bracing has been shown to influence the somatosensory inflow from the skin around the knee.57

22. In individuals with PFP, an improvement in the control of the tibiofemoral joint with both bracing and neutral patella taping has been demonstrated.51

23. Taping has been shown to reduce the amount of superior translation14 of the patella in extension, which would likely lead to increased contact area. Additionally, the change in lateral shift, lateral tilt, and varus rotation with taping has been demonstrated to be dependent on the value of these kinematic parameters in the untaped state.14

Alterations in the Quadriceps

24. Quadriceps weakness and atrophy30 and vastus medialis obliquus (VMO) atrophy39 have been associated with idiopathic PFP, but evidence to the contrary has also been reported.10

25. Although impaired VMO function (as assessed by EMG signal magnitude and timing) has been implicated in PFP,12,59,63 this finding has not been consistent across all studies.8,41

26. Recent in vivo work demonstrated that the largest component of the vastus medialis moment arm relative to the patella center of mass is in the anterior direction, with a secondary component in the superior direction.62 Thus, for every unit force within this muscle, the largest torques will result in patella varus rotation, with the secondary torque resulting in medial tilt. The same holds true for the vastus lateralis, with the largest torque resulting in valgus rotation with secondary torque production causing lateral tilt.

27. Recent work comparing the in vivo patellofemoral kinematics before and after a motor branch block to the VMO demonstrated that a loss of force in the VMO could explain some, but not all, of the kinematic changes typically observed in patients with PFP.52 This confirms the speculations of an earlier anatomical study.1
Where Do We Need to Go in the Future?

It is widely accepted that PFP is multifactorial and that individuals can arrive at a painful state through multiple mechanisms. Yet, there remains no consensus on causative relationships between chronic idiopathic PFP and any of these mechanisms. Thus, future studies must work at developing a direct link between tissue stress and pain. Specific attention should be given to tissues that are the likely sources of pain.

As part of providing this direct link, future studies evaluating potential factors leading to PFP should focus on obtaining a large database of individuals with pain (eg, greater than 50) along with an appropriate control group of the same size, to capture a true representation of the spectrum of individuals experiencing PFP. These studies should make every attempt to explain the pathway to pain for each subject (or subgroup of patients) within the study, as opposed to assuming that individuals who do not fit within the primary theories being tested are “outliers” and can be eliminated from the analysis or ignored in discussing the results.

It has been hypothesized that “periodic short episodes of ischemia due to vascular bending” could be 1 source of PFP.46 Clinically, this may be related to a subgroup of patients whose pain is associated with low environmental temperatures and poor rehabilitation outcomes.49 Further work is needed to substantiate these hypotheses.

Because PFP can arise from surgery and other injuries, the relationship of the pain experienced by these individuals to that of individuals with idiopathic PFP should be investigated.

Future studies need to include clear definitions of the eligibility criteria (eg, idiopathic pain, traumatic onset of pain, pain on activity, previous surgery, total knee replacement, previous history of dislocation, instability without any history of dislocation, PFP following other specific knee injuries), along with justifications for the inclusion/exclusion criteria.

Because it is known that the level of quadriceps force, as well as the knee angle, affects patellofemoral bone and cartilage contact kinematics, studies focused on exploring the pathomechanics of PFP should do so under dynamic conditions, with high quadriceps loads, in regions of the greatest patellofemoral instability.

Clinical diagnostic tests need to be developed that differentiate the potential pathological parameters that lead to PFP. Specifically, a system of relatively simple clinical tests for the classification of patients needs to be developed to facilitate targeted patient-specific treatment options. As part of this, the relationship between complex imaging and modeling techniques should be related to more available clinical measures.

Because in vivo measures of patellofemoral cartilage stress are unavailable, there is a need to develop neuromusculoskeletal computational models that are validated and accurate to provide greater assessment of contact mechanics under physiological loading conditions. As this area continues to advance, proper validation, accuracy, and sensitivity studies will be crucial to maintain clinical relevance.

The current image-based alignment and kinematics assessment methodologies need to be transferred to the clinic. Relationships must be developed that explain the variation across experimental paradigms (eg, weight bearing versus non-weight bearing, static versus dynamic). In each of these, a clear understanding of accuracy, precision, and repeatability is required. In addition, a clear, consistent definition of the anatomical references used to define the kinematics is essential for reducing variability and enhancing cross-study comparisons.9,54

Further development of imaging modalities (eg, MR spectroscopy, water-fat differentiating MRI, PET, CT), as well as other tools, that will enhance the diagnosis of underlying mechanisms of PFP is needed.

Metrics of maltracking should consider the underlying geometry of the articulating surfaces to infer the influence of maltracking on contact areas and joint stress.

Long-term, prospective studies are needed to investigate the long-term sequelae of PFP.

The interrelationships between proximal, distal, and local factors need to be better understood.

Taping and bracing have been shown to improve proprioception at the knee.11 Future work is needed to determine if this improvement in proprioception can be directly correlated with improved knee function or a reduction in PFP.

References
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