Patellofemoral joint osteoarthritis: An individualised pathomechanical approach to management




Abstract


Patellofemoral joint integrity is maintained by an optimal interaction of passive, dynamic and structural restraints. Disruption of these mechanics can lead to structural joint damage and subsequent patellofemoral osteoarthritis, which is a prevalent and disabling condition with few effective conservative management strategies. Due to the influential role of biomechanics in this disease, targeting the specific pathomechanics exhibited by an individual is logical to improve their likelihood of a positive treatment outcome. This review summarises the effect of different pathomechanical factors on the presence and progression of patellofemoral osteoarthritis. It then presents a synthesis of mechanical effect of treatment strategies specifically addressing these pathomechanics. Identifying the pathomechanics and clinical characteristics of individuals with patellofemoral osteoarthritis that respond to treatment may assist in the development of individualised treatment strategies that alleviate symptoms and slow structural damage.


Introduction


It is increasingly acknowledged that osteoarthritis (OA) is a complex and multidimensional disease. OA has the fastest growing prevalence of all musculoskeletal diseases and of these conditions was recently found to attract the greatest indirect health costs in terms of years of healthy life lost due to disease and disability adjusted life years . Of the weight-bearing joints, the knee is the most commonly affected by OA and is characterised by joint space narrowing, loss of articular cartilage, osteophyte formation, subchondral bone cysts and synovitis. While the majority of prognostic and intervention studies have focused on the medial tibiofemoral (TF) joint, OA of the patellofemoral (PF) joint, either in isolation or combined with TF OA, is reported to be more prevalent . This is concerning as PF OA is a significant source of knee pain and disability .


Older age, female gender, high body mass index and previous anterior cruciate ligament injury are risk factors of both PF and TF OA . However, PF OA has unique clinical characteristics that differentiate it from TF OA, such as difficulty descending stairs and pain on compression of the PF joint ( Fig. 1 ). It is also independently associated with lower self-perceived functional scores . This unique disease burden could be due to the unique mechanics of the PF joint. Unlike the TF joint, the PF joint is not loaded during level walking. Rather, the PF joint reaction forces gradually increase up to 90° of knee flexion and can reach up to 8 times body weight depending on the type of activity (i.e. stair climbing, squatting etc.) . During loaded activities, the PF joint shows maximal contact area and maximal cartilage thickness between 20° and 90° of knee flexion, where the compressive loads are highest . This balance is dependent on optimal interaction of passive, dynamic and structural restraints and can be easily disturbed, resulting in structural joint damage . Thus, PF OA is largely biomechanically mediated and it seems logical that the specific biomechanical factors that are disrupted in a particular individual need to be addressed when designing a treatment strategy.




Fig. 1


Risk factors for the presence and progression of PF OA at an individual level and at a joint level.


Designing treatment strategies that are individualised to target patients’ specific pathomechanics follows current recommendations for the management of PF OA . Due to the diversity of knee OA with respect to aetiology, clinical and radiographic presentation, one-size-fits-all treatment approaches are suboptimal. Rather, tailoring management to the individual is preferred in order to maximise the likelihood of achieving a positive outcome. A novel approach to tailored management, gaining interest in low back pain research (another prevalent musculoskeletal disorder ), is a model of stratified care or subgrouping. Stratified care phenotypes patients based on clusters of signs and symptoms in order to direct clinical decision making towards the most effective management strategies . This approach was recently found to result in greater health benefits than standard-of-care .


Patient phenotyping is increasingly encouraged in OA literature . Pathoanatomical phenotyping based on the presence and magnitude of osteophytes, joint space narrowing or cartilage damage facilitates a common language and standardisation between investigators. However, its utility in treatment design is limited due to a disconnect between the pathoanatomical feature and movement impairment or treatment response . In contrast, Eyles et al. reviewed literature that used a prognostic approach to determine particular clinical features exhibited by individuals with hip and knee OA that were predictive of positive outcomes in response to different conservative therapies. The three features with moderate evidence of association with positive outcomes were the absence of depressive symptoms, signs of inflammation and knee alignment. This highlights the importance of person-level and systemic characteristics in the management of any type of OA. While the lack of strong predictive value of mechanical characteristics in this review was surprising, most clinical trials regard patients with knee OA as a homogenous group and this could potentially mask phenotype-specific effects. Hinman and Crossley have previously called for PF OA to be treated as a specific subgroup of knee OA due to unique PF biomechanical function, its prevalence of structural damage and considerable association with pain and disability. With increasing research into PF OA, a synthesis of PF OA pathomechanics and their potential treatments is timely in order to inform clinicians tailoring treatment to individuals for greater effectiveness. Principles of these treatments are likely to be beneficial for other forms of OA, particularly those at weight bearing joints.


This narrative review will summarise the available evidence regarding the pathomechanics of PF OA that have been associated with disease presence, severity and poor prognosis. We will also discuss pathomechanics based on findings from patellofemoral pain syndrome (PFPS) literature, as there is increasing evidence that it may be related to the development of PF OA . Finally, we will describe the effect of specific treatment strategies specifically addressing these pathomechanics and their clinical efficacy in the context of OA-related pain and function. The literature presented in this review was sourced through literature searches up to November 2013 using Medline, PubMed, Scopus and Cinahl electronic databases limited to English-language human-based studies. Relevant reference lists were also searched and authors with multiple publications in the field were contacted for non-Pubmed indexed abstracts.




Pathomechanics of the patellofemoral joint


Framework of contributors to patellofemoral OA


The pathomechanical issue most commonly cited with the presence and progression of PF OA is abnormal PF joint stress ( Fig. 2 ). This abnormality can be due to either excessive magnitude of stress and/or aberrant dispersion of forces. Such abnormalities can contribute to disease progression by disrupting the balance between breakdown and repair of joint tissues . Higher PF joint stress has also been correlated with reduced functional scores on the Knee Osteoarthritis Outcome Survey (KOOS) . Further, increased contact pressure and shear stress have been reported in individuals with PFPS, suggesting that altered joint stress may occur prior to structural damage . The cause of abnormal stress in the PF joint is multifactorial consisting of local and person-level contributors ( Fig. 1 ). At a person-level, increased BMI increases the load on the joint by increasing the external joint moments . Being of female gender is also associated with increased joint stress, particularly during knee flexion and activities or occupations that involve frequent knee flexion dictate the frequency of stress application . While all of these factors are important, they are beyond the scope of this review. Locally, the extensor mechanism, soft tissue restraints from muscles, ligaments and retinaculum, articular geometry and dyskinesia and lower limb alignment interact to influence PF joint stress . In addition, there is evidence of proximal and distal kinetic chain influences such as rearfoot mobility, hamstring, iliotibial band tightness and hip muscle activation and force . These factors will be discussed below.




Fig. 2


Free body diagram of patellofemoral joint reaction force when an individual ascends a step. CoG = centre of gravity; kJR = knee joint reaction force; m 1 = quadriceps force; m 2 = patellor tendon tesion; PFJR = patellofemoral joint reaction force; x = flexor level arm.


Proposed mechanical contributors to the presence of patellofemoral OA


Cross-sectional studies examining pathomechanics, such as patella malalignment and maltracking, muscle force and activation and lower limb alignment use the presence of joint space narrowing, cartilage damage, osteophytes and bone marrow lesions as indicators of structural joint damage ( Table 1 ). While these studies are limited in their ability to draw conclusions regarding cause and effect, many studies calculate odd ratios to express the risk of structural joint damage when a variable of interest is present ( Fig. 3 a, b).



Table 1

Details of PF OA studies included in the review.






























































































































































































































Authors Type of study Comparator group Follow-up period (range) N Imaging methods Risk factor Disease marker
Type View Knee angle Grading system
Amin et al. Longitudinal n/a 30 months 265 MRI Sagittal, coronal and axial WORMS (modified) Quadriceps strength Articular cartilage loss
Baker et al. Cross-sectional n/a n/a 1396 X-ray Weight-bearing skyline 30° KL grade Quadriceps strength Joint space narrowing, osteophytes
Cahue et al. Longitudinal n/a 18 months 211 a X-ray Weight-bearing skyline 30° OARSI Varus-Valgus alignment Joint space narrowing
Crossley et al. Cross-sectional Healthy controls ( N = 18) n/a 60 X-ray Weight-bearing skyline 30–40° KL Altered hip abductors muscle activation Joint space narrowing, osteophytes, subchondral bone cysts
Elahi et al. Cross-sectional n/a n/a 292 X-ray Weight-bearing skyline 30° OARSI Varus-Valgus alignment Joint space narrowing
Fok et al. Cross-sectional Healthy controls ( N = 21) n/a 30 Joint kinematics, joint moments, muscle force and joint reaction force American College of Rheumatology clinical criteria, osteophytes
Gross et al. Cross-sectional n/a n/a 1903 MRI Sagittal, coronal and axial WORMS Pes planus Articular cartilage damage
Gross et al. Cross-sectional n/a n/a 2940 b MRI Sagittal, coronal and axial WORMS Varus-Valgus alignment Articular cartilage damage
Hart et al. Cross-sectional Healthy controls ( N = 11) n/a 22 X-ray MRI Skyline Coronal, axial KL Quadriceps cross-sectional area Joint space narrowing, osteophytes, subchondral bone cysts
Hunter et al. Longitudinal n/a 36 months (24–60) 595 X-ray Weight-bearing skyline 30–40° OARSI Patellofemoral geometry and alignment Joint space narrowing
Kalichman et al. Cross-sectional n/a n/a 213 MRI X-ray Sagittal, coronal and axial weight-bearing skyline 30° 4-point scale Patellofemoral geometry and alignment Joint space narrowing, osteophytes
Kalichman et al., Cross-sectional n/a n/a 213 MRI Sagittal, coronal and axial WORMS Patellofemoral geometry and alignment Articular cartilage loss and bone marrow lesions
McWalter et al. Cross-sectional n/a n/a 10 MRI KL Varus-Valgus alignment Patella kinematics
Sharma et al. Longitudinal n/a 18 months 171 X-ray Weight-bearing skyline 30° OARSI Quadriceps strength Joint space narrowing
Stefanik et al. Longitudinal n/a 30 months 907 c X-ray MRI Weight-bearing lateral axial 20–50° WORMS Patellofemoral geometry and alignment Cartilage thickness, cartilage defects, bone marrow lesions, subchondral bone attrition
Stefanik et al. Cross-sectional n/a n/a 807 MRI Sagittal, coronal and axial WORMS Quadriceps weakness Articular cartilage damage and bone marrow lesions
Stefanik et al. Cross-sectional n/a n/a 881 MRI Sagittal, coronal and axial WORMS Trochlear morphology Joint space narrowing, bone marrow lesions

MRI = Magnetic Resonance Imaging, KL = Kellgren Lawrence grading, OARSI = Osteoarthritis research society international, WORMS = Whole organ magnetic resonance imaging score.

a Participant numbers, total of 397 knees.


b Participant numbers, total of 3432 knees.


c Total knees included.




Fig. 3


A: Odds ratios and 95% confidence intervals for the presence of lateral PF compartment OA for specific pathomechanical characteristics based on cross-sectional studies. An odds ratio of 1 represents equal risk of the presence of pathoanotomical feature. BML bone marrow lesion, CD cartilage damage, CL cartilage loss, JSN Joint space narrowing, Osteo osteophytes. B: Odds ratios and 95% confidence intervals for the presence of medial PF compartment OA for specific pathomechanical characteristics based on cross sectional studies. An odds ratio of 1 represents equal odds of the presence of pathoanotomical feature. BML bone marrow lesion, CD cartilage damage, CL cartilage loss, JSN Joint space narrowing, Osteo osteophytes.


Patellofemoral joint geometry and dyskinesia


Alterations in patella height (alta and baja), tilt and displacement have been associated with joint space narrowing, cartilage loss and bone marrow lesions ( Fig. 4 ). At the femoral side of the articulation, a shallow trochlea, particularly the lateral trochlea surface, has also been associated with increased odds PF cartilage damage and lateral PF compartment bone marrow lesions . The relationships between the type of alteration in PF joint geometry and presence of PF OA differs markedly between the medial and lateral PF compartments. Lateral displacement of the patella, shallow trochlear groove and decreasing lateral patella tilt have all been linearly associated with the magnitude of joint space narrowing, cartilage damage and bone marrow lesions in the lateral compartment . In one study, the odds ratio between lateral patella displacement and lateral joint space narrowing and lateral PF osteophytes indicated an 8- and 3-fold increase in the odds respectively ( Fig. 3 a). In contrast, increasing lateral patella tilt is the only pathomechanical characteristic that has been consistently linearly related with medial joint space narrowing and cartilage damage (there were no correlates with medial bone marrow lesions) ( Fig. 3 b). This has important implications for treatment design, as even small correction in PF joint geometry could reduce the odds of lateral PF OA damage, however this is not the case for those with medial compartment disease.




Fig. 4


Schematic demonstrating measurements of patellofemoral malalignment indices. (a) Patella height measured by Insall-Salvati ratio = length of patella tendon (b): superior–inferior length of the patella (a), with examples of patella alta and baja. (b) Medial–lateral patella displacement relative to the femur as measured by the bisect offset (c) Trochlear groove depth as measured by the sulcus angle, which is defined by joining the highest points of the medial and lateral femoral condyles with the lowest point of the intercondylar sulcus or, when the groove lacks discernable depth, defined by a perpendicular line projected anteriorly from the posterior condylar line. (c) Lateral patella tilt measured as the angle between the patella and posterior femoral condyles.


It is theorised that increased mobility of the patella, by being altered in shape and not confined to the trochlear groove, increases shear forces and joint stress . Farrokhi et al. provided evidence that peak and mean joint pressure and shear stress at the patella and femur are increased when individuals with PFPS performed a squatting task. The authors theorised that shear stress reflects the portion that tends to distort joint tissue and is the possible risk factor for cartilage breakdown. There is little in vivo evidence for the specific patella and femoral geometry risk factors identified above. However, in cadaveric knees, experimentally induced lateral displacement and tilt of the patella significantly increased mean lateral facet pressure . This effect was strongest near extension. A similar effect was reported in a mechanical model study of the biomechanical effect of patella height. Patella baja significantly increased patella contact pressures in knee extension whereas patella alta increased the magnitude and duration of patella contact forces during flexion . While the latter study did not specify whether the medial or lateral compartment was experiencing greater stress, the studies suggest that individuals displaying altered PF geometry characteristics may be experiencing increased joint stress at times when the PF joint is not normally loaded.


Muscle force and activation


The quadriceps, hip abductors, gluteals, hamstrings and iliotibial band (ITB) have all been implicated in the presence of increased PF joint stress. The majority of research has focused on quadriceps strength, as the peak PF joint reaction force is primarily influenced by the knee flexion angle and magnitude of quadriceps force . Hart et al. reported cross sectional areas of the vastii and rectus femoris were reduced in individuals with PF OA, implying that their force generating capacity was reduced. This findings has been supported by numerous studies indicating that individuals with PF OA negotiate stairs with decreased quadriceps force , that quadriceps weakness was positively associated with lateral cartilage damage and bone marrow lesions and that strong quadriceps reduce the odds of the presence of lateral PF OA ( Fig. 3 a). Interestingly, these associations were not found for medial PF OA. The controversy in these findings, however, is their relationship to joint stress and OA symptoms. Evidence regarding the association between peak quadriceps force and pain is inconsistent, with one paper finding no relationship and another concluding there is an interconnected relationship .


Of the remaining muscles, only hip abductors and gluteal force have been studied in individuals with PF OA . In these studies it was found that individuals with PF OA, produce significantly less gluteus medius and minimus force than healthy controls during level walking and descending stairs . They also exhibit significantly reduced hip abductor strength . The potential increase in femoral internal rotation could result from decreased hip abductor strength may lead to an increase in lateral displacement of the patella in the trochlear groove. In cadaveric models, increases in lateral displacement, produced by increased load on hamstrings and ITB, have been reported to shift force and pressure toward the lateral patella facet and increase joint stress by a minimum of 5% .


Patella flexion also increases with tight hamstrings as the tibia and patella tendon are translated posteriorly, subsequently increasing PF compression forces – even more so when combined with weakened quadriceps . Similarly, a tight ITB can pull on its lateral retinaculum attachment and increase lateral tilt of the patella . In a study of 16 healthy men, those with tight hamstrings exhibited significantly greater lateral PF compartment joint stress and significantly reduced medial PF compartment contact area during a squat task . While these studies offer an explanation for how specific muscles contribute to PF joint stress, results are not in vivo or in knees with PF OA damage. Forces applied by muscles in vivo, particularly the ITB, are unknown. Therefore, cadaver studies may over or underestimate the amount of force required in their experiments and may not have clinically meaningful consequences. Ward and Powers examined contributions to PF joint stress in a PFPS population and found results that differed considerably to previous cadaveric studies. Further, the magnitude of PF joint stress may differ between healthy individuals and those with PF joint pain in some tasks, such as walking , but not others such as negotiating stairs . This suggests that data from modelling studies and healthy cohorts may over or under represent the implications for PF OA populations and should be interpreted with caution.


Lower limb alignment and kinematics


Varus or valgus alignment, tibiofemoral rotation and foot morphology have all been cited as contributors to PF OA due to their potential influence on the Q-angle. The Q angle adds a strong, laterally directed component to the PF contact force, resulting in the majority of medial-lateral PF joint load to be on the lateral compartment . Several authors have reported that valgus alignment was associated with between two- and four-fold increase in odds of lateral PF OA and varus alignment increased the odds of medial PF OA ( Fig. 3 a, b). A simple mechanical explanation is that valgus decreases the Q-angle, increasing the lateral PF forces and varus alignment increases the Q-angle and thus increases medial PF forces. McWalter et al. added to this explanation by reporting patella kinematics (patella flexion, anterior translation and spin) differ during knee flexion depending on whether an individuals with knee OA exhibit varus or valgus alignment. However, these authors also observed inconsistencies in patella tilt and lateral translation within malalignment groups, suggesting that correction of malalignment may not necessarily correct the force distribution at the PF joint. Several other cross-sectional studies report medial PF bone marrow lesions and cartilage damage is prevalent in individuals with valgus and neutral alignment, as well as those in varus . Thus, the summation of evidence suggests that other alignment and kinematic factors need to be considered.


The influence of tibia and femur alignment and kinematics on PF mechanics has been well documented in cadaver models and individuals who are healthy or have PFPS. Individuals with PFPS have been found to exhibit significantly increased femoral internal rotation in knee extension and flexion compared with healthy controls . Increases in patella lateral tilt and translation were also observed in this study and in a study of healthy individuals who landed from a jump in increased femoral internal rotation . However, the magnitudes of internal femoral rotation reported in these studies were shy of the reported 20°–30° threshold required to increase joint contact pressure in cadaver models . Thus, it appears the hypothesis of Powers et al. that the primary contributor to lateral patella instability is femoral rotation, may only be valid if there is co-existing tibial external rotation.


External tibial rotation increases lateral patella shift and tilt in cadaver models and increases PF contact pressure in the lateral compartment . Combined tibiofemoral rotation independently explains 29% of variance in PF joint contact area in individuals with PFPS . Similarly, increasing internal tibial rotation increased contact pressure on the medial PF compartment, although increases are much less than those experienced in the lateral compartment . The lack of large influence of tibial internal rotation on PF compartment pressure may explain why the presence of pes planus was not associated with medial or lateral PF cartilage damage , despite the coupling of rearfoot eversion and internal tibial rotation. The lack of association may also be due to data being collected in static positions given that rearfoot-tibia coupling is most evident during running gait .


Proposed mechanical contributors to the progression of patellofemoral OA


Patellofemoral joint geometry and dyskinesia


Similar to cross-sectional data, a longitudinal study demonstrated lateral displacement of the patella was linearly associated with odds of increasing lateral PF joint space narrowing over 35-month period ( Fig. 5 ). Patella alta also linearly increased the odds of progression of medial and lateral cartilage damage and lateral bone marrow lesions even when the influence of lateral patella tilt and displacement were adjusted for . In contrast to cross-sectional data, where large lateral patella tilt increased the odds of exhibited medial PF joint space narrowing, the same relationship was not found for studies of PF OA progression. A single study reported that increasing lateral tilt had a linear protective effect on medial PF joint space narrowing and no effect on narrowing in the lateral compartment. There are several theories that could explain this contrast. Increasing patella tilt could reflect laxity in the structures that hold the patella in a lateral tilt resulting in greater mobility and shear stress on the medial compartment. However, as PF OA progresses, it is unlikely that a single source of stress would be present in isolation. Thus concomitant tightening of the ITB or altered patella kinematics may influence patella tilt in a manner that reduces stress on the medial compartment.




Fig. 5


Odds ratios and 95% confidence intervals for the risk of PF OA progression for specific pathomechanical characteristics based on longitudinal data. An odds ratio of 1 represents equal odds of progression. BML = bone marrow lesion, CD = cartilage damage, CL = cartilage loss, JSN = Joint space narrowing, Osteo = osteophytes.


A further difference between medial and lateral PF OA progression was their relationship with the depth of the trochlear groove. When individuals exhibited progression in lateral PF joint space narrowing, their sulcus angle was more likely to be in the first and fourth quartile, indicating the deepest or shallowest trochlear grooves . Whereas the greatest odds of medial PF OA progression were for those whose trochlear groove depth placed them in the middle quartiles. While there was no correlation between trochlea groove depth or lateral patella displacement and pain , this indicates that treatments aimed at altering the femoral articulating surfaces may adversely affect one PF compartment for the sake of the other.


Muscle force and activation


Longitudinal studies examining the influence of muscle strength and activation on the progression of PF OA have focussed on the quadriceps ( Table 1 ). Quadriceps activity can promote cartilage health and stabilise the knee joint, however it may also increase the joint reaction forces . Over time, individuals with PFPS may modify their walking behaviour in an attempt to reduce this force. This is particularly the case for vastus medialis, which can be inhibited by knee pain Ref. . Two studies have evaluated the influence of quadriceps strength on PF structural progression and pain over 15–30 months. Neither study found a linear association between strength and joint space narrowing or cartilage loss ( Fig. 5 ). However, Amin et al. , observed the proportion of cartilage loss, pain and disability were less when quadriceps strength was high. Participants in both studies exhibited either PF or TF OA, thus results may over or under represent the influence of quadriceps strength for individuals with PF OA. In addition, the apparent protective effect was no longer evident when Amin et al. stratified participants based on the presence of varus alignment.


Lower limb alignment and kinematics


Over 18 months, valgus alignment resulted in a 1.6-fold increase in the odds of isolated lateral compartment progression ( Fig. 5 ). Varus alignment was associated with a two-fold increase in the odds of medial PF OA compartment progression. Further, as the severity of varus alignment increased, the odds of medial PF progression also increased. A potential explanation for the correlation between alignment and structural damage is that joint laxity increases with increasing malalignment, leading to greater shear stress a the PF joint. Sharma et al. explored this explanation in their longitudinal examination of TF OA progression. These authors hypothesised that if laxity influences OA progression, controlling for it during the analysis should decrease the strength of the alignment-progression relationship. This did not occur, suggesting that laxity may not be a mechanism for the effect of varus alignment on TF OA progression. While the generalizability of these results to PF OA is questionable, it suggests that other alignment and kinematic factors may influence knee OA progression. However, the influence of other potentially contributing factors, such as tibiofemoral rotation or patella kinematics, has not been longitudinally examined.




Pathomechanics of the patellofemoral joint


Framework of contributors to patellofemoral OA


The pathomechanical issue most commonly cited with the presence and progression of PF OA is abnormal PF joint stress ( Fig. 2 ). This abnormality can be due to either excessive magnitude of stress and/or aberrant dispersion of forces. Such abnormalities can contribute to disease progression by disrupting the balance between breakdown and repair of joint tissues . Higher PF joint stress has also been correlated with reduced functional scores on the Knee Osteoarthritis Outcome Survey (KOOS) . Further, increased contact pressure and shear stress have been reported in individuals with PFPS, suggesting that altered joint stress may occur prior to structural damage . The cause of abnormal stress in the PF joint is multifactorial consisting of local and person-level contributors ( Fig. 1 ). At a person-level, increased BMI increases the load on the joint by increasing the external joint moments . Being of female gender is also associated with increased joint stress, particularly during knee flexion and activities or occupations that involve frequent knee flexion dictate the frequency of stress application . While all of these factors are important, they are beyond the scope of this review. Locally, the extensor mechanism, soft tissue restraints from muscles, ligaments and retinaculum, articular geometry and dyskinesia and lower limb alignment interact to influence PF joint stress . In addition, there is evidence of proximal and distal kinetic chain influences such as rearfoot mobility, hamstring, iliotibial band tightness and hip muscle activation and force . These factors will be discussed below.




Fig. 2


Free body diagram of patellofemoral joint reaction force when an individual ascends a step. CoG = centre of gravity; kJR = knee joint reaction force; m 1 = quadriceps force; m 2 = patellor tendon tesion; PFJR = patellofemoral joint reaction force; x = flexor level arm.


Proposed mechanical contributors to the presence of patellofemoral OA


Cross-sectional studies examining pathomechanics, such as patella malalignment and maltracking, muscle force and activation and lower limb alignment use the presence of joint space narrowing, cartilage damage, osteophytes and bone marrow lesions as indicators of structural joint damage ( Table 1 ). While these studies are limited in their ability to draw conclusions regarding cause and effect, many studies calculate odd ratios to express the risk of structural joint damage when a variable of interest is present ( Fig. 3 a, b).



Table 1

Details of PF OA studies included in the review.






























































































































































































































Authors Type of study Comparator group Follow-up period (range) N Imaging methods Risk factor Disease marker
Type View Knee angle Grading system
Amin et al. Longitudinal n/a 30 months 265 MRI Sagittal, coronal and axial WORMS (modified) Quadriceps strength Articular cartilage loss
Baker et al. Cross-sectional n/a n/a 1396 X-ray Weight-bearing skyline 30° KL grade Quadriceps strength Joint space narrowing, osteophytes
Cahue et al. Longitudinal n/a 18 months 211 a X-ray Weight-bearing skyline 30° OARSI Varus-Valgus alignment Joint space narrowing
Crossley et al. Cross-sectional Healthy controls ( N = 18) n/a 60 X-ray Weight-bearing skyline 30–40° KL Altered hip abductors muscle activation Joint space narrowing, osteophytes, subchondral bone cysts
Elahi et al. Cross-sectional n/a n/a 292 X-ray Weight-bearing skyline 30° OARSI Varus-Valgus alignment Joint space narrowing
Fok et al. Cross-sectional Healthy controls ( N = 21) n/a 30 Joint kinematics, joint moments, muscle force and joint reaction force American College of Rheumatology clinical criteria, osteophytes
Gross et al. Cross-sectional n/a n/a 1903 MRI Sagittal, coronal and axial WORMS Pes planus Articular cartilage damage
Gross et al. Cross-sectional n/a n/a 2940 b MRI Sagittal, coronal and axial WORMS Varus-Valgus alignment Articular cartilage damage
Hart et al. Cross-sectional Healthy controls ( N = 11) n/a 22 X-ray MRI Skyline Coronal, axial KL Quadriceps cross-sectional area Joint space narrowing, osteophytes, subchondral bone cysts
Hunter et al. Longitudinal n/a 36 months (24–60) 595 X-ray Weight-bearing skyline 30–40° OARSI Patellofemoral geometry and alignment Joint space narrowing
Kalichman et al. Cross-sectional n/a n/a 213 MRI X-ray Sagittal, coronal and axial weight-bearing skyline 30° 4-point scale Patellofemoral geometry and alignment Joint space narrowing, osteophytes
Kalichman et al., Cross-sectional n/a n/a 213 MRI Sagittal, coronal and axial WORMS Patellofemoral geometry and alignment Articular cartilage loss and bone marrow lesions
McWalter et al. Cross-sectional n/a n/a 10 MRI KL Varus-Valgus alignment Patella kinematics
Sharma et al. Longitudinal n/a 18 months 171 X-ray Weight-bearing skyline 30° OARSI Quadriceps strength Joint space narrowing
Stefanik et al. Longitudinal n/a 30 months 907 c X-ray MRI Weight-bearing lateral axial 20–50° WORMS Patellofemoral geometry and alignment Cartilage thickness, cartilage defects, bone marrow lesions, subchondral bone attrition
Stefanik et al. Cross-sectional n/a n/a 807 MRI Sagittal, coronal and axial WORMS Quadriceps weakness Articular cartilage damage and bone marrow lesions
Stefanik et al. Cross-sectional n/a n/a 881 MRI Sagittal, coronal and axial WORMS Trochlear morphology Joint space narrowing, bone marrow lesions

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Nov 10, 2017 | Posted by in RHEUMATOLOGY | Comments Off on Patellofemoral joint osteoarthritis: An individualised pathomechanical approach to management

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