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Research Review By Dr. Brynne Stainsby©


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Date Posted:

June 2016

Study Title:

Is there a biomechanical link between patellofemoral pain & osteoarthritis? A narrative review


Wyndow N, Collins N, Vicenzino B et al.

Author's Affiliations:

Departments of: Physiotherapy, School of Health and Rehabilitation Sciences, The University of Queensland, Australia; Mechanical Engineering, Melbourne School of Engineering, The University of Melbourne, Australia; School of Biomedical Sciences, The University of Queensland, Australia; School of Allied Health, College of Science, Health and Engineering, Latrobe University, Australia.

Publication Information:

Sports Medicine 2016; 46: 1797-1808.

Background Information:

As a leading cause of pain and disability, knee osteoarthritis (OA) affects approximately 33% of people over the age of 60 (1, 2). The three knee compartments are: the medial and lateral tibiofemoral (TF) and the patellofemoral (PF). While each of the knee compartments may be affected individually, mixed medial and PF is the most common, impacting 40% of people with knee OA (3-10). Isolated PF OA has been found in up to 36% of people (9-12) and incidence rates in those with knee pain range from 29-31% (12, 13). Interestingly, radiographic evidence of PF OA has been associated with greater pain and disability than similar degrees of TF OA (14). In addition, PF OA is a marker for the future development of arthritic changes in the TF compartments (15).

Given the prevalence and clinical impact of PF OA, little is known about the development of this condition. The authors of this review have hypothesized that a continuum may exist between patellofemoral pain (PFP) and PF OA. Specifically, they explore how abnormal loading may cause PFP, and eventually lead to a biomechanical framework for the development of PF OA.

Clinically, patients with PF pain present with anterior knee pain that is aggravated by flexion and loading of the knee, and have no other symptoms that would be attributed to another diagnosis (16, 17). It is considered a diagnosis of exclusion when other internal knee derangements have been ruled out. Patients with PF OA also present with anterior knee pain with activities that load the PF joint, such as squatting or climbing stairs. This supports the authors’ hypothesis that abnormal lower limb biomechanics and neuromuscular control in patients with PFP may lead to altered loading patterns and structural damage, which may cause PF OA.



Traditionally, PFP has been viewed as a self-limiting condition; however, it may progress to a chronic condition in up to 90% of individuals (18-22). Particularly, patients with a longer duration of baseline pain or more intense knee pain were more likely to have poorer outcomes at three and 12 month follow-ups in a prior study (22). Further, pain that was severe enough to limit activity was reported by 8-36% of study participants up to 18 years after diagnosis (19-21).

From a radiographic perspective, in a study of 125 patients aged 35-54 with chronic knee pain, 33% had radiographic PF OA and over a seven-year period, a further 31% developed PF OA (13). In another study of 888 women over the age of 45, a history of anterior knee pain and PF crepitus were risk factors for PF OA on MRI (7). Finally, in a study of 150 patients undergoing arthroplasty for isolated PF OA, 22% reported anterior knee pain in adolescence and early adulthood (23).

Relationship between PF Loads and PF OA

Altered joint loading has been hypothesized to contribute to the development of both PFP and PF OA. In a healthy joint, forces are evenly distributed over the joint surface to minimize stress on the cartilage and subchondral bone (24) and the joint responds by increasing cartilage thickness and bone density (25, 26). In patients with PFP however, increased focal areas of force have been identified which may result in greater magnitude of force and increased frequency of loading; both of which can exceed tissue thresholds and cause repetitive joint damage (25-28). In patients with PFP, it is possible that altered cartilage (softening, fissuring and fibrillation) and subchondral bone stress may result in a degenerative response (29-37). Early OA has also been associated with articular cartilage changes, specifically collagen breakdown and the loss of proteoglycans (28, 36, 37).

With greater duration or severity of PFP, patients may adopt movement modifications to alter PF loading and decrease pain (38-41). For example, during gait and ambulating up or down stairs, reduced knee flexion angles have been demonstrated compared to asymptomatic controls (38-43). This altered knee flexion has been related to reduced joint reaction forces and though effective in the short term, may lead to reduced quadriceps and gluteal function, which have been observed in patients with PF OA (44-46).

Functional and Structural Factors Influencing PF Joint Stress

Movement at the PF joint (flexion/extension) is affected by the anatomy of the patella and femoral trochlea, and neuromuscular control of the lower extremity. A shallow femoral trochlea, patellar tilt and patella alta have been associated with patellar instability, cartilage and bony damage in patients with PFP (47-51). The same parameters have been found in patients with OA (4, 45, 52, 53).

It is also possible that static varus/valgus alignment of the TF joint and the Q-angle may impact patellar kinematics, but a relationship between these factors and the development of either PFP or PF OA has not yet been demonstrated. Dynamic knee valgus has been associated with increased PF stress in PFP and PF OA (54-56). During MRI studies, patients with PFP may demonstrate internal rotation of the femur during a squat, and this may decrease PF contact and create focal areas of increased load (22, 57, 58), though this has not been demonstrated in all studies (59). It is unknown if this is a biomechanical contributing factor, an adaptive strategy or the result of arthrogenic inhibition, and has not been demonstrated in patients with PF OA.

In patients with PFP, quadriceps torque has been found to be lower than asymptomatic controls, which may be an attempt to minimize pain during knee extension activities (48, 60-63) or due to arthrogenic inhibition (64, 65). Quadriceps atrophy has also been found in patients with PFP and PF OA when measured on MRI, though thigh girth measured clinically has not been related to the diagnosis of these conditions (66).

The activation of vastus medialis obliquus (VMO) has been demonstrated to be delayed or decreased relative to vastus lateralis (VL), and may increase stress on the lateral patella in patients with PFP; however, this has been demonstrated in subjects without PFP as well (67). Theoretically, local coordination and altered medial stabilization of the patella could affect patellar kinematics and PF joint stress, but have not been demonstrated in all patients with PFP. In patients with PF OA, differences in VMO and VL activation have not been demonstrated (68, 69). Altered activation of the medial and lateral hamstrings may also occur in patients with PFP, such that adolescents with PFP recruit the lateral hamstrings earlier than the medial (70-72), however this has not been investigated in patients with PF OA.

Altered muscle activation in the hip and pelvic muscles have also been reported in patients with PFP, such that gluteus medius demonstrates delayed onset while there is greater activation of gluteus maximus when climbing stairs (73). In patients with PF OA, isometric hip abductor strength (74), and peak force during walking and stair descent (39,75) has also been demonstrated to be lower than in age-matched controls. It is not clear from these studies, however, if these findings are the cause or effect of PFP or PF OA. Further, when examining rear-foot mechanics, no studies have identified factors that contribute to the development of PFP or PF OA. In the midfoot, increased mobility has been observed in patients with PFP (16,76-79), but has not been studied in patients with PF OA. Finally, reduced ankle dorsiflexion has been observed in patients with PFP and may contribute to altered PF joint mechanics (80-83). However, patients aged 16-18 with PFP have been found to have greater ankle dorsiflexion when compared to controls (16), thus a causal biomechanical relationship between ankle dorsiflexion and PFP cannot be identified. This relationship has not been studied in patients with PF OA.

Clinical Application & Conclusions:

This review identifies the biomechanical similarities between PFP and PF OA, though fails to identify a direct biomechanical relationship. While it is certainly possible that altered biomechanics and loading may suggest a continuum of disease exists between the two conditions, there is currently a lack of evidence to support this conclusion.

Future research is needed to identify risk factors for the development of PF OA, prevention strategies and treatment programs. Given the relationship between radiographic PF OA and clinical pain and disability, interventions intending to alter PF loads may mitigate the progression of the condition and provide patients with relief. A trial of care aiming to improve lower limb biomechanics, strengthen the surrounding musculature and improve gait would be warranted with careful monitoring of symptom progression.

Study Methods:

  • A literature search was conducted using PubMed and the University of Queensland Library master search function “Summon” from earliest records to September 2015.
  • The authors used relevant search terms and also combined them.
  • Articles were screened for relevance.
  • Hand searches of references lists from relevant were also performed.
  • Due to the paucity of literature, the authors believed a systematic review would not be appropriate.
  • No details regarding critical appraisal, data extraction or consensus were provided.

Study Strengths / Weaknesses:


The authors provided a helpful overview of the prevalence of knee OA, and the relative frequencies of OA in each compartment. Further, they outlined the impact of PF OA in terms of pain and functional limitations. The paper offered a well-organized and thorough outline of the current literature as it relates to PFP and PF OA. Lastly, they appropriately described how altered lower limb movement patterns may be caused by or causing joint degeneration.

  • The primary limitation of this study is the lack of described methodology. Though it provided a brief summary of the literature search, without an understanding of the research question, search strategy or appraisal methods used, the results must be interpreted with some degree of caution.
  • While the authors did note the paucity of high-quality literature regarding PF OA, the comment was found at the end of the methodology. A decision to complete a systematic review or narrative should have been made a priori.
  • The quantity of the available literature should not be the determining factor in the type of review performed.
  • Appraisal of strengths and weaknesses of the included studies is not included.

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