Identifying the origins of patellofemoral pain could help create consensus about its cause and treatment, saving patients from a therapeutic merry-go-round. Researchers using MRI and computer modeling techniques are closing in on these origins and are using imaging to chart biochemical changes that might trigger anatomic changes that produce pain.
Identifying the origins of patellofemoral pain could help create consensus about its cause and treatment, saving patients from a therapeutic merry-go-round. Researchers using MRI and computer modeling techniques are closing in on these origins and are using imaging to chart biochemical changes that might trigger anatomic changes that produce pain.
Contributing factors to patellofemoral pain (PFP) include overuse and overload of the patellofemoral joint, biomechanical problems, and muscular dysfunction. The differential diagnosis of anterior knee pain is extensive and includes prepatellar bursitis, patellar and quadriceps tendinitis, patellofemoral arthrosis, patellar subluxation and dislocation, and knee ligamentous and meniscal pathology.
Sharmila Mujumdar, Ph.D., director of the Musculoskeletal and Quantitative Imaging Research Group at the University of California, San Francisco, has been using high-resolution MR to image cartilage and 3D model studies to determine kinematics. The team has recorded wide variability of data between subjects and controls but has not reached any conclusion regarding the origins of PFP.
"We often find that marathon runners, for example, have no pain but exhibit signs of cartilage damage on MRI. We are trying to reconcile these results," Mujumdar said.
While multiple potential causes of PFP exist, thinning cartilage is one likely factor. Computer modeling has shown a correlation between thinning cartilage and increased cartilage stress. To test this hypothesis in vivo, researchers at Stanford University used upright weight-bearing MRI for patella tracking to capture the dynamic nature of the disorder. No previous studies have examined articular cartilage thickness in young adults with PFP, said coauthor Dr. Garry Gold, an assistant professor of radiology at Stanford. The study is scheduled for publication in OsteoArthritis and Cartilage.
The Stanford team evaluated 34 patients with PFP and 16 controls (average age 24 years). Researchers used 1.5T MR for supine imaging to measure cartilage thickness and a 0.5T system for upright weight-bearing imaging to measure cartilage contact area in 0 degrees , 30 degrees , and 60 degrees of knee flexion. They calculated cartilage stress with the help of a 3D finite element model analysis of biomechanical forces.
Overall, males with PFP had thinner cartilage than male controls, while no such correlation was found among the females. The patellofemoral joint contact area increased, not unexpectedly, with load and knee flexion. Subjects with thinner cartilage tended to have a smaller contact area.
"Knowing the contact area between the two cartilage plates is key to determining how the stress might be distributed," Gold said. "A maltracking patella will likely have a lower contact area than a patella that does not maltrack. If both patellas experience the same forces, the maltracking one will have higher stress."
Changes in cartilage are caused by multiple factors, Majumdar said. For example, alterations in components proteoglycan and collagen can be seen with MRI. Researchers now want to know how these changes manifest themselves longitudinally in terms of cartilage thinning. Another potential mitigating factor to PFP is bone marrow, which shows signs of water content. Researchers may be able to track bone marrow changes with MRI and correlate them with cartilage variance.
"What we are aiming for is predicting early degeneration in articular cartilage, so that when disease modifying therapies are available, one can immediately decide which component in the knee joint to treat," she said.
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