Background: Anterior knee pain without clinical and radiologic abnormalities has primarily been explained from a purely structural view. A recently proposed biologic and homeostatic explanation questions the malalignment theory. No objective measurement of the pathophysiology responsible for changes in local homeostasis has been presented.
Hypothesis: Flexing the knee joint interferes with the perfusion of the patellar bone in patellofemoral pain syndrome.
Study design: Case control study; Level of evidence, 4.
Methods: Pulsatile blood flow in the patella was measured continuously and noninvasively using photoplethysmography. Measurements were made with the patient in a resting position with knee flexion of 20 degrees and after passive knee flexion to 90 degrees. In total, 22 patients with patellofemoral pain syndrome were examined bilaterally, and 33 subjects with healthy knees served as controls.
Results: The pulsatile blood flow in the patient group decreased after passive knee flexion from 20 degrees to 90 degrees (systematic change in position, or relative position [RP] = -0.32; 95% confidence interval for RP, -0.48 to -0.17), while the response in the control group showed no distinct pattern (RP = 0.17; 95% confidence interval for RP, -0.05 to 0.31). The difference between the groups was significant (P = .0002). The median change in patients was -26% (interquartile range, 37).
Conclusions: Pulsatile patellar blood flow in patellofemoral pain syndrome patients is markedly reduced when the knee is being flexed, which supports the previous notion of an ischemic mechanism involved in the pathogenesis of this pain syndrome.