Abstract
BackgroundLittle is known about the relationships of circulating levels of biomarkers of cartilage degradation with biomechanical outcomes relevant to knee osteoarthritis (OA) or biomarker changes following non-pharmacological interventions. The objectives of this exploratory, pilot study were to: 1) examine relationships between biomarkers of articular cartilage degradation and synthesis with measures of knee joint load during walking, and 2) examine changes in these biomarkers following 10 weeks of strengthening exercises.MethodsSeventeen (8 male, 9 female; 66.1 +/- 11.3 years of age) individuals with radiographically-confirmed medial tibiofemoral OA participated. All participants underwent a baseline testing session where serum and urine samples were collected, followed by a three-dimensional motion analysis. Motion analysis was used to calculate the external knee adduction moment (KAM) peak value and impulse. Following baseline testing, participants were randomized to either 10 weeks of: 1) physiotherapist-supervised lower limb muscle strengthening exercises, or 2) no exercises (control). Identical follow-up testing was conducted 11 weeks after baseline. Biomarkers included: urinary C-telopeptide of type II collagen (uCTX-II) and type II collagen cleavage neoepitope (uC2C), serum cartilage oligomeric matrix protein (sCOMP), serum hyaluronic acid (sHA) and serum C-propeptide of type II procollagen (sCPII). Linear regression analysis was used to examine relationships between measures of the KAM and biomarker concentrations as baseline, as well as between-group differences following the intervention.ResultsKAM impulse predicted significant variation in uCTX-II levels at baseline (p = 0.04), though not when controlling for disease severity and walking speed (p = 0.33). KAM impulse explained significant variation in the ratio uCTX-II;sCPII even when controlling for additional variables (p = 0.04). Following the intervention, changes in sCOMP were significantly greater in the exercise group compared to controls (p = 0.04). On average those in the control group experienced a slight increase in sCOMP and uCTX-II, while those in the exercise group experienced a reduction. No other significant findings were observed.ConclusionsThis research provides initial evidence of a potential relationship between uCTX-II and knee joint load measures in patients with medial tibiofemoral knee OA. However, this relationship became non-significant after controlling for disease severity and walking speed, suggesting further research is necessary. It also appears that sCOMP is amenable to change following a strengthening intervention, suggesting a potential beneficial role of exercise on cartilage structure.Trial registrationClinicaltrials.gov NCT01241812
Highlights
Little is known about the relationships of circulating levels of biomarkers of cartilage degradation with biomechanical outcomes relevant to knee osteoarthritis (OA) or biomarker changes following non-pharmacological interventions
Home exercise adherence rates were high with a mean (SD) of 83% (17%) of the exercise days completed
Though the knee adduction moment (KAM) is a well-accepted and valid measure of medial compartment joint load [10] with significant relationships with many clinical outcomes specific to knee OA in the medial compartment [8,24,25,26,27,28,29], it does not represent the total load within the knee joint [30] nor does it account for any potential changes in joint contact force that may result from increased muscle activity [31]
Summary
Little is known about the relationships of circulating levels of biomarkers of cartilage degradation with biomechanical outcomes relevant to knee osteoarthritis (OA) or biomarker changes following non-pharmacological interventions. Magnetic resonance imaging (MRI) has been used to assess changes in the morphology of the bone and cartilage to supplement radiographical findings [1] Though these approaches are reliable and well-established clinically, their use for the monitoring of changes in cartilage over time is limited by the fact that these changes take place over long periods of time and detail soft tissue damage that has already occurred [2]. Given that significant changes in symptoms and joint structure can occur over the course of 2 years, coupled with the fact that most non-surgical and non-pharmacological interventions are conducted over months instead of years, improved methods of assessing changes in cartilage structure and outcomes following shorter-terms treatments over shorter periods of time are needed
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