The Use of Biomarkers to Quantify Clinical Response to Total Knee Arthroplasty Interventions: A Systematic Review.

The primary objective of this review was to determine whether the attenuation of the postoperative inflammatory response (PIR) after total knee arthroplasty (TKA) leads to a notable improvement in clinical outcome scores. The secondary objective of this review was to determine the optimal approach in using inflammatory biomarkers, clinical inflammatory assessments, and imaging to quantify the PIR. A systematic literature search of eight major databases was conducted using a predetermined search strategy. C-reactive protein (CRP), interleukin-6 (IL-6), erythrocyte sedimentation rate (ESR), knee surface temperature (KST), and clinical outcome data were collected and graphically displayed. Eighty-six percent of the studies that reported a statistically significant decrease in inflammatory biomarkers in their treatment group demonstrated a concordant notable improvement in clinical outcome scores. Mean CRP, IL-6, ESR, and KST values peaked on postoperative day (POD) 2, POD1, POD7, and POD 1-3, respectively. The PIR is correlated with early pain and function recovery outcomes. Future studies comparing TKA surgical methodologies and perioperative protocols should assess PIR by incorporating inflammatory biomarkers, such as CRP and IL-6, and clinical inflammatory assessment adjuncts, to provide a more comprehensive comparison.

A single dose of exercise stimulates skeletal muscle mitochondrial plasticity in myotonic dystrophy type 1.

AIM: Myotonic dystrophy type 1 (DM1) is the second most common muscular dystrophy after Duchenne and is the most prevalent muscular dystrophy in adults. DM1 patients that participate in aerobic exercise training experience several physiological benefits concomitant with improved muscle mitochondrial function without alterations in typical DM1-specific disease mechanisms, which suggests that correcting organelle health is key to ameliorate the DM1 pathology. However, our understanding of the molecular mechanisms of mitochondrial turnover and dynamics in DM1 skeletal muscle is lacking. METHODS: Skeletal muscle tissue was sampled from healthy and DM1 mice under sedentary conditions and at several recovery time points following an exhaustive treadmill run. RESULTS: We demonstrate that DM1 patients exhibit an imbalance in the transcriptional apparatus for mitochondrial turnover and dynamics in skeletal muscle. Additionally, DM1 mice displayed elevated expression of autophagy and mitophagy regulators. A single dose of exercise successfully enhanced canonical exercise molecular pathways and skeletal muscle mitochondrial biogenesis despite failing to alter the cellular pathology in DM1 mice. However, treadmill running stimulated coordinated organelle fusion and fission signaling, as well as improved alternative splicing of Optic atrophy 1. Exercise also evoked autophagy and mitophagy pathways in DM1 skeletal muscle resulting in the normalized expression of autophagy- and lysosome-related machinery responsible for the clearance of dysfunctional organelles. CONCLUSION: Collectively, our data indicate that mitochondrial dynamics and turnover processes in DM1 skeletal muscle are initiated with a single dose of exercise, which may underlie the adaptive benefits previously documented in DM1 mice and patients.