Abstract

Osteoarthritis of the knee (OAK) is a chronic degenerative disease and progresses with an imbalance of cytokines and macrophages in the joint. Studies regarding the use of platelet-rich plasma (PRP) as a point-of-care treatment for OAK have reported on its effect on tissue repair and suppression of inflammation but few have reported on its effect on macrophages and macrophage polarization. Based on our clinical experience with two types of PRP kits Cellaid Serum Collection Set P type kit (leukocyte-poor-PRP) and an Autologous Protein Solution kit (APS leukocyte-rich-PRP), we investigated the concentrations of humoral factors in PRPs prepared from the two kits and the effect of humoral factors on macrophage phenotypes. We found that the concentrations of cell components and humoral factors differed between PRPs purified using the two kits; APS had a higher concentration of M1 and M2 macrophage related factors. The addition of PRP supernatants to the culture media of monocyte-derived macrophages and M1 polarized macrophages revealed that PRPs suppressed M1 macrophage polarization and promoted M2 macrophage polarization. This research is the first to report the effect of PRPs purified using commercial kits on macrophage polarization.

Highlights

  • Erythrocyte concentration was negligible for LP-platelet-rich plasma (PRP) while it was lower for Autologous Protein Solution (APS) compared to whole blood

  • Platelet concentrations were higher for both Leukocyte-poor PRP (LP-PRP) and APS compared to whole blood and did not significantly differ between LP-PRP and APS

  • A comparison of the ratio of leukocyte types contained in whole blood and APS revealed that in APS, the ratios of neutrophils and eosinophils were higher while the ratios of monocytes and lymphocytes were lower (Figure 1C)

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Osteoarthritis of the knee (OAK) is a chronic degenerative disease that damages articular cartilage. OAK is characterized by aberrant cartilage metabolism, osteophyte formation, synovial tissue thickening, and macrophage infiltration. These changes contribute to the progress of OAK, resulting in joint pain and dysfunction [1,2]. There are about 25 million patients with

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