Abstract

Platelet-rich plasma (PRP) is injected within tendons to stimulate healing. Metabolic alterations such as the metabolic syndrome, diabetes, or hyperuricemia could hinder the therapeutic effect of PRP. We hypothesise that tendon cells sense high levels of uric acid and this could modify their response to PRP. Tendon cells were treated with allogeneic PRPs for 96 hours. Hyperuricemic PRP did not hinder the proliferative actions of PRP. The gene expression pattern of inflammatory molecules in response to PRP showed absence of IL-1b and COX1 and modest expression of IL6, IL8, COX2, and TGF-b1. IL8 and IL6 proteins were secreted by tendon cells treated with PRP. The synthesis of IL6 and IL8 proteins induced by PRP is decreased significantly in the presence of hyperuricemia (P = 0.017 and P = 0.012, resp.). Concerning extracellular matrix, PRP-treated tendon cells displayed high type-1 collagen, moderate type-3 collagen, decorin, and hyaluronan synthase-2 expression and modest expression of scleraxis. Hyperuricemia modified the expression pattern of extracellular matrix proteins, upregulating COL1 (P = 0.036) and COMP (P = 0.012) and downregulating HAS2 (P = 0.012). Positive correlations between TGF-b1 and type-1 collagen (R = 0.905, P = 0.002) and aggrecan (R = 0.833, P = 0.010) and negative correlations between TGF-b1 and IL6 synthesis (R = −0.857, P = 0.007) and COX2 (R = −0.810, P = 0.015) were found.

Highlights

  • The use of platelet-rich plasma (PRP) to treat tendon pathology has widely expanded in the last five years [1]

  • After 96 hours in culture, PRP significantly enhanced tendon cell proliferation when compared to FBS (P = 0.008)

  • The population doubling time of the cells cultured in PRP was 40.40 hours (SD = 6.105); the doubling time of the population of cells cultured in hyperuricemic PRP was 39.97 hours (SD = 5.265) (Figure 1)

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Summary

Introduction

The use of platelet-rich plasma (PRP) to treat tendon pathology has widely expanded in the last five years [1]. PRP is injected within tendons aiming at healing, reducing pain, and improving tendon function [2]. A recent meta-analysis has shown a significant reduction of pain at three years, six years, and one year after PRP treatment in different tendons [3]. Despite a higher risk of suffering tendinopathy [4], patients with metabolic diseases are often excluded from the clinical trials testing PRP efficacy [5, 6]. Whether metabolic disorders should be an exclusion criterion from PRP therapies is open to question

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