Platelet-rich plasma releasate inhibits inflammatory processes in osteoarthritic chondrocytes

Am J Sports Med. 2011 Nov;39(11):2362-70. doi: 10.1177/0363546511419278. Epub 2011 Aug 19.


Background: Platelet-rich plasma (PRP) has recently been postulated as a treatment for osteoarthritis (OA). Although anabolic effects of PRP on chondrocytes are well documented, no reports are known addressing effects on cartilage degeneration. Since OA is characterized by a catabolic and inflammatory joint environment, the authors investigated whether PRP was able to counteract the effects of such an environment on human osteoarthritic chondrocytes.

Hypothesis: Platelet-rich plasma inhibits inflammatory effects of interleukin-1 (IL-1) beta on human osteoarthritic chondrocytes.

Study design: Controlled laboratory study.

Methods: Human osteoarthritic chondrocytes were cultured in the presence of IL-1 beta to mimic an osteoarthritic environment. Medium was supplemented with 0%, 1%, or 10% PRP releasate (PRPr, the active releasate of PRP). After 48 hours, gene expression of collagen type II alpha 1 (COL2A1), aggrecan (ACAN), a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)4, ADAMTS5, matrix metalloproteinase (MMP)13, and prostaglandin-endoperoxide synthase (PTGS)2 was analyzed. Additionally, glycosaminoglycan (GAG) content, nitric oxide (NO) production, and nuclear factor kappa B (NFκB) activation were studied.

Results: Platelet-rich plasma releasate diminished IL-1 beta-induced inhibition of COL2A1 and ACAN gene expression. The PRPr also reduced IL-1 beta-induced increase of ADAMTS4 and PTGS2 gene expression. ADAMTS5 gene expression and GAG content were not influenced by IL-1 beta or additional PRPr. Matrix metalloproteinase 13 gene expression and NO production were upregulated by IL-1 beta but not affected by added PRPr. Finally, PRPr reduced IL-1 beta-induced NFκB activation to control levels containing no IL-1 beta.

Conclusion: Platelet-rich plasma releasate diminished multiple inflammatory IL-1 beta-mediated effects on human osteoarthritic chondrocytes, including inhibition of NFκB activation.

Clinical relevance: Platelet-rich plasma releasate counteracts effects of an inflammatory environment on genes regulating matrix degradation and formation in human chondrocytes. Platelet-rich plasma releasate decreases NFκB activation, a major pathway involved in the pathogenesis of OA. These results encourage further study of PRP as a treatment for OA.

MeSH terms

  • ADAM Proteins / biosynthesis
  • ADAMTS4 Protein
  • Aggrecans / biosynthesis
  • Cells, Cultured
  • Chondrocytes / metabolism*
  • Collagen Type II / biosynthesis
  • Cyclooxygenase 2 / biosynthesis
  • Gene Expression Profiling
  • Glycosaminoglycans / analysis
  • Humans
  • Inflammation Mediators / antagonists & inhibitors*
  • Interleukin-1beta / antagonists & inhibitors
  • Male
  • Matrix Metalloproteinase 13 / biosynthesis
  • NF-kappa B / metabolism
  • Nitric Oxide / metabolism
  • Osteoarthritis / metabolism*
  • Platelet-Rich Plasma / metabolism*
  • Procollagen N-Endopeptidase / biosynthesis
  • Up-Regulation


  • Aggrecans
  • COL2A1 protein, human
  • Collagen Type II
  • Glycosaminoglycans
  • IL1B protein, human
  • Inflammation Mediators
  • Interleukin-1beta
  • NF-kappa B
  • Nitric Oxide
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • ADAM Proteins
  • MMP13 protein, human
  • Matrix Metalloproteinase 13
  • Procollagen N-Endopeptidase
  • ADAMTS4 Protein
  • ADAMTS4 protein, human