Michael P Fice1, J Chance Miller2, Robert Christian3, Charles P Hannon4, Niall Smyth5, Christopher D Murawski6, Brian J Cole1, John G Kennedy7. 1. Section of Cartilage Restoration and Sports Medicine, Department of Orthopaedics, Rush University Medical Center, Chicago, Illinois, U.S.A. 2. College of Physicians and Surgeons, Columbia University, New York, New York, U.S.A. 3. Department of Orthopaedic Surgery, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, U.S.A. 4. Section of Cartilage Restoration and Sports Medicine, Department of Orthopaedics, Rush University Medical Center, Chicago, Illinois, U.S.A.. Electronic address: charles.p.hannon@gmail.com. 5. Department of Orthopaedic Surgery, Miami University School of Medicine, Miami, Florida, U.S.A. 6. School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, U.S.A. 7. Department of Orthopaedic Surgery, Hospital for Special Surgery, New York, New York, U.S.A.
Abstract
PURPOSE: To review the basic science studies on platelet-rich plasma (PRP) for cartilage and determine whether there has been an improvement in methodology and outcome reporting that would allow for a more meaningful analysis regarding the mechanism of action and efficacy of PRP for cartilage pathology. METHODS: The PubMed/MEDLINE and EMBASE databases were screened in May 2017 with publication dates of January 2011 through May 2017 using the following key words: "platelet-rich plasma OR PRP OR autologous conditioned plasma (ACP) OR ACP AND cartilage OR chondrocytes OR chondrogenesis OR osteoarthritis OR arthritis." Two authors independently performed the search, determined study inclusion, and extracted data. Data extracted included cytology/description of PRP, study design, and results. RESULTS: Twenty-seven studies (11 in vitro, 13 in vivo, 3 in vitro and in vivo) met the inclusion criteria and were included in the study. All of the studies (100%) reported the method by which PRP was prepared. Two studies reported basic cytologic analysis of PRP, including platelet, white blood cell, and red blood cell counts (6.7%). Nine studies reported both platelet count and white blood cell count (30.0%). Twelve studies reported platelet count alone (40.0%). Nine studies (30.0%) made no mention at all as to the composition of the PRP used. PRP was shown to increase cell viability, cell proliferation, cell migration, and differentiation. Several studies demonstrated increased proteoglycan and type II collagen content. PRP decreased inflammation in 75.0% of the in vitro studies reporting data and resulted in improved histologic quality of the cartilage tissue in 75.0% of the in vivo studies reporting data. CONCLUSIONS: Although the number of investigations on PRP for cartilage pathology has more than doubled since 2012, the quality of the literature remains limited by poor methodology and outcome reporting. A majority of basic science studies suggest that PRP has beneficial effects on cartilage pathology; however, the inability to compare across studies owing to a lack of standardization of study methodology, including characterizing the contents of PRP, remains a significant limitation. Future basic science and clinical studies must at a minimum report the contents of PRP to better understand the clinical role of PRP for cartilage pathology. CLINICAL RELEVANCE: Establishing proof of concept for PRP to treat cartilage pathology is important so that high-quality clinical studies with appropriate indications can be performed.
PURPOSE: To review the basic science studies on platelet-rich plasma (PRP) for cartilage and determine whether there has been an improvement in methodology and outcome reporting that would allow for a more meaningful analysis regarding the mechanism of action and efficacy of PRP for cartilage pathology. METHODS: The PubMed/MEDLINE and EMBASE databases were screened in May 2017 with publication dates of January 2011 through May 2017 using the following key words: "platelet-rich plasma OR PRP OR autologous conditioned plasma (ACP) OR ACP AND cartilage OR chondrocytes OR chondrogenesis OR osteoarthritis OR arthritis." Two authors independently performed the search, determined study inclusion, and extracted data. Data extracted included cytology/description of PRP, study design, and results. RESULTS: Twenty-seven studies (11 in vitro, 13 in vivo, 3 in vitro and in vivo) met the inclusion criteria and were included in the study. All of the studies (100%) reported the method by which PRP was prepared. Two studies reported basic cytologic analysis of PRP, including platelet, white blood cell, and red blood cell counts (6.7%). Nine studies reported both platelet count and white blood cell count (30.0%). Twelve studies reported platelet count alone (40.0%). Nine studies (30.0%) made no mention at all as to the composition of the PRP used. PRP was shown to increase cell viability, cell proliferation, cell migration, and differentiation. Several studies demonstrated increased proteoglycan and type II collagen content. PRP decreased inflammation in 75.0% of the in vitro studies reporting data and resulted in improved histologic quality of the cartilage tissue in 75.0% of the in vivo studies reporting data. CONCLUSIONS: Although the number of investigations on PRP for cartilage pathology has more than doubled since 2012, the quality of the literature remains limited by poor methodology and outcome reporting. A majority of basic science studies suggest that PRP has beneficial effects on cartilage pathology; however, the inability to compare across studies owing to a lack of standardization of study methodology, including characterizing the contents of PRP, remains a significant limitation. Future basic science and clinical studies must at a minimum report the contents of PRP to better understand the clinical role of PRP for cartilage pathology. CLINICAL RELEVANCE: Establishing proof of concept for PRP to treat cartilage pathology is important so that high-quality clinical studies with appropriate indications can be performed.
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