Platelet-rich plasma (PRP) may be defined as an autologous blood product produced by the centrifugation of whole blood, yielding a concentration of platelets that is increased above baseline values (1). It is the physiological role of platelets in the body’s healing response that has led to interest in PRP as a treatment for a variety of indications (2).

Additionally, the autologous nature of PRP and its ease of production have led to an ever increasing popularity in its use, with the market value expected to reach 126 million USD by 2016 in the United States alone (3).

 

While PRP has been examined for a wide variety of pathologies, ranging from alopecia to erectile dysfunction (4, 5), it is for musculoskeletal indications that its use has been most thoroughly investigated. In this regard, the use of PRP has been controversial, as its widespread use has continued without supporting evidence established by high-quality randomised controlled clinical trials. To date, PRP has been used in the orthopaedic setting to treat Achilles tendinopathy, anterior cruciate ligament tears, plantar fasciitis and epicondylitis, as well as to augment spinal fusion, bone healing, rotator cuff repair, arthroplasty, and cartilage regeneration (6-15). A recent meta-analysis regarding the use of PRP in orthopaedics concluded that a lack of standardization across studies complicated the current literature, however there is a trend favouring PRP (16). 

 

The basic science evidence regarding the use of PRP for certain orthopaedic indications shows promise. Using cartilage pathology as an example, PRP has been shown to improve chondrocyte viability, proliferation, as well as proteoglycan and type II collagen deposition (17,18). Additionally, PRP may mediate the catabolic effects of inflammatory cytokines present in an articulating joint in a pathological state (19,20). However, translating these results into clinical practice is challenging. One aspect of PRP that has become clear is that not all PRP is created equal. The PRP produced by different commercially available centrifugation systems shows a wide variability in its cytological and molecular composition (21). Mazzocca et al (22) published further evidence that highlights the variance in PRP. The authors drew blood from eight individuals at three different time points and following centrifugation using a commercially available system to produce PRP, measured the concentration of platelets, WBCs, and growth factors. The results of the study demonstrated that the concentration of the biologically active constituents in PRP demonstrate both inter- and intra-individual variability.

We, as clinicians and scientists, have yet to determine the optimal concentrations of the key cytological components of PRP. With regard to platelet counts, increasing levels may not necessarily translate into a better outcome. We have also yet to come to a consensus as to whether a leukocyte-rich or a leukocyte-poor PRP product may be more beneficial, as different PRP systems may produce either. Additionally, it stands to reason that no single formulation of PRP should be used for all indications, as the biology of cartilage is very different from that of a tendon. The old science adage “the more you know, the more you don’t” holds ever true with platelet-rich plasma.

The future of PRP in medical practice lies in adequately characterising its cytological and molecular make-up and then tailoring it to suit specific indications. We anticipate that as the body of evidence regarding its use grows, the suitable indications for the implementation of PRP will narrow. 

 

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