Platelet-rich plasma (PRP) is an injectable preparation made by taking a sample of the patient's own blood, concentrating the platelets by centrifugation, and injecting that concentrate into an injured tendon, joint or other soft tissue with the aim of improving pain and healing. It is the most widely used orthobiologic in sport and exercise medicine (SEM), it is heavily marketed, and athletes frequently ask for it by name. The evidence is far less settled than the marketing suggests: for the conditions studied most rigorously, well-conducted placebo-controlled trials have not shown clinically important benefit, and in the UK it is not routinely commissioned as standard care. This page covers what PRP is and how it is prepared, what the evidence does and does not show, and how to counsel an athlete honestly, including the anti-doping position.
PRP is an autologous preparation, meaning it is made from the patient's own blood. A sample of venous blood, with the volume set by the system and the target rather than by a single standard, is drawn into a tube containing an anticoagulant such as citrate and spun in a centrifuge. Spinning separates the blood by density into red cells at the bottom, a buffy coat containing platelets and leucocytes, and plasma above. Exactly what is then harvested depends on the system: leucocyte-rich preparations collect at or near the buffy coat, whereas leucocyte-poor preparations usually collect platelet-containing plasma while deliberately avoiding much of it. Injection may be ultrasound-guided, particularly for tendon and precise soft-tissue targets, while joint injections may be landmark-guided or image-guided. The rationale is that platelets contain alpha granules rich in growth factors, including platelet-derived growth factor, transforming growth factor beta and vascular endothelial growth factor, and that delivering a concentrated dose of these may influence cell recruitment, proliferation and matrix formation. This is a plausible biological rationale rather than a demonstrated clinical mechanism in humans.
A crucial point for the exam and for practice is that PRP is not one product. Preparations differ in the final platelet concentration, in leucocyte content, in whether the platelets are deliberately activated before injection, in the spin protocol and number of spins, and in the injected volume and number of injections given. Different commercial systems produce measurably different products from the same patient's blood. This heterogeneity is one of the main reasons trial results conflict and why pooled analyses are difficult to interpret: studies that all describe themselves as testing PRP may in fact be testing quite different injectates delivered by different protocols. When reading or quoting a PRP study, the preparation and protocol matter as much as the result.
The honest summary is that where PRP has been tested most rigorously, the results have been disappointing, even though earlier smaller and open studies looked promising. In knee osteoarthritis, a large rigorous placebo-controlled trial found no clinically important symptomatic or structural benefit over saline injection, while the wider evidence base remains heterogeneous rather than uniformly negative. UK guidance reflects this uncertainty: for PRP in knee osteoarthritis specifically, safety raises no major concerns but the evidence on efficacy is limited in quality, so the procedure should be used only with special arrangements for clinical governance, consent, and audit or research, with clinicians informing their governance leads, supporting shared decision making, and auditing outcomes including the methods used to prepare and administer the injection. In mid-portion Achilles tendinopathy, placebo or sham-controlled trials of single-injection protocols have not shown a meaningful advantage when both groups follow a loading programme, and progressive loading remains core treatment.
Elsewhere the picture is mixed rather than settled. In lateral elbow tendinopathy the trial evidence is inconsistent; some studies report better outcomes than corticosteroid at longer follow-up, but that does not establish efficacy over placebo, because corticosteroid is an active comparator with its own time-dependent course, including a well-recognised tendency to worse longer-term outcomes. For plantar heel pain, gluteal tendinopathy and patellar tendinopathy the evidence varies by condition and protocol but remains insufficient to establish routine use, and the preparation and protocol heterogeneity across these studies prevents confident condition-by-condition conclusions. Several factors explain why trials conflict: preparations and protocols differ, blinding is frequently inadequate, many studies compare an injection against no injection rather than against a credible placebo, co-interventions such as rehabilitation are inconsistently controlled, and outcome measures and follow-up periods vary. For an exam answer, the safe position is that PRP is an adjunct under investigation whose benefit is unproven for the conditions tested most rigorously, and that it does not replace progressive loading, weight management or the other core measures that do have evidence behind them.
Practical use in the UK is governed by honesty, consent and governance rather than by routine protocol. PRP is not routinely commissioned as standard National Health Service (NHS) care for these indications, and local commissioning and governance arrangements vary, so it is usually accessed privately. That creates an obvious commercial pressure the clinician must handle transparently. Where it is offered, the standards are that the diagnosis is secure, core management including a progressive loading programme has genuinely been tried, the patient understands that the magnitude and certainty of benefit are condition-specific and remain uncertain and that they may pay for no benefit, governance arrangements are followed where they apply, and outcomes are audited. Consent should avoid describing PRP as regenerative or as something that heals or reverses tissue damage, because that claim outruns the evidence. Practically, a local injection-site flare of pain for a few days can occur and should be discussed in advance so it is not mistaken for a complication.
Safety is generally reassuring, which is part of why the treatment persists despite weak efficacy data. Because PRP is autologous, there is no donor-transmitted infection or alloimmune risk, although contamination, procedural infection, bleeding and tissue injury remain possible, as with any injection. Reported harms are mostly local: pain and swelling at the site, a self-limiting flare, and bruising. Rare complications include nerve injury, deep infection after tendon or soft-tissue injection, and septic arthritis after intra-articular injection. Avoiding non-steroidal anti-inflammatory drugs around the time of injection is a theoretical, protocol-dependent practice rather than standard mandatory care, and decisions should reflect the indication, bleeding risk and local protocol. On anti-doping, the position is clear and worth memorising: PRP and related platelet-derived procedures are not prohibited under the current World Anti-Doping Agency (WADA) Prohibited List. Any added or separately administered substance must still be checked, since purified growth factors and other prohibited substances remain prohibited when given separately, and the current list should always be consulted.
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