Platelet-Rich Plasma (PRP) & Orthobiologics

• Rapid clinical uptake ahead of robust evidence makes it a favourite viva theme - the examiner is testing judgement, not enthusiasm.
• The science is examinable: the growth factors, their platelet alpha-granule source, and the leukocyte axis are concrete facts.
• The evidence is uneven: strong for knee OA (PRP beats HA), mixed for tendinopathy, weak/low-level for most other uses.
• Standardisation is the recurring criticism - and the reason PAW/Mishra reporting systems exist.

Platelet-rich plasma (PRP) is an autologous preparation in which the patient's own blood is centrifuged to concentrate platelets (commonly several-fold above the whole-blood baseline) into a small plasma volume. Platelets store growth factors in their alpha-granules; on activation they release PDGF, TGF-β, VEGF, IGF-1, EGF and bFGF, among others. The rationale is that delivering a bolus of these factors to an injured or degenerate tissue promotes cell proliferation, matrix synthesis, angiogenesis and modulation of inflammation — augmenting the local healing environment.

PRP is made at the point of care: anticoagulated whole blood is centrifuged so it separates by density into plasma (top), a thin buffy coat of platelets and leukocytes (middle), and red cells (bottom). A single spin ('soft') concentrates platelets in plasma while keeping some red/white cells; a double spin ('hard') achieves higher platelet concentration and lets the operator include or exclude the leukocyte layer to make leukocyte-rich or leukocyte-poor PRP. The product may be used as a liquid (often activated with calcium chloride/thrombin to trigger granule release) or as a fibrin matrix (PRF).

Across all orthobiologics the limiting issue is lack of standardisation and regulation: dose, cell/platelet content, processing and activation vary between systems and studies, outcomes are heterogeneous, and many indications rest on low-level evidence. The mature position is to use the best-supported indications (e.g. LP-PRP for knee OA), specify the preparation, counsel honestly about uncertainty and cost, and avoid overselling unproven uses.

• PRP = autologous concentrated platelets releasing PDGF, TGF-β, VEGF, IGF-1, EGF, bFGF from alpha-granules.
• Leukocyte-poor vs leukocyte-rich is the key axis — LP intra-articular (less inflammatory), LR sometimes for tendinopathy.
• Knee OA: level-1 evidence PRP beats HA at 6–12 months; LP-PRP over LR-PRP; no extra adverse events.
• Tendinopathy (e.g. lateral epicondylitis): mixed evidence, used when conservative care fails.
• Reporting systems: PAW (DeLong), Mishra, PLRA.
• The central caveat: lack of standardisation — always specify the preparation and counsel honestly.

Two level-1 meta-analyses anchor the knee-OA story: intra-articular PRP outperforms hyaluronic acid for pain and function at 6 and 12 months without more adverse events, and leukocyte-poor PRP does better than leukocyte-rich intra-articularly. In Belk et al. (18 level-1 RCTs) the mean WOMAC improvement was 44.7%PRP versus 12.6%HA.

PRP is autologous and very safe, but examiners expect the practical caveats. Relative/absolute contraindications include active infection (local or systemic), active malignancy (especially at the injection site), critical thrombocytopenia or platelet-function disorders, and significant anaemia; anticoagulation is a relative contraindication. The key drug interaction: NSAIDs and aspirin inhibit platelet COX and granule release, so they are usually withheld around the procedure (commonly about a week before and one-to-several weeks after), and a recent intra-articular corticosteroid may blunt the anabolic response, so the two are spaced apart. The main adverse effect is a self-limiting post-injection pain/inflammatory flare (more common with leukocyte-rich PRP); serious complications such as infection are rare. Counsel about the transient flare, the need to pause anti-inflammatories, and the out-of-pocket cost.