CLAUDIA MCGLOIN
Claudia McGloin is a registered nurse holding dual registration in both the UK and Ireland. McGloin is the clinical director and nurse practitioner at The New You Clinic in Sligo. She is one of Ireland’s leading platelet-rich plasma experts and has performed thousands of PRP treatments.
While widely used to reduce inflammation, PRP therapy can sometimes cause or exacerbate it...
PRP is prepared by centrifuging the patient’s blood to isolate a plasma fraction rich in platelets, typically three to five times the normal platelet concentration. Platelets contain alpha granules loaded with growth factors such as platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-ß), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF). Upon activation, these platelets release their growth factors, which play crucial roles in modulating inflammation, promoting angiogenesis, recruiting stem cells, and stimulating collagen synthesis.
The goal of PRP therapy is to accelerate healing by enhancing the body’s natural repair processes. But while the growth factors are intended to reduce inflammation and promote regeneration, the injection of PRP can paradoxically cause an inflammatory reaction.
WHY DOES PRP CAUSE INFLAMMATION?
Inflammation is a natural and necessary stage of tissue healing. PRP injections often induce a mild, acute inflammatory response as part of the body’s healing cascade. When PRP is injected into injured tissue, it acts as a stimulus that attracts immune cells, such as neutrophils and macrophages, to the site. These cells release cytokines and other inflammatory mediators that clear debris and bacteria and set the stage for tissue regeneration. This initial inflammation is usually transient and considered a normal part of the therapeutic process.
Although PRP is rich in growth factors, it also contains inflammatory mediators. Upon activation, platelets release not only healing factors but also pro-inflammatory cytokines like interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-ß), and chemokines. These substances recruit more immune cells and may contribute to local swelling, redness, warmth, and pain. Depending on the PRP preparation method and the tissue injected, the inflammatory reaction can vary in intensity.
VARIABILITY IN PRP PREPARATIONS
PRP is not standardised and its composition can differ significantly depending on how it’s prepared. Some PRP formulations contain leukocytes (white blood cells), which can enhance the inflammatory response. Leukocyte-rich PRP (LR-PRP) tends to cause more inflammation compared to leukocyte-poor PRP (LP-PRP). Leukocytes are part of the immune system and release enzymes and cytokines that can promote inflammation and tissue breakdown if not balanced properly.
The mechanical process of injecting PRP itself can cause minor tissue trauma, leading to an inflammatory reaction. Needle insertion disrupts tissue and small blood vessels, which triggers the release of inflammatory mediators as part of the injury response. This mechanical injury may amplify the inflammatory effects of the PRP injection.
Individual differences in immune response, underlying conditions such as autoimmune diseases or chronic inflammation, and genetic predispositions can affect how the body responds to PRP. Some patients may experience exaggerated inflammatory reactions, including prolonged pain, swelling, or even adverse reactions such as sterile abscess formation.
CLINICAL IMPLICATIONS OF PRP-INDUCED INFLAMMATION AND MANAGEMENT STRATEGIES
While mild inflammation following a PRP injection is expected and often signals the body’s healing process, excessive or prolonged inflammation can lead to negative outcomes. A heightened inflammatory response may cause increased pain and swelling, temporarily limiting a patient’s mobility and function. Inflammation that becomes too intense or chronic can delay healing by causing further tissue damage, fibrosis, or scar formation. In rare cases, PRP injections can provoke more serious adverse reactions such as infections or granuloma formation, especially if sterile technique is compromised. Additionally, excessive post-treatment inflammation can lower patient satisfaction and confidence in the therapy.
To optimise outcomes and minimise unwanted inflammation, clinicians employ several strategies. These include selecting the appropriate type of PRP for example, leukocyte-poor PRP for conditions where reducing inflammation is crucial, like osteoarthritis, and leukocyte-rich PRP when a stronger inflammatory stimulus may be beneficial, such as in tendon repair. Proper injection techniques, including the use of ultrasound guidance and gentle administration, help reduce tissue trau ma. Post-injection care recommendations like rest, ice application, and cautious use of non-steroidal anti-inflammatory drugs (NSAIDs) aim to manage pain without suppressing the regenerative inflammation necessary for healing. Lastly, patient selection is critical; screening for underlying inflammatory or autoimmune disorders helps identify those who might be prone to exaggerated inflammatory responses.
Understanding the inflammatory mechanisms triggered by PRP allows clinicians to tailor treatments, minimise adverse effects, and improve patient outcomes.