prp and nsaids cover

PRP, NSAIDs and take-home instructions


Platelet-rich plasma (PRP) is currently used to treat many different conditions, ranging from sports injuries to androgenic alopecia.  It has been very popular in the sports medicine arena the past one to two decades.  Many providers are aware of the instructions after a PRP treatment but may have not looked further into the reasoning behind them.

PRP is a biologic therapy is thought to promote healing by delivering the concentrated growth factors to damaged tissues and augment the natural healing process with mitogenesis or cellular proliferation through mitosis, chemotaxis, and other cellular processes.  To release these restorative molecules, platelets must be activated. This complex process begins with binding of myriad agonists to platelet G-protein-coupled receptors (GPCRs) or immunoreceptor tyrosine-based activation motif complexes [1].  These lead to signaling cascades and platelet responses, including regulating surface receptors, and releasing growth factors into the environment through degranulation.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are thought to inhibit growth factor release by competitively and irreversibly inhibiting cyclooxygenase (COX) 1 and 2. More specifically, this is thought to occur through the inability of arachidonic acid (AA) to allow downstream thromboxane-A2 (TxA2) binding to TxA2 receptor to allow for platelet activation. Consequently, many physicians recommend cessation of antiplatelet and anti-inflammatory drugs before initiating PRP therapy [1].

A 2022 systematic review recently reviewed the information regarding growth factors and different types of NSAIDs.   While the results were not definitive, it appeared that the use of CaCl2 or TBN alone as activation agents for PRP was, in general, not significantly affected by antiplatelets, and the use of collagen, ADP, and AA as activation agents showed a reduction in growth factors. There are limited high-quality data on the subject currently, and future clinical research is warranted [2].

Another recent review evaluated platelet function and aggregation for some common medications.  In 73 patients, statin therapy did not result in a significant decrease in maximal platelet aggregation. Although there was not a significant difference in platelet aggregation with statin treatment when compared with control patients, treatment with statins did trend toward a significant decrease in aggregation.  This is not one of the common medications that patients are told to hold before or after PRP injections [3]. Older studies have shown that ACE inhibitors can inhibit platelet function and some providers will recommend holding these if possible.  Depending on the usage and level of comorbidities, this may be a case-by-case basis.

Table 1.  Key Regenerative growrth factors in PRP.  Adopted from [10].

A single study with 13 patients involving acetaminophen (13 patients) showed that the drug inhibited platelet inhibition in a dose-dependent manner, presumably because of its ability to weakly inhibit COX-1 [4]. Few other studies exist that describe the effects of acetaminophen on platelets, and the ones that do show conflicting findings [5]. 

Most patients treated with differing doses of aspirin (268 patients) showed a significant decrease in platelet aggregation [6]. However, there was one study with 48 patients that failed to exhibit decreased platelet aggregation [7].

In the review, patients who took NSAIDs (172 patients) demonstrated significantly decreased platelet aggregation only when treated with nonselective formulations. Interestingly, those treated with COX-2–selective NSAIDs showed no significant difference in platelet aggregation.  This supports that COX selectivity plays a crucial role in determining whether NSAID use causes platelet dysfunction. This finding coincides with the knowledge that COX-1 plays a significant role in thrombosis, whereas COX-2 plays a more significant role in the inflammation cascade [8].

In a separate 2018 study, naproxen diminished several biologic factors in LR-PRP.  It was also shown in this study that one week without naproxen was shown to be sufficient to recover from this diminished activity.  Many growth factors were evaluated in this including PDGF-AA, PDGF-AB, TNF-A, IL-1b, FGF-2 and IL-6.  This study recommended the discontinuation of NSAIDs one week before any PRP treatment. 

Table 2.  Clinical use of PRP.  Adopted from [10].

The use of cryotherapy or ice is also frequently mentioned when discussing PRP and take-home instructions.  Most providers will recommend against icing initially because cryotherapy has been shown to have anti-inflammatory effects.  Other medications are also similar and thought to have a more anti-inflammatory effect.  These medications include gingko biloba, garlic, flax oil, cod liver oil, vitamin A, vitamin E, or any other essential fatty acids.  There is limited data regarding its use directly after PRP, however.

Figure 3.  General physical therapy and action plan following PRP for the shoulder.

Figure 4.  Further take home instructions after PRP injection.

Figure 5.  Final page of take home instructions after PRP injection.


In conclusion, aspirin, acetaminophen, and nonselective NSAIDs should be stopped before a PRP injection because of their potential to diminish the effects of the injection. COX-2–selective NSAIDs and statins may possibly be continued following PRP injection.  Other medications and modalities have limited data and many providers do recommend holding any other medications that have anti-inflammatory effects.


  1. Yun SH, Sim EH, Goh RY, Park JI, Han JY. Platelet activation: the mechanisms and potential biomarkers. Biomed Res Int. 2016;2016:9060143.
  2. Kao DS, Zhang SW, Vap AR. A Systematic Review on the Effect of Common Medications on Platelet Count and Function: Which Medications Should Be Stopped Before Getting a Platelet-Rich Plasma Injection? Orthopaedic Journal of Sports Medicine. 2022;10(4).
  3. Munsterhjelm E, Munsterhjelm NM, Niemi TT, Ylikorkala O, Neuvonen PJ, Rosenberg PH. Dose-dependent inhibition of platelet function by acetaminophen in healthy volunteers. Anesthesiology. 2005;103(4):712–717.
  4. Lages B, Weiss HJ. Inhibition of human platelet function in vitro and ex vivo by acetaminophen. Thromb Res. 1989;53(6):603–613. 
  5. Trettin A, Böhmer A, Suchy MT, et al. Effects of paracetamol on NOS, COX, and CYP activity and on oxidative stress in healthy male subjects, rat hepatocytes, and recombinant NOS. Oxid Med Cell Longev.2014;2014:212576. 
  6. Feuring M, Haseroth K, Janson CP, Falkenstein E, Schmidt BM, Wehling M. Inhibition of platelet aggregation after intake of acetylsalicylic acid detected by a platelet function analyzer (PFA-100). Int J Clin Pharmacol Ther. 1999;37(12):584–588.
  7. Vaturi M, Vaduganathan M, Bental T, Solodky A, Kornowski R, Lev EI. Relation of aspirin response to age in patients with stable coronary artery disease. Am J Cardiol. 2013;112(2):212–216. doi:10.1016/j.amjcard.2013.03.022
  8. Morita I. Distinct functions of COX-1 and COX-2. Prostaglandins Other Lipid Mediat. 2002;68-69:165–175.a
  9. Moser, Lynette, et al. “ACE inhibitor effects on platelet function in stages I-II hypertension.” Journal of cardiovascular pharmacology4 (1997): 461-467.
  10. Peter, I., et al. “Platelet-rich plasma.” Physical Medicine and Rehabilitation Clinics4 (2016): 825-853.