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PRP ≠ Inflammation

  • Jul 29
  • 6 min read

Updated: Jul 30

Samuel G Oltman, ND, RMSK


Platelet Rich Plasma (PRP) is not an attempt to create inflammation. It is an effort to direct a specific immune response that stimulates healing. By “healing”, I mean anabolism, proliferation, regeneration, and inflammation resolution. The inflammatory response is fundamental to our physiology and helps us maintain health but the semantics and language around it have made it difficult to discuss. Understanding exact PRP mechanisms helps to clarify this confusion and dispel many misconceptions about what to take and not to take around PRP treatments (and any other regenerative treatment like prolotherapy or MFAT).


Inflammation is not one thing. It is an umbrella term describing a myriad of biochemical processes, some of which heal and some of which harm. We want to heal from injuries but we want to harm infectious microbes. The inflammatory response is responsible for both of these situations. 


The difference between types of inflammatory responses depends on the biochemical signals (cytokines and prostaglandins) and the subsequent cellular action (neutrophil and macrophage polarization). The biochemical signals are determined by the triggering event (infection or injury) and the overall health of the individual (baseline systemic inflammation, nutrient levels, stress, etc). These biochemical signals are also where various drugs and compounds exert their effect on the inflammatory response. 

prp inflammation
Macrophage Polarization. All of this is "inflammation", but M1 is degenerative/destructive and M2 is regenerative/healing. The same type of distinction happens with Neutrophils, a different type of white blood cell.

Within both common parlance and within the medical community there are biochemical processes we discuss as “anti-inflammatory parts of the inflammatory response” and “pro-inflammatory inflammation”. It doesn’t make sense and creates deep confusion. It’s all inflammation. 


For processes/compounds/signals that are commonly called “anti-inflammatory”, the more accurate term is regenerative (or anabolic, or healing). For processes/compounds/signals that are commonly called “pro-inflammatory”, the more accurate term is degenerative (or catabolic, or destructive). So we don’t have anti-inflammatory inflammation and pro-inflammatory inflammation. We have regenerative inflammation and degenerative inflammation, which more accurately describes their processes and end results.


PRP doesn’t work by just creating inflammation broadly. It works by promoting the specific subtype of regenerative inflammation to heal injured tissue (1, 2, 3). This is why the guidance around PRP is so often wrong and oversimplified: Not everything that is “anti-inflammatory” needs to be avoided– only compounds that directly interfere with the specific healing process that PRP is promoting. 


Cyclooxygenase (COX) activity is a special consideration in this conversation because COX inhibition is how most over-the-counter pain meds like Advil work. COX-1 inhibiting NSAIDs block platelet activation, cartilage synthesis and slow healing. COX-2 inhibitors do not have the same negative effect (4, 5). Here's the full breakdown: 

AVOID with PRP

OK/Neutral

ENCOURAGED with PRP

COX-1 NSAIDs

  • Ibuprofen (Advil)

  • Naproxen (Aleve)

  • Aspirin

  • Indomethacin

COX-2 NSAIDs

  • Meloxicam

  • Celecoxib (Celebrex)

Anti-Inflammatory Mediterranean Diet

Steroidals

  • Prednisone

  • Cortisone

Plant Compounds

  • Caffeine

  • Cannabinoids

Botanical Medicine

  • Turmeric

  • Ginger

  • Boswelia

  • Bromelain

Food

  • Alcohol

  • High Sugar


Nutrients

  • Omega-3 (fish oil)

  • Vitamin E

  • Polyphenols

  • Flavonoids



There have not been any studies showing that taking the nutrients in the right column negatively impacts PRP. The entire basis of the recommendation relies on extrapolating basic mechanistic studies which is fraught with error. When you look closely at the studies on how these compounds work, they are complex, multi-faceted, and in many cases enhance PRP outcomes. For example:

  • Turmeric is a COX-2 inhibitor (OK to take with PRP) along with having antioxidant, neuroprotective, and many other properties like promoting M2 polarization in macrophages (see graphic above). Studies that look at combining turmeric with PRP find that turmeric enhances PRP outcomes and speeds healing (6, 7, 8, 9, 10, 11).

  • Ginger is a COX-2 inhibitor (among other mechanisms) with zero COX-1 inhibition that promotes regenerative inflammation (12).

  • Bromelain is a COX-2 inhibitor (among other mechanisms) with zero COX-1 inhibition that promotes regenerative inflammation (13).

  • Vitamin E decreases platelet aggregation, which has no effect on growth factor release. Studies looking at Vitamin E combined with PRP find that Vitamin E enhances PRP outcomes and speeds healing (14).

  • Fish Oil/Omega-3 fatty acids have some COX-1 inhibition but also increase the signaling molecules the promote the regenerative inflammatory response. Whereas COX-1 NSAIDs block cartilage growth, fish oil preserves it. No study has every shown worse PRP outcomes in patients who are taking fish oil. Furthermore, diets high is omega-3s result in better PRP results (15, 16).


You Make Your Own Medicine


prp inflammation

If we then zoom out away from microscopic mechanism rationale and instead look at big-picture outcomes, we find the same thing: healthier patients do better with PRP than unhealthy patients. People who eat healthy, do better (17,18). “Healthy” meaning, good metabolic markers and low systemic inflammation primarily determined by diet, movement, and sleep. Eating an "anti-inflammatory diet" does not negatively impact the benefit of PRP-- it enhances it. What nutrients is the Mediterranean Diet high in? Omega-3s, Vitamin E, polyphenols, herbal antioxidants, etc.



If all we wanted was increased inflammation, why don't we recommend patients go on a beer-and-pizza-bender the night before PRP treatment? That would increase inflammation but it was be degenerative inflammation. The flip side is that an "anti-inflammatory diet" doesn't suppress inflammation, it promotes regenerative inflammation.


When we begin seeing the whole forest instead of just individual trees, the evidence suggests that we should be encouraging the regenerative healing process via these “anti-inflammatory” and “anti-platelet” compounds and that the labeling is misleading. For regenerative medicine procedures like PRP, we want to promote the healing response with compounds that promote the regenerative inflammation response-- not just avoid everything with the "anti-inflammatory" label. 


From my years of reviewing the evidence, my personal experience receiving PRP, and my 10 years of helping patients heal with PRP, I strongly believe this distinction around “anti-inflammatory” and “anti-platelet” compounds is a false assumption. With PRP you are making your own medicine. You want your platelets, your immune system, and your whole body to be ready to initiate the regenerative inflammatory process. Priming your system to heal can be aided by lifestyle and nutritional compounds that are misunderstood and mislabeled. Forget the inflammation label, think "what helps my body heal?"


See our Treatment Guidelines here:

References:

  1. Lana JF, Huber SC, Purita J, et al. Leukocyte-rich PRP versus leukocyte-poor PRP - The role of monocyte/macrophage function in the healing cascade. Journal of Clinical Orthopaedics and Trauma. 2019;10(Suppl 1):S7. doi:10.1016/j.jcot.2019.05.008

  2. Chaintreuil P, Kerreneur E, Bourgoin M, et al. The generation, activation, and polarization of monocyte-derived macrophages in human malignancies. Frontiers in Immunology. 2023;14:1178337. doi:10.3389/fimmu.2023.1178337

  3. Moussa M, Lajeunesse D, Hilal G, et al. Platelet rich plasma (Prp) induces chondroprotection via increasing autophagy, anti-inflammatory markers, and decreasing apoptosis in human osteoarthritic cartilage. Exp Cell Res. 2017;352(1):146-156. doi:10.1016/j.yexcr.2017.02.012

  4. Ludwig HC, Birdwhistell KE, Brainard BM, Franklin SP. Use of a cyclooxygenase-2 inhibitor does not inhibit platelet activation or growth factor release from platelet-rich plasma. Am J Sports Med. 2017;45(14):3351-3357. doi:10.1177/0363546517730578

  5. Lisowska B, Kosson D, Domaracka K. Positives and negatives of nonsteroidal anti-inflammatory drugs in bone healing: the effects of these drugs on bone repair. Drug Design, Development and Therapy. 2018;12:1809. doi:10.2147/DDDT.S164565

  6. Ahmad RS, Hussain MB, Sultan MT, et al. Biochemistry, safety, pharmacological activities, and clinical applications of turmeric: a mechanistic review. Evidence-based Complementary and Alternative Medicine : eCAM. 2020;2020:7656919. doi:10.1155/2020/7656919

  7. Comparison of combined therapy (Curcumin + prp) versus curcumin alone prp alone in terms of quality of life improvement in osmf | journal of neonatal surgery. Published online November 4, 2025. Accessed July 28, 2026.

  8. Ahmad RS, Hussain MB, Sultan MT, et al. Biochemistry, safety, pharmacological activities, and clinical applications of turmeric: a mechanistic review. Evidence-based Complementary and Alternative Medicine : eCAM. 2020;2020:7656919. doi:10.1155/2020/7656919

  9. Ozorowski M, Wiciński M, Liczner G, Wójcicki J, Włodarczyk E. The effects of curcumin on vascular endothelial function, lipid metabolism, inflammation and neuroprotection—a review. Nutrients. 2026;18(7):1032. doi:10.3390/nu18071032

  10. Deng T, Xu J, Wang Q, et al. Immunomodulatory effects of curcumin on macrophage polarization in rheumatoid arthritis. Front Pharmacol. 2024;15:1369337. doi:10.3389/fphar.2024.1369337

  11. Zavala A, Martinez PC, Gutierrez GG, Vara MD, Pawlikowski WD. The combined use of curcumin and platelet-rich plasma enhances axonal regeneration in acute nerve injuries: an experimental study in a rat model. Journal of Hand and Microsurgery. 2020;15(1):31. doi:10.1055/s-0040-1721562

  12. Breemen RB van, Tao Y, Li W. Cyclooxygenase-2 inhibitors in ginger (Zingiber officinale). Fitoterapia. 2010;82(1):38. doi:10.1016/j.fitote.2010.09.004

  13. Insuan O, Janchai P, Thongchuai B, et al. Anti-inflammatory effect of pineapple rhizome bromelain through downregulation of the nf-κb- and mapks-signaling pathways in lipopolysaccharide (Lps)-stimulated raw264. 7 cells. Current Issues in Molecular Biology. 2021;43(1):93. doi:10.3390/cimb43010008

  14. Yarahmadi A, Saeed Modaghegh MH, Mostafavi-Pour Z, et al. The effect of platelet-rich plasma-fibrin glue dressing in combination with oral vitamin E and C for treatment of non-healing diabetic foot ulcers: a randomized, double-blind, parallel-group, clinical trial. Expert Opin Biol Ther. 2021;21(5):687-696. doi:10.1080/14712598.2021.1897100

  15. Norris PC, Dennis EA. Omega-3 fatty acids cause dramatic changes in TLR4 and purinergic eicosanoid signaling. Proceedings of the National Academy of Sciences of the United States of America. 2012;109(22):8517. doi:10.1073/pnas.1200189109

  16. Cordingley DM, Cornish SM. Omega-3 fatty acids for the management of osteoarthritis: a narrative review. Nutrients. 2022;14(16):3362. doi:10.3390/nu14163362

  17. Platzer H, Bork A, Gantz S, et al. Dietary patterns are associated with blood cell profiles and the molecular composition of platelet-rich plasma. Nutrients. 2026;18(1):163. doi:10.3390/nu18010163

  18. Platzer H, Kubon KD, Diederichs S, et al. [Platelet-rich plasma (Prp) : Compositional analysis with different dietary habits and timing of blood sampling]. Orthopadie (Heidelb). 2023;52(11):907-915. doi:10.1007/s00132-023-04442-x

 
 
 

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