PRP and Rheumatoid arthritis

Ross Hauser, MD

Inflammatory arthritis, or rheumatoid arthritis, generally occurs when the body attacks itself by making antibodies against itself. Antibodies are proteins, made by the immune system, that fight microorganisms such as bacteria that invade the body. In these instances, this inflammation is counterproductive because the body is reacting against its own immune system.

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Rheumatoid arthritis treatment involves use of medications that inhibit tumor-necrosis factor such as Enbrel® and Humira® (or generics etanercept and adalimumab) which have been shown to enhance quality of life and slow the arthritic process.

Tumor-Necrosis factor (TNF‑α) is cell signalling protein (cytokine), which communicates the commands to create inflammation in Rheumatoid arthritis joint swelling. The medical thinking is if you can block TNF and other inflammatory factor production or at least inhibit it, joint swelling will be reduced and hopefully the amount of articular cartilage breakdown resulting from a toxic, over inflamed joint environment will be slowed.

Medications have shown that they indeed can slow and reduce inflammation, however,  the articular cartilage still breaks down even as the medications become more sophisticated.

In our opinion, treatment should be geared at repairing the cause of the joint swelling, not the chemistry of the joint swelling.
Halting joint swelling with a drug makes no sense.

The RICE protocol and NSAIDs can stop a joint from swelling for the short-term. Use of more sophisticated drugs such as interleukin-1 blockers or corticosteroid injections (or for that matter, interleukin injection blockers) just limit joint swelling for a longer period of time, but you leave the joint vulnerable to further injury and degeneration.

In a new paper (July 2017) doctors at Shanghai Jiaotong University in China have published the results of their findings suggesting that Platelet-rich plasma exhibits beneficial effects for rheumatoid arthritis by suppressing inflammatory factors.

The research which appears in the medical journal Molecular medicine reports suggests in animal study that:

  • Platelet-rich plasma (PRP), a multifunctional blood product containing highly concentrated platelets, and various cell growth factors which promote cell proliferation and differentiation exhibited benefits in injurious articular cartilage repair and the removal of inflammatory factors in clinical studies.
  • In the present study, the therapeutic effects and primary mechanism of PRP on a type II collagen‑induced arthritis mouse model was investigated.
    • The therapeutic efficacy of PRP in this study demonstrated that treatment with PRP alleviated arthritis, and reduced humoral and cellular immune responses.
    • Mice treated with PRP exhibited downregulated expression of various inflammatory markers including the interleukin family of immune system stimulators (inflammatories) IL‑6, IL‑8, IL‑17A, IL‑1β, TNF‑α, receptor activator for nuclear factor‑κB (regulates and creates messages to begin inflammation) and IFN‑γ (interferon) in inflammatory tissue.
    • In addition healing factors listed below were shown to increase:
      • Vascular Endothelial Growth Factor (VEGF) Helps new blood vessel formation, thereby increasing vascularity in injured areas,
      • Platelet-Derived Growth Factor (PDGF) Attracts immune system cells to the area and stimulates them to proliferate. Has been shown to enhance ligament and tendon healing.
      • Transforming Growth Factor-β (TGF-β) Secreted by and affects all major cell types involved in healing. Similar affects as PDGF.
      • Insulin-like growth factor-1 (IGF-1) a growth factor mediator.
  • Conclusion: mice treated with PRP exhibited beneficial effects, including decreased joint inflammation, cartilage destruction and bone damage, and increased repair of joint tissue. The results of the present study suggested that PRP may be an effective therapeutic agent for Rheumatoid Arthritis.1

In January 2017, this same research team investigated the beneficial anti-inflammatory effect of PRP on synovial fibroblasts in Rheumatoid Arthritis.2 In joint swelling caused by rheumatoid arthritis an increase in cytokines, such as tumor-necrosis factor and interleukin-1, occurs in the joint fluid, PRP was shown to reduce these increases.

In their research, doctors in Germany wrote in the medical journal Arthritis and rheumatism that in their animal study, PRP alleviated inflammatory arthritic changes in pig knee joints.3

Understanding rheumatoid arthritis treatment

Autoimmune disorders are not a prednisone or NSAID deficiency. Correcting the underlying cause of why the body is attacking itself is key to reversing these conditions. This can include investigating the possibility of leaky gut syndrome, poor diet, food sensitivities, heavy metals, fatty acid or other nutrient deficiency, underlying infection such as Lyme disease or mycoplasma, and unresolved trauma. Treatment may involve a comprehensive approach to diet and supplements, hormones, IV nutrients, oxygen therapies, mind-body therapies, and more. It is for this reason that people suffering from these painful chronic conditions should seek the care of a Natural Medicine physician so the cause of the condition can be treated.

Questions about PRP and Rheumatoid arthritis? Get help and information from our Caring Medical Staff

1 Tong S, Zhang C, Liu J. Platelet-rich plasma exhibits beneficial effects for rheumatoid arthritis mice by suppressing inflammatory factors. Molecular Medicine Reports. 2017 Jul 27. [Pubmed] [Google Scholar]

2 Tong S, Liu J, Zhang C. Platelet-rich plasma inhibits inflammatory factors and represses rheumatoid fibroblast-like synoviocytes in rheumatoid arthritis. Clinical and experimental medicine. 2017 Jan 24:1-9. [Pubmed] [Google Scholar]

3 Lippross S, Moeller B, Haas H, Tohidnezhad M, Steubesand N, Wruck CJ, Kurz B, Seekamp A, Pufe T, Varoga D. Intraarticular injection of platelet‐rich plasma reduces inflammation in a pig model of rheumatoid arthritis of the knee joint. Arthritis & Rheumatology. 2011 Nov 1;63(11):3344-53. [Pubmed] [Google Scholar]




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