Anti-inflammatory medications have damaged your joints. Can that damage be repaired?
Understanding the possibilities of non-surgical treatments and how they work
There are many reasons why you have osteoarthritis. At the top of your list is perhaps:
- A physically demanding job,
- High level of sports activities,
- Accident/Injury trauma
- Medical treatments
Medical treatments always seem to bring a raised eye-brow to some when we suggest to the patient in our examination room that their past treatments accelerated his/her arthritic pain. To others they have long recognized that their treatments were causing damage to their joints. This list of treatments includes:
- arthroscopic surgery
- opioid prescriptions
- oral anti-inflammatory prescriptions
- cortisone injections
- and over-the-counter pain medications.
Patients are aware of the risk that their arthroscopic surgery will bring or have brought about osteoarthritic changes in their joints. They were told this before there surgery. They may not have been quite so aware that their pain relief programs would in fact make their situation worse. Intuitively, you are probably aware that these pills are not really helping you.
If you need the research, you can find a lot of research in our articles on how your pain medications are making your situation worse.
- When NSAIDs make pain worse
- The Acceleration of Articular Cartilage Degeneration in Osteoarthritis by Nonsteroidal Anti-inflammatory Drugs
When anti-inflammatories leads to surgery
The body’s healing response is inflammation. Inflammation fixes injuries. Inflammation will turn on and continue staying on until the joint injury is healed.
But what if the joint does not heal because the degenerative injury has become too severe for the body to heal on its own?
- Then the inflammatory mechanism will be stuck in the “open” position, chronic inflammation will continue trying to heal something it can’t.
- Naturally occurring inflammation is filled with quick acting chemicals.
- Let’s stress that these are quick acting and not “long-term.” One characteristic of inflammation is its use of powerful corrosives to remove dead and dying tissue.
- If inflammation becomes chronic, naturally occurring powerful corrosives start eating away at your joint. This is the degenerative process.
Can you prevent joint collapse
In our office we do not use stem cell therapy on every patient. In fact, we rarely use stem cell therapy. Why? Because it is not necessary to achieve the type of joint repair and rebuilding that the patient and our team will find successful. However, in cases of advanced degenerative disease stem cells may be offered.
- Stem cells are an injection therapy. The treatment works by taking stem cells from other areas of your body and reintroducing them into the damaged areas. Your stem cells have an ability to change into the building blocks of cartilage and help repair and assist the cells like the chondrocytes, already in the joint, to complete the repair.
- The goal of our stem cell therapy is to get patients back to doing the things that they want to do without pain and without the need of surgery.
You did not wake up one morning with advanced degenerative joint disease, nor is it something that will go away overnight
People may have an unrealistic expectation of what stem cell therapy can do. For some, they believe that a one time injection will reverse years of degenerative damage. This is not a realistic expectation. Some will be told that they will need 2 or 3 injections for the treatment to work. While this is a more realistic expectation, it is not for many a reality that will help them avoid surgery.
Advanced joint degeneration requires advanced joint regeneration.
A single injection given once a month for three months will help some, but it is not the type of treatment that should be expected to prevent an eventual joint replacement or fusion surgery.
Let’s explore what degenerative treatments are doing to your joints and the ability of stem cell therapy to heal that damage.
NSAIDs – What is the damage?
In 2010, this is what Ross Hauser, MD wrote in his paper in the Journal of Prolotherapy entitled: The Acceleration of Articular Cartilage Degeneration in Osteoarthritis by Nonsteroidal Anti-inflammatory Drugs:
It is clear from the scientific literature that NSAIDs have a significant negative effect on cartilage repair and formation which causes an acceleration of the deterioration of articular cartilage in osteoarthritic joints.
- The overwhelming evidence shows that NSAIDs have no beneficial effect on articular cartilage and accelerate the very disease for which they are most used and prescribed.
- The long-term consequence of the deterioration of the joint is a need for joint replacement.
- Massive NSAID use in osteoarthritic patients since their introduction is one of the main causes of the rapid rise in the need for hip replacements and knee replacements both now and in the near future.(1)
This was later supported in the medical research which not only showed how NSAIDs destroyed joints, but could negatively impact stem cell therapy’s ability to fix that damage.
- Doctors in Canada wrote in the journal Arthritis research & therapy: (2) NSAIDs makes pain worse and interferes with stem cells healing capabilities. NSAIDs do this by inhibiting stem cells’ ability to regrow bone. Further, residual NSAID presence in the joints may weaken bone, causing structural instability. This is supported by research from McGill University reporting on Naproxen’s effect on bone healing.
- This research is from doctors at Maastricht University Medical Centre and Boston University. In this study published in the journal Public Library of Science one (3) is a discussion of the NSAID COX-2 inhibitor. (COX or cyclooxygenase, are two enzymes (COX-1 and COX 2) that promote inflammation). COX inhibitors shut off inflammation and directly cause suppression of cartilage cell growth and natural repair of articular cartilage growth.
- Doctors at Oxford University, writing in the journal Maturitas (4) examining elderly patients with non-healing bone fractures found the treatment of post-fracture pain with NSAIDs put the patient at the greatest risk for non-union of the fracture and questioned whether stem cells introduced into treatment could help these patients.
- In the Journal of gastroenterology and hepatology, (5) researchers examined the digestive and gastrointestinal distress caused by NSAIDs and found that they may have their origin in the patient’s low anti-oxidant inner milieu. In other words, the immune system is too compromised to fight off the NSAIDs side-effects including ulcers. This can also suggest that the immune system is too compromised to heal joints.
Clearly, NSAIDs inhibit and suppress the growth of bone and collagen, the stuff of ligaments, tendons, and cartilage. If a patient has a long history of NSAIDs this should be addressed prior to stem cell therapy and a treatment plan discussed.
If you have questions about how stem cells heal degenerative joint disease after years of cortisone and painkillers, get help and information form our Caring Medical staff
1. Hauser RA. The Acceleration of Articular Cartilage Degeneration in Osteoarthritis by Nonsteroidal Anti-inflammatory Drugs: Journal of Prolotherapy. 2010;(2)1:305-322. [Google Scholar]
2. Salem O, Wang HT, Alaseem AM, Ciobanu O, Hadjab I, Gawri R, Antoniou J, Mwale F. Naproxen affects osteogenesis of human mesenchymal stem cells via regulation of Indian hedgehog signaling molecules. Arthritis Res Ther. 2014 Jul 17;16(4):R152. doi: 10.1186/ar4614. [Google Scholar]
3. Caron MM, Emans PJ, Sanen K, Surtel DA, Cremers A, Ophelders D, van Rhijn LW, Welting TJ. The role of prostaglandins and COX-enzymes in chondrogenic differentiation of ATDC5 progenitor cells. PloS one. 2016 Apr 6;11(4):e0153162.[Google Scholar]
4. Foulke BA, Kendal AR, Murray DW, Pandit H. Fracture healing in the elderly: A review. Maturitas. 2016 Oct 31;92:49-55.[Google Scholar]
5. Kono Y, Kawano S, Takaki A, Shimomura Y, Onji M, Ishikawa H, Takahashi S, Horii J, Kobayashi S, Kawai D, Yamamoto K. Oxidative stress controlling agents are effective for small intestinal injuries induced by non‐steroidal anti‐inflammatory drugs. Journal of gastroenterology and hepatology. 2017 Jan 1;32(1):136-45. [Google Scholar]
6. Hernigou P, Trousselier M, Roubineau F, Bouthors C, Chevallier N, Rouard H, Flouzat-Lachaniette CH. Stem cell therapy for the treatment of hip osteonecrosis: a 30-year review of progress. Clinics in orthopedic surgery. 2016 Mar 1;8(1):1-8. [Google Scholar]
7. Wyles CC, Houdek MT, Wyles SP, Wagner ER, Behfar A, Sierra RJ. Differential cytotoxicity of corticosteroids on human mesenchymal stem cells. Clinical Orthopaedics and Related Research®. 2015 Mar 1;473(3):1155-64. [Google Scholar]
8 Wang M, Yuan Z, Ma N, Hao C, Guo W, Zou G, Zhang Y, Chen M, Gao S, Peng J, Wang A. Advances and prospects in stem cells for cartilage regeneration. Stem cells international. 2017;2017. [Google Scholar]
9 Deorosan B, Nauman EA. The Role of Glucose, Serum, and Three-Dimensional Cell Culture on the Metabolism of Bone Marrow-Derived Mesenchymal Stem Cells. Stem Cell International. 2011; Article ID 429187, 12 pages. Doi:10.4061/2011/429187 . [Google Scholar]
10 Pei M. Environmental preconditioning rejuvenates adult stem cells’ proliferation and chondrogenic potential. Biomaterials. 2017 Feb 1;117:10-23. [Google Scholar]