Paradox in pain management

 Anti-inflammatory drugs are medicines commonly use for treating pain in injuries, arthritis, backache and many diseases. But do these really help in tissue healing? Answer is BIG “no”. Rather these drugs are delaying or stopping natural repair of various tissues like ligaments, muscles, tendons, cartilages and bones other then dangerous systemic side effects like-

•           Stomach pain and heartburn

•           Stomach ulcers

      A tendency to bleed more

•          

Ringing in the ears

•           Allergic reactions such as rashes, wheezing, and throat swelling

•           Liver or kidney problems

•           High blood pressure

•           Leg swelling

Treating or Suppressing Joint Pain?

Why have researchers failed to develop effective and safe disease modifying osteoarthritis drugs (DMOADs) for the millions of patients suffering from this serious and disabling disease? Because drugs do not repair damaged cartilage in joints.

The treatment assumption is that stopping inflammation assists recovery.

Mostly because of a lack of adequate information provided by the prescribing physician, many patients are under the mistaken impression that these drugs not only reduce pain, but also promote healing. Nothing could be further from the truth. Inflammation is an integral part of the healing process.

NSAIDs (Nonsteroidal Anti-inflammatory Drugs) and the acceleration of the arthritis process-

NSAIDs are truly anti-inflammatory in their mechanism of action. Since all tissues heal by inflammation, one can see why long-term use of these medications will have harmful effects. Osteoarthritis and other chronic pain disorders are not an ibuprofen or other NSAID deficiency. Their chronic long-term use will not cure, and will actually hamper soft tissue healing and accelerate the arthritic process.

For those using NSAIDs compared to the patients who do not use them, joint replacements occur earlier and more quickly and frequently. Massive NSAID use in osteoarthritic patients since their introduction over the past forty years is one of the main causes of the rapid rise in the need for hip and knee replacements, both now and in the future.

Other authors agree:

•       “NSAIDs have been one of the most frequently used drugs for over 30 years with 80% of rheumatologists prescribing NSAIDs for symptomatic osteoarthritis.”

•       “It has been questioned whether there is a correlation between the sudden increase in OA: with replacement surgeries between 1997 and 2005 significantly rising: knee replacement climbing by 69%, hip replacements by 32% and spinal fusion surgeries increasing by 73%.”

•       Another group investigated the association of NSAIDs and the risk of atrial fibrillation in a prospective study of elderly individuals, and found that the use of NSAIDs was associated with an increased atrial fibrillation risk.

Below is a quote from new research in the medical journal Pain. In this statement doctors suggest that the reason joint replacement is recommended and performed is because NSAIDs do not work.

 “Difficulty in managing advanced osteoarthritis pain often results in joint replacement therapy. Improved understanding of mechanisms driving NSAID-resistant ongoing osteoarthritis pain might facilitate development of alternatives to joint replacement therapy.”

Other new research on failings of NSAIDs: The bullet points:

•       In a new study NSAID prescription were frequently given to patients with early axial spondyloarthritis, (inflammation of the sacroiliac joints and spine). Patients took low doses and gave up on them over time even though pain remained. Doctors concluded spondyloarthritis should not be treated with treated with NSAIDs. They don’t work.

•       In our practice we see patients of all ages. We see the high school athlete, we see the great-grand parent. If both have knee problems – from sports related injury or age deterioration, both prior to their visit with us, they will likely be prescribed an NSAID. Why? Because doctors believe that NSAIDs still offer the best of both worlds – an anti-inflammatory medication and a pain reliever.

•       As such, NSAIDs are still considered the first-line treatment for osteoarthritis related pain despite significant side effects including PREVENTING HEALING and ACCELERATE osteoarthritis and joint deterioration.

No available evidence suggests that NSAIDs are able to promote the healing process-

•       NSAIDs such as Ibuprofen, Piroxicam, Flurbiprofen and Indomethacin. One of the damaging side effects of NSAIDs is the inhibition of the healing process of soft tissues. The long term detrimental effects far outweigh the temporary positive effect of decreased pain.

•       NSAIDs inhibit proteoglycan synthesis –  a component of ligament and cartilage tissue regeneration and repair.

Non-steroidal anti-inflammatory drugs all inhibit release of prostaglandins and the healing process of soft tissues.

When a ligament or tendon is injured, prostaglandins are released which initiate vasodilation in non-injured blood vessels.

This enables healthy blood vessels to increase blood flow and immune cell flow to the injured area to begin the repair process.

The use of anti-inflammatories inhibits the release of prostaglandins thus ultimately decreasing the blood flow to the injured area.

Proteoglycans are essential for the elasticity and compressive stiffness of articular cartilage and suppression of their synthesis has significant adverse effects on the joint.

The key question regarding the healing of any injury is, “What exactly does any therapy do to the fibroblastic cells that actually grow the ligament and tendon tissue?” Treatments that stimulate fibroblast proliferation will cause ligament and tendon repair and will help with healing (Prolotherapy). Therapies that interfere with or destroy fibroblastic growth will be detrimental to the healing (NSAIDs)

Recently doctors reported that the use of NSAIDs prevented post-surgical healing,7 and as far back as 1995, in a classic study from the University of North Carolina, School of Medicine, Division of Orthopaedic Surgery, Sports Medicinesection found how detrimental NSAIDs use was in healing soft tissue. They separated study patients into groups:

•       Group I was the control in which no treatment was done;

•       Group II- the tendons were exercised;

•       Group III- the tendons were exercised and anti-inflamed with Indomethacin; and

•      

•       Group III- the tendons were exercised and anti-inflamed with Indomethacin; and

•       Group IV- the tendons were just anti-inflamed with the Indomethacin.

All the tendons underwent injury through repetitive motion, similar to what would happen to an athlete in training. Seventy-two hours after the injury, it was noted that compared to controls the only group that showed increased levels of prostaglandins (inflammation) was the exercised group. The group that was exercised and received the NSAID, as well as the NSAID group, had statistically significant lower levels of prostaglandins (specifically Prostaglandin E2) in the tendons.

•       This showed that the NSAID blocked the inflammatory healing.

•       The tendonitis that was treated with just the NSAID had almost no prostaglandins in the sample, signaling a complete inhibition of the inflammatory healing process.

The researchers also measured DNA synthesis in the fibroblasts (repair mechanism). This showed which fibroblasts were proliferating. Again, the exercised group was the only group that exhibited elevated levels of DNA synthesis in the fibroblasts. Compared to the control group there was 100 percent more growth of fibroblasts in the exercise group. The tendons treated with NSAIDs had no DNA synthesis noted.

This showed there was no fibroblastic growth occurring. The group that exercised and took the NSAID showed a little bit of growth. The paper also stated a fact that many researchers in this field are wondering, “Despite the lack of scientific data, NSAIDs are widely used, often as the mainstay of treatment.”  More than twenty years later – little has changed.

Bibliography –

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