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NSAIDs | Why we don’t recommend chronic pain medications

Prolotherapy

Ross Hauser, MD

In this article, Ross Hauser MD explains why chronic NSAIDs use and their side-effects can be detrimental in helping the patient with chronic joint and back pain.

The American medical care system is focused on providing relief of symptoms rather than prevention or dealing with underlying causes. Thus when a patient presents with an acute sports injury, or chronic pain, the first thing they do is prescribe non-steroidal anti-inflammatory drugs (NSAIDs) under the assumption that quelling 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. In reality, nothing could be further from the truth. As every Prolotherapist (but apparently very few orthopedic and family physicians) knows, inflammation resulting from injury is an integral part of the healing process. So it may not be so wise to interfere with it.

Furthermore, no available evidence suggests that NSAIDS are able to promote the healing process independent of the body’s inflammatory reaction.

  • Nonsteroidal anti-inflammatory drugs (NSAIDS) include examples 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 have been shown in studies to produce short-term pain relief. The studies, however, also demonstrate the long-term damaging effects on healing and an acceleration of soft tissue degeneration.
  • NSAIDs inhibit proteoglycan synthesis, a component of ligament and cartilage tissue regeneration and repair.

Non-steroidal anti-inflammatory drugs all inhibit the healing process of soft tissues. The long term detrimental effects far outweigh the temporary positive effect of decreased pain. 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).

In spite of the widespread use of NSAIDs there is substantial evidence that they hamper soft tissue healing.

As far back as 1993, a study from the University of North Carolina, School of Medicine, Division of Orthopaedic Surgery, Sports Medicine section 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 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 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 of even the tendon injuries that were exercised or rehabilitated. 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 effect was even more pronounced at 108 hours.

The researchers also measured DNA synthesis in the fibroblasts. 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 Indomethacin 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 authors concluded, “Motion and prostaglandin release in Group II were associated with increased DNA synthesis. Inhibition of prostaglandin by Indomethacin also coincided with a decrease in DNA synthesis… Inhibition of prostaglandin synthesis, and thereby DNA synthesis, may not be desirable during the proliferative stage of a soft tissue injury, when DNA synthesis for cell division of fibroblasts is needed to heal the injury to the tendon.”

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.”1

The administration of NSAIDs, in combination with the RICE treatment, nearly eliminates the body’s ability to heal.

NSAIDs have been shown to delay and hamper the healing in all of the soft tissues, including muscles, ligaments, tendons, and cartilage. Anti-inflammatories can delay healing and delay it significantly, even in muscles with their tremendous blood supply. In one study on muscle strains, Piroxicam essentially wiped out the entire inflammatory proliferative phase of healing (days 0-4). At day two there were essentially no macrophages (cells that clean up the area) in the area and by day four after the muscle strain, there was very little muscle regeneration compared to the normal healing process. The muscle strength at this time was only about 40 percent of normal.2

Almekinders and his associates also confirmed the above, by showing that at day 28 after injury the muscle regenerative process was still delayed. The muscles of a group treated with Flurbiprofen (NSAID) were significantly weaker. The muscle fibers were shown under the microscope to have incomplete healing because of the medication.1

NSAIDs are the mainstay treatment for acute ligament and tendon injuries, yet efficacy in their usefulness is lacking.

What about ibuprofen

In a study in The Journal of Hand Surgery, it was found that the ibuprofen doses used in the study caused the strength of the flexor tendons to decrease. 3

NSAIDS decrease pain, but at the expense of diminishing the healing ability of the injured soft tissue

From the above studies, it is clear that NSAIDs inhibit the fibroblastic growth process and thus diminish the individual’s chance of healing. NSAIDs are used because they decrease pain, but they do so at the expense of hurting the healing of the injured soft tissue. A good example of this is a study on the use of Piroxicam in the treatment of acute ankle sprains in the Australian military.

Compared with the placebo group, the subjects treated with Piroxicam had less pain, were able to resume training more rapidly, were treated at lower cost, and were found to have increased exercise endurance on resumption of activity. At first glance in reviewing this study, NSAIDs appear to be great, but the real question is did they help the ligament injury heal? To test ligament healing the ankles were tested via the anterior drawer test. During this test the ankle was moved forward to determine the laxity in the ligaments. In this study at every date of testing after the initial injury, days three, seven, and fourteen, the Piroxicam-treated group demonstrated greater ligament instability. At the time of the initial injury the ligament instability in the Piroxicam group and the control group were exactly the same. This study showed that the NSAID stopped ligament healing, yet the person felt better. The authors noted, “This result is of concern in that it may reflect a paradoxically adverse effect of the NSAID-derived analgesia in allowing subjects to resume activity prematurely.”4

NSAIDS 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.

In our own research article The Acceleration of Articular Cartilage Degeneration in Osteoarthritis by Nonsteroidal Anti-inflammatory Drugs, we noted: “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.”5

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 OA.”6
  • “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’s climbing by 69%, hip replacements by 32% and spinal fusion surgeries increasing by 73%.”7
  • Another group investigated the association of non-steroidal anti-inflammatory drugs (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 risk of atrial fibrillation.8

Our research continues, “Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used drugs in the world for the treatment of osteoarthritis (OA) symptoms, and are taken by 20-30% of elderly people in developed countries. Because of the potential for significant side effects of these medications on the liver, stomach, gastrointestinal tract and heart, including death, treatment guidelines advise against their long-term use to treat OA. One of the best documented but lesser known long-term side effects of NSAIDs is their negative impact on articular cartilage.”5

The following human study demonstrates the impact of NSAIDs on the acceleration of the progression of OA of the knee and the radiological deterioration of joint space:

“After 1 year of treatment with indomethacin compared to placebo on 376 patients: the indomethacin group showed 47% progression of radiographic modifications of OA, while placebo demonstrated only 22%.” Of 170 available patients at the 3rd interim analysis, 40 of 85 receiving indomethacin had deteriorated compared to19 of 85 receiving placebo, a statistically significant difference. Indomethacin increased the rate of radiological deterioration of joint space in patients with OA of the knee.”9

Prolotherapy, because it stimulates inflammation, helps the body heal. Prolotherapy stops the arthritic process and helps eliminate the person’s chronic pain, often permanently. NSAIDs should not be taken while undergoing Prolotherapy because they inhibit the inflammation caused by the treatment. For that matter, anyone with chronic pain should seriously consider stopping NSAIDs and starting Prolotherapy.

1. Almekinders, L. An in vitro investigation into the effects of repetitive motion and nonsteroidal anti-inflammatory medication on human tendon fibroblasts. American Journal of Sports Medicine. 1995; 23:119-123.
2. Greene, J. Cost-conscious prescribing of nonsteroidal anti-inflammatory drugs for adults with arthritis. Archives of Internal Medicine. 1992; 152:1995-2002.
3. Kulick, M. Oral ibuprofen: evaluation of its effect on peritendinous adhesions and the breaking strength of a tenorrhaphy. The Journal of Hand Surgery. 1986; 11A:100-119.
4. Slatyer, M. A randomized controlled trial of Piroxicam in the management of acute ankle sprain in Australian regular army recruits. American Journal of Sports Medicine. 1997; 25:544-553.
5. Hauser RA. The Acceleration of Articular Cartilage Degeneration in Osteoarthritis by Nonsteroidal Anti-inflammatory Drugs. Journal of Prolotherapy. 2010; 1(2):305-322.
6. Hochberg MC, Perlmutter DL, Hudson JI, Altman RD. Preferences in the management of osteoarthritis of the hip and knee: results of a survey of community-based rheumatologists in the United States. Arthritis Care Res. 1996;9(3):170–176.
7. Merrill C, Elixhauser A. Hospital stays involving musculoskeletal procedures, 1997–2005: statistical brief #34. Healthcare Cost and Utilization Project (HCUP) Statistical Briefs. 2006 MD, USA.
8. Krijthe BP, Heeringa J, Hofman A, Franco OH, Stricher BH. Non-steroidal anti-inflammatory drugs and the risk of atrial fibrillation: a population-based follow-up study. BMJ Open. 2014; 4(4): doi:10.1136/bmjopen-2013-004059
9. Huskisson EC, Berry H, Gishen P, Jubb RW, Whitehead J. Effects of antiinflammatory drugs on the progression of osteoarthritis of the knee. LINK study group. longitudinal investigation of nonsteroidal antiinflammatory drugs in knee osteoarthritis. J. Rheumatol. 1995;22(10):1941–1946.

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