Anti-inflammatories may not help tendon injuries

NewsBot · Feb 18, 2006

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Reuters are reporting:
Anti-inflammatories may not help tendon injuries
Fri Feb 17, 2006 03:35 PM ET

NEW YORK (Reuters Health) - Anti-inflammatory painkillers like ibuprofen and naproxen may be ineffective in many cases of tendon injury, according to researchers.

Pain relievers known collectively as nonsteroidal anti-inflammatory drugs, or NSAIDs, are often used to treat sore muscles and joints because the body's inflammatory reaction to injury contributes to pain.

However, UK researchers write in a new report, there is no reason to believe that NSAIDs aid tendon injuries known as tendinopathy.

Tendinopathy is a general term for disorders of the tendons, bands of fibrous tissue that connect muscle to bone. The Achilles tendon, tendons in the shoulder and the patellar tendon in the kneecap are commonly affected areas.

While the initial injury that leads to these tendon problems may involve inflammation in the first several days, there is no evidence of ongoing inflammation in chronic tendinopathy. Nor is there evidence that NSAIDs are an effective therapy, according to Drs. Merzesh Magra and Nicola Maffulli of Keele University School of Medicine in Hartshill.

"The available evidence would suggest that in the absence of an overt inflammatory process, there is no rational basis for the use of NSAIDs in chronic tendinopathy," the researchers write in the Clinical Journal of Sports Medicine.

What's more, while NSAIDs may bring some pain relief from tendinopathy, there's no evidence that they aid the healing process -- and they may, in fact, hinder it, according to Magra and Maffulli.

Lab research suggests, for example, that while NSAIDs decrease certain inflammatory chemicals, they may increase the production of substances called leukotrienes that could actually further damage the tendon.

Unfortunately, it's hard for doctors, let alone patients, to tell whether an injury is tendinopathy or an inflammatory injury that might be helped by NSAIDs, according to Maffulli.

So the "simplest advice," he told Reuters Health, is to use an analgesic that does not act as an anti-inflammatory, like acetaminophen, the active ingredient in Tylenol and some other brand names.

A visit to the doctor is the best course of action, according to Maffulli, though tendinopathy can be difficult to discern, and many physicians may end up prescribing an NSAID anyway.

But a trip to the physician can open up other therapy options as well. According to Maffulli, tactics that have been shown to help at least some types of tendinopathy include strengthening exercises and topical glyceryl trinitrate patches.

Doctors also often use injections of cortisone, an anti-inflammatory drug. But, Maffulli said, cortisone has the same issues as NSAIDs, and there is evidence that the injections can make tendons more vulnerable to rupture.
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Atlas · Feb 18, 2006

Mechanical problems have mechanical solutions.

NewsBot · Feb 1, 2019

Oral Ibuprofen Interferes with Cellular Healing Responses in a Murine Model of Achilles Tendinopathy
Adam Bittermann et al
J Musculoskelet Disord Treat. 2018; 4(2): 049.

Background:
The attempted healing of tendon after acute injury (overloading, partial tear or complete rupture) proceeds via the normal wound healing cascade involving hemostasis, inflammation, matrix synthesis and matrix remodeling. Depending on the degree of trauma and the nature of the post-injury milieu, a variable degree of healing and recovery of function occurs. Post-injury analgesia is often achieved with NSAIDs such as Ibuprofen, however there is increasing evidence that NSAID usage may interfere with the healing process. This study aimed to investigate the cellular mechanism by which IBU therapy might lead to a worsening of tendon pathology.

Methods:
We have examined the effect of oral Ibuprofen, on Achilles tendon healing in a TGFb1-induced murine tendinopathy model. Dosing was started 3 days after initial injury (acute cellular response phase) and continued for 22 days or started at 9 days after injury (transition to matrix regeneration phase) and given for 16 days. Cellular changes in tendon and surrounding peritenon were assessed using Hematoxylin/Eosin, chondroid accumulation with Safranin O and anti-aggrecan immunohistochemistry, and neo-vessel formation with GSI Lectin histochemistry. Markers of inflammation included histochemical localization of hyaluronan, immunohistochemistry of heavy chain 1 and TNFα-stimulated glycoprotein-6 (TSG6). Cell responses were further examined by RT-qPCR of 84 NFκB target genes and 84 wound healing genes. Biomechanical properties of tendons were evaluated by tensile testing.

Results:
At a clinically-relevant dosage, Ibuprofen prevented the process of remodeling/removal of the inflammatory matrix components, hyaluronan, HC1 and TSG6. Furthermore, the aberrant matrix remodeling was accompanied by activation at day 28 of genes (Col1a2, Col5a3, Plat, Ccl12, Itga4, Stat3, Vegfa, Mif, Col4a1, Rhoa, Relb, F8, Cxcl9, Lta, Ltb, Ccl12, Cdkn1a, Ccl22, Sele, Cd80), which were not activated at any time without the drug, and so appear most likely to be involved in the pathology. Of these, Vegfa, Col4a1, F8, Cxcl9 and Sele, have been shown to play a role in vascular remodeling, consistent with the appearance at 25 days of vasculogenic cell groups in the peritenon and fat pad stroma surrounding the Achilles of the drug-dosed mice. Tensile stiffness (p = 0.004) and elastic modulus (p = 0.012) were both decreased (relative to age-matched uninjured and non-dosed mice) in mice dosed with Ibuprofen from day 3 to day 25, whether injured or not.

Conclusion:
We conclude that the use of Ibuprofen for pain relief during inflammatory phases of tendinopathy, might interfere with the normal processes of extracellular matrix remodeling and cellular control of expression of inflammatory and wound healing genes. It is proposed that the known COX2-mediated anti-inflammatory effect of ibuprofen has detrimental effects on the turnover of a pro-inflammatory HA matrix produced in response to soft-tissue injury, thus preventing the switch to cellular responses associated with functional matrix remodeling and eventual healing.
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NewsBot · Mar 22, 2021

No Additive Clinical or Physiological Effects of Short-term Anti-inflammatory Treatment to Physical Rehabilitation in the Early Phase of Human Achilles Tendinopathy: A Randomized Controlled Trial
Nikolaj M. Malmgaard-Clausen, MD, Oscar H. Jørgensen, BSc, Rikke Høffner, PT, MSc, ...
The American Journal of Sports Medicine March 15, 2021

Background:
Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in the treatment of Achilles tendinopathy, but whether they have any additive clinical effect on physical rehabilitation in the early phase of tendinopathy remains unknown.

Purpose/Hypothesis:
To investigate whether an initial short-term NSAID treatment added to a physical rehabilitation program in the early phase of Achilles tendinopathy would have an additive effect. We hypothesized that the combination of NSAID and rehabilitation would be superior to rehabilitation alone.

Study Design:
Randomized controlled trial; Level of evidence, 1.

Methods:
A total of 69 patients with early phase Achilles tendinopathy (lasting <3 months) were randomly assigned to either a naproxen group (7 days of treatment; 500 mg twice daily; n = 34) or a placebo group (7 days of placebo treatment; n = 35). Both groups received an identical 12-week physical rehabilitation program. The clinical outcome of the study was evaluated using the Victorian Institute of Sports Assessment–Achilles (VISA-A) questionnaire and a numerical rating scale (NRS), and the physiological outcome was evaluated using ultrasonography, magnetic resonance imaging (MRI), and ultra-short time to echo T2* mapping MRI (UTE T2* MRI). Follow-up was performed at 1 week, 3 months, and 1 year. Time effects are presented as mean difference ± SEM.

Results:
No significant differences were found between the 2 treatment groups for any of the outcome measures at any time point (P > .05). For the VISA-A score, a significant time effect was observed between baseline and 3-month follow-up (14.9 ± 2.3; P < .0001), and at 1-year follow-up, additional improvements were observed (6.1 ± 2.3; P < .01). Furthermore, the change in VISA-A score between baseline and 3-month follow-up was greater in patients with very short symptom duration (<1 month) at baseline compared with patients who had longer symptom duration (>2 months) (interaction between groups, 11.7 ± 4.2; P < .01). Despite clinical improvements, total weekly physical activity remained lower compared with preinjury levels at 3 months (–2.7 ± 0.5 h/wk; P < .0001) and 1 year (–3.0 ± 0.5 h/wk; P < .0001). At baseline, ultrasonography showed increased thickness (0.12 ± 0.03 cm; P < .0001) and vascularity (0.3 ± 0.1 cm2; P < .005) on the tendinopathic side compared with the contralateral side, but no changes over time were observed for ultrasonography, MRI, or UTE T2* MRI results.

Conclusion:
Clinical symptoms in early tendinopathy improved with physical rehabilitation, but this improvement was not augmented with the addition of NSAID treatment. Furthermore, this clinical recovery occurred in the absence of any measurable structural alterations. Finally, clinical improvements after a physical rehabilitation program were greater in patients with very short symptom duration compared with patients who had longer symptom duration.
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