Tag: Achilles tendon

Categories : Pain ManagementTags : 30/10/26Achilles tendonLeave a comment

Corticosteroid Achilles Injections Show no Meaningful Benefit over Placebo

On October 30, 2026October 30, 2026 By ModernMedia

Results suggest short lived benefit with steroid injections, but no sustained improvement and possible longer term harm 

Commonly used injections for Achilles tendinopathy – pain, stiffness and swelling in the Achilles tendon – offer no meaningful clinical advantage over placebo (sham) treatment, finds a clinical trial published by The BMJ.

The results show that high volume injections – delivering saline, local anaesthetic, and sometimes a low dose of corticosteroid around the Achilles tendon – did not improve pain and disability compared with sham injection at 12 months, and therefore do not support routine use.

Achilles tendinopathy is a leading cause of persistent lower limb pain that affects around 6% of people during their lives and disrupts everyday activities such as walking. While exercise based therapy is recommended, up to 44% of patients do not recover and many seek alternative options, including injection therapy.

Some data suggest that corticosteroid containing injections may provide short term symptom improvement, but the longer term clinical effects and cost effectiveness of high volume injections with or without corticosteroid remains uncertain.

To address this, researchers enrolled 192 adults (mean age 49; 55% male) with midportion Achilles tendinopathy from a radiology clinic in Melbourne, Australia between December 2019 and July 2022. Participants were randomly assigned to three groups: sham injection (64), high volume injection without corticosteroid (63), or high volume injection with corticosteroid (65).

All groups received the same exercise programme, education and activity modification advice.

The main outcome of interest was self-reported pain and disability at 52 weeks based on the Victoria Institute of Sport Assessment-Achilles (VISA_A) scale (0-100, where 100 is no pain or disability). Cost per quality-adjusted life-year (QALY) – a combined measure of quantity and quality of life – was also assessed.

At the start of the trial, participants reported moderate to high pain and disability (mean VISA-A score 48.7) and a median symptom duration of two years.

VISA-A data for 181 of 192 (94%) participants at 12 months showed no clear differences between sham and high volume injection either with or without corticosteroid, and between the two injections.

High volume injection with no corticosteroid showed no benefit over sham at any timepoint. High volume injection with corticosteroid provided small, short term improvements over sham at six weeks, but worse outcomes than high volume injection without corticosteroid at 26 weeks.

High volume injection with corticosteroid was more effective (QALYs gained) and less costly than sham, but the overall clinical findings do not support routine use. No serious trial related adverse events were recorded.

The authors acknowledge that they recruited participants primarily via social media, potentially limiting generalisability, they were unable to mask injection providers, and there is a risk that some effects may reflect chance rather than true treatment effects.

However, they say this evidence “should prompt clinicians to reconsider the rationale for using these injections in people with Achilles tendinopathy.”

Corticosteroids are neither all-good, nor all-bad and must be used only in the correct context (where short term needs predominate over longer term needs), says John Orchard at the University of Sydney in a linked editorial.

Crucially, he stresses that a patient should never be told that a corticosteroid will fix or cure a tendinopathy.

“All clinicians recommending or performing corticosteroid injections for tendinopathy need to understand this trade-off and make every effort to explain the broader overview to the patient as part of the informed consent process,” he concludes.

Source: BMJ Group

Categories : Pain ManagementTags : 18/2/26Achilles tendon

Scientists Find Hidden Trigger Behind Achilles Pain and Tennis Elbow

On February 18, 2026February 18, 2026 By ModernMedia

Complaints such as pain in the Achilles tendon, tennis elbow, swimmer’s shoulder and jumper’s knee are familiar to many young sportspeople, as well as to older individuals. These conditions are all caused by overloading of tendons and are generally very painful.

“Tendons are fundamentally susceptible to overuse,” explains Jess Snedeker, a professor of orthopaedic biomechanics at ETH Zurich and Balgrist University Hospital in Zurich. “They must withstand powerful loads, with all the forces of our muscles being concentrated to the relatively thin tendons that transmit these forces into movement of our skeleton.”

In medical terms, the aforementioned conditions are known as tendinopathies. They are some of the most frequent conditions seen by orthopaedic specialists, but treatment options are extremely limited. Although physiotherapy can help, there are many serious cases for which this treatment does not achieve much. Scientists are therefore keen to research these tendon problems in greater depth with a view to developing effective treatments.

Not just correlation – causation

Now, a team of researchers led by Snedeker and by Katrien De Bock, professor of exercise and health at ETH Zurich, has reached a new milestone. In the HIF1 protein, they have identified a central molecular driver of tendon problems of this kind. A part of HIF1 acts as a transcription factor, which controls the activity of genes in cells.

This protein was already known to be present at elevated levels in diseased tendons. However, it was unclear whether the increase was simply a concomitant phenomenon or whether the conditions are actually triggered by the protein. In experiments in mice and with tendon tissue from humans, the team of researchers has now shown the latter to be the case.

Treatment before it is too late

In mouse experiments, the researchers either activated the HIF1 protein permanently or switched it off completely. Whereas they observed tendon disease even without overloading in the mice with permanently activated HIF1, no tendon disease occurred in the mice if HIF1 was deactivated in tendons, even in the case of overloading.

Both in the mice and in the experiments with human tendon cells, which the researchers obtained from tendon surgeries at the hospital, they were able to show that elevated HIF1 levels in the tissue leads to a pathogenic remodelling of the tendons: More crosslinks form within the collagen fibres that make up the basic structure of the tendons.

“This makes the tendons more brittle and impairs their mechanical function,” explains Greta Moschini, a doctoral student in De Bock and Snedeker’s groups and lead author of the study. In addition, blood vessels and nerves growth into the tendon tissue. “This could be the explanation for the pain commonly observed in tendinopathy,” says Moschini.

“Our study not only provides new insight into how the disease develops. It also shows that it’s important to treat tendon problems early,” says Snedeker. He is thinking particularly of young athletes, who frequently struggle with tendinopathies. In these cases, it is often still possible to treat the problems. “However, the damage caused by HIF1 in tendon tissue can accumulate and become irreversible over time. Physiotherapy then no longer helps, and the only treatment at this moment is to surgically remove the diseased tendon.”

A starting point to search for treatments

The fact that HIF1 has now been identified as a molecular driver raises the question whether it is possible to develop medicines that deactivate HIF1 and therefore can prevent or cure tendon disease. It is not quite that easy, explains ETH Professor De Bock. In many organs of the body, HIF1 is responsible for detecting hypoxia and activating a physiological adaptation. “Switching HIF1 off throughout the body would likely lead to side effects,” she says.

It may be possible to look for methods that specifically deactivate HIF1 only in the tendon tissue. In De Bock’s view, however, the more promising approach would be to explore the biochemical processes around HIF1 in the cells in greater detail. This could help to identify other molecules that are influenced or controlled by HIF1 and that could be more suitable targets for the treatment of tendinopathy. The researchers will now embark on precisely that search.

Source: ETH Zurich