Green tea and tendinopathy – should we be recommending it?

Peter Malliaras6th of March 2016home / blog / tendinopathy-updates / green-tea-and-tendinopathy-should-we-be-recommending-it

Hi all,

Welcome to tendinopathy blog 10. Have been learning lots from Ben Cormack (@CorKinetic) on his Functional Therapeutic Movement course, hosted at our clinic this weekend, great stuff.

This week I will email subscribers a powerpoint lecture with audio recording of a simplified view of tendon management – how to identify key elements, not to sweat the minutia, but also not ignore the complexity! Subscribe if you would like to receive it.

Here are links to Lower Limb Tendinopathy Courses in Melbourne, Perth over the next few weeks, and June in the UK.

Until next time, keep joining the dots



Let them have green tea!

What they did: Vieira et al. investigate the effects of green tea and glycine in tendon healing in rats. They argue that ‘Green tea (GT) (Camellia sinensis) has been widely used for therapeutic purposes due to its beneficial properties, including antimuta-genic, antidiabetic, anti-inflammatory and antioxidant effects’ (e.g. Sharangi 2009). The mechanisms are thought to be inhibition of TNF-a synthesis and other cytokines involved in inflammation - some of these cytokines are also involved in tendon pathology (e.g. Cao 2007), so we can see the rationale for use in tendinopathy. Glycine is the most prevalent amino acid in the collagen triple helix and 5% glycine supplementation has been shown to improve collagen organisation in tendon pathology in rats (Vieira 2015). For these reasons the authors sought to investigate the effects of GT + glycine supplementation on tendon pathology in rats.

The right Achilles tendon of a group of rats was injected with collagenase (an enzyme that breaks down collagen) to induce tendon pathology. Rats were then divided into groups that had nothing vs GT vs GT + Glycine for 7 or 21 days – this made 6 groups in total. There was also a control group that did not have the collagenase induced tendon pathology. 700mg/kg/day of GT extract was given orally, and 5% glycine diet introduced into the relevant groups. After the 7 or 21 days of diet supplementation animals Achilles tendons were removed and the structure and biomechanics as well as some biochemcials in the tissue were investigated.

What they found: Hydroxiproline is an amino acid that helps to stabilise the collagen triple helix. In this study it was used as a marker of collagen concentration. As seen in the graph below it was consistently elevated after both 7 and 21 days of GT treatment (C: control group; G1: tendinitis in seven days; G2: tendinitis supplied with green tea; G3: tendinitis supplied with green tea and glycine diet in seven days; G4: tendinitis in 21 days group; G5: tendinitis supplied with green tea in 21 days and G6: tendinitis supplied with green tea and glycine diet in 21 days). There were also some reported improvement in tendon structure and organisation (under polarised light microscope) at 7 day follow up ie improved with GT and improved even further with GT+glycine. By 21 days the no supplement group had caught up. Biomechanical tests on the rat Achilles demonstrated increased tensile strength but only in 1 group – the group with GT supplementation for 21 days versus the group with no supplementation for 21 days.

 Screen Shot 2016-09-08 at 11.28.41 am.png

Clinical interpretation: This study suggests that maybe the mechanism of green tea and glycine supplementation are related to the tissue. The authors suggest that perhaps the GT effect on cytokines such as TNFa slow down matrix degradation and explain the positive effects in this study. The interest in green tea probably stems from the paper by Fallon et al. where they propose the polypill of ibuprofen (400mg 3x/day) and doxycycline (100mg per day). Doxycycline mainly for its anti TNF effects and ibuprofen to inhibit PGE2 that may also drive enzymes that break down the matrix. They also in passing suggest green tea and omega 3 fatty acids because of their reported anti-TNFa actions.

Obvious limitations are that it is a collagenase induced tendinopathy (the authors refer to it as tendinitis) so it is surely different to human load induced tendinopathy. So far there are no human data on green efficacy and mechanisms in treating tendinopathy. Perhaps the mechanisms are related to changing tendon structure or biochemicals? Or maybe obscure mechansims via systemic inflammation and reducing pain sensitivity? Or maybe placebo? Regardless there is no harm in green tea extracts (more the better presumably). What you must do as a minimum is screen patient expectations regarding supplements and at least give it to the the ones who believe most in it’s effects!


Are statins harmful for tendon?

What they did: Teichtahl et al. have reviewed evidence for statin involvement in tendinopathy. Definitely a worthy topic because there is that association in many clinicians and patients’ minds – ie statins cause or at least contribute to tendon injury.  So what is the truth? They conducted a systematic review according to the 2009 PRISMA statement and included studies that reported a comparison of a tendinopathy outcome between participants exposed to statins and those not exposed to statins. They included randomised controlled trials and cross-sectional, cohort or case-control studies. The level of evidence of studies was determined in conjunction with the quality score calculated for each study (see box below). ’The Bradford-Hill criteria were used to determine whether there was adequate evidence of causal relationship between statin use (the risk factor) and tendinopathy (the disease).

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What they found: They identified 3 cohort studies and 1 case-control study that were eligible for inclusion. Tendon rupture was the primary outcome in 3 studies and rotator cuff disease in 1 study. Exposure to statins varied from the preceding 12 months, to atleast 12 months and a minimum of 28 days in 1 study. Three of the four studies were considered to be high quality. In the largest cohort study (34,749 participants) there was no association between statin use and tendon rupture. The smallest study reported an association between tendon rupture and statin therapy in women but based on small numbers. Another study reported a trend of association between spontaneous distal biceps tendon rupture and statin therapy, but the direction of the result was changed when age was taken into account in a multivariate model. Two studies found that simvastatin was protective against rupture or rotator cuff disease. Overall, the best evidence synthesis indicated limited evidence to conclude there was no association between statin therapy and tendon rupture. There was strong evidence that simvastatin was associated with a reduced risk of tendon rupture or rotator cuff disease.

The authors also found, ‘at best, weak evidence for a cause effect relationship (based on Bradford-Hill criteria- see below). And go on to say that ‘the paucity of data in this field makes adequate interpretation of the Bradford Hill criteria difficult.’

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Clinical interpretation: Overall, although data are limited, it is unlikely that statin has a causative mechanism on tendon rupture/tendinopathy. Two of the largest studies showed the opposite – statin use was protective. These authors excluded case reports and case series that tend to suggest a link between statin use and tendon disease/rupture – this is where a lot of the bad press probably comes from. The biggest likely confounder in the relationship between statin use and tendon pathology/rupture is the fact that people that take statins take them because of elevated lipid levels, and we know that lipid imbalance is a risk factor for tendon disease (Tilley 2015). As Gaida et al. has put it (in a response to a letter about this paper), ‘persons prescribed a statin have, in all likelihood, had abnormal lipids for many years. Over time, this may have adversely affected the tendons of these people before taking their first tablet.’ So maybe let them have statins too, it may do them some good!


Plantaris and medial Achilles pain

What they did: Masci et al. included 18 patients with midportion Achilles symptoms (5 with bilateral so N = 23 tendons) referred for surgical opinion. They assessed tenderness and site of pain, as well as ultrasound (gray scale and Doppler) and Ultrasound Tissue Characterisation (UTC). UTC discriminates 4 different echo-types: ‘Type I pixels (green) represent intact, continuous and aligned collagen bundles (fibres and fascic- uli); type II (blue) indicates less continuous and/or more swollen and/or more wavy collagen bundles (fibres and fasciculi); type III (red) is generated by disintegration with ten- don tissue replaced by mainly disorganised, fibrillar matrix; type IV (black) is generated by complete disintegration with tendon tissue replaced by an amorphous matrix and fluid’. They then performed surgery including plantaris excision (soleus muscle tendon junction to calcaneum) and scrapping of the anterior Achilles tendon.

What they found: A plantaris tendon was identified in ALL patients at surgery. In 21 it was in close proximity to the medial side of the Achilles tendon midportion, with richly vascularised fatty tissue between them (see figure below - left). In two cases the plantaris tendon invaginated the medial Achilles tendon. There was activity related pain and tenderness specifically at the medial Achilles tendon in 20/23 (activities that bought on pain are not discussed). On US the plantaris was seen in 20/23 cases and there was medial Achilles hypoechoic changes/Doppler flow (see figure below - centre) (the remaining 3 had these changes on the medial and lateral side). On UTC 19/23 tendons were focally disorganised (grade 3 or 4) on the medial side (see images below - right) (the remaining 4 had these changes on the medial and lateral side).

 Screen Shot 2016-09-08 at 11.29.23 am.png

Clinical interpretation: These authors show that in their case series medial Achilles pain/tenderness is associated with pathology that may be related to plantaris involvement (they define the imaging presentation nicely) – ie medial Achilles pathology. They suggest the plantaris compresses the medial Achilles, which is plausible. It is also possible that there are other reasons, such as increased load on the medial Achilles tendon, that explain this pain/pathology site presentation. Key points are 1) consider plantaris with medial sided Achilles pain and 2) US can be used to visualise plantaris and UTC is better for objectively assessing adjacent medial Achilles structural changes (UTC cannot visualise the plantaris).

A consideration is that we can have medial Achilles pain that is not related to plantaris involvement (e.g. localised medial paratenon pain). And of course sometimes the pathology features described in this study may be asymptomatic. But I know this study was not assessing the diagnostic utility of medial Achilles pain/tenderness. Another important consideration is how does knowing there is a plantaris component change our management? Surgery is one option (Masci 2015), some will respond to good rehab and conservative management…a story for another time. And there are also questions about how common plantaris involvement is. I see mainly tertiary referrals and I do see it but in no more than 5-10% of Achilles cases. Lorenzo Masci and Hakan Alfredson have great expertise in this area so they may see more.

As always, look forward to comments and discussion


Peter Malliaras
Tendinopathy Rehabilitation