The 3rd International Scientific Tendon Symposium Oxford (UK) 2014

I would like to welcome a fantastic clinical academic, Seth O’Neil, to the biomechanics blog. He is doing some fantastic research related to the management of Achilles Tendinopathy, and until I met him recently in the UK, based on twitter I actually thought he was an Achilles tendon (see twitter handle). With some assistance from @Peter_Gettings and @oliw_physio Seth has provided us all with an amazing summary of the tendon symposium. After putting this together, I felt like I was there! I think we all owe them a beer, and I look forward to some great research output going forward.

I will now pass it over to Seth ……….

This was my first major conference and quite daunting. The conference attendance list read like a “who’s who” of tendon research (oh yeah and a few tendon geeks off twitter, me included). There were over 200 attendees with the organisers planning for 80!! I think part of this was probably the European location and also the tendon-geek chats on twitter and various podcasters increasing awareness of the event. One of my favourite pre-conference elements was the hashtag vote on twitter- great fun, loved #TendonMania2014 shame it didn’t win.

There were 115 posters submitted to the conference and all 115 abstracts can be found here, many of the posters can be viewed by having a check through my feed from the 5th and 6th of September or viewing #Tendons2014 on twitter. In case you don’t know how to do that – open the search and type in #Tendons2014.

So let’s get to the main event itself – view full program

You will notice the conference lay out was a mix of plenary speakers (see their biogs here) interspersed by podium presentations from researchers. Abstracts presented by each speaker are linked to their names during the below discussions. Where know, speaker twitter handles have also been included to help facilitate further discussion.

Rather than blindly report what was said I have tried to play devil’s advocate and ask questions for some of the talks I could understand. These are not “digs” at anyone but rather my brain trying to make sense of findings or linking with other literature.


George Murrell’s plenary talk on aetiology of tendinopathy

This talk was predominately about the Shoulder and rotator cuff pathology and if there is one thing to take away from ISTS2014 it’s that the upper limb (especially shoulder) is a very different beast to the lower limb. Clinically we see far more central changes with widespread pain, there is also much more reserve capacity in the shoulder where other muscles/tendons can compensate for functional deficits in another. This talk suggested shoulder laxity in swimmers was not associated with tendinopathy, but tendinopathy was likely to result in positive impingement signs.

George then went on to explain how overuse/tendon stress alters protein kinases which in turn increases apoptosis (programmed cell death), eventually leading to tendinopathy. It appears that stress induces hypoxia, which switches on collagen type III genes. This leads to a loss of collagen matrix and many of the characteristics of tendinopathy.

His talk got the conference off to a good start and encouraged questions from the basic cellular scientists and the clinical groups present, this interaction was exceptionally useful and provided some interesting discussions. Check the twitter feed for questions and responses.


Podium session on risk factors and UTC imaging

George’s talk was followed by 6 podium presentations by researchers. This included 4 presentations using UTC.

  1. Astrid De Vries presented data on a survey completed in basketball players to explore patellar Tendinopathy risk factors. The key clinical message here was male subjects who participated in heavy work were the highest risk for Patella tendinopathy. Interestingly load related data appeared not to link but this may be due to difficulties with measuring load (see roald Bahrs BJSM commentary and work on jumping levels in volleyball).
  2. Lorenzo Masci  (@lorenzo_masci) presented a study showing Plantaris involvement in mid-tendon tendinopathy using UTC. This involved some lovely images prior to patients undergoing surgery by Hakan Alfredson. Lorenzo clearly highlighted that Plantaris appears to be present in all of us, despite some of the old medical text books suggesting otherwise. I can certainly vouch for that as we see it in all of our cadaveric dissections except where the students have been “heavy handed”. The suggestion is that pain may arise from the fat pad between Plantaris and the Achilles tendon.
  3. Lorenzo Masci had another abstract which showed how the tendon recovered after Hakan Alfredson’s surgical scraping. There were some great clinical tips here with clinical signs reported as sudden onset of medial pain, recurrent pain, different to usual tendon type pain and occasionally associated with flicking sensations around the medial aspect. The Monash clinical session on Sunday highlighted that the pain may be felt a little higher up than normal mid-tendon tendinopathy. The MONSTERS (Monash) guys suggested that treatment should be like an insertional tendinopathy avoiding end range dorsiflexion.

My too pennies is can we be sure Plantaris is causing compression of the medial portion of the tendon or could the medial portion be receiving extra tensile load leading to the development of tendon changes?

We already know that Plantaris anatomy is highly varied and this may help explain why some people go on to develop a problem and may be worth considering in prospective studies that use US or UTC scanning.

Also it’s worth considering the role of Plantaris, the tendon has more Golgi tendon organs per area than any other tendon, suggesting it may have an important proprioceptive role. Does something go wrong with this prior to onset of symptoms allowing the person to stay in more dorsiflexion?

  1. Sean Docking (@SIDocking) was next and talked about Donuts (see pic here). Actually it was UTC and the Monash guys describe the viable tendon as the donut and tendinopathic region as the hole) suggested that tendon size increases with tendon disorganisation in an attempt to maintain adequate levels of aligned fibres. A nice logical explanation showing tendons can adapt and they do this not by remodelling the “hole” but by increased the “donut” (healthy tendon fibrils).
  2. Mathijis Van Ark used UTC to measure tendon change during a 5 day Volleyball competition with players playing around 8 games during this time. His study showed that UTC characterized content did change but this was not statistically significant. The change in echo patterns only occurred in those with pre-existing changes suggesting that prior changes increase susceptibility to future changes. However, this study did not measure player loading as suggested recently by Roald Bahr (some players jump huge volumes whist others do not).
  3. Noel Pollock (@DrNoelPollock) presented the 4th of the UTC presentations, using it to monitor elite UK track and field athletes. Noel highlighted that there is a steep learning curve with UTC and it has taken them a while to determine exactly what they are doing. This study monitored the percentage of echo types in the tendon in female and male participants. The results showed a difference in UTC echotype between males and females, potentially explained by oestrogens influence on tendon health. However they found no difference between symptomatic tendons (or previously symptomatic tendons) and non-symptomatic tendons. This study raised some important questions about UTC and how good it is at distinguishing between those with and without pain. However we must remember the measures were of a very large area of the tendon (from calcaneus to soleus insertion) and averaged out the percentage of the various echo types. It would be interesting to know what the AP diameter or cross sectional area (CSA) was as this may be more relevant – Sean Docking’s earlier talk.


Paul Ackermann’s plenary talk about pain therapies

Paul brought up some contentious issues about the location of neural ingrowth, suggesting it was intratendon, with justification based on animal modelling involving surgical induced tendinopathy or rupture. Hakan Alfredson disagreed during the question time suggesting it is really in the paratenon, which seemed to be the general consensus of the audience. There was a detailed explanation of the chemical cascade linked to neural ingrowth, and up-regulation of various genes and chemicals like glutamate. Paul talked briefly about the effect of eccentrics on the neural system, but is it only eccentrics that influence this? Probably not. He briefly mentioned central sensitisation, and you could hear all the physios hold their breath, unfortunately this was not expanded upon. One of his main clinical comments was the suggestion that shockwave therapy denervates the tendon! This offers at least one mechanism for the clinically observed effects. He went on to highlight the possible involvement of Nitric oxide and Mg2+ blockers but the clinical application of these as treatment interventions needs further modelling. He went on to suggest a role of Epsom salts as a possible intervention to effect block MG2+ receptors and also ketamine as a pain reliever but neither myself or @oliw_physiocan recall the exact mechanism of effect.


Podium session on cell biology, tendinopathy incidence and gene variants….

  1. Peter Clegg looked at Transriptomic signatures of tendon ageing.  In aging many genes are down-regulated but few are up-regulated. Peter’s work showed that aging appears to alter protein isoforms in the tendon linked to degradation, cytokines and growth factors. Some elements are up-regulated some down regulated.
  2. Stephanie Dakin looked at the diversity of macrophage signatures across a spectrum of supraspinatus pathology. Basically this work showed increased macrophages in tendinopathic tissue and supported inflammatory type changes but this is not known/found in the Achilles/patella so may be the key is RC tendinopathy is different from lower limb. Further research is clearly needed.
  3. Sophie Albers looked at the incidence and prevalence of lower extremity tendinopathy in the general population. This was a nice presentation based on a survey of Dutch GP’s. The study used computer coding but also case notes to cross match diagnosis. Whilst this approach cannot be 100% accurate the study does highlight that in the general population lateral hip pain seems to be most prevalent closely followed by Achilles Tendinopathy and plantar fasciopathy. Anyone interested in recreating this study in the UK? l
  4. Michael Posthumus  presented some work by Louis on the COL5A1 gene and risk of Achilles tendon pathology in a British Cohort. The study showed that it COL5A1 gene is associated with male tendinopathy and not female the reason for this is unknown.


Malcom Collins’ plenary talk on genetics of Tendinopathy: Translation of basic science

This presentation for me was fantastic, a stand out performance by a polished presenter. Most importantly he made the information clinically relevant and accessible to all despite its complex nature. One of the scary parts of his talk was the fact that some companies are offering genetic testing for the general population despite the fact this data does not yet predict risk!! It can only be a matter of time before we start seeing people turning up in our clinics with this information so be prepared to explain how this does/does not link to problems. His main take home message was that tendinopathy is a multifactorial disease. He also highlighted that they are currently studying whether this can predict injury (ACL cohort).


Britt Wildemann’s plenary talk on Cell biology and growth factors

Britt highlighted that fatty infiltration of muscle alters collagen I production and cell proliferation and that BMP 2 and 7 stimulate tendon healing/growth. This was quite cell/biology based talk but offered some interesting discussions about how this may transfer to clinical work. During question time a member of the audience pointed out how the dosages in this work are huge and not possible in vivo and there may be issues with Osteogenesis.


Podium session focussed on the cells and chemical influences

  1. Chavaunne Thorps looked at the characterisation of the proteome of the tendon interfascicular matrix. This talk highlighted that tendons also allow interfascicular sliding not just stretching of fibrils. They also showed clusters of various proteins (including type III collagen) within the interfasicular space. Their work supported later work showing that there is an increased number of cells within the interfascicular space.
  2. Margaret Smith looked at the effects of high glucose and metformin on tendon explants: a role for fibrosis in tendinopathy. This was a great talk. As we know in human studies that Diabetes seems to link to tendinopathy but we do not yet understand why. Margaret showed us the background work regarding advanced glycation end products AGES (further info) and their effects on collagen. This work showed that the effects of stress deprivation were profound with effects on all collagen modification enzymes whilst increased glucose levels provided a similar response. The work then went on to administer Metformin and showed this prevented much of the negative consequences of unloading or glucose levels. Further work is ongoing but this looks promising. Interesting to read about versican in the abstract and how it may be important for interfasciular sliding, this is something that may explain some of the issues associated with GAG/PG changes in tendinopathy.
  3. Rouhollah Mousavizadeh reported on Angiopoietin like 4, a novel mechanoresponse protein involved in tendinopathy. This talk was very cell biology based and showed how mechanical strain may influence angiogenic activity. The clinical application of this to our load based treatments needs further investigation.
  4. Ewa Spiesz reported on early inflammatory response of tenocytes to overload. This study supported the fact that cells appear to concentrate in the interfascicular spaces rather than within fascicles. Loading induced rapid remodelling (cell reactions) within the Interfacisicular spaces.  It would be interesting to know whether these cells migrate into the fascicles proper? This may be a good question for @tendonresearch and @DrMobs as its too advanced for my understanding and knowledge of the area). In summary the interfasicular matrix appears to be very rich in cells and show acute response to load involving inflammatory components, but as @tendonpain so eloquently tweeted at the time “what does the term inflammation mean? Cells?, Substances?, Cascade?, Vessels?”


James Wang’s plenary talk on Tendon Stem/Progenitor cell and its role in the development of degenerative tendinopathy

Overall this was a highly interesting talk but also served to highlight how little we know about stem cells and whether these techniques might work in humans!


Off to posters and Dinner

Check out the abstracts on the BJSM website as there are some really interesting studies there, I tweeted pics of a good few that I managed to get around early on prior to the proper poster presentations, to see these check the #tendons2014 for these.



Day 2

Nelly Andarawis Puri’s plenary presentation on promoting repair in fatigue damages tendons

The key messages were that collagen altered with loading, and that with moderate loading tendon stiffness dropped by 20%. Her other key messages were increased “damage” led to alterations in gene expression especially MMP2, and that a sedentary lifestyle was as harmful for tendons as unaccustomed activity. This loss of tendon stiffness remained a debatable element and there was some discussion about how this was measured- it was somewhat unclear.


Liz Laird’s plenary presentation on synthesis and assembly of the collagenous extracellular matrix in tendon

This talk really got down to the finer detail of interfasciular bundles within tendons but was, for obvious reasons, focussed on animal tissue. It would be superb to see this detail in human tendons.  She included some stunning pictures of tendons (check my timeline for these) and abstract 64. Again this talk highlighted that cells are much more abundant in the interfasicular space when compared with the fascicule. Unfortunately this data was largely derived from rat tails and not energy storage tendons, however it was supported by others work later. During the tweeting for this talk the speakers explained that the animals had no symptoms but Jamie Gaida (@tendonresearch) pointed out Mice/rats (prey animals) will not limp when observed, but if using hidden cameras they will. This made some of the findings possibly incorrect.


Podium session on cell biology

  1. Daniel Rowson presented on primary cilia in tenocytes from the inter-fascicular matrix and the fascicular matrix. This talk was about cilia on the end of tenocytes and how they can change cilia length. No direct clinical application at present but may explain how tenocytes are sensitive to mechanical stimulus?
  2. Maria kuzma-Kuzniarska presented on in vitro and ex vivo assessment of gap junction function in the tendon using a complex technique of fluorescence recovery after photobleaching or FRAP for short. This study highlighted that tenocytes respond to load by reducing gap junction communication. Have a look at the abstract.


Graham Riley’s plenary presentation on mechanotransduction- the tenocyte and its response to strain in the stressful environment

Interestingly a few of his early slides showed the strain in the human Achilles tendon versus horse (see Table below). Superficial digital flexor tendon (SDFT) tendon: You will notice that human load is greater than much of the measures in horses.

Human Achilles Horse SDFT
Max Load 9,000 Newtons (12.5x BW) 7500-12400 Newtons
Peak Strain 7.5-9.9% 12-17%
Peak Stress 59(walk) – 111 (run) MPa 65-109MPa

Graham’s main point was despite knowing the load we do not know the load on the tenocyte. He went on to explain that many of the studies applying load to tenocytes (including his own) effectively pluck a number out of the air and use that. Obviously this raises some potential doubts about the accuracy of these studies.


Roger Smith’s plenary presentation on stem cell therapy for tendinopathy – What’s the evidence from animal models?

An interesting and stimulating look at the research completed by Roger Smith and his team using Stem cells.. Again this talk highlighted the hypercellular nature of tendinopathic tissue. Their horse data shows fibrosis and increased tendon stiffness. Is this what we see in humans? Is there a consensus on whether tendinopathic tissue has increased/decreased stiffness in humans yet, your thoughts? Roger’s stem cell studies show some good promise in horses but caution is needed prior to human studies, especially since they use bone marrow stem cells which may revert to type and lead to osteogensis within tendons (this was according to some other experts in the audience). He did report they have not seen this in their studies.


Podium presentation on clinical interventions, diagnosis and biomechanics

  1. Peter Malliaris (@DrPeteMalliaras) presented on high volume injection, platelet rich plasma and placebo in chronic Achilles tendinopathy – a double blind prospective study. Pete presented data on an RCT that showed HVI to have better clinical outcomes short term, whilst PRP and HVI were comparable in the longer term. Both were superior to placebo. This was a nice study and timely. I would love to see a sham placebo controlled study at some stage as the process of HVI and PRP injections have lots of “theatre” to them and it is important we attempt to determine what effects are due to this or the mechanics/biochemical reaction. It will also be important to ascertain whether treatment effect is the same without any corticosteroids in the HVI. Certainly the take home message was: “if you are going inject go HVI”.
  2. Hio-Teng Leong presented on supraspinatus tendinopathy: association of subacromial space and scapular muscle strengths. This study took us back to impingement and assessed the mechanical components possibly involved. The study concluded that the scapula muscles were weaker in those with impingement like symptoms and that there was a significant difference between the subjects with symptoms and those without, although my retrospective review of the abstract leaves me unclear about which position this occurred in.
  3. Alison Grimaldi (@alisongrimaldi) presented on Gluteal tendinopathy- clinical diagnosis vs MRI diagnosis? This was a nice clinical study that took patients with lateral hip pain and examined several tests to determine how these clinical tests compared to MRI scans for Gluteal Tendinopathy. The study reported the sensitivity, specificity, PPV and NPV values for all tests. The best tests involved simple palpation – high sensitivity but low specificity. Other tests involving stretching the gluteals over the Trochanter and then contracting them were recorded as best.  The reference standard was the MRI scan, it was unclear how we can be clear that the MRI results were related to symptoms (e.g. was the MRI finding of tendinopathy an asymptomatic finding?)- This was highlighted by a question from the audience.


Jo Gibson’s plenary presentation on the challenge of pain: Is it all about load

Jo delivered a tremendously clinical relevant talk related to management of upper limb tendinopathy. It was super to hear about how the brain and central sensitization can influence changes. This was nicely linked to psychosocial factors and was the “elephant in the room” for the previous day’s talks. Jo nicely described the lack of correlation between structure and pain. She then went on to how elements like tactile discrimination, pressure pain threshold, body schema and tactile discrimination are associated with upper limb tendinopathy. One of her nice clinical gems was central adaption (with treatment) may be greatest with bilateral movements- sounds like a nice idea for a study………

As some of you know I am a fan boy of pain literature and central adaptations (especially the group) so it was great to see patients beliefs, expectations, context of pain and imaging discussed in relation to the patient. This is something so often missing in the management of tendinopathy and something I feel is critical to successful management.

As Angie Fearon (@angefearon) tweeted Load, Exs, LANGUAGE


Andrew Carr’s presentation on Pain- Central sensitization

This talk was primarily about a study on shoulder (RC tendinopathy) problems and identification of centrally mediated changes in this particular cohort, the key focus was on using QST testing particularly monofilament (Von Frey Hairs) testing to identify central changes. He also recommended the PainDETECT questionnaire.


Podium presentations on isometrics, power deficits and intratendon tears

At this point I’ll thank Oli Williamson (@oliw_physio)for writing the summary of the next sessions, I was not really able to concentrate as was trying to get in the zone………….

Ebonie Rio (@tendonpain) Exercise reduces pain immediately and affects cortical inhibition in patellar tendinopathy.

Ebonie starts her presentation by suggesting that health care professionals have traditionally favoured eccentric muscle contractions to relieve acute tendon pain. However it is thought that eccentrics are poorly adhered to (due to pain or in some cases worse outcomes). Therefore Ebonie speculates that we can’t be sure if prescribing eccentrics are the most effective interventions to relieve acute tendon pain. She highlights that there is a need to investigate other interventions that reduce pain, enabling participation in season without effecting muscle fatigue and performance. Recently there has been some speculation regarding the positive effects of isometric contractions upon central sensitisation and its potential role into relieving tendon pain. Therefore the purpose of Ebonie’s study was to compare the effects of isometric Vs isotonic muscular contractions upon immediate tendon (PT) pain relief and function.

Participants = volleyball players who had sustained “severe” in season patella tendon pain. Subjects were split into two groups via a cross over design. Prior to receiving heavy open chain (leg extension) isometric (5×45s at 70% MVIC) and isotonic (4×8 repetitions (3s concentric phase and 4s eccentric phase) at 100% of their 8RM) interventions, baseline scores of SL decline squat tendon pain were recorded.

Outcome Measures:

  1. Pain (out of ten) whilst performing a SL decline squat
  2. Transcranial magnetic stimulation measures to ascertain corticospinal excitation/inhibition
  3. Maximal voluntary isometric contraction (MVIC) torque upon rectus femoris muscle whilst performing isometric leg extension

The results demonstrated that heavy isometric contractions significantly reduced SL decline squat patella tendon pain as well as cortical inhibition compared to the isotonic contractions at 0mins and 45mins post intervention. It was also noted that MVIC increased post isometric contraction intervention whereas isotonic contractions seemed to decrease MVIC.

Take home messages from Ebonie:

Heavy isometric contractions seem to….

  1. Reduce patella tendon pain
  2. Decrease motor inhibition
  3. Increase rectus femoris strength and SL decline squat function
  4. You must load the effected tendon- no cross over response (@Peter_Gettings)

This study suggests that heavy isometric contractions could be the preferable intervention for an in season athlete who suffers from patella tendon pain.


Seth again- A superb study which highlights a novel aspect to motor output in tendinopathy, I am sure that this study will change our ongoing management and we must congratulate Ebonie on winning the BJSM award for best young  researcher.

Whilst this study is likely to be replicable we need to cautious as this was a small sample (n=6) and only of patella tendinopathy patients. Whilst it is likely to be no different in other tendons we have to consider the patella as slightly different due to the patella (bone-tendon-bone).


Seth O’Neill (me) presented on Plantarflexor muscle power deficits in runners with Achilles tendinopathy.

Seth opened up his presentation by stating that a significant risk factor for runners sustaining an Achilles tendinopathy (AT) is plantar flexor weakness and highlights Mahieu’s 2006 paper as an excellent reference.

Seth suggests that at present we don’t know which muscle contraction (concentric/eccentric) is more favourable and whether knee position is important when considering interventions to reduce plantarflexor deficits.  Therefore the purpose of Seth study is to compare the triceps surae power at 0° and 80° knee flexion upon runners with and without AT.

Participants = 41 runners with AT and 27 runners without history of AT. Each runner had their plantarflexor strength measured during concentric and eccentric contractions (90°/sec) using an isokinetic dynomometer. Knee flexion angle was fixed to 0° and 80° to differentiate gastrocnemius and soleus involvement.

Outcome measures = peak plantarflexor power @ 90°/sec

The results highlighted that the AT group had significantly reduced plantarflexor power at 0° and 80° knee flexion during both eccentric and concentric contractions when compared with the control group.

The deficits observed in plantarflexor power within the AT group at both 0° and 80° knee flexion suggest that soleus strength (concentric and eccentric) is the likely culprit for deficits in plantarflexor power for runners reporting AT pain. It was also worth noting that no pain was reported in the AT group when testing peak power, so pain is unlikely to have limited performance.

This opens up further discussion into the notion that central inhibition could play a significant role in reducing plantarflexor peak power. However Seth did highlight that the unaffected side also observed similar results. Therefore, it is likely that a reduction in soleus strength is responsible for the deficit.

Take home messages from Seth

  1. Runners with AT have significantly reduced plantarflexor peak power
  2. Increasing soleus strength may help runners with AT reduce plantarflexor power deficit
  3. We must consider concentric and eccentric strengthening
  4. Strengthening the soleus may reduce the incidence of reported AT related pain within the running population.

My own comment would be to direct you to the intervention study of 24 subjects from this cohort to show you how eccentrics failed to fully resolve all the identified deficits.


Dylan Morrisey (@DrDylanM) presented on intratendinous tears of the Achilles tendon- A new pathology? Analysis of a large 4 year cohort- poster here.

Dylan highlighted that intratendinous pathologies have traditionally been reported as Achilles tendionopathy or Achilles rupture. However are we missing an additional pathology? For example what do we diagnose when patients have an acute instant onset of Achilles pain? Is this intratendinous in nature?

The study in question looked at US reports and images of all patients who attended for presumed Achilles tendinopathy (AT) between 2005 and 2012. The patients were categorised into groups based on the findings.

  1. No pathology
  2. Mid tendon AT
  3. Insertional AT
  4. Partial tear
  5. Achilles Rupture
  6. Intratedinous tear (ITT) -  Defined as a clearly visualised echopoor area situated centrally in the tendon or extending to, but not through the tendon periphery, with pain on palpation and no clinical findings consistent with Achilles rupture)

Out of 740 patients 37 had an ITT (5%) – elite sports men were more highly represented in the ITT group

Dylan speculated that that suspicion of an ITT must be high when an acute onset has occurred, normally antero-medial in origin. These patients can train sub maximally but struggle to sprint and load maximally. Could this be due to torn fascicles within the tendon?

With regards to treatment – Dylan suggests that in the acute onset a 1ml Dextrose injection (immobilised) can be used along with an offload via 4-6cm heel wedge. Loading must be gradual with the athlete looking at around 3 months prior to competition.

Take home message from Dylan:

  1. Be suspicious of ITT when an elite athlete (especially male) presents with an acute onset of antero-medial Achilles pain with associated loss of maximal loading power (i.e. can train but not able sprint).
  2. There seems to be a strong association of ITT with mid tendon tendinopathic presentation therefore we must be able to differentiate.
  3. Accurate diagnosis can only be made with a combination of clinical suspicion and characteristic US findings.


Seth again – I like this further discrimination of tendinopathy to include intratendon tears. This work directly links with one of the spin offs from my Soleus argument and the involved fascicles. It will be interesting to see how this develops.

There was a final discussion session which was filmed and will be realised on the BJSM website and also as a podcast (my understanding at least).

In summary this was an amazing conference, and a MUST attend for anyone seriously interested in tendinopathy. I wonder where the next one will be……………………….

A big heads up to @Peter_Gettings and @oliw_physio for reviewing and adding a few tweaks to the review, particularly missing take home messages. I would also like to thank the MACP for funding my attendance at the conference!! Big thanks.