Everything the busy sports practitioner needs to know. Main overview by Ryan Shulman
Among the wide variety of overuse syndromes that sports practitioners encounter, a significant proportion affect the tendons of the rotator cuff, patella and Achilles, and the origins of forearm flexors and extensors. Our understanding of the pathology of these tendon overuse injuries has come a long way in the past 10 years. But not far enough: I still find it common to hear patients and friends talk of their patellar or Achilles ‘tendinitis’.
I suspect, too, that if the prevalence of the term among research papers and discussion is anything to go by, many practitioners are still using this term, incorrectly, to define their clients’ pathophysiologies. This may be because it requires little explanation – ‘tendinitis’ is such a common term within the sports injury vernacular that clients will readily accept it as a diagnosis.
However, the suffix ‘itis’ suggests an inflammatory process. We now know that most of what we deal with in overuse tendinopathy has little to do with inflammation; what many people describe as chronic tendinitis is, in fact, tendinosis, which is a degenerative process. It is really important therefore that sports therapists start to adopt the correct terminology, so that they can also start to think differently about management and client education.
Chronic tendinitis does exist as a separate medical entity, but it is a rare presentation (see below). We should adopt the term ‘tendinopathy’ to describe the common sporting conditions we see in our clinics.
The training effect on protein metabolism in both muscle and tendon has been studied in detail. It appears that immediately after training, there is a period of catabolism (protein breakdown) in preparation for remodelling, followed by a period of protein synthesis, one to three days later. If training is occurring too frequently the athlete may remain in a state of extended catabolism(1). Chronic overtraining or perhaps irregular high intensity training sessions may contribute to an extended state of catabolism, which in turn may affect the ability of tendon cells to repair damage or result in their death.
Tendinosis was first described more than a quarter of a century ago and numerous studies have contributed to our understanding of the pathological process. Tendinosis is a non-inflammatory condition involving collagen breakdown and disorganisation, neovascularisation(2) (the abnormal growth of capillaries into the substance of the tendon), calcification and occasional death of tendon tissue.
As degenerative changes evolve, the forces through the inherently weakened tendon can cause partial or complete tears of the tendon(3). These acute injuries can trigger a local inflammatory response, thus explaining how an inflammatory process can coexist with this condition. As mentioned above, overuse tendinitis does occasionally occur, but it is rare to see it clinically. Most authorities suggest treating the initial presentation of tendinopathy as tendinosis.
The repetitive loading of tendon collagen beyond its yield strength causes microfailure of the fibres. This initiates a repair process in which tendon cells produce extra healing collagen. Unfortunately this process is very slow: experimental animal models show that complete healing takes between 4 and 14 months. If further microtrauma occurs before healing is complete, excess strain may cause the tendon cells to die, which decreases the inherent ability of the tendon to heal itself and makes it vulnerable to further injury(1). The ingrowth of new capillaries shows evidence of the body’s healing response to deliver oxygenated blood to the damaged area.
There are other theories attempting to explain the development of tendinosis. One theory proposes decreased blood supply to the tendon as an initiator of the process, but this is controversial, and seemingly contradicted by the fact that heavy eccentric exercise improves the condition.
Another theory suggests that tendinosis is in fact a disease of underuse rather than overuse. Loading of a tendon insertion is not uniformly distributed, and it appears that tendinopathy usually occurs in areas of a tendon where this loading is lowest. It is hypothesised that the placing of repeatedly increasing forces through a tendon will preferentially load the stronger areas, theoretically shielding other areas of the tendon. These shielded areas, prone to tendinosis, are therefore ‘underused’.
Clinically it is thought that tendinopathy is initially asymptomatic(5). In fact, imaging of many athletes with Achilles tendinosis on one side will show early changes indicative of tendinosis in the opposite asymptomatic Achilles tendon(6). These findings suggest that an underlying process of tendinosis may be responsible for apparently spontaneous tendon rupture(7).
Local pain receptor thresholds are also thought to undergo change. While local trauma may contribute to a patient’s chronic symptoms, basic science research has identified abnormal amounts of glutamate(8) and substance P (both are pain-related neurotransmitter substances)(9) within affected tendons, which may excite the peripheral nerve endings in their soft tissue coverings. It also seems that new nerve endings accompany neovascularisation(10). These blood vessels and nerves are the targets of sclerosant therapy (see below).
Other contributors to tendinopathies include:
* some medications
* collagen diseases (eg Marfan’s)
* genetics (eg blood group ‘O’)
* medical conditions such as rheumatoid arthritis or diabetes mellitus.
Local biomechanics, environmental factors such as footwear, and occupation can also predispose certain individuals to tendinopathy.
How a client will present obviously depends on which tendon is causing trouble. The athlete with patellar tendinopathy often has anterior knee pain and tenderness localised to the tendon’s proximal insertion. Functional testing can include getting the client to perform decline squats on a wedge (decline board), which can elicit pain after a few repetitions.
Achilles tendinopathy typically causes pain at one of two sites – mid-portion or insertion. They are slightly different entities and prognosis for mid-portion tendinopathy is much better than for insertional, where complications include retrocalcaneal bursitis and posterior impingement syndromes. Mid-portion tendinopathy will usually cause tenderness in the tendon itself, rather than pain in other structures. The therapist should be sure always to rule out Achilles rupture (palpable defect, positive Simmon’s squeeze test).
The athlete with tennis elbow (or more appropriately ‘lateral elbow tendinopathy’) has pain radiating from the lateral forearm to the insertion of extensor carpi radialis brevis (ECRB) at the lateral epicondyle (outer elbow edge) of the humerus. Resisted wrist extension and gripping actions will elicit pain. The therapist should be alert to other disorders that mimic this pain, such as C5/C6/C7 nerve root symptoms and posterior interosseus nerve entrapment.
Regardless of the site of the tendinopathy, the history is likely to be similar, and can usually be plotted against increased loading of the tendon. Symptoms develop gradually. Many clients will admit to a recent change in training volume and/or intensity. Pain and stiffness are often worse first thing in the morning, particularly after a hard training session the previous day, and will improve once they ‘get moving’. Pain at the onset of activity that settles during performance and worsens again afterwards is typical. As the condition intensifies, clients may report pain throughout training and competition and, in the worst cases, during rest. Often functional exercises are required to elicit pain.
The recent questionnaires developed by the Victorian Institute of Sport Assessment are an excellent method of monitoring the progress of patients with Achilles (VISA-A) and patella (VISA-P) tendinopathies. Both questionnaires are available for free download at www.clinicalsportsmedicine.com/ publications.htm
Diagnosticians now have the luxury of detailed imaging of the tendon with the use of ultrasound and magnetic resonance imaging (MRI). It is important to consider the possible differential diagnosis in each case.
Plain x-rays are useful in narrowing the differential diagnoses. In the knee, for instance, they can help to identify loose bodies, patellofemoral joint disease, calcific tendinitis, and traction apophysitis conditions.
Ultrasound is a cheap, easy and noninvasive imaging tool, suited to tendons that are close to the skin surface. Tendon thickening, partial tears and collagen disorganisation can be inferred from typical changes on ultrasonography. The use of Doppler ultrasound is now being recognised as very useful for identifying the growth of new blood vessels into the tendon substance. Doppler is used when delivering sclerosants and autologous blood (see below).
MRI is similarly sensitive for detecting tendon thickening and can sometimes show partial tears. In the knee, fine-slice MRI also provides excellent detail of other local structures, such as articular cartilage, menisci and fat pads.
Therapists should be aware that even where an athlete is asymptomatic, changes suggestive of tendinopathy can show up on both ultrasound(11) and MRI. In other words, changes may be present on a scan that are not always contributing to the patient’s presenting complaint. Moreover, changes in patients whose symptoms have resolved after surgery for tendinosis continue to show pathological changes on ultrasound and MRI(12). We do not yet understand why this happens. Clearly, imaging findings should only be used to support the working diagnosis.
Historically, conservative management has been the mainstay of treatment. Yet despite a wide variety of management options, few have delivered consistently effective results. Many advocated rest only, others relied too heavily on electrotherapeutics. Today most experts would still advocate an initial period of conservative management – but the emphasis is not on rest; rather, it involves considerable training and an understanding that symptoms can take many months to improve.
Initial investigation into simple causes such as poor training technique, inappropriate training loads, training surfaces or unsuitable equipment (shoes, poorly designed orthotics etc), may allow the therapist, coach and/or athlete to alter the pathological biomechanics sufficiently to enable the tendon to heal. Physical examination may elicit evidence of poor flexibility (eg hamstrings, iliotibial band), overpronation, weakness and imbalance (eg gastroc-soleus complex ,vastus medialis obliquus, proximal hip stabilisers). While stretching of the affected tendon itself is not useful, it may well be helpful to stretch those structures that are affecting good biomechanics.
The therapist (together with the coach, if possible) should analyse the athlete’s performance and make appropriate changes to technique, including the use of orthotics (eg heel raise) or braces for initial deloading and pain relief.
Once a client has presented with a tendinopathy, practitioners should normally recommend rest from full competitive activities(13) to allow the athlete to focus on a comprehensive conservative treatment plan, with biomechanical correction at its core.
Eccentric loading programmes have shown good results. These include the use of a wedge (decline board) in decline squats (for patellar tendinopathy), and heel drops (in Achilles tendinopathy). In both programmes the client is instructed to use their arms to assist in the concentric part of the exercise, and use their entire body weight during the eccentric phase. It is expected that the athlete will experience some discomfort while doing these exercises(13). The client needs to be highly motivated, because many eccentric loading regimes involve twice-daily repetitions, seven days a week for 12 weeks or more (14).
Beyond eccentric loading
Clients may respond to strengthening alone and should gradually return to competition with improved or altered technique. Those who fail or who are slow to respond may find additional alternatives useful, but the therapist should examine the options with care.
NSAIDs are useful for acute symptoms only and there is no evidence to suggest that their use improves outcomes for tendinopathies. In fact, in the clinical management of chronic tendinopathy, the ubiquitous use of NSAIDs may mask symptoms and consequently hamper the necessary therapeutic management(15).
Corticosteroid use comes into the same category. Of course there are some cases when the use of injected corticosteroid has reduced the athlete’s pain; yet trials have not only found little benefit but have shown that after injection the risk of acute rupture increases significantly.
Many authors have advocated deep transverse friction massage. A Cochrane systematic review in the UK has, however, found no significant evidence that this improves outcomes(16).
Ice is useful for analgesia, and theoretically will decrease blood flow through abnormal blood vessels, but no evidence exists on protocols or outcomes.
Extracorporeal shock wave therapy is used predominantly to treat calcific tendinopathy and seems to be of benefit only to patients with advanced disease where calcium deposits are hampering rehabilitation. Some studies have shown modest improvements in tendon healing with laser, electrotherapy, electromagnetic fields and ultrasound. However, most of these studies have not been performed on athletes or very active people, so are of limited value as a guide to therapeutic options.
Newer treatments have started to show promising results. Ultrasound-guided dry needling and autologous (patient’s own) blood injection have been examined, with James et al(17) reporting a mean increase in VISA-P (patella) scores of 34.5 (from 39.8 to 74.3) at an average follow-up time of 14.8 months.
This procedure involves the insertion of a needle into the degenerative area of the tendon under ultrasound control. Multiple stabs are made into the area, which is then infiltrated with a small amount of venous blood from the patient. Results from this study showed significant subjective improvement in patients’ pain, yet intriguingly, ultrasound imaging post-procedure showed little improvement in the tendon’s appearance.
Similar excellent results have been reported, albeit in a small study, with injection of platelet-rich plasma in lateral elbow tendinopathy. Mishra(18) found that patients who received the injection had a 60% improvement in their visual analogue score (subjective pain assessment), compared to a 16% improvement in the placebo group. The improvement increased to 81% at six months and 93% at final follow-up.
Substances known as sclerosants can be injected into the sites of new vessel ingrowth. They act to destroy the abnormal capillaries and adjacent nerve networks. Studies show the effectiveness of these substances over non-sclerosants(19), though there are no trials comparing this treatment with others such as autologous blood injection.
Small studies have shown improvements in subjective and objective outcome scores with the use of topical nitric oxide (NO). Glyceryl trinitrate (GTN) patches (normally used for management of angina) are placed over the damaged tendon. Their use is supported by basic science data, which shows a transient increase in NO in damaged tendon and an absence of NO in normal tendon. Animal models have shown that tendon healing improves with the addition of NO(20). Any therapist considering trying these patches should consult a sports physician first.
Options for the surgical treatment of tendinopathy generally involve cutting out the degenerate material; occasionally obvious fissures in the tendon are repaired. Arthroscopic debridement (cleaning up) is advocated, because the procedure is minimally invasive.
It is hard to make any meaningful assessment of the relative merits of surgical versus conservative management, because surgical approaches vary widely, in terms of techniques adopted, inclusion and exclusion criteria and the specific experience of the surgeon. The variety of techniques in use suggests that outcomes aren’t ideal with any particular technique.
Success rates in some series approach 80%, but some of these studies have been criticised for inadequate design. There are currently no well designed randomised controlled trials examining the most appropriate surgery for tendinopathy, so we cannot reach any sound conclusions about their effectiveness(15).
Experimental research has examined the use of apoprotein (an inhibitor of collagen breakdown), stem cells, growth factors and synthetically engineered tissue to assist in the repair of the degenerate tissue.
Tendinopathy does pose a clinical dilemma for the sports practitioner. Recovery is slow, rehabilitation requires dedication and the process can be frustrating for the athlete, their coach and the treating team. Leaders in sports medicine such as Karim Khan(2,3,7,12) have provided us with a better understanding of the pathology and its healing. At least we should be better equipped by now to educate our patients and hopefully improve their chances of a successful return to activity at some level.
1. Ohberg L, Lorentzon R, Alfredson H ‘Neovascularisation in Achilles tendons with painful tendinosis but not in normal tendons: an ultrasonographic investigation’. Knee Surg Sports Traumatol Arthrosc 2001; 9: 233-8.
2. Khan KM, Maffulli N, Coleman BD, Cook JL, Taunton JE. ‘Patellar tendinopathy: some aspects of basic science and clinical management’. Br J Sports Med 1998;32:346-355.
3. Khan KM, Cook JL et al ‘Overuse Tendinosis, Not Tendinitis Part 1: A New Paradigm for a Difficult Clinical Problem’. The Physician and Sportsmedicine 2000 28(5).
4. Lian O, Holen KJ et al ‘Relationship between symptoms of jumper’s knee and the ultrasound characteristics of the patellar tendon among high level male volleyball players’. Scand J Med Sci Sports 1996;6:291-296.
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8. Alfredson H, Forsgren S et al ‘In vivo microdialysis and immunohistochemical analyses of tendon tissue demonstrated high amounts of free glutamate and glutamate NMDAR1 receptors, but no signs of inflammation, in jumper’s knee’. J Orthop Res 2001; 19: 881-6.
9. Gotoh M, Hamada K et al ‘Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases’. J Orthop Res 1998;16:618–21.
10. Ackermann PW, Li J et al ‘Autonomic innervation of tendons, ligaments and joint capsules: a morphologic and quantitative study in the rat’. J Orthop Res 2001; 19: 372-8.
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12. Khan KM, Visentini PJ et al ‘Correlation of ultrasound and magnetic resonance imaging with clinical outcome after patellar tenotomy: prospective and retrospective studies. Victorian Institute of Sport Tendon Study Group’. Clin J Sport Med 1999; 9: 129-37.
13. Visnes H , Bahr R ‘The evolution of eccentric training as treatment for patellar tendinopathy (jumper’s knee): a critical review of exercise programmes’. Br J Sports Med 2007;41:217–223.
14. Rees JD, Wilson AM , Wolman RL ‘Current concepts in the management of tendon disorders’. Rheumatology 2006;45:508–521.
15. Peers KHE, Lysens RJJ ‘Patellar tendinopathy in athletes current diagnostic and therapeutic recommendations’. Sports Med 2005; 35 (1): 71-87.
16. Brosseau L, Casimiro L et al ‘Deep transverse friction massage for treating tendinitis’. Cochrane
Database Syst Rev 2002;4:CD003528. 17. James SLJ, Ali K et al ‘Ultrasound guided dry needling and autologous blood injection for patellar tendinosis’. Br J Sports Med 2007;41:518–522.
18. Mishra A, Pavelko T ‘Treatment of chronic elbow tendinosis with buffered platelet-rich plasma’. Am J Sports Med 2006;34:1774–8.
19. Alfredson H, Ohberg L ‘Sclerosing injections to areas of neovascularisation reduce pain in chronic Achilles tendinopathy: a double-blind randomized controlled trial’. Knee Surg Sports Traumatol Arthrosc 2005;13:338–44.
20. Murrell GAC ‘Using nitric oxide to treat tendinopathy’. Br. J. Sports Med. 2007;41;227-231.