Tendinopathy

Home Conditions Recovery Exercise Products Veterinarians Contact Links

Tendinopathy (tendonitis, tendinosis, rupture, sprained tendon)

Tendinopathies are common in performance individuals, both animal and human. Terminologies can be exhaustive and confusing, and there appears to be a great deal of grey area and overlap between conditions such as tendonitis and tendinosis. Tendinosis is a relatively new term, and is absent in many if not most of classic medical and veterinary reference and textbooks.

Normal tendons are well organised hierarchical structures that are predominantly made up of long strands of Type I collagen. The collagen is enveloped by ground substance that is mainly comprised of small proteglycans with hydrophilic glycosaminoglycan chains, supplied by a sparse, but functionally adequate, neurovascular structure (Kountouris and Cook, 2007).

Leadbetter (1992) separates the injury response of a tendon to either an acute macrotraumatic injury or a chronic microtraumatic injury. In the microtraumatic tendon injury the main histological features represent a degenerative tendinopathy thought to be due to a hypoxic degenerative process. Inflammatory cell infiltration as seen in macrotrauma is absent or aborted. An acute injury should therefore be differentiated from a non-traumatic, chronic overuse condition in which the classic signs of inflammation after injury are not always present or identifiable (Williams, 1986).

Tendonitis is best described as an induced inflammation of a tendon following injury or destruction to its tissues, and there is an active inflammation response (Leadbetter, 1992), and normally follows on from a sprain or partial rupture of the tendon (Thomson et al., 1994 and Corrigan and Maitland, 1994). Tendonitis is further classed as acute (< 2 weeks), subacute (2-6 weeks) or chronic (> 6 weeks) (Puddu et al., 1976). Histological changes are further categorized as either

1. Purely inflammation with acute haemorrhage and tear

2. Inflammation superimposed upon pre-existing degeneration

3. Calcification and tendinosis changes in chronic conditions

Thus, tendinosis is assumed to be synonymous with descriptions of chronic tendonitis. Resent research has found that true tendonitis is quite rare, as histological analysis of biopsies retrieved form various tendons affected by tendonitis reveal that in the majority of the cases there is no active inflammatory response (Ashe et al., 2004 and Yuan et al., 2003).

Tendinosis refers to intratendinous degeneration caused by aging, accumulated and repetitive microtrauma and vascular compromise, and is recognised by the absence of an active inflammatory response. There is presence of non-inflammatory collagen degeneration, with fibre separation, collagen disorientation and disorganisation, hypocelluarity, scattered vascular ingrowth, and occasional local necrosis or calcification (Kahn et al., 1999). Clinically there may be a palpable tendon enlargement which may or may not be symptomatic and/or tender. Tendinosis is reported to be asymptomatic in 1/3 of subjects (Alfredson and Lorentzon, 2000), and is thought to result from chronic overuse and consistent mechanical overload (Kahn et al., 2000).

Tendonitis is mostly an acute condition following trauma, either direct or indirect, and the patient can normally identify the causative factor (fall, kick, long run). Clinical signs of inflammation such as swelling, heat, erythema and pain are present. Tendinosis on the other hand can be of obscure aetiology and present asymptomatic. It is thought that spontaneous tendon ruptures are often caused by pre-existing tendinosis (Roe, 1998), and rupture of the Supraspinatus or Achilles tendon being prime examples of this.

It is clear that the respective tendinopathies will not respond the same to any given treatment. Tendonitis is reported to respond favourably to classic treatment with ice, compression, elevation and NSAIDs or corticosteroids. The same treatment however will not achieve much in tendinosis. Clinically it can be difficult to differentiate between the two conditions, and there may also be an obscure transition.

Tendinosis have in several sources been reported to respond well to loaded eccentric exercise (Alfredson and Lorentzon, 2000). This is thought to encourage realignment and increased collagen synthesis. One study also looks at the ethics of going thought that pain threshold for this group, as the most effective treatment (eccentric exercise) is prone to trigger an inflammatory (but beneficial) pain response. This is extrapolated from human data, which obviously can be informed and then consent to the anticipated pain component. However, animals cannot have such an interaction with the therapist, and it then lies on the individual therapist’s interpretation as to how to translate this information and apply it to animals.

back

References

Alfredson H and Lorentzon R (2000) Chronic Achilles tendinosis recommendations for treatment and prevention. Sports Medicine. 29 (2), pp135-146

Ashe MC, McCauley T, Kahn KM (2004) Tendinopathies in the upper extremity; a paradigm shift. Journal of Hand Therapy. 17 (2) pp 329-334

Corrigan B and Maitland GD (1994) Practical Orthopaedic Medicine. Butterworth-Heinemann Ltd. Oxford.

Khan KM, Cook JL, Bonar F (1999) Histopathology of common tendinopathies: update and implication for clinical management. Sports Medicine 27(6), pp 393-408

Khan KM, Cook JL, Taunton JE, Bonar F (2000) Overuse tendinosis, not tendonitis. The Physician & Sports Medicine. 28(5) pp38-48

Kountouris A, Cook J. (2007) Rehabilitation of Achilles and patellar tendinopathies. Best Practice & Research Clinical Rheumatology. 21(2), pp 295-316

Leadbetter WB (1992) Cell-matrix response in tendon injury. Clinical Sports Medicine. 11, pp 533-578

Puddu G, Ippolito E, Postacchini P (1976) A classification of Achilles tendon disease. American Journal of Sports Medicine. 4, pp 145-150

Roe SC (1998) Injury and disease of tendons. In: Bloomberg MS, Dee JF, Taylor RA (Eds.) Canine sports medicine and surgery. WB Saunders Company, Philadelphia

Williams JGP (1986) Achilles tendon lesions in sports. Sports Medicine. 3, pp114-135

Yuan J, Wang XZ, Murrell GAC (2003) Cell death and tendinopathy. Clinics in Sports Medicine. 22, pp 693-701