Do you have clients suffering from Tennis Elbow or Patellar Tendinitis?

Back in the 1990s there was a major shift in thinking regarding chronic tendinopathies. Histologic data pointed to a lack of acute inflammatory cells in the load-bearing regions of tendons, and some studies noted collagen separation and thinning without inflammatory cell infiltrates1,2,3,4.

As the thinking changed to ‘chronic tendinopathies are caused by an unknown degenerative process without inflammation,’ treatment strategies soon shifted away from anti-inflammatory modalities (NSAIDS, corticosteroids) and toward peritendinous injections of autologous blood products and shock wave therapies.

Today, however, the evidence for a non-inflammatory degenerative process behind chronic tendinopathies remains weak – and there is strong evidence that an ongoing inflammatory response is behind much of the pathology. When thinking about tendons, inflammation deserves a second thought.

The Myth of Tendinitis

An editorial in the BMJ entitled “Time to abandon the tendinitis myth” urged practitioners to adopt a new perspective and language in referring to chronic tendinopathies and stop attributing the condition to inflammation, noting that histologically there was little in common with inflammatory diseases like Rheumatoid Arthritis. Based on the evidence, this recommendation was likely both misleading and detrimental to patient care. The shift to treating chronic tendinopathies as non-inflammatory and rather degenerative led to the adoption of four main categories of treatment: (a) physical eccentric exercises and progressive loading, (b) blood products to induce remodeling, (c) pain reduction injections (sclerosants), and (d) extracorporeal shock wave therapy (ESWT), none of which address inflammation. Recent studies have failed to replicate the early success rates of eccentric exercises6 and level 1 evidence for PRP for Achilles tendinopathy has shown the practice to be ineffective7. Studies repeatedly fail to demonstrate reliable efficacy from ESWT. Are we missing something?

The Case for Inflammation

The myth of tendinitis arose from histological data suggesting the lack of acute inflammatory cells (e.g., neutrophils and macrophages), but advances in immunohistochemistry in the last 10 years suggests something else: there is in human and animal models a significant inflammatory reaction in both chronic tendinopathies and the early overloading response. A 2006 study by Schubert8 noted the presence of macrophages and T and B lymphocytes in chronic Achilles tendinopathy using monoclonal antibodies. Other studies found significant levels of macrophage-derived interleukin-1 (IL-1), cyclo-oxygenase (COX-1 and COX-2), IL-6, transforming growth factor beta, and high levels of substance p9,10,11,12,13. Almost all histological studies of tendon pathology make note an increased concentration of larger than normal tenocytes, a sign of cytokines and growth factor influence. In addition, in arthritis it is generally accepted that neovascularity is a sign of active inflammation, and neovascularization is seen commonly on doppler studies of symptomatic tendons. As recent evidence grows of an ongoing inflammatory component to chronic tendinopathies it seems like the time has come to reconsider the ‘myth’ of tendinitis and adjust our thinking.


Though mechanical overload is still a major factor in tendinopathies, modern immunopathology suggests that the pathology in both acute and chronic cases is in fact mediated by an ongoing inflammatory process that must also be addressed. Re-thinking the ‘myth’ of tendinitis opens up the possibility of treating such conditions with additional modalities that address specifically the inflammatory component (NSAIDS, Anti-TNF-a agents, substance p and glutamate inhibitors, and daily R.I.C.E. therapy), and this strategic approach seems likely to improve patient care outcomes.

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  1. Puddu G, Ippolito E, Postacchini F. A classification of Achilles tendon disease. Am J Sports Med 1976;4:145–50.
  2. Aström M, Rausing A. Chronic Achilles tendinopathy. A survey of surgical and histopathologic findings. Clin Orthop Relat Res 1995;316:151–64.
  3. Józsa L, Kannus P. Histopathological findings in spontaneous tendon ruptures. Scand J Med Sci Sports 1997;2:113–18.
  4. Khan KM, Cook JL, Bonar F, et al. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Med 1999;27:393–408.
  5. Khan KM, Cook JL, Maffulli N, et al. Time to abandon the “tendinitis” myth. BMJ 2002;16:626–7.
  6. Rompe JD, Nafe B, Furia JP, et al. Eccentric loading, shock-wave treatment, or a wait-and-see policy for tendinopathy of the main body of tendo Achilles: a randomized controlled trial. Am J Sports Med 2007;35:374–83.
  7. De Vos RJ, Weir A, van Schie HTM, et al. Platelet-rich plasma injection for chronic Achilles tendinopathy. JAMA 2010;303:144–9.
  8. Schubert TE, Weidler C, Lerch K, et al. Achilles tendinosis is associated with sprouting of substance P positive nerve fibres. Ann Rheum Dis 2005;64:1083–6.
  9. Gotoh M, Hamada K, Yamakawa H, et al. Significance of granulation tissue in torn supraspinatus insertions: an immunohistochemical study with antibodies against interleukin-1 beta, cathepsin D, and matrix metalloprotease-1. J Orthop Res 1997;15:33–9.
  10. Sullo A, Maffulli N, Capasso G, et al. The effects of prolonged peritendinous administration of PGE1 to the rat Achilles tendon: a possible animal model of chronic Achilles tendinopathy. J Orthopaed Sci 2001;6:349–57.
  11. Zhang J, James H-C. Wang production of PGE2 increases in tendons subjected to repetitive mechanical loading and induces differentiation of tendon stem cells into non-tenocytes. J Orthop Res 2010;28:198–203.
  12. Khan MH, Li Z, Wang JH. Repeated exposure of tendon to prostaglandin-E2 leads to localized tendon degeneration. Clin J Sport Med 2005;15:27–33.
  13. Legerlotz K, Jones ER, Screen HR, et al. Increased expression of IL-6 family members in tendon pathology. Rheumatology (Oxford) 2012;51:1161–5.

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