Tendinopathy

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Original Editors - Matthias Verlinden

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Search Strategy[edit | edit source]

Engine: Pubmed, Articledatabase, Web of Knowledge
Keywords: Tendinopathy, review, (tendinitis, tendinosis)
Inclusion criteria: <10years – April 2011, English, accessible
Exclusion criteria: Non-English

Definition/Description[edit | edit source]

Tendinopathy is a failed healing response of the tendon, with haphazard proliferation of tenocytes, intracellular abnormalities in tenocytes, disruption of collagen fibers, and a subsequent increase in noncollagenous matrix.[1][2][3]  1 The term tendinopathy is a generic descriptor of the clinical conditions ( both pain and pathological characteristics) associated with overuse in and around tendons.[4]

Clinically Relevant Anatomy
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Healthy tendons are brilliant white in color and have a fibroelastic structure. Within the extracellular network , tenoblasts and tenocytes constitute about 90% to 95% of the cellular elements of tendons.[5] The remaining 5% to 10% of the cellular elements of tendons consists of chondrocytes at the bone attachment and insertion sites, synovial cells of the tendon sheath, and vascular cells, including capillary endothelial cells and smooth muscle cells of arterioles.
The oxygen consumption of tendons and ligaments is 7.5 times lower than that of skeletal muscles. The low metabolic rate and well-developed anaerobic energy-generation capacity are essential to carry loads and maintain tension for long periods, reducing the risk of ischemia and subsequent necrosis. However, a low metabolic rate results in slow healing after injury.[6]

Epidemiology /Etiology[edit | edit source]

Tendinopathic tendons have an increased rate of matrix remodeling, leading to a mechanically less stable tendon that is probably more susceptible to damage.[7] Histological studies of surgical specimens from patients with established tendinopathy consistently show either absent or minimal inflammation.[8][9][10] They generally also show hypercellularity, a loss of the tightly bundled collagen fiber appearance, an increase in proteoglycan content, and commonly neovascularization.[11][12] Inflammation seems to play a role only in the initiation, but not in the propagation and progression, of the disease process.[13] Failed healing and tendinopathic features have been associated with chronic overload, but the same histopathological characteristics also have been described when a tendon is unloaded: stress shielding seems to exert a deleterious effect.[8] Unloading a tendon induces cell and matrix changes similar to those seen in an overloaded state and decreases the mechanical integrity of the tendon.[14][15][16]

Characteristics/Clinical Presentation[edit | edit source]

Tendinopathy is usually seen in:

  • Lateral Epicondylitis
  • Medial Epicondylitis
  • Patellar tendon
  • Achilles Tendon
  • Rotator cuff

Differential Diagnosis[edit | edit source]

Location specific.

Diagnostic Procedures[edit | edit source]

  Location specific.

Outcome Measures[edit | edit source]

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Examination[edit | edit source]

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Medical Management
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Location specific.

Physical Therapy Management
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Location specific.

Key Research[edit | edit source]

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Resources
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Clinical Bottom Line[edit | edit source]

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Recent Related Research (from Pubmed)[edit | edit source]

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References[edit | edit source]

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  1. ↑ Maffulli et al. Novel Approaches for the Management of Tendinopathy. J Bone Joint Surg Am. 2010;92:2604-2613. doi:10.2106/JBJS.I.01744 (Evidence level A1)
  2. ↑ Maffulli N, Longo UG, Maffulli GD, Rabitti C, Khanna A, Denaro V. Marked pathological changes proximal and distal to the site of rupture in acute Achilles tendon ruptures. Knee Surg Sports Traumatol Arthrosc. 2010 Jun 19 [Epub ahead of print]. (Evidence level B)
  3. ↑ Maffulli N, Longo UG, Franceschi F, Rabitti C, Denaro V. Movin and Bonar scores assess the same characteristics of tendon histology. Clin Orthop Relat Res. 2008; 466:1605-11. (Evidence level A2)
  4. ↑ Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy. 1998;14:840-3.
  5. ↑ Kannus P, Jozsa L, Jarvinnen M. Basic science of tendons. In: Garrett WE Jr, Speer KP, Kirkendall DT, editors. Principles and practice of orthopaedic sports medicine. Philadelphia: Lippincott Williams and Wilkins; 2000. p 21-37. (Book)
  6. ↑ Williams JG. Achilles tendon lesions in sport. Sports Med. 1986;3:114-35.
  7. ↑ Arya S, Kulig K. Tendinopathy alters mechanical and material properties of the Achilles tendon. J Appl Physiol. 2010;108:670-5. (Evidence level B )
  8. ↑ 8.0 8.1 Longo UG, Franceschi F, Ruzzini L, Rabitti C, Morini S, Maffulli N, Forriol F, Denaro V. Light microscopic histology of supraspinatus tendon ruptures. Knee Surg Sports Traumatol Arthrosc. 2007;15:1390-4. (Evidence level B)
  9. ↑ Longo UG, Franceschi F, Ruzzini L, Rabitti C, Morini S, Maffulli N, Denaro V. Characteristics at haematoxylin and eosin staining of ruptures of the long head of the biceps tendon. Br J Sports Med. 2009;43:603-7.
  10. ↑ Longo UG, Franceschi F, Ruzzini L, Rabitti C, Morini S, Maffulli N, Denaro V. Histopathology of the supraspinatus tendon in rotator cuff tears. Am J Sports Med. 2008;36:533-8. (Evidence level B)
  11. ↑ Longo UG, Ronga M, Maffulli N. Acute ruptures of the Achilles tendon. Sports Med Arthrosc. 2009;17:127-38.
  12. ↑ Longo UG, Ronga M, Maffulli N. Achilles tendinopathy. Sports Med Arthrosc. 2009;17:112-26.
  13. ↑ Rees JD, Maffulli N, Cook J. Management of tendinopathy. Am J Sports Med. 2009;37:1855-67. (Evidence level B)
  14. ↑ Lewis JS. Rotator cuff tendinopathy: a model for the continuum of pathology and related management. Br J Sports Med. 2010 Jun 11.
  15. ↑ Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med. 2009;43:409-16
  16. ↑ Louis C. et al. Strain patterns in the patellar tendon and the implications for patellar tendinopathy. Knee Surg, Sports Traumatol, Arthrosc (2002) 10 :2–5 (Evidence level B)


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