Tendinopathy

Author(s): Julio Martinez-Silvestrini, MD and Hans Knopp, MD

Originally published:11/11/2011

Last updated:04/04/2017

1. DISEASE/DISORDER:

Definition

Any painful condition affecting the tendon or paratenon. May be acute but is typically a chronic overuse and degenerative condition, exacerbated by mechanical loading. Tendinitis typically refers to tendon related pain, since thereis only a low grade inflammatory response with tendinopathy. Tendinosis refers to chronic, degenerative tendinopathy.

Etiology

  • Typically overuse with poor or altered mechanics. Contributing factors include an altered healing response, relative ischemia and apoptosis of tenocytes. Repeated mechanical stress and recurrent injuries with an absent or blunted inflammatory process may lead to the development of angiofibroblastic hyperplasia (fibroblasts and vascular granulation tissue).1-4

Epidemiology including risk factors and primary prevention

  • The pathology is extremely common; incidence depends on the affected area, most often occurring in 30- to 60-year-olds.
  • Risk factors may be divided into intrinsic (related to tendon itself) and extrinsic (environmental) factors and depend on the site affected and relate to biomechanics. Flouroquinolone use is also a major risk factor.

Patho-anatomy/physiology

  • Normally tendon fiber bundles are composed of fascicles consisting of tropocollagen (triple helix polypeptide chain) and blood vessels arranged parallel to the fascicles. The portion of the tendon that bears stress during mechanical loading is composed of three main components: Type 1 collagen, cells, mainly fibroblasts, and a noncollagenous matrix4
  • Pathologic changes include macrostructural thickening and increased vascularity. Microstructure changes include degeneration and disorganization of collagen fibers, increased cellularity, minimal inflammation.1 The build-up of mucopolysaccharide in fibrous tendon sheath leads to mucoid (myxoid) degeneration. This cycle repeats leaving globular degeneration and the production of matrix metalloproteinases (MMPs), tenocyte apoptosis, chondroid metaplasia of the tendon, and expression of protective factors such as insulin-like growth factor 1 (IGF-1) and nitric oxide synthetase (NOS) causing recurrent and chronic pain.5-9 In addition, there is increased COX-2 and IL-6 expression indicating a low grade inflammatory response.10

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

  • New onset/acute phase could begin as tendinitis with inflammation of the tendon or paratenon, followed by a blunted inflammatory process. Onset may be acute, traumatic, or insidious, presenting as an acute tear, often related to unaccustomed activity or a single instance of exertion. The healing process may be altered due to relative ischemic or other factors.
  • The subacute or chronic nature of tendinopathy repeats the blunted inflammatory cycle resulting in a thickened and degenerated tendon that is more prone to pain or an acute tear. 4

Specific secondary or associated conditions and complications

  • The variant of calcific tendinosis (calcific tendinitis) is a hydroxyapatite crystalline deposition into tendon, often affecting specific tendons such as the supraspinatus, and progresses through stages including fibrocartilage ingrowth, calcium formation, resorption and healing. Calcific tendinopathy is most painful during the resorptive phase and improves during tendon healing.
  • Fatty infiltration can occur as the degenerated tendon vacuolizes and space is filled presumably with the proliferation of the areolar tissue in the adjacent paratenon.
  • Tendon rupture can be a complication of rapid and/or forceful eccentric strain in the setting of advanced tendinopathy. Rupture can sometimes be the initial event signaling the presence of tendinopathy (eg, Achilles tendon). Injection of corticosteroid, particularly intratendinous may predispose a tendon to rupture.

2. ESSENTIALS OF ASSESSMENT

History

  • Symptoms are often described as a dull, aching, at times sharp pain. Usually pain is focal, non-radiating, improves with rest, ice, may improve with nonsteroidal anti-inflammatory drugs (NSAIDs), and worsens with activity, or using the affected area.
  • Important historical points include prior injury of the affected limb, repetitive use, systemic illnesses, and recent medications including fluoroquinolones.
  • Other presentations could include a history of an acute rupture (due to underlying tendinopathy), or complaints of an intermittent or chronic snapping tendon.

Physical examination

  • Inspection is often normal, but can reveal fullness or focal thickening over superficial tendons. Alignment, observing activities, and inspecting for posture and biomechanics are important to identify predisposing factors.
  • Palpation reveals tenderness anywhere from the enthesis to the myotendinous junction. Adjacent soft tissues or bursae may also be tender.
  • Range of motion, active and passive, may be decreased or elicit end-range pain (eg, elbow extension lag in severe lateral epicondylitis).
  • Neurologic exam should be thorough and normal. Strength deficits, if present, should be pain-limited only.
  • Special tests that can reproduce pain include passive stretching of affected tendon, or resisted active motion of the tendon.

Functional assessment

  • Evaluate for functional activities and ROM of adjacent and nearby joints. It is important to evaluate at least one joint above and below the lesion.
  • Evaluate the, posture, form, biomechanics, repetitive motions or other issues that may prevent a recurrence or worsening in athletes or workers. Workplace or ergonomic evaluation may also be helpful.
  • Fully evaluate the kinetic chain for range of motion (ROM) deficits, strength, alignment, mechanical and functional issues.

Laboratory studies

  • May be necessary when multiple sites of tendon pain are identified to look for inflammation. Evaluate for conditions such as rheumatoid arthritis or collagen vascular diseases.
    • An example of this is the association of HLA-B27 with bilateral Achilles tendinopathy.

Imaging

  • Radiographs may help determine the presence of intra-tendinous calcifications, calcified tendon insertions (enthesophytes), or concomitant articular or bone pathology such as fracture or apophysitis.
  • Magnetic resonance imaging (MRI) is generally not indicated unless grading a tear is necessary or evaluation of adjacent structures or concomitant pathology is needed.
  • Musculoskeletal ultrasound is a low cost point-of-care dynamic imaging modality that can be very helpful in assessing tendon tears, degenerative changes, calcifications and associated neovascularity. It is useful fto evaluateextra-articular soft-tissue pathology and compare to the opposite limb. Limitations include ultrasonographer skill, equipment deficiencies, or availability.11

Supplemental assessment tools

Differential diagnosis

  1. Depends on the site or surrounding tissue.
  2. Local inflammatory causes such as bursitis, synovitis, paratenonitis, or apophysitis; local degenerative causes such as arthropathy, cartilage injury,, muscle/tendon tears, or other intra-articular pathology; tumorogenic, infectious or vascular causes could be considered, in addition to referred or radicular pain.

Instruments to measure strength distal to the affected tendon over time can demonstrate treatment effects.

Early predictions of outcomes

Functional outcome measures, some joint specific, can be utilized to chart the success, or lack thereof, of treatment12.

Environmental

Work- or sport-specific tasks in the environment can lead to or worsen tendinopathy.

Social role and social support system

Persons with tendon pain may suffer depression or other mood disorders if they cannot participate in vocational or avocational activities. In such cases activity adaptations or appropriate multidisciplinary treatment is required.

Professional Issues

Patients with chronic recalcitrant tendinopathy may seek out unproven treatments and should be counseled appropriately.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

There are no established treatment guidelines specifically for tendinopathy.

At different disease stages

New onset/acute tendinopathy

  1. Initial treatment should be tailored to the patient’s needs or desire to return to activity, symptom relief, the chronicity severity of tendinopathy, and the frequency of recurrence.
  2. Acute exacerbations may be managed with relative rest, NSAIDs, and physical modalities, including ice. Other modalities such as iontophoresis, phonophoresis, ultrasound, low-level laser therapy, shock wave therapy, and electrical stimulation have limited, if any, utility. Topical treatments including aspirin or diclofenac cream may be helpful, and have a small amount of systemic absorption. Glyceryl trinitrate patch may decrease pain and enhance healing.10 Tendon sheath corticosteroid injections could give temporary partial pain relief, though their use is controversial. Intra-tendinous injections are not recommended, as may result in tendon tears.Physical therapy could also include transverse friction massage, correcting biomechanics, ergonomic adjustments, and therapeutic exercises.

Subacute/chronic

  1. Strategies for secondary prevention and recurrence management could include early recognition of recurrent pain due to tendinopathy and enrollment in a program of eccentric training and symptomatic management as described above. Often tendinopathy is only first recognized in the subacute or chronic stage. More advanced treatments include prolotherapy, sclerotherapy for neovessels, percutaneous tenotomy, extracorporeal shockwave therapy, tendon hydrodissection and surgery.
  2. Rehabilitation strategies could include preserving adjacent joint range of motion, improving flexibility or kinetic chain deficits and optimizing function in order to return to activity.
  3. iii. An alternative strategy for patients recalcitrant to conservative care is to palliate symptoms during times of exacerbation, and optimize prevention strategies as discussed above.
  4. iiii. An eccentric strengthening program has been demonstrated as potentially curative for Achilles tendinopathy, yet found similar to ice and stretching for lateral epicondylitis.13, 14

Coordination of care

  • Coordinated and interdisciplinary: Patients with recalcitrant tendinopathy causing sustained disability due to pain and secondary weakness will require a coordinated interdisciplinary treatment approach.
  • Integrated: Physical and occupational therapy, vocational counseling and rehabilitation psychologists can all play a role in treatment.
  • Multidisciplinary: In cases of tendon tear or rupture a surgical consultation or debridement/repair of severe tendinopathy may be needed.

Patient & family education

  • Family and societal roles may change due to disabling conditions.
  • Often important to recovery in chronic cases is helping patients reestablish their role in the family through active rehabilitation exercises.

Emerging/unique Interventions

Impairment-based measurement

Patients with work limitations may require capacity exams to quantify their work tolerance.

Measurement of patient outcomes

Joint specific functional outcome measures, when needed

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Physicians may learn and integrate into their practice newer techniques described to treat tendinopathy, including biologics.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

  • Injection of substances under ultrasound and fluoroscopic guidance has increased accuracy. Guidance improves the accuracy of diagnostic injections.
  • Injection of biologics including platelet rich plasma (PRP) and stem cells offer alternatives to those who have failed conservative care.
  • Peritendinous hydrodissection may place a role in treating tendnoopathies with neovascularity in adjacent fat pads.

Emerging/unique interventions

  • Interventions directed at restoring normal tendon anatomy such as PRP, amniotic growth factor injections, and stem cell therapy are emerging treatments. PRP can be applied with or without tenotomy

5.GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

  • Injection of corticosteroid under imaging guidance has not been sufficiently studied to show increased efficacy.
  • Controlled studies are required to establish the efficacy of injecting biologics including PRP and stem cells or tenotomy alone vs tenotomy and PRP.

References

  1. Khan KM, Cook JL, Bonar F, Harcourt P, Astrom M. Histopathology of common tendinopathies. Update and implications for clinical management.Sports Med. 1999;27:393-408.
  2. Ljung BO, Forsgren S, Friden J. Substance P and calcitonin gene-related peptide expression at the extensor carpi radialis brevis muscle origin: implications for the etiology of tennis elbow. J Orthop Res. 1999;7:554-559.
  3. Soslowsky LJ, Thomopoulos S, Tun S, Flanagan CL, Keefer CC, Mastaw J, Carpenter JE. Neer Award 1999. Overuse activity injures the supraspinatus tendon in an animal model: a histologic and biomechanical study. J Shoulder Elbow Surg. 2000;9:79-84.
  4. Scott, Alex, Ludvig J. Backman, and Cathy Speed. “Tendinopathy: update on pathophysiology.” journal of orthopaedic & sports physical therapy 45.11 (2015): 833-841.
  5. Jones GC, Corps AN, Pennington CJ, Clark IM, Edwards DR, Bradley MM, Hazleman BL, Riley GP. Expression profiling of metalloproteinases and tissue inhibitors of metalloproteinases in normal and degenerate human achilles tendon. Arthritis Rheum. 2006;54:832-842.
  6. Lian O, Scott A, Engebretsen L, Bahr R, Duronio V, Khan K. Excessive apoptosis in patellar tendinopathy in athletes. Am J Sports Med. 2007;35:605-611.
  7. Scott A, Cook JL, Hart DA, Walker DC, Duronio V, Khan KM. Tenocyte responses to mechanical loading in vivo: a role for local insulin-like growth factor 1 signaling in early tendinosis in rats. Arthritis Rheum. 2007;56:871-881.
  8. Szomor ZL, Appleyard RC, Murrell GA. Overexpression of nitric oxide synthases in tendon overuse. J Orthop Res. 2006;24:80-86.
  9. Yuan J, Murrell GA, Wei AQ, Wang MX. Apoptosis in rotator cuff tendonopathy. J Orthop Res. 2002;20:1372-1379.
  10. Robert-Jan de Vos, Adam Weir, Lodewijk P. J. Cobben, Johannes L. Tol The value of power Doppler ultrasonography in Achilles tendinopathy: a prospective study.Am J Sports Med. 2007 Oct; 35(10): 1696–1701.
  11. Andres BM, Murrell GAC. Treatment of tendinopathy: what works, what does not, and what is on the horizon. Clin Orthop Relat Res. 2008;466(7):1539-54.
  12. Newcomer K. Martínez-Silvestrini JA. Gay R. White K. A Comparison of the Patient-Rated Forearm Questionnaire with Other Outcome Measurement Tools for Lateral Epicondylitis. Journal of Hand Therapy 2005; 18(4):400-405.
  13. Alfredson H, Cook J. A treatment algorithm for managing Achilles tendinopathy: new treatment options. Br J Sports Med. 2007;41:211-216.
  14. Martínez-Silvestrini JA. Newcomer K. Gay R. White K. A clinical trial of concentric and eccentric strengthening for chronic lateral epicondylitis. Journal of Hand Therapy. 2005; 18(4):411-419.

Original Version of the Topic

Chris Visco, MD. Tendinopathy. 04/05/2013

Author Disclosures

Julio Martinez-Silvestrini, MD
Nothing to Disclose

Hans Knopp, MD
Nothing to Disclose

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