1. Disease/Disorder:
    1. Chronic local degenerative change in the macrostructure of tendon.
    2. Overuse syndrome of chronic intermittent tendon pain with use.
    1. Overuse with poor or altered mechanics. Other theorized 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).1-3
    Epidemiology including risk factors and primary prevention
    1. The pathology is extremely common; incidence depends on the affected area, most often occurring in 30- to 60-year-olds.
    2. Risk factors depend on the site affected and relate to biomechanics; for instance, overuse of gripping at the wrist may result in common extensor tendinopathy.
    1. Normally tendon fiber bundles are composed of fascicles consisting of tropocollagen (triple helix polypeptide chain) and blood vessels arranged parallel to the fascicles.
    2. 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.4-8
    Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
    1. New onset/acute
      1. The initial cycle 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.
    2. The variant of calcific tendinosis (calcific tendinitis) is a hydroxyapatite crystaline deposition into tendon, often affecting specific tendons such as the supraspinatus, and progresses through stages including fibrocartilage ingrowth, calcium formation, resorption and healing.
    3. 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.
    Specific secondary or associated conditions and complications
    1. 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. Calcific tendinopathy is most painful during the resorptive phase and improves during tendon healing. 
    3. 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.
  2. Essentials of Assessment
    1. 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.
    2. Important historical points include prior injury of the affected limb, systemic illnesses, and recent medications including fluoroquinolones.
    3. 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
    1. Inspection is often normal, can reveal fullness over superficial tendons. Alignment, observing activities, and inspecting for posture and biomechanics are important to identify predisposing factors.
    2. Palpation reveals tenderness anywhere from the enthesis to myotendinous junction. Adjacent soft tissue may also be tender.
    3. Range of motion, active and passive, may be decreased or elicit end-range pain (eg, elbow extension lag in severe lateral epicondylitis).
    4. Neurologic exam should be thorough and normal. Strength deficits, if present, should be pain-limited only.
    5. Special tests that can reproduce pain include passive stretching of affected tendon, or resisted active motion of the tendon (Cozen test at the wrist).
    Functional assessment
    1. Evaluate for functional activities and ROM of adjacent and nearby joints. It is important to evaluate one joint above and below the lesion.
    2. Evaluate the biomechanics, posture, form, repetitive motions or other issues that may prevent a recurrence or worsening in athletes or workers. Workplace or ergonomic evaluation may also be helpful.
    3. Fully evaluate kinetic chain for range of motion (ROM) deficits, strength, alignment or possible mechanical and functional issues.
    Laboratory studies
    1. 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.
    1. Radiographs may help determine the presence of intra-tendinous calcifications, or concomitant articular or bone pathology such as fracture, enthesophyte, or apophysitis.
    2. Magnetic resonance imaging (MRI) is generally not indicated unless grading a tear is necessary or evaluation of adjacent structures or concomitant pathology is needed (eg, evaluating extensor carpi ulnaris tendinopathy in the setting of a triangular fibrocartilage complex (TFCC) tear.
    3. Musculoskeletal ultrasound is an excellent imaging modality to evaluate for tendinopathy, particularly to compare to the unaffected limb/tendon and evaluate extra-articular soft-tissue pathology.  However, limitations may be present due to  ultrasonographer skill, equipment limitations, or availability.
    Supplemental assessment tools
    1. 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, enthesopathy, muscle/tendon tears, or other intra-articular pathology; tumorogenic, infectious or vascular causes could be considered, in addition to referred or radicular pain.
    2. Instruments to measure strength distal to the affected tendon over time can demonstrate treatment effects.
    Early predictions of outcomes
    1. Functional outcome measures, some joint specific, can be utilized to chart the success, or lack thereof, of treatment.
    1. Work- or sport-specific tasks in the environment can lead to or worsen tendinopathy.
    Social role and social support system
    1. Persons with tendon pain may suffer depression if they cannot participate in vocational or avocational activities. In such cases appropriate multidisciplinary treatment is required.​
    Professional Issues
    1. 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
    1. There are no established treatment guidelines specifically for tendinopathy.​
    At different disease stages
    1. 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.9 Corticosteroid injections could give temporary partial pain relief, though their use is controversial. Prolotherapy, an increasingly popular injection modality, may offer some sustained relief.
      3. An eccentric strengthening program has been demonstrated as potentially curative for Achilles tendinopathy.10

        Physical therapy could also include transverse friction massage, correcting biomechanics, ergonomic adjustments, and therapeutic exercises.
    2. 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 sclerotherapy for neovessels, percutaneous tenotomy and surgery.
      2. Rehabilitation strategies could include preserving adjacent joint range of motion, flexibility, and optimizing function in order to return to activity.
      3. An alternative strategy for patients recalcitrant to conservative care is to palliate symptoms during times of exacerbation, and optimize prevention strategies as discussed above.
    Coordination of care
    1. Coordinated and interdisciplinary: Patients with recalcitrant tendinopathy causing sustained disability due to pain and secondary weakness will require a coordinated interdisciplinary treatment approach.
    2. Integrated: Physical and occupational therapy, vocational counseling and rehabilitation psychologists can all play a role in treatment.
    3. Multidisciplinary: In cases of tendon tear or rupture a surgical consultation or debridement/repair of severe tendinopathy may be needed.
    Patient & family education
    1. Family and societal roles may change due to disabling conditions.
    2. 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

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

    Measurement of patient outcomes

    1. Functional outcome measures, joint specific when needed
    Translation into practice: practice "pearls"/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
    1. Physicians may learn and integrate into their practice newer techniques described to treat tendinopathy.
  4. Cutting edge/emerging and unique concepts and practice
    Cutting edge concepts and practice
    1. Injection of substances under imaging guidance (ultrasound and fluoroscopic) has increased accuracy. Guidance improves the accuracy of diagnostic injections.
    2. Injection of biologics including PRP and stem cells offer alternatives to those who have failed conservative care.

    Emerging/unique interventions

    1. Interventions directed at restoring normal tendon anatomy such as platelet rich plasma (PRP), growth factor treatment, and stem cell therapy are emerging treatments. PRP could be applied with or without tenotomy. More studies are needed to establish the effectiveness of PRP treatment.
  5. Gaps in the evidence-based knowledge
    Gaps in the evidence-based knowledge
    1. Injection of cortisone under imaging guidance has not been sufficiently studied to show increased efficacy.
    2. Controlled studies are required to establish the efficacy of injecting biologics including PRP and stem cells.
    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. 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.
    5. 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.
    6. 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.
    7. Szomor ZL, Appleyard RC, Murrell GA. Overexpression of nitric oxide synthases in tendon overuse. J Orthop Res. 2006;24:80-86.
    8. Yuan J, Murrell GA, Wei AQ, Wang MX. Apoptosis in rotator cuff tendonopathy. J Orthop Res. 2002;20:1372-1379.
    9. Alfredson H, Cook J. A treatment algorithm for managing Achilles tendinopathy: new treatment options. Br J Sports Med. 2007;41:211-216.
    10. 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.
Clinical Topic Detail
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