Tendinopathy is a broad term used to describe any problem involving a tendon. While many use tendinopathy as an umbrella term to describe all tendon pathology, others may use it to describe a chronic tendon condition that fails to resolve (see tendinosis).
The prevalence of tendinopathy in the general population is 2-5%. Active and sporting individuals are at increased risk of tendinopathy although it is also commonly seen in non-active individuals. The prevalence in some populations can be high, e.g. patellar tendinopathy in up to 40% of volleyball players, however, sites and prevalence will depend on the sport and level played .
Tendinopathy is a clinical syndrome consisting of pain, tenderness, tendon swelling and impaired function .
The pathophysiology of tendinopathy is yet to full elucidated but one popular theory is the continuum model with inflammation rather than degeneration implicated :
- reactive tendinopathy
- tendon dysrepair (also known as "failed healing")
- degenerative tendinopathy
Tenocyte proliferation occurs with adaptive chondrometaplasia. Mucin deposition in connective tissues, fiber disruption of collagen and vascular proliferation. Deposition of fat or calcification may occur.
Risk factors can be intrinsic or extrinsic :
- sex: increased in female
- age: increases with age
- medications, e.g. fluoroquinolones, local and systemic glucocorticoids
- metabolic, e.g. obesity, type 2 diabetes mellitus, dyslipidemia, hypercholesterolemia
- poor muscle strength
- excessive tendon beyond tendon capacity, in particular, activities with a high-energy storage component (e.g. jumping in basketball, kicking sports)
- amount of loading (e.g. increased training time, overuse)
- change in loading
- "abusive loading" (i.e. unaccustomed activity) in non-active individuals
Ultrasound is the mainstay of imaging tendinopathy, with MRI as the second-line investigation. Plain radiograph and CT have a limited role, sometimes used to assess for calcification or associated avulsion injuries.
Plain radiographs have a low sensitivity for tendinopathy but localized soft tissue swelling and calcifications/ossification may be seen. Calcified insertional tendinopathy is usually well seen and is a common incidental finding.
Specific features will depend on the site of tendinopathy but general features include :
- early changes: tendon thickening, contour change, echotexture change
- progressive changes: further tendon thickening, loss of normal fibrillary pattern with hypoechoic heterogeneity
- may be focal or diffuse
- color Doppler may demonstrate neovascularity
The above changes can be seen in asymptomatic individuals but prominent, tendon thickening, loss of fibrillary pattern and neovascularity are more commonly seen in symptomatic patients .
There is overlap in the imaging features on ultrasound with tendon thickening and contour change present .
- T1: hyperintense
- T2: hyperintense
- GRE: hyperintense (often before T1 spin-echo hyperintensity)
- T1C+: enhancement
Unfortunately, these features are indistinguishable from myxoid degeneration.
Chronic insertional tendinopathy may demonstrate a tear with adjacent bony proliferation at the tendon insertion, with our without marrow edema.
- adjacent capsular or ligamentous injuries
- tendon instability
- on ultrasound, anisotropy artifact can mimic hypoechoic tendinopathic changes
- on MRI, magic angle artifact can mimic hyperintense tendinopathic changes