Rotator Cuff Tendinosis
Rotator cuff tendinosis is a chronic degenerative condition of the rotator cuff tendons—most commonly the supraspinatus—characterized by tendon degeneration without rupture, caused by repetitive mechanical stress, impingement, and hypovascularity, resulting in pain during overhead activities and weakness. 1
Pathophysiology
Rotator cuff tendinosis represents a chronic degenerative process rather than acute inflammation. 1 The condition develops through several mechanisms:
Mechanical impingement: Repeated compression of the supraspinatus tendon occurs between the humeral head and the coracoacromial arch during arm abduction, particularly when the humerus is simultaneously abducted and internally rotated. 1
Hypovascularity: The region proximal to the supraspinatus tendon insertion has poor blood supply, which impairs healing and predisposes to degeneration. 1
Repetitive microtrauma: Eccentric stress on the supraspinatus, external rotators, and scapular stabilizers leads to cumulative tendon damage, particularly in throwing athletes and overhead workers. 2
Scapular dyskinesis: Poor coordination of scapular movements during arm elevation contributes to abnormal biomechanics and progressive tendon wear. 2
Clinical Presentation
The hallmark features include:
Pain location: Anterior or anterolateral shoulder pain that worsens with overhead activities and arm elevation between 70-120 degrees (the "painful arc"). 1, 2
Weakness: Focal weakness during shoulder abduction and external rotation, though strength may be preserved at approximately 4/5 in early tendinosis without complete tear. 2, 3
Decreased range of motion: Particularly during abduction with external or internal rotation. 2
Night pain: Common complaint that disrupts sleep, especially when lying on the affected shoulder. 3
Diagnostic Features on Imaging
MRI findings show tendon signal abnormalities without focal disruption:
Tendinous enlargement with heterogeneous signal pattern demonstrating diffuse increased signal intensity on T1 weighting, often with slight increase on T2 weighting. 1
No focal tendon disruption distinguishes tendinosis from partial- or full-thickness tears. 1
Associated findings may include subacromial bursal thickening and morphologic abnormalities of the acromion. 1
Ultrasound is equivalent to MRI for detecting rotator cuff abnormalities when performed by experienced operators, showing tendon thickening and altered echogenicity. 1, 4
Physical Examination Findings
Hawkins' test: Pain with forcible internal rotation at 90 degrees forward flexion (92% sensitive, 25% specific for impingement). 1, 2
Neer's test: Pain with full forward flexion between 70-120 degrees (88% sensitive, 33% specific). 1, 2
Preserved passive range of motion distinguishes tendinosis from adhesive capsulitis. 4
Epidemiology and Risk Factors
Prevalence: Affects approximately 1 in 50 adults (2% of the population). 1
Age: Most common after 40 years of age, with increasing prevalence in older decades. 1
Occupational risk: Particularly common in laborers working with arms overhead and athletes who throw repetitively. 1
Dominant arm involvement: Occurs more frequently in the dominant arm due to repetitive use. 1
Key Distinction from Other Conditions
Tendinosis differs from tendon tears: Tendinosis shows signal abnormality without focal disruption, while partial-thickness tears demonstrate focal fiber discontinuity and full-thickness tears show signal extending from inferior to superior tendon surface on all MRI sequences. 1
Tendinosis differs from acute tendinitis: The term "tendinosis" specifically indicates chronic degenerative changes rather than acute inflammation, as the role of inflammation in chronic tendon conditions is unclear. 1
Common Pitfalls
Do not assume all rotator cuff pain represents tendinosis: 10% of rotator cuff tears are asymptomatic and present only with morphologic changes on imaging, while symptomatic tendinosis may exist without imaging abnormalities. 1
Avoid misinterpreting secondary impingement: In younger patients, rotator cuff weakness combined with ligamentous laxity causes dynamic instability (secondary impingement), which differs mechanically from primary structural impingement in older adults. 2
Do not overlook scapular dyskinesis: This is a primary contributor that must be addressed in treatment, as poor scapular coordination perpetuates the impingement cycle. 2, 4