Supraspinatus Tendonitis

Updated: Nov 06, 2023
  • Author: Thomas M DeBerardino, MD, FAAOS, FAOA; Chief Editor: Sherwin SW Ho, MD  more...
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Practice Essentials

Supraspinatus tendonitis is often associated with shoulder impingement syndrome. The common belief is that impingement of the supraspinatus tendon leads to supraspinatus tendonitis (inflammation of the supraspinatus/rotator cuff tendon and/or the contiguous peritendinous soft tissues), which is a known stage of shoulder impingement syndrome (stage II) as described originally by Neer in 1972. [1]

The causes of supraspinatus tendonitis can be broken down into extrinsic and intrinsic factors. [2, 3, 4]  Extrinsic factors are further broken down into primary impingement, which is a result of increased subacromial loading, and secondary impingement, which is a result of rotator cuff overload and muscle imbalance. In athletes whose sport involves stressful repetitive overhead motions, a combination of causes may be found.

Signs and symptoms

Pain is usually reported in the lateral, superior, anterior shoulder; occasionally it is referred to the deltoid region.

See Presentation for more detail.


Standard radiographic studies are used to rule out glenohumeral/acromioclavicular arthritis and os acromiale.

Magnetic resonance imaging (MRI) is considered the imaging study of choice for shoulder pathology.

See Workup for more detail.


The goals of the acute phase are to relieve pain and inflammation, prevent muscle atrophy without exacerbating the pain, reestablish nonpainful range of motion, and normalize the arthrokinematics of the shoulder complex. This includes a period of active rest, eliminating any activity that may cause an increase in symptoms.

The initial goals of the rehabilitation phase are to normalize range of motion and shoulder arthrokinematics, perform symptom-free activities of daily living, and improve neuromuscular control and muscle strength. Range-of-motion exercises are progressed to active exercises in all planes and self-stretches, concentrating on the joint capsule, especially posteriorly.

See Treatment and Medication for more detail.



Causes include the following:

  • Extrinsic causes

    • Primary impingement

      • Increased subacromial loading

      • Trauma (direct macrotrauma or repetitive microtrauma)

      • Overhead activity (athletic and nonathletic)

    • Secondary impingement

      • Rotator cuff overload/soft tissue imbalance

      • Eccentric muscle overload

      • Glenohumeral laxity/instability

      • Long head of the biceps tendon laxity/weakness

      • Glenoid labral lesions

      • Muscle imbalance

      • Scapular dyskinesia

      • Posterior capsular tightness

      • Trapezius paralysis

  • Intrinsic causes

    • Acromial morphology (ie, hooked acromion, presence of an os acromiale or osteophyte, calcific deposits in the subacromial space, all of which predispose to primary impingement)

    • Acromioclavicular arthrosis (inferior osteophytes)

    • Coracoacromial ligament hypertrophy

    • Coracoid impingement

    • Subacromial bursal thickening and fibrosis

    • Prominent humeral greater tuberosity

    • Impaired cuff vascularity

    • Aging (primary)

    • Impingement (secondary)

    • Primary tendinopathy

    • Intratendinous

    • Articular side partial-thickness tears

    • Calcific tendinopathy



United States statistics

Supraspinatus tendonitis is a common cause of shoulder pain in athletes whose sports involve throwing and overhead motions.

International statistics

From 23% to 38% of swimmers experience shoulder injuries within a 1-year period, and 23% of volleyball players have dominant shoulder pain during the season. [5]


Functional Anatomy

The shoulder consists of 2 bones (ie, humerus, scapula), 2 joints (ie, glenohumeral, acromioclavicular), and 2 articulations (ie, scapulothoracic, acromiohumeral). Several interconnecting ligaments and layers of muscles join these bones. The relative lack of bony stability in the shoulder permits a wide range of motion. Soft tissue structures are the major glenohumeral stabilizers.

The static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. The dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles such as the pectoralis major, latissimus dorsi, and serratus anterior.

The rotator cuff consists of 4 muscles, which control 3 basic motions: abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor for controlling external rotation, and the subscapularis for controlling internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head on the glenoid fossa, forming a force couple with the deltoid to allow elevation of the arm. It is responsible for 45% of abduction strength and 90% of external rotation strength.

The supraspinatus outlet is a space formed by the acromion, coracoacromial arch, and acromioclavicular joint on the upper rim and the humeral head and glenoid below. It accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been identified as a cause of impingement syndrome and rotator cuff tendonitis.

Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described that variations in acromial size and shape can contribute to impingement. From cadaveric studies, 3 different variations in the morphology of the acromion are described. Type I is flat, type II is curved, and type III is anteriorly hooked. Although the curved configuration is the most common (43% prevalence, compared with 17% for flat and 40% for hooked), the hooked configuration is associated most strongly with rotator cuff pathology.

Other sites of impingement in the supraspinatus outlet space include the coracoacromial ligament, where thickening can occur, and the undersurface of the acromioclavicular joint, where osteophytes can form. Only rarely is the medial coracoid involved. These impingement sites in the supraspinatus outlet are compressed further when the humerus is placed in the forward flexed and internally rotated position, forcing the greater tuberosity of the humerus into the undersurface of the acromion and coracoacromial arch.

Nonoutlet impingement can also occur. The causes may be loss of normal humeral head depression either from a large rotator cuff tear or weakness of the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. Another way this may occur is with thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.


Sport-Specific Biomechanics

Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff tendonitis. Shoulder pain and rotator cuff tendonitis are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, tennis).

Secondary impingement

Supraspinatus tendonitis is often attributed to impingement, which is seldom mechanical in athletes. Rotator cuff tendonitis in this population may be related to subtle instability and therefore may be secondary to such factors as eccentric overload, muscle imbalance, and glenohumeral instability or labral lesions. This has led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint.

Secondary impingement may be the most common cause in young athletes who use overhead motions and who frequently place repetitive large stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures and leading to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendon. These increased demands may lead to rotator cuff pathology such as partial tearing or tendonitis, and, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging on the coracoacromial arch, which leads to rotator cuff inflammation. In these patients, treatment should be directed at the underlying instability.

Glenoid impingement

Recently, the concept of glenoid impingement has been suggested as an explanation for partial-thickness rotator cuff tears in throwing athletes, particularly those tears involving the articular surface of the rotator cuff tendon. Such tears might occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon either from abnormal motion of the glenohumeral joint or from increased forces on the rotator cuff necessary to stabilize the shoulder.

Arthroscopic studies of these patients have noted impingement between the posterior superior edge of the glenoid and the insertion of the rotator cuff tendon with the arm placed in the throwing position, abducted and externally rotated. Lesions are noted along the area of impingement at the posterior aspect of the glenoid labrum and articular surface of the rotator cuff. This concept is believed to occur most commonly in throwing athletes and must be considered when assessing for impingement and rotator cuff tendonitis.



A study by Millar et al suggested proinflammatory cytokines may have a role in supraspinatus tendinopathy. [6] The investigators used custom micro-arrays to assess rat supraspinatus tendinopathy produced by running overuse. In addition, samples of torn supraspinatus tendon and matched intact subscapularis tendon from patients undergoing shoulder surgery for rotator cuff tears, as well as control samples of subscapularis tendon from 10 individuals with normal rotator cuffs undergoing arthroscopic shoulder stabilization, were collected and examined with semiquantitative reverse transcription polymerase chain-reaction (RT-PCR) and immunohistochemistry. [6] The presence of significant upregulation of proinflammatory cytokines and apoptotic genes was found in the rat samples (P = 0.005) as well as in the supraspinatus and subscapularis tendons obtained from the patients with rotator cuff tears (P = 0.0008).



In general, the prognosis is good for rotator cuff tendonitis that is promptly and correctly diagnosed and treated. Of patients, 60-90% improve and are free of symptoms with conservative treatment. Surgical outcomes are also very promising for patients in whom a full trial of conservative therapy fails.


If rotator cuff tendonitis is not diagnosed and treated promptly and correctly, it can progress to rotator cuff degeneration and eventual tear. A study by Quinlan et al found that in patients treated conservatively for rotator cuff tendinopathy, the rates of progression to full or partial tear at 1-2 years, 2-5 years, and over 5 years between MRI scans were 32%, 37%, and 54%, respectively. [7] Other complications may include progression to adhesive capsulitis, cuff tear arthropathy, and reflex sympathetic dystrophy. Complications may also result from surgery, injections, physical therapy, or medications.


Patient Education

Patient education may improve the outcome because the patient is educated regarding avoidance of provocative activities, pathology, and proper shoulder arthrokinematics. Education should also stress proper warm-up techniques, specific strengthening techniques, and warning signs of early impingement. A proper home exercise program should be formulated and encouraged to prevent recurrence of symptoms.