Rotator cuff pathology can be caused by extrinsic or intrinsic causes. Extrinsic examples include a traumatic tear in tendons from a fall or accident. Overuse injuries from repetitive lifting, pushing, pulling, or throwing are also extrinsic in nature. Intrinsic factors include poor blood supply, normal attrition or degeneration with aging, and calcific invasion of tendons. Impingement of the rotator cuff relative to the acromion, age, smoking and diabetes mellitus are commonly associated with rotator cuff disease.
Rotator cuff dysfunction is typically a continuum of pathology ranging from tendonitis and bursitis, to partial tearing, to a complete tearing in one or more of the tendons. Although the earlier stages may resolve with conservative care, actual tearing of the tendon can be more problematic. These tears most commonly occur at the tenoperiosteal (tendon-to-bone) junction. Since this area has a relatively poor blood supply, injury to the tendon at this location is very unlikely to actually heal. Additionally, the constant resting tension in the muscle-tendon unit, or muscle tone, pulls any detached fibers away from the bone, preventing their reattachment. Finally, joint fluid from within the shoulder may seep into the tear gap and prevent the normal healing processes from occurring.
Once a supraspinatus tendon defect is established, it typically propagates posteriorly through the remainder of the supraspinatus tendon, then into the infraspinatus muscle. With the increasing defect of the cuff tendon, the spacer effect of the cuff tendon is lost (as well as its stabilizing effect), allowing the humeral head to displace superiorly, placing increased load on the biceps tendon. As a result, the breadth of the long head tendon of the biceps is often greater in patients with cuff tears in comparison with uninjured shoulders. In chronic cuff deficiency, the long head tendon of the biceps frequently is ruptured.
Clinically, a rotator cuff rupture is characterized by painful or impaired active abduction, with reduced strength in abduction, external rotation and elevation. However, a degenerative rotator cuff rupture may also be asymptomatic. Ten percent of the population has an atraumatic and subclinical rotator cuff rupture in their fourth decade of life; this increases to 50% in the sixth decade and 80% in the eighth decade. Fifty percent of patients over 50 years of age with an asymptomatic rotator cuff rupture become symptomatic within 5 years.
Milgrom et al. studied the integrity of the rotator cuff in both dominant and non-dominant shoulders of 90 asymptomatic adults between the ages of 30 and 99 years using ultrasound. The criteria for diagnosis had been validated on unembalmed cadaver specimens. The authors found no statistically significant difference in the incidence of impingement findings between dominant and non-dominant arms, or between genders or exertional shoulder activities. This is an important finding in relation to occupational rotator cuff problems which have been attributed to repetitive motion injuries. The prevalence of partial- or full-thickness tears increased markedly after 50 years of age: these were present in over 50% of dominant shoulders in the seventh decade and in 80% of subjects over 80 years of age. The authors concluded that the results indicated that rotator cuff lesions are a natural correlate of aging, and are often present without symptoms.
Numerous studies have been conducted to look at the etiology of rotator cuff tears. The general consensus, as noted above, seems to be that the cause is multifactorial. However, it is generally believed that in non-athletes above the age of 40 without a defined acute traumatic shoulder injury, age-related degeneration is the primary factor responsible for rotator cuff tears.
One such study was conducted by Hashimoto et al. The authors performed histopathologic, histochemical, and morphometric studies on 80 medial stumps of torn rotator cuff tendons to clarify the cause of tears. A high prevalence and diffuse distribution of degenerative changes were observed in the rotator cuff tendons including thinning and disorientation of collagen fibers, myxoid degeneration, hyaline degeneration, chondroid metaplasia, calcification, vascular proliferation, and fatty infiltration. No distinct inflammatory reaction was observed. Thinning and disorientation of collagen fibers, myxoid degeneration, and hyaline degeneration were seen in all cases. All changes except vascular proliferation and fatty infiltration were more pronounced in the middle to deep layers of the tendons than in the superficial layer. The collagen fibers were disoriented in the deep layer of the tendons, shown by microscopic image analysis. The frequency and distribution of thinning and disorientation of collagen fibers, myxoid degeneration, and hyaline degeneration suggested that these were early degenerative processes. Chondroid metaplasia and calcification may be chronic pathologic changes that occur after tearing regardless of the type of tear. The authors concluded that preexisting degenerative change in the middle and deep layers of the tendon in association with microtrauma seemed to be the main cause of rotator cuff tears.
Degenerative muscular changes associated with rotator cuff tears include fatty infiltration and atrophy. This has led to the specific study of the natural history of fatty infiltration and atrophy of the supraspinatus muscle in rotator cuff tears with the goal of better defining the relationship between the symptomatic time period before diagnosis of rotator cuff tear and the development of fatty infiltration and atrophy among various tear patterns.
Melis et al. retrospectively reviewed 1688 patients with rotator cuff tears and recorded the following: number of tendons torn, etiology of the tear, time between onset of shoulder symptoms and diagnosis of rotator cuff tear. Fatty infiltration of the supraspinatus was graded using either CT or MRI classification. Muscular atrophy was measured indirectly using the tangent sign. Overall, the onset of fatty infiltration was earlier, and its progression was faster in patients with more than one tear. The time between the onset of rotator cuff symptoms and diagnosis of rotator cuff tear played a major role in the development of muscular changes.
The authors observed that the fatty infiltration was minimal in small tears and minimal or absent in asymptomatic small tears. Greater supraspinatus fatty infiltration was observed with longer delay between symptom onset and the diagnosis of rotator cuff tear on imaging studies. With all rotator cuff tear types in this study, moderate fatty infiltration developed at an average of 4 years (45.7 months ± 61.8 months) after the onset of symptoms. Severe fatty infiltration appeared at an average of 6 years (70.3 months ± 74 months) after the onset of symptoms. Nevertheless, for patients who experienced traumatic rotator cuff tears, moderate fatty infiltration appeared at an average of 3 years (34.8 ± 55.7 months) after the initial incident/onset of symptoms. Severe fatty infiltration (stage 3 or 4) developed at an average of 5 years (57.7 ± 66.7 months) after the initial incident/onset of symptoms.
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