Table of Contents
- 01. Rotator Cuff
- 1. Anatomy and Function
- 2. Pathogenesis
- 3. Terminology
- 4. Natural History
- 5. Ultrasound Technique
- 6. Spectrum of Findings
- 7. Ultrasound Pitfalls
- 8. References
- 02. Postoperative Rotator Cuff
- 03. Long Head of Biceps Brachii Tendon
- 04. Bursae
- 05. Joint Spaces
- 1. Acromioclavicular Joint
- 2. Glenohumeral Joint
- 3. Sternoclavicular Joint
- 4. Scapulothoracic
- 5. References
- 06. Fractures
- 07. Os acromiale
- 08. Adhesive Capsulitis
- 09. Deltoid
- 10. Pectoralis Major
- 11. Web Exclusive: Sternocostal Joints
- 12. Web Exclusive: Musculoskeletal Ultrasound Educational Videos
- a. Best Original Manoeuver
- b. Snapping Film Direction
- c. Actor in a Leading Role
- d. Actress in a Leading Role
- e. Actor in a Supporting Role
- f. Actress in a Supporting Role
- g. Best Correlation Between Clinical and Sonographic Findings
- h. Joint Instability Short Film Documentary
- i. Unedited Film
- j. Real Time Impingement Short Film
- k. Nerve Compression Short Film
- l. Doppler Feature Special Award for Lifetime Achievements
- m. Interventional Feature Special Award for Distinguished Body of Work
- n. Honorary Award
6.2. Rotator Cuff Ultrasound: Calcific Tendinopathy
The histopathological changes in chronic tendinopathy are well recognized and consist of a predominant degenerative pattern characterized by disorganization of tendon fibers, increased granulation tissue, and absence of inflammatory cells.112-120 Fibrocartilaginous metaplasia, often accompanied by calcium deposits, is also common. What truly compose the calcium deposits in rotator cuff tendon disease is carbonate apatite.121 Two different types of carbonate apatite can be found and defined as A-type and B-type,122 depending on the position which carbonate ions occupy in the hydroxyapatite.123
Three main theories have emerged in an attempt to explain the mechanisms involved in tendon calcification. The first theory is the theory of reactive calcification and involves an active cell-mediated process,124 usually followed by spontaneous resorption by phagocytosing multinucleated cells showing a typical osteoclast phenotype.125 Such osteoclasts play a critical role in establishing the acidic environment that is essential for the resorption of mineral deposition.126 Osteopoitin, a potent regulator of calcium deposition on connective tissues, is also observed surrounding tendon calcification, but its role in calcific tendinopathy is unknown.127,128 The second theory suggests that calcium deposits are formed by a process resembling endochondral ossification. The mechanism involves regional hypoxia, which transforms tenocytes into chondrocytes.39,129. Insertional Achilles and patellar calcific tendinopathies are good prototypes for this theory. In insertional Achilles calcific tendinopathy, bone spurs occur after fibrocartilage cells arise from metaplasia of tenocytes.130 In patellar tendinopathy, calcification is associated with a marked increase of type-X collagen, a marker of endochondral pathway.131 Endochondral ossification may also apply to rotator cuff since animal models have been shown an increased expression of a fibrocartilage phenotype over a tendon phenotype related to repeated compression of the supraspinatus.132,133 The third theory involves ectopic bone formation from metaplasia of mesenquimal stem cells normally present in tendon tissue into osteogenic cells.134,135 The stimulus that causes this erroneous differentiation is still elusive, and a genetic susceptibility has been postulated in some individuals.136-140 As no single theory is satisfactory to explain all cases, calcific tendinopathy is currently believed to be multifactorial.
It is unknown why some tendons develop reactive calcification, while others undergo endochondral ossification or metaplasia of mesenquimal stem cells. Similarly, it is not clear if degeneration of the involved tendon is a requisite39,141-144 or not129 for calcification to develop. The self-limiting course of calcific tendinopathy suggests that deposition of calcium is an active cell-mediated process and mitigates against tendon degeneration as a requisite (table 1-3). Another compelling evidence against degeneration as a critical step comes from the description of calcium deposits in children.145-147 Clinical practice also does not support tendon degeneration as a requisite since many cases of calcific tendinopathy seen at US occur in otherwise normal tendons. The leading theory at present is that most cases of calcific tendinopathy correspond to a reactive process, and the tendon degeneration occasionally associated best considered the result of the reparative response to calcic deposition rather than the cause of presentation.
Table 1-3. Stages of calcific tendinopathy.Ϯ
Rotator cuff calcific tendinopathy is frequent and reported in 8 to 20% of adults on the basis of radiographs.167 Clinically, patients may be asymptomatic or may present with either acute or chronic pain.
The sonographic appearance of calcific tendinopathy is variable (table 1-4).168 In the formative phase, calcium deposits are depicted as an arciform echogenic structure with marked acoustic shadow (figure 1-25) or fragmented thin echogenic foci with variable shadowing (figure 1-26). In the resting phase, calcium deposits are thicker, more nodular, and typically show no shadowing (figure 1-27). Finally, in the resorptive phase, calcium deposits show bold echogenic wall surrounding a hypo-anechoic area or layering content (figure 1-28). Increased vascularity may be observed at any stage and reflects active reparative process (figure 1-29; videos 1-6 and 1-7). It is believed that the calcific tendinopathy becomes more symptomatic and vascularized when the calcium deposit undergoes resorption.169 Symptoms at this stage include severe pain and restriction of movement, usually for about two weeks.169
Table 1-4. Correlation of sonographic phase, morphology and symptoms during calcific stage of calcific tendinopathy.
Figure 1-28. Calcific supraspinatus tendinopathy in the resorptive phase.
Calcific tendinopathy involves supraspinatus, infraspinatus (figure 1-30), subscapularis (figure 1-31), and teres minor (figure 1-32) in decreasing order of frequency. Calcifications located in the subscapularis, infraspinatus (video 1-8), or teres minor tendons may be difficult to demonstrate radiographically because of the overlapping shadow of the humerus (figure 1-33). Calcium deposits may likewise be overlooked on MRI because it is not easily distinguished from the tendon. The reason why some calcium deposits involve the main body of the tendon, while others are insertional (figure 1-34) or even protrude from the tendon and collect beneath the subacromial-subdeltoid bursa is not clear (figure 1-35; video 1-9).
Figure 1-30. Calcific infraspinatus tendinopathy.
The erosive form is considered a variant presentation of calcific tendinopathy that is associated to poorer outcomes,170,171 and believed to result from active inflammation at the tendon insertion induced by calcium deposits (figure 1-36).172 Imaging findings may resemble those observed in rim-rent tears (see section 7.3), but the calcific material is usually thicker and longer when compared to the stria associated to partial-thickness tears (figure 1-37).
6.2.1. Grading of Calcific Tendinopathy
The most intuitive way of grading calcific tendinopathy is to report the size of calcium deposit, and there is some evidence to suggest that the it may correlate with shoulder pain in both preoperative173 and postoperative setting.174 However, this relationship is not free of controversy, especially because anecdotal experience during contralateral comparison suggests that the size of calcium deposit does not correlate with symptoms in many individuals. As a prognostic marker, the preoperative size of calcium deposit is irrelevant and clinical response after surgery correlates only with the absence of residual calcification.173
Hence, we generally do not report the size of calcium deposit because (1) there is no solid evidence indicating that this information is clinically relevant for management, (2) it induces the referring physician to mathematize the condition for follow-up, and (3) sonographic measurements may not correlate with the volume of calcium because of shadowing (figure 1-38). We, however, do our best to report the stage of calcific tendinopathy because it correlates with clinical symptoms and may influence management, but this can be challenging since the abnormality is often multifocal and not necessarily synchronic.175
6.2.2 Follow-up of Calcific Tendinopathy
Serial evaluation of calcific tendinopathy reveals a predictable pattern of morphologic changes, from precalcific to calcific and postcalcific stages. In the calcific stage, there is also a predictable pattern of changes, from formative to resting and resorptive phases. A prolonged time frame is typically required to obviate these changes, in the range of several months, not just few weeks.