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Calcium Apatite Deposition Disease: Diagnosis and Treatment Hindawi Publishing Corporation Radiology Research and Practice Volume 2016, Article ID 4801474, 16 pages http://dx.doi.org/10.1155/2016/4801474 Review Article Calcium Apatite Deposition Disease: Diagnosis and Treatment Nicholas M. Beckmann Department of Diagnostic and Interventional Imaging, UT Health, Houston, TX, USA Correspondence should be addressed to Nicholas M. Beckmann; [email protected] Received 28 September 2016; Accepted 24 October 2016 Academic Editor: Ali Guermazi Copyright © 2016 Nicholas M. Beckmann. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Calcium apatite deposition disease (CADD) is a common entity characterized by deposition of calcium apatite crystals within and around connective tissues, usually in a periarticular location. CADD most frequently involves the rotator cuff. However, it can theoretically occur in almost any location in the musculoskeletal system, and many different locations of CADD have been described. When CADD presents in an unexpected location it can pose a diagnostic challenge, particularly when associated with pain or swelling, and can be confused with other pathologic processes, such as infection or malignancy. However, CADD has typical imaging characteristics that usually allows for a correct diagnosis to be made without additional imaging or laboratory workup, even when presenting in unusual locations. This is a review of the common and uncommon presentations of CADD in the appendicular and axial skeleton as well as an updated review of pathophysiology of CADD and current treatments. 1. Overview is unknown. Several authors have speculated that the forma- tion may be the result of tendon degeneration, while others Calcium apatite deposition disease has been given many have proposed that the calcifications are a cell-mediated reac- names (calcific periarthritis, calcific bursitis, periarthritis cal- tive process [11–14]. Uhthoff and Loebr proposed a natural carea, periarthritis calcarea, and hydroxyapatite rheumatism) progression of calcific tendinitis that can be divided into four butismostcommonlyknownascalcifictendinitis.Itisarel- phases: precalcific, formative, resorptive, and postcalcific [15]. atively common phenomenon characterized by formation of In the precalcific phase, collagen fibers of the tendon undergo calcium deposits both in and around tendons and other con- metaplasia into fibrocartilage tissue. During the formative nective tissue structures. Calcific tendinitis most commonly phase, chondrocytes begin to develop within the areas of occurs in between the ages of 30–60, although cases have been fibrocartilage formation with eventual formation of calcified described in patients as young as 3 years old [1, 2]. A large apatite crystals. After the formative phase, the area of calci- majority of cases of calcific tendinitis occur at the shoulder, fication can remain asymptomatic in a “resting state” for an particularly involving the supraspinatus and infraspinatus indefinite period of time. Typically, however, the calcifi- tendons. The hip is the next most common location of cationswillprogresstoaninflammatoryresorptivephase involvement, followed by the spine. Although rarely reported, characterized by the appearance of leukocytes, lymphocytes, calcific tendinitis has been described involving numerous and giant cells forming a “calcium granuloma.” Finally, the other sites as well [3–6]. calcification will enter the postcalcific phase where a repar- Historically, calcium deposits in calcific tendinitis have ative process incites new capillary and collagen fiber forma- been thought to represent collections of hydroxyapatite crys- tion. tals leading to the used of the term hydroxyapatite deposition Calcific tendinitis typically presents with a single site disease (HADD) to describe this disease process [7, 8]. How- of involvement. However, bilateral presentation of shoulder ever, more recent studies by Hamada et al. in 2001 and 2006 calcific tendinosis is not uncommon, occurring in anywhere demonstrated the calcium deposits of calcific tendinitis to be from 5 to 23% of patients in larger studies of rotator cuff cal- composed of carbonate apatite instead of hydroxyapatite as cific tendinitis [16–18]. Bilateral involvement has been rarely previously thought [9, 10]. The exact etiology of these deposits described in the hip [19], and bilateral involvement has not 2 Radiology Research and Practice been described in any other joint. There is a slight female excludes other etiologies of pain when the presenting symp- predilection for calcific tendinitis with calcific tendinitis toms are atypical. MRI appearance of the calcifications varies occurring approximately 50% more frequently in women depending on the radiographic appearance of the calcifica- than men [2]. A study by Harvie et al. showed an association tions, and the degree of soft tissue inflammation depends between estrogen and thyroid hormone disorders and the on the stage of the calcifications. In the acutely symptomatic development of calcific tendinitis, which may account for at phase, soft tissue edema will typically be seen surrounding least a portion of the female predilection [17]. Sengar et al. the region of calcification (Figure 3(a)) [4, 15, 29]. Discrete, discovered an association between the HLA-A1 gene and homogeneous calcifications on radiographs appear as homo- calcific tendinitis, suggesting a genetic predisposition to the geneous signal voids on all MRI sequences (Figure 3(b)), disease [20]. An association has also been found between while ill-defined inhomogeneous calcifications on radio- adult onset diabetes and calcific tendinitis [21]. graphs appear as heterogeneous low and intermediate signal on both T1 and fluid sensitive MRI sequences (Figure 3(a)). 2. Clinical Presentation Ultrasound is not commonly needed to make the diag- nosis of calcific tendinitis, but it is commonly used in image- Calcium apatite deposition is often seen incidentally on guided treatment of the calcifications. Four morphologies of radiographs in asymptomatic patients. When patients are tendon calcification have been described on ultrasound (Fig- symptomatic, symptoms can vary from an acute episode ure 4): arc-shaped (echogenic arc of calcification with deep of severe pain to chronic mild discomfort. Typically, acute acoustic shadowing), nodular (single echogenic focus of cal- episodes of pain are single occurrences that resolve sponta- cification without acoustic shadowing), fragmented (two or neously, although patients can experience recurrence of pain more echogenic foci of calcification with or without acoustic months after the initial episode [22]. Occasionally, patients shadowing), and cystic (hyperechoic wall with anechoic will present with symptoms of neuropathy [5, 6, 23]. These region, weakly hypoechoic region, or layering content) [30]. acute episodes of pain are what frequently lead to patients The nodular, fragmented, and cystic morphologies on ultra- presenting for treatment and can be a diagnostic challenge sound are associated with the acute, symptomatic phase of for clinicians. Acute episodes of calcific tendinitis frequently calcific tendinitis while the arc morphology is more sugges- present with severe pain along with mild swelling and warmth tive of the chronic or asymptomatic phase [30]. Increased of the affected tissue, which can be easily mistaken for infec- flowonpowerDopplerisstronglyassociatedwithacute tion [24, 25]. Restricted range of motion may or may not be symptomatic calcific tendinopathy but is present in only present. Laboratory and vital signs are usually normal; how- about one-third of cases [31]. In the rotator cuff, thickening of ever,itisnotuncommonforpatientstohavemildlyelevated the subacromial-subdeltoid bursa is strongly associated with inflammatory markers, mild leukocytosis, or low grade fever, acute symptomatic calcific tendinopathy but is present in less which can also raise the concern for infection [4, 25–27]. than one-third of cases [31]. Furthermore, it is not uncommon for acute calcific tendinitis Nuclear medicine exams are rarely used to diagnose episodes to be preceded by low level trauma, and the amor- calcific tendinitis. Not surprisingly, cases of calcific tendinitis phous calcifications may be mistaken for a neoplastic process have been described as demonstrating increased radiotracer [4, 24, 26]. activity on both positron emission tomography and techne- tium-99m bone scans (Figure 5) [32–34]. This increased 3. Imaging activity is likely related to the inflammatory phase of calcific tendinitis and can be confused for malignancy or bony The diagnosis of calcific tendinitis is most frequently made metastatic disease. on radiographs. Calcifications have been described typically Rarely, calcific tendinitis can extend to involve the under- appearing as fluffy, ill-defined, and inhomogeneous or as lying bone at the tendon attachment site. Approximately 80% discrete, homogeneous, and well defined (Figure 1) [8, 15, 28]. ofosseousinvolvementbycalcifictendinitisoccursatthepro- The fluffy, ill-defined calcifications are associated withthe ximal femur and proximal humerus with the femur diaphy- acutely symptomatic phase of calcific tendinitis, while the sis most commonly involved followed by the humerus tuber- better defined, homogeneous calcifications tend to be present osities. Cortical erosion
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