Calcific tendinopathy of the shoulder

INTRODUCTION — Calcific tendinopathy is a disorder of the shoulder of unknown etiology. It is characterized by the formation of deposits of calcium crystals in one or several of the rotator cuff tendons, leading to pain and dysfunction [1,2]. Many cases resolve spontaneously or with conservative management. In cases with persistent symptoms, invasive treatment measures may be required.

This topic will review the pathophysiology, diagnosis, and management of calcific tendinopathy of the shoulder. Shoulder pain and other conditions of the rotator cuff are discussed separately. (See "Evaluation of the adult with shoulder complaints" and "Subacromial (shoulder) impingement syndrome" and "Rotator cuff tendinopathy" and "Presentation and diagnosis of rotator cuff tears".)

TERMINOLOGY — Calcific tendinopathy is a disorder of the shoulder of unknown etiology characterized by the formation of deposits of calcium crystals in one or several of the rotator cuff tendons [1]. Tendon inflammation located around the deposits and increased intratendinous pressure are thought to contribute to pain [3]. Different terms such as calcific tendinopathy, calcific tendinitis, calcific shoulder periarthritis, calcific tendonitis, or rotator cuff calcification disease are used in the literature to refer to the condition. In this topic, we use the term "calcific tendinopathy."

ETIOLOGY — The cause of calcific tendinopathy remains unknown. Most experts agree that it is not caused by trauma or overuse, and it is rarely part of a systemic disease, although it may be associated with diabetes, thyroid disorders, or kidney stones [4,5].

Some reports suggest there is a genetic predisposition for the development of intratendinous calcific deposits, a claim supported by the relatively high frequency of bilateral occurrence. However, to the authors' knowledge, clear proof of this has not been presented.

PATHOPHYSIOLOGY AND NATURAL COURSE — Our understanding of the pathogenesis of rotator cuff disorders is incomplete. The pathophysiology of chronic tendon disorders is discussed separately. (See "Overview of overuse (persistent) tendinopathy".)

The pathophysiology of calcific tendinopathy of the shoulder remains controversial. The calcific deposits consist of poorly crystallized hydroxyapatite, an inorganic component of bone tissue. An early hypothesis described calcification as a consequence of age-related tendon degeneration. However, this is not supported by several findings, including the relatively young patient age at the peak incidence, the spontaneous healing and resolution that occurs in many cases (in stark contrast with degenerative tendinopathy), and the development of the condition in healthy, untraumatized tissue.

In 1997, Uhthoff and Loehr proposed that calcific tendinopathy was a disease that progressed through four distinct phases, with correlating pathologic and clinical findings [2]. This scheme remains the most common way to describe the disease:

●In the formative phase, a portion of the tendon undergoes a fibrocartilaginous transformation, and calcification occurs in the transformed tissue. Calcific deposits enlarge during this stage.

●In the resting phase, the calcific deposits remains stable. These deposits may or may not become painful. If large enough, they may cause mechanical symptoms.

●In the resorptive phase, an inflammatory reaction may occur. Vascular tissue develops around the deposit, and macrophages and giant cells absorb the deposit. The calcific deposit occasionally leaks into the subacromial bursa, which often causes extreme pain. The trigger for the resorptive phase remains unknown [6].

●In the post-calcific phase, the deposit has been resorbed and fibroblasts reconstitute the normal collagen pattern of the tendon. However, on sonography, small punctiform hyper-echogenicities can be seen in the area of the former deposit, even long after resorption.

While this description of the phases of the disease is generally accepted, the severity and duration of symptoms vary considerably among patients. In some patients painful periods alternate with pain free periods, while in others severe pain can develop acutely (so-called acute calcific tendinopathy), probably as a consequence of leakage of calcific crystals into the overlying bursa. Overall, approximately 50 percent of patients become pain free spontaneously or with conservative treatment during the first three months, and an additional 20 percent become pain free during the first year, while 30 percent develop persistent pain or repeated episodes of pain over several years.

Pain may be caused by impingement, inflammation, and other effects. Mechanically, calcium deposits can reduce the space between the rotator cuff and the acromion causing subacromial soft tissues to become impinged. The deposits and reduced space can also impair the normal function of the rotator cuff. Inflammation during resorption of calcific deposits can produce pain. In addition, increased intratendinous pressure may contribute to a patient's symptoms. (See "Subacromial (shoulder) impingement syndrome" and "Rotator cuff tendinopathy".)

The variable time course of symptomatic calcific tendinopathy is reflected in observational studies, of which only a limited number are available. The authors of one observational study reported that 50 percent of patients with chronic calcific tendinopathy were pain-free after six months [7]. According to another retrospective study of 159 patients, 70 percent were pain-free by 49 months [8].

In observational studies, factors found to be associated with a negative prognosis among patients treated conservatively included bilateral occurrence, localization to the anterior portion of the acromion, medial (subacromial) extension, and a high volume of calcific deposits [9]. In one study, additional factors included dominant arm involvement, bilateral disease, longer duration of symptoms, female gender, and multiple calcifications [10].

Of the 30 percent of patients who do not improve spontaneously or with conservative treatment, approximately two-thirds have been reported to improve with barbotage or extracorporeal shockwave therapy, and the remaining 10 percent referred for surgery. However, these improvement rates were drawn from cohort studies without adequate control groups, and it is unclear whether they reflect the natural history of the condition or the effects of placebo or treatment interventions. The effectiveness of treatments is discussed below. (See 'Management' below.)

EPIDEMIOLOGY — Shoulder pain is a common presenting complaint among adults, with lifetime prevalence estimates reported to be as high as 67 percent [11]. Most such patients present with subacromial pain, as is the case with calcific tendinopathy. The prevalence of the calcific tendinopathy has been reported to be 3 to 10 percent in the general population [2,12], and 7 to 17 percent among individuals with shoulder pain [13]. Approximately 50 percent of all calcific deposits are asymptomatic. The condition is bilateral in 10 to 40 percent and is most common among females in the fourth to sixth decades of life. Women of this age with subacromial pain and a calcific deposit >1.5 cm in length have the highest risk of symptomatic calcific tendinopathy of the rotator cuff.

Associations between calcific tendinopathy of the shoulder and endocrine disease, including diabetes mellitus, disorders of the thyroid, estrogen metabolism, and nephrolithiasis, have been reported in several observational studies [4,5,14]. Contrary to popular belief, individuals involved in strenuous manual labor or athletic activities are not more commonly affected than those who are sedentary [15].

CLINICAL PRESENTATION — The clinical presentation of calcific tendinopathy varies with the extent of the calcification and the phase of the condition. Each phase is described above. In the authors' experience, the presentation of calcific tendinopathy of the shoulder does not vary by age. (See 'Pathophysiology and natural course' above.)

Patients with symptomatic calcific tendinopathy typically describe shoulder pain similar to that experienced by patients with rotator cuff tendinopathy or shoulder impingement syndrome. Pain is the cardinal symptom and is localized on the top or lateral aspect of the shoulder or both, often with radiation towards the insertion of the deltoid. The onset of pain is gradual and unassociated with trauma. Most patients report increased pain at night and an inability to lay on the affected shoulder. Daily activities involving overhead motions, such as putting on a shirt or brushing hair, can be painful. In many cases symptoms resolve spontaneously over three to six months. (See "Subacromial (shoulder) impingement syndrome" and "Rotator cuff tendinopathy".)

A more chronic course, with symptoms persisting for a year or longer, is seen in approximately one-third of patients. In these cases, pain-free periods may be interrupted by episodes of pain that can vary widely in severity and duration. Management of these patients often entails invasive measures. (See 'Management' below.)

Some patients in the resorptive phase of the condition present with a dramatic, acute increase in shoulder pain (acute calcific tendinopathy). They commonly hold the arm in a protective manner close to the body and sometimes are not willing to move the shoulder at all. The acute phase may be the result of a spontaneous leakage of calcium crystals from the deposit into the overlying bursa. It typically lasts for 10 to 14 days and is often followed by significant clinical improvement.

PHYSICAL EXAMINATION — The general evaluation of the patient with shoulder pain, the shoulder examination, and other specific shoulder problems are discussed separately. (See "Evaluation of the adult with shoulder complaints" and "Physical examination of the shoulder" and "Rotator cuff tendinopathy" and "Subacromial (shoulder) impingement syndrome" and "Overview of the management of overuse (persistent) tendinopathy" and "Presentation and diagnosis of rotator cuff tears".)

On examination, patients with calcific tendinopathy typically experience pain when the shoulder is moved actively through its normal arc of abduction, or there may be a pain-related decrease in the range of abduction. Scapular dyskinesis can be seen when lowering the arm from abduction. In patients with such dyskinesis, the clinician will note asynchronous scapular movement – rapid, wobbly motion of the scapula during shoulder movement. Passive movement of the shoulder is usually unaffected. Pain inhibition can give an impression of muscular weakness. One or several of the commonly used impingement tests, such as the Hawkins test or Neer test, is usually positive [16,17]. (See "Physical examination of the shoulder", section on 'Assessment of abduction and the supraspinatus' and "Physical examination of the shoulder", section on 'Special tests for shoulder impingement'.)

Patients suffering from an acute episode of pain due to calcific tendinopathy often refuse to move their shoulder, holding their arm close to their bodies in internal rotation, and do not allow a shoulder examination to be performed.

DIAGNOSTIC IMAGING — Diagnostic imaging, typically plain radiographs and ultrasound (US), is necessary to distinguish calcific tendinopathy from other conditions that cause subacromial pain.

Initial imaging: Plain radiography — Standard plain radiographs of the shoulder are often adequate for initial imaging of the patient with suspected calcific tendinopathy of the shoulder. Anteroposterior (AP), outlet, and internal and external rotation views should be obtained. These enable the clinician to assess the size, location, morphology, and "texture" of any deposit.

Typically, the calcification is located somewhat proximal to the greater tubercle (image 1). Deposits that are localized in the infraspinatus or subscapularis tendon can be hidden by the humeral head but are often visible on internal or external rotation views. Even small calcifications can be seen on radiographs, but it is important to distinguish between the cloud-like appearance of calcific tendinopathy and calcifications that appear as fine lines located at tendon insertions. The latter are typical of insertional tendinopathy of the shoulder (image 2).

Plain radiographs are helpful for determining the stage of the disease (eg, resting (image 3) or resorptive (image 1)). In the resting phase, the deposit typically appears dense and homogeneous with well-defined limits and sometimes consists of multiple fragments. In the resorptive phase, the deposit has a more fluffy appearance with poorly defined limits and in some cases with an area of increased density at its center.

Repeat plain radiographs obtained during follow-up allow the clinician to see whether the deposit has changed appearance or disappeared. Some authors have developed classification schemes for the deposits according to their radiologic morphology, but none have been widely adopted [18,19].

Ultrasound — US is a useful tool for diagnosing calcific tendinopathy of the shoulder, as it is highly sensitive for detecting calcifications. In the resting phase, calcifications usually appear as hyperechoic lesions with acoustic shadowing (image 4). In the resorptive phase the deposit may appear more fluffy, fragmented, or punctuated (image 5). Pain caused by compression from the transducer while a calcific deposit is visualized suggests the deposit is contributing to the patient's symptoms. In addition to diagnosing calcific tendinopathy, US is useful for identifying many associated rotator cuff injuries and bursitis.

Magnetic resonance imaging — While calcific deposits can be detected using magnetic resonance imaging (MRI), routine use of MRI is not indicated for calcific tendinopathy. Depending upon the clinical scenario, MRI may be useful if other shoulder pathologies, such as labral or rotator cuff tears, are suspected. (See "Superior labrum anterior to posterior (SLAP) tears" and "Presentation and diagnosis of rotator cuff tears".)

LABORATORY STUDIES — Calcific tendinopathy is not associated with abnormal laboratory findings. Serum concentrations of calcium, phosphate, and alkaline phosphatase are within normal limits. Thus, laboratory studies are not indicated as routine tests for the diagnosis or management of calcific tendinopathy.

DIAGNOSIS — The diagnosis of calcific tendinopathy can be made reliably based on a suggestive history and clinical findings, and diagnostic imaging (generally, plain radiographs or ultrasound) that reveals calcific deposits. Typically, patients report a gradual onset of shoulder pain unassociated with trauma. Individuals involved in strenuous manual labor or athletic activities are not at increased risk. Pain is the cardinal symptom and is localized on the top or lateral aspect of the shoulder or both, often with radiation towards the insertion of the deltoid. Most patients report increased pain at night and an inability to lay on the affected shoulder. In daytime, use of the arm above shoulder height causes pain. Plain radiographs or ultrasound reveal characteristic calcific deposits. (See 'Diagnostic imaging' above.)  

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of shoulder pain is broad and the approach to these patients is discussed separately. Several diagnoses sometimes mistaken for calcific tendinopathy of the shoulder are discussed briefly below. (See "Evaluation of the adult with shoulder complaints".)

Distinguishing clinically between calcific tendinopathy and some of the conditions listed below is difficult as symptoms may be similar. However, in the large majority of cases, calcific tendinopathy can be distinguished from other causes of subacromial pain by demonstrating the presence of one or more calcific deposits using plain radiographs or ultrasound (US).

●Rotator cuff tear – US or magnetic resonance imaging (MRI) examination can be performed to differentiate shoulder pain caused by a full-thickness rotator cuff tear from calcific tendinopathy. With US, calcific deposits are seen as hyperechoic areas with shadow, and the rotator cuff tendon can be visualized. Conversely, a full-thickness rotator cuff tear appears as a hypoechoic area within the tendon or the tendon cannot be visualized, and no calcific deposits are identified. The sonographic appearance of a calcific deposit is so characteristic that a negative study nearly excludes the diagnosis. On MRI, a calcific deposit is seen as a hypointense (black) signal, in contrast to a rotator cuff tear which is characterized by a hyperintense signal corresponding to fluid.

A partial-thickness rotator cuff tear cannot be excluded definitively by a negative US or MRI, as both have limited sensitivity and specificity for the condition. However, either study can exclude the presence of calcific tendinopathy and thus can be of value in some cases. Patient history may be helpful for differentiating the two conditions as partial tears sustained by patients younger than 50 years are typically related to trauma while calcific tendinopathy is not. (See "Presentation and diagnosis of rotator cuff tears".)

●Cervical radiculopathy ‒ Cervical radiculopathy can mimic the pain from calcific tendinopathy, but it is typically accompanied by neurologic symptoms in the affected upper extremity, such as numbness, tingling, burning, or weakness, and by radiation to the neck region. (See "Clinical features and diagnosis of cervical radiculopathy".)

●AC osteoarthritis and biceps tendinopathy ‒ Osteoarthritis of the acromioclavicular (AC) joint and bicipital tendinopathy can be distinguished from calcific tendinopathy by the differing locations of pain and tenderness (focal at the AC joint or over the proximal biceps tendon, respectively). Calcific deposits are absent on radiographs or US in both conditions. AC joint arthritis has a characteristic appearance on both plain radiograph and US. Biceps tendinopathy is readily identified with US. (See "Acromioclavicular joint disorders" and "Biceps tendinopathy and tendon rupture".)

●Glenohumeral osteoarthritis ‒ Glenohumeral osteoarthritis has distinctive features on plain radiograph, not including calcific deposits, and nearly always causes some motion restrictions that are not related to pain. (See "Clinical manifestations and diagnosis of osteoarthritis", section on 'Shoulder'.)

●Frozen shoulder ‒ Distinguishing between an acute attack of calcific tendinopathy and the early, painful phase of frozen shoulder can be difficult. However, in patients with calcific tendinopathy, active and passive shoulder motion improve after an intrabursal or subacromial injection of anesthetic, while stiffness persists in patients with frozen shoulder. Musculoskeletal ultrasound is useful for distinguishing between the two conditions. The typical fluffy, fragmented, or punctuated appearance of deposits in calcific tendinopathy is absent in frozen shoulder. (See "Frozen shoulder (adhesive capsulitis)".)

MANAGEMENT

Initial therapy — Calcific tendinopathy of the shoulder is often self-limited with a relatively benign clinical course. Therefore, first-line therapy should be conservative and focused on symptom relief. Initial treatments may include oral anti-inflammatory and analgesic medication, glucocorticoid injection, and physical therapy.

Little evidence is available to guide the selection of conservative measures or to determine which should be preferred. Interventions are often performed with a "try it and see" approach. Glucocorticoid injection may be prompted by the presence of severe pain, sonographic findings of a fluid collection within a thickened bursa overlying a calcific deposit, or by increased signal around the deposit when assessed with power Doppler, all suggesting the presence of acute inflammation that may respond to glucocorticoid injection. The contributors to this topic have found glucocorticoid injection to provide effective short-term pain relief.

Physical therapy should focus on correction of upper body posture and restoration of scapulothoracic and glenohumeral strength and function, and it should not cause undue pain. Physical therapy for scapulothoracic and glenohumeral dysfunction is reviewed separately. (See "Rehabilitation principles and practice for shoulder impingement and related problems".)

Two prospective observational studies reported success rates of 73 percent (306 of 420 patients) and 72 percent (66 of 87 patients), respectively, after a minimum of three months of conservative treatment [9,20]. In the larger of these studies, negative prognostic factors for a successful outcome included the following:

●Calcific deposits in both shoulders

●Large volume deposits (eg, ≥1500 mm³)

●Localization of deposits near the anterior portion of the acromion

●Subacromial extension of the deposits

Therapy of an acute attack of calcific tendinopathy — Patients who present with an acute episode of severe pain from calcific tendinopathy can often be treated effectively with a subacromial injection of a glucocorticoid. Suitable medications for injection include triamcinolone 20 to 40 mg or methylprednisolone 20 to 40 mg. We prefer to dilute the glucocorticoid with a local anesthetic such as lidocaine. (See "Intraarticular and soft tissue injections: What agent(s) to inject and how frequently?", section on 'Use of glucocorticoid injections'.)

Therapies for refractory cases — If symptoms fail to improve despite appropriate conservative treatment for one year or even longer, alternative treatment options may be entertained. These include extracorporeal shockwave therapy (ESWT) and ultrasound (US)-guided lavage and needling (barbotage), although high-quality evidence supporting these interventions is limited. Selection of either intervention will vary based upon local resources and preferences.

If the patient remains symptomatic following ESWT or barbotage, surgical treatment may be performed. Possible surgical interventions include acromioplasty, removal of the deposit, or some combination of each.  

Extracorporeal shock wave therapy — ESWT uses acoustic waves to fragment calcific deposits in the rotator cuff. According to limited observational evidence, resolution of symptoms and improvement in shoulder function may occur in up to 70 percent of patients treated with ESWT following an unsuccessful trial of conservative therapy [21,22]. Two systematic reviews of randomized trials assessing the effectiveness of ESWT have concluded that it yields significant reductions in pain and improvements in function when compared with placebo [23,24]. Another systematic review with broader inclusion criteria reported trends toward improvement but emphasized that all trials were susceptible to bias [25]. High-quality, randomized trials directly comparing ESWT using higher energy with barbotage are lacking.

ESWT protocols differ in dose (low or high energy), duration (impulses), and the interval of administration. Proponents disagree about the optimal approach. Most studies comparing different protocols report better results with medium- to high-dose therapy [21,26-30]. However, an optimum value for the total cumulative dose of energy that should be administered has not yet been defined [23,26-29]. While the procedure is generally well tolerated with newer equipment, it can be performed under local anesthesia or following administration of oral analgesics if patients experience undue discomfort.

Barbotage — Barbotage is an ultrasound-guided lavage technique that involves breaking up and then aspirating pieces of the calcific deposit. This approach may be used for chronic or acute, painful cases of calcific tendinopathy. While barbotage may not be as effective as previously thought, the contributors to this topic believe the procedure benefits some patients whose symptoms persist despite conservative management and continues to be an appropriate therapeutic option.

Ultrasound-guided barbotage is performed on an outpatient basis, often in combination with a glucocorticoid injection. This combination of interventions both removes part or all of the calcification and treats the resulting inflammation. Aspiration of calcium is possible in most but not all cases. Sometimes, the deposit is too hard to aspirate. However, the amount of calcium that can be removed may not affect outcomes, and a decrease in the size of the deposit over time is seen regardless of how much calcium is aspirated initially [31].

Barbotage is technically straightforward. It is performed under local anesthesia, generally well tolerated, and requires about 20 minutes to complete. Consequently, many clinics that manage calcific tendinopathy of the shoulder use barbotage as their preferred treatment following failed conservative management. A video of the barbotage procedure can be seen at the following link: video barbotage procedure [32].

The overall effectiveness of barbotage is unclear. While cohort studies have reported good to excellent results in approximately 65 to 75 percent of patients [33-38], the most rigorous study to date, a multicenter randomized trial, found no long-term differences in outcome [39]. In this trial, 220 adults with calcific tendinopathy of at least three months duration were randomly assigned to one of three treatment arms: barbotage plus injection with glucocorticoid and analgesic, sham barbotage plus injection with glucocorticoid and analgesic, or sham barbotage plus injection of analgesic alone (ie, no glucocorticoid). At four months, patients in all three groups experienced moderate improvement in shoulder symptoms and function as measured by the Oxford Shoulder Score, but no significant differences were noted among treatment groups, while at 24 months no intervention was superior to sham treatment. In a previous randomized trial of 48 patients, no difference in clinically important outcomes was noted at five-year follow-up between barbotage and glucocorticoid injection alone [40].

Earlier studies suggested greater benefit. A systematic review of 15 studies involving 1450 shoulders concluded that barbotage is a "safe and effective procedure" for the treatment of calcific tendinopathy [41]. Another systematic review limited to eight randomized trials (published prior to the multicenter trial described above) involving 617 cases reached similar conclusions but mentioned limitations in methodology [42]. In a small number of comparison studies with a one year follow-up, barbotage appeared to yield better results than glucocorticoid injection alone [43] or ESWT [44].

Inconsistencies in reports of the effectiveness of barbotage may stem from a lack of clarity about appropriate selection criteria. Interventions and baseline characteristics reported to be associated with good short- or medium-term outcomes following barbotage include glucocorticoid injection with the barbotage procedure (better result at three-month follow-up compared with barbotage alone) [45,46]. While earlier studies reported that retrieval of calcific material during barbotage and larger deposit size were associated with improved outcomes, the multicenter trial described above found no such association [39].

Surgery — Approximately 10 percent of patients with calcific tendinopathy of the shoulder do not respond to conservative treatment, ESWT, or barbotage, and may be candidates for surgical treatment [47]. Surgery is usually performed arthroscopically and interventions may include removal of the calcification without acromioplasty, acromioplasty without removal of the calcification, or acromioplasty and removal of the calcification.

While evidence is limited to small, observational studies, good results have been reported with all three approaches, and none has proven superior [1,48-55]. Follow-up of patients treated with acromioplasty shows disappearance of deposits in the majority of cases after two years and good clinical results [50,51]. A point of debate is whether the tendon defect caused by arthroscopic calcium removal should be repaired. While some authors believe that repair is not required, others recommend tendon repair if the defect size exceeds 1 cm [1,49].

Unproven therapies — A number of therapies for calcific tendinopathy are under investigation. Dry needling has been studied in a small number of trials, but its effectiveness is unproven [56].

Compared with glucocorticoid injection, adjunct therapy with platelet-rich plasma (PRP) injection was found to produce no clinically significant differences in functional outcome at two-year follow-up in a well-blinded, randomized trial of 80 patients, all of whom were treated with needle aspiration of calcific deposits [57]. While the group treated with glucocorticoid had better scores on functional assessments at six weeks and lower morbidity, the PRP group had higher rates of complete calcium resorption (84 versus 66 percent). Given the low cost, low morbidity, and comparable long-term outcomes of glucocorticoid, it remains the preferred adjunct treatment for calcific tendinopathy. (See "Biologic therapies for tendon and muscle injury".)

FOLLOW-UP CARE — Follow-up with the supervising clinician and subsequent management varies according to the stage of the disease, at what point treatment was initiated, and the response to treatment. Common scenarios are discussed below.

Follow-up of patients treated conservatively — For patients being managed with physical therapy, with or without analgesic medication, follow-up should be performed at approximately four months, after completion of the physical therapy program. A clinical examination focused on assessing shoulder mobility and strength should be performed at that time. Repeat imaging by sonography and plain radiographs can be reserved for patients with persistent symptoms, as findings on imaging help to guide treatment decisions in these cases. Patients with persistent symptoms after three to six months of physical therapy and a calcific deposit still demonstrable on imaging should be evaluated for further treatment, such as extracorporeal shockwave therapy (ESWT), barbotage, or surgery.

Patients with persistent symptoms but minimal or no calcific deposits on imaging should be treated for a subacromial pain syndrome (ie, shoulder impingement). (See "Subacromial (shoulder) impingement syndrome" and "Rehabilitation principles and practice for shoulder impingement and related problems".)

Follow-up after barbotage and ESWT — Patients treated with barbotage or ESWT should follow a post-treatment physical therapy exercise program aimed at restoring shoulder mobility and function. Follow-up with the supervising clinician can be performed after approximately four months of physical therapy, and should include clinical examination and reimaging, preferably by ultrasound (US).

Patients with persistent symptoms or dysfunction despite treatment with barbotage or ESWT should be assessed for a second barbotage treatment if sonography reveals a persistent, dense calcific deposit of more than 5 mm in diameter. If the deposit has disappeared or is 5 mm or less, and symptoms persist despite an appropriate physical therapy program, patients should be referred for possible surgery.

A return to manual labor or sport that places significant demands on the shoulder should only be permitted when the shoulder is pain-free during and after the performance of the activities entailed in the sport or work. The final stage of physical therapy should include tasks that closely simulate the demands to be placed on the shoulder by the patient's sport or work.

Follow-up after treatment of an acute painful episode — For patients experiencing acute, painful episodes of calcific tendinopathy, follow-up should be early, typically after one or two weeks, and should include a shoulder examination to assess mobility and strength, along with repeat plain radiographs or US of the shoulder. Clinical examination should be identical to the initial assessment and findings from the two examinations should be compared. If a glucocorticoid injection was given at the initial visit and was effective (ie, pain absent or substantially reduced), we recommend a wait-and-see approach together with the initiation of a gentle physiotherapy exercise program. If the patient is better but still symptomatic, and deposit volume and density are unchanged or only slightly reduced, early barbotage treatment may be performed after discussion of the benefits and risks with the patient. If significant pain persists, a second glucocorticoid injection may be performed, supplemented by oral pain medication. These patients are reassessed in another one to two weeks and the same treatment approach described here can be followed.

PROGNOSIS AND COMPLICATIONS — The prognosis for calcific tendinopathy of the shoulder is generally good, with deposits spontaneously resorbed and therapeutic measures leading to a resolution of symptoms in the large majority of cases. (See 'Pathophysiology and natural course' above.)

Complications can be related to the condition itself or to treatment measures [58,59]. Some patients develop adhesive capsulitis due to a spontaneous leakage of calcium crystals into the overlying bursa, or following arthroscopic removal of the deposit or, in a very small percentage of cases, following barbotage, when it is likely caused by residual calcium debris around the tendon.

An association between calcific tendinopathy and rotator cuff tears has been reported [59]. Whether the coexistence of the two pathologies is incidental or one causes the other remains unclear. It is not unusual for partial-thickness rotator cuff tears to be sustained during arthroscopic removal of calcific deposits. The size of such tears depends upon the extent of the resection necessary to remove the deposit. If the procedure causes a large tear, surgical repair may be needed. (See "Presentation and diagnosis of rotator cuff tears" and "Management of rotator cuff tears".)

Osteolysis of the greater tuberosity is a rare complication of calcific deposits that lie in contact with or close to the greater tuberosity [59]. This condition is associated with a more prolonged and severe course of calcific tendinopathy and can be diagnosed with magnetic resonance imaging. Ossifying tendinitis is another rare complication of surgical removal of calcific deposits [60].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General issues in muscle and tendon injury diagnosis and management" and "Society guideline links: Shoulder soft tissue injuries (including rotator cuff)".)

SUMMARY AND RECOMMENDATIONS

●Definition and etiology – Calcific tendinopathy is a disorder of the shoulder of unknown etiology characterized by the formation of deposits of calcium crystals in one or several of the rotator cuff tendons. The condition does not appear to be related to trauma or overuse. (See 'Terminology' above and 'Etiology' above.)

●Pathophysiology and disease course – Calcific tendinopathy is thought to progress through four distinct phases, which are described in the text. The severity of symptoms and duration of each phase can vary substantially. Pain may be caused by impingement, inflammation, increased intratendinous pressure, and other effects. In most cases symptoms resolve spontaneously over three to six months. A more chronic course, with symptoms persisting for a year or longer, is seen in approximately one-third of patients. (See 'Pathophysiology and natural course' above.)

●Clinical presentation – Patients with symptomatic calcific tendinopathy typically describe shoulder pain similar to that experienced by patients with rotator cuff tendinopathy or shoulder impingement. Pain is the cardinal symptom, develops gradually in most cases, and is localized on the top or lateral aspect of the shoulder or both, often with radiation towards the insertion of the deltoid. Most patients report increased pain at night and an inability to lay on the affected shoulder. Daily activities involving overhead motions can be painful. (See 'Clinical presentation' above.)

●Physical examination – Patients typically experience pain when the shoulder is moved actively through its normal arc of abduction, or there may be a pain-related decrease in the range of abduction. Scapular dyskinesis can be seen when lowering the arm. Passive movement of the shoulder is usually unaffected. Common tests of shoulder impingement (eg, Neer, Hawkins) are usually positive. Patients suffering from an acute episode of pain may be unwilling to move their shoulder. (See 'Physical examination' above.)

●Diagnostic imaging and diagnosis – Diagnostic imaging, typically plain radiographs and ultrasound (US), is necessary to distinguish calcific tendinopathy from other conditions that cause subacromial pain. The diagnosis of calcific tendinopathy can be made reliably based on a suggestive history and clinical findings, and diagnostic imaging that reveals calcific deposits (image 2). (See 'Diagnostic imaging' above and 'Diagnosis' above.)

●Differential diagnosis – The differential diagnosis for calcific tendinopathy of the shoulder includes: rotator cuff tear, cervical radiculopathy, acromioclavicular osteoarthritis, biceps tendinopathy, glenohumeral osteoarthritis, and frozen shoulder. (See 'Differential diagnosis' above.)

●Initial treatment – For initial management, we suggest a conservative approach focused on symptom relief (Grade 2B). Initial treatments may include oral anti-inflammatory and analgesic medication, glucocorticoid injection, and physical therapy. Patients who present with an acute episode of severe pain can often be treated effectively with a subacromial injection of a glucocorticoid (eg, triamcinolone 20 to 40 mg; methylprednisolone 20 to 40 mg). (See 'Initial therapy' above.)

●Treatment of refractory disease – For patients whose symptoms fail to improve despite appropriate conservative management, we suggest treatment with either extracorporeal shockwave therapy (ESWT) or US-guided lavage and needling (barbotage) (Grade 2C). The decision of which to use largely depends on patient preference and local expertise and equipment. If neither ESWT nor barbotage is effective, surgical referral is appropriate. (See 'Therapies for refractory cases' above.)