Version July 2025
INTRODUCTION —
Basic calcium phosphate (BCP)-associated musculoskeletal syndromes can be organized into calcific periarthritis and arthritis associated with BCP crystals. The predominant mineral type in BCP-associated musculoskeletal pathology is carbonated hydroxyapatite [1].
The term "basic calcium phosphate" refers to a trio of submicron-sized calcium phosphate crystals. These include partially carbonate-substituted hydroxyapatite, octacalcium phosphate, and tricalcium phosphate (whitlockite). The terms "calcium phosphate" and "hydroxyapatite" are often used synonymously with the more accurate term "basic calcium phosphate." BCP crystals are similar in composition to the normal mineral found in bones and teeth as well as to the pathologic mineral found in atherosclerotic plaques and calcinosis cutis.
An overview of the pathogenesis of BCP-associated musculoskeletal syndromes and the clinical manifestations, diagnosis, and treatment of BCP-associated calcific periarthritis, also termed calcific tendinitis or tendinopathy, will be discussed here. Calcific tendinopathy of the shoulder and BCP-associated arthritis are presented in detail separately. (See "Calcific tendinopathy of the shoulder" and "Basic calcium phosphate (BCP) crystal arthritis, including Milwaukee shoulder syndrome".)
PATHOGENESIS OF BCP-ASSOCIATED MUSCULOSKELETAL SYNDROMES —
The etiology of pathologic basic calcium phosphate (BCP) crystal formation is not fully understood [2]. BCP mineral formation often occurs at sites of local tissue damage associated with injury or inflammation. Once formed, BCP crystals can produce symptoms and mediate tissue damage by several mechanisms, including the induction of a vigorous inflammatory response, biomechanical disruption, and through direct interactions with nearby cells, resulting in tissue damage in the absence of inflammation [3-7]. Relatively little is known about the factors that specifically initiate symptomatic arthritis or periarthritis associated with BCP crystals.
There are several contributors to BCP crystal formation, which together with locally high levels of extracellular calcium and phosphate tip the balance of pro- and antimineralization factors to allow BCP crystals to form. These include chondro- or osteometaplasia, which may serve as an inciting factor in BCP mineral formation at sites of local tissue damage [8]. Cytokines and growth factors found at sites of tissue damage [9] and alterations in extracellular matrix proteins may also contribute to BCP crystal formation [10].
Once formed, BCP crystals can produce symptoms and mediate tissue injury in several ways. Under certain circumstances, BCP crystals induce a vigorous inflammatory response [3]. The mechanism linking BCP crystals to inflammation may involve innate immune pathways, which are shared by other particulates, including monosodium urate (MSU) and calcium pyrophosphate (CPP) crystals. Factors that modulate the inflammatory potential of crystals include crystal size, the type and amount of protein coating the crystals, and the presence of nearby tissue trauma.
Little is known about the factors that initiate symptomatic arthritis or periarthritis associated with BCP crystals. One theory is that BCP tissue deposits are asymptomatic until something triggers their dissolution and subsequent osteoclast-mediated resorption introduces pain-producing factors into the surrounding tissues. BCP crystal deposition also disrupts normal tissue biomechanics [4]. Lastly, BCP crystals can directly interact with resident connective tissue cells, even in the absence of an inflammatory response, to produce destructive cytokines, growth factors, and enzymes. As an example, BCP crystals directly induce synovial fibroblasts to increase mitogenesis [5] and secrete tissue-damaging factors such as collagenase and prostaglandin E2 (PGE2) [6]. BCP crystals have also been shown to promote osteoclastogenesis, resulting in local bone destruction [7].
EPIDEMIOLOGY AND RISK FACTORS —
Calcific periarthritis most often affects healthy, middle-aged patients. Trauma, metabolic, and genetic factors may each be associated with increased risk of basic calcium phosphate (BCP)-associated calcific periarthritis.
●Epidemiology – Calcific periarthritis most often develops in middle-age but can be seen across the age spectrum, including rare case reports in children [11]. Case series demonstrate that two- to threefold more females are affected than males [12,13].
●Exogenous or acquired risk factors – Most patients with calcific periarthritis are in good general health and have no known risk factors. Some patients report a history of recent trauma or overuse as an antecedent to symptomatic periarthritis.
Diabetes [14], altered estrogen states, and thyroid disease [15] have been suspected as risk factors for calcific periarthritis, but sufficient evidence is lacking to establish clear associations with these conditions.
The metabolic abnormalities associated with end-stage kidney disease (ESKD) have also been implicated in causing symptomatic periarthritis, but this association is not well documented by population-based studies. This issue is complicated by metabolic abnormalities, such as secondary hyperparathyroidism, that produce systemic elevations of calcium and phosphate and cause widespread BCP mineral deposition known as calciphylaxis. (See "Calciphylaxis (calcific uremic arteriolopathy)".)
●Genetic risk factors – A number of genetic disorders, including some affecting phosphate metabolism, have been associated with calcific periarthritis. As examples, some adult patients with familial recurrent calcific periarthritis have subtle forms of hypophosphatasia caused by a congenital deficiency of alkaline phosphatase [16] (see "Skeletal dysplasias: Specific disorders", section on 'Hypophosphatasia'). In addition, symptomatic calcific periarthritis has been reported in patients with CD73 deficiency [17] and in family members of several kindreds with an Augustine-null blood type related to mutations in the equilibrative nucleoside transporter 1 (ENT1) [18].
Dramatic familial presentations with large periarticular calcified masses are usually associated with congenital causes of hyperphosphatemia. These patients typically present in childhood and have mutations of GLANT3 or the genes encoding fibroblast growth factor 23 (FGF23) or alpha-Klotho. Calcific periarthritis may be the first manifestation of these syndromes in patients with milder phenotypes. (See "Overview of the causes and treatment of hyperphosphatemia".)
Other forms of familial calcific periarthritis have been described in association with mutations that produce spondyloepiphyseal dysplasia [19]. These cases are distinguished from other syndromes by the presence of short stature. (See "Skeletal dysplasias: Specific disorders", section on 'Spondyloepiphyseal dysplasia congenital' and "Skeletal dysplasias: Specific disorders", section on 'Spondyloepiphyseal dysplasia tarda'.)
CLINICAL MANIFESTATIONS —
Calcific periarthritis typically causes the acute onset of severe pain involving a single joint, tendon, or bursal area; it can occur around both large and small joints as well as in the spine [20]. The affected joints are focally tender with a variable degree of warmth and swelling. Erythema may be present. Joint effusions are typically absent, and the area of tenderness may not correlate with the typical location of the joint line. Patients sometimes report fever and chills.
Attacks are self-limited, lasting a few weeks to several months. There are case reports of more chronic symptoms, but it remains unclear whether persistent radiographically evident calcifications contribute to such persistent symptoms [21].
More common syndromes include the following:
●Large joint involvement – Shoulder involvement is the most commonly recognized and best-studied form of calcific periarthritis [22]. Typically, patients report a gradual onset of shoulder pain without trauma. Pain 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 lie on the affected shoulder, while during the day, use of the arm above shoulder height causes pain. This condition is described in detail separately (see "Calcific tendinopathy of the shoulder"). Elbow involvement is uncommon and typically involves the distal biceps tendon [23].
Calcific periarthritis around the hip has been well described, but its prevalence is not known. It most frequently involves the rectus femoris, the gluteus maximus, or the gluteus minimus tendon, usually near the femoral insertions [24]. Symptoms from rectus femoris involvement include pain and tenderness near the anterior-inferior iliac spine and are exacerbated by hip flexion. Snapping hip syndrome has been associated with calcific deposits in the rectus femoris. Involvement of the gluteus maximus produces pain in the proximal thigh, while gluteus minimus involvement causes pain in the low back, buttock, or posterolateral thigh. Iliopsoas involvement is less common and can produce pain in the hip or knee. Knee involvement is uncommon and, when it does occur, can affect any of the ligaments, bursae, and tendons around the knee [25].
●Small joint involvement – Calcific periarthritis may develop around the small joints of the hands and feet. Hand involvement often occurs at the flexor carpi ulnaris but may affect any of the hand tendons. Involvement of the wrist or base of the thumb may cause acute onset of symptomatic carpal tunnel syndrome [26], and trigger finger has been reported [27].
Foot involvement is most frequently reported at the first metatarsal phalangeal joint, where it typically presents with symptoms at the plantar aspect of that joint. This syndrome has been referred to as "hydroxyapatite pseudopodagra" and may be particularly common in young women [28]. Calcific periarthritis of the foot less commonly involves the peroneus longus tendon or the navicular insertion of the tibialis posterior tendon (image 1A-B).
●Other sites of involvement – Retropharyngeal calcific tendinitis involves the longus colli high in the cervical spine and can present with acute onset of neck pain and stiffness associated with dysphagia and odynophagia [29].
LABORATORY TESTING —
Acute phase responses (as indicated by the erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP] levels) are elevated in some symptomatic patients. Other laboratory studies, including complete blood count (CBC), basic chemistries, and levels of calcium, phosphorus, and alkaline phosphatase are typically normal.
IMAGING
●Plain film radiography – Radiographs show amorphous-appearing extraarticular calcifications. These are often in or near tendons or bursae. Calcifications may be present in tendons, bursae, ligaments, or soft tissues (image 1A and image 1B). Bone erosions may occur adjacent to the calcific density [30]. Periarticular calcific densities are often described as amorphous or "cloud-like" when they are acute, while chronic calcifications may be denser and more homogeneous. Grading systems have been developed that are based upon the radiographic density of the calcification [31]. However, the size and grade of calcification correlates poorly with clinical manifestations or outcomes [21,24].
●Ultrasonography – Ultrasonography is helpful in expert hands and has been well studied in calcific tendinitis of the shoulder [32]. In the resting phase, calcifications usually appear as hyperechoic lesions with acoustic shadowing (image 2). In the resorptive phase, the deposit may appear more fluffy, fragmented, or punctuated (image 3). (See "Calcific tendinopathy of the shoulder", section on 'Ultrasound'.)
●Magnetic resonance imaging – Magnetic resonance imaging (MRI) cannot readily distinguish calcified material from other types of tissue damage. T2 and short tau inversion recovery (STIR) images on MRI often demonstrate edema in the area around the calcific deposit.
●Computed tomography – Computed tomographic (CT) scanning, by contrast with MRI, readily identifies calcifications, and CT scans can be used to confirm the anatomic location of the calcific deposit.
●Other – Bone scanning with technetium-99m and positron emission tomography (PET) scanning show concentrated tracer at sites of inflammation around basic calcium phosphate (BCP) deposits that may mimic the appearance of malignant lesions [33].
HISTOPATHOLOGY —
Careful handling of specimens is necessary in order to prevent dissolution of calcium phosphate by methods commonly used for tissue staining and preservation. There are few histopathologic studies of calcific periarthritis. In one study, a predominantly histiocytic infiltrate was demonstrated on most pathologic samples from patients with calcific periarthritis, but some tissue samples had neutrophilic infiltrates [12]. Most calcifications appear as granular and psammoma-like, while larger amorphous calcifications were less common [30].
DIAGNOSIS
Diagnosis and diagnostic evaluation
●All patients – The diagnosis of calcific periarthritis is based upon the presence of a characteristic clinical presentation and typical findings on plain radiographs; the most typical presentation is of an acute onset of pain and swelling around a single joint in a healthy young or middle-aged woman (see 'Clinical manifestations' above). On physical examination, there is no obvious joint effusion, and tenderness may not be located at the joint line. The presence of periarticular calcifications on plain radiographs of symptomatic areas are usually sufficient to confirm the diagnosis of calcific periarthritis, and no further diagnostic testing is necessary in typical cases. (See 'Imaging' above.)
●Selected patients – Further imaging such as computed tomography (CT) scanning may be necessary to visualize calcific deposits in deep structures, such as the iliopsoas or retropharyngeal areas, or to more accurately localize calcification in areas where two-dimensional imaging with conventional radiographs is inadequate. (See 'Imaging' above.)
A biopsy of the involved tissues with culture and histopathologic analysis may be helpful in patients with an atypical presentation, increased concern for infection, or in the absence of radiographic findings of calcification [12]. (See 'Histopathology' above.)
Postdiagnostic evaluation — Multiple episodes or multiple sites of calcific periarthritis should prompt a thorough family history as well as an evaluation for metabolic disorders. In patients with any of these features, further testing should include serum levels of calcium, phosphate, and alkaline phosphatase, and these results may prompt genetic testing.
DIFFERENTIAL DIAGNOSIS —
Calcific periarthritis is frequently misdiagnosed. It is most often mistaken for acute gouty arthritis, acute calcium pyrophosphate (CPP) crystal arthritis, or infectious arthritis. Each of these is a true arthritis, and thus either physical examination or imaging studies should demonstrate a synovial effusion. Other conditions may also be mistaken for calcific periarthritis.
●Acute crystal arthritis (gout and calcium pyrophosphate deposition [CPPD] disease) – Acute pain in the region of the joint may be present with both calcific periarthritis and acute gout or acute CPP arthritis. However, the demographics of gout and CPP crystal arthritis are quite different from those of calcific periarthritis. Gout typically develops in older men with other comorbidities, including metabolic syndrome, and acute CPP crystal arthritis is rare in people under the age of 60. (See "Gout: Clinical manifestations and diagnosis" and "Calcium pyrophosphate crystal deposition (CPPD) disease: Clinical manifestations and diagnosis".)
Calcified tophi can be confused with periarticular calcifications and have a rim of calcification rather than the cloud-like appearance seen in calcific periarthritis (image 4); however, these typically appear in patients with well established gout.
●Infectious arthritis – Both infectious arthritis and calcific periarthritis can cause pain and swelling in the region of the joint, as well as fever and chills. Unlike periarthritis, infections that involve the joint are associated with demonstrable joint effusions, and infections involving the soft tissues or bursae rarely cause radiographic calcifications. (See "Septic arthritis in adults".)
●Osteosarcoma and chondrosarcoma – Calcifications with nearby osseous erosions on radiograph can be mistaken for osteo- or chondrosarcomas. The correct diagnosis is established by biopsy of these lesions. (See "Osteosarcoma: Epidemiology, pathology, clinical presentation, and diagnosis" and "Chondrosarcoma".)
●Trauma and fracture – Trauma, particularly around the small joints of the hands and feet, should also be considered in the differential diagnosis. Metatarsal fractures, for example, can present with pain, swelling, and erythema in the forefoot or midfoot without a clear history of injury, similar to the findings of calcific periarthritis. Avulsion fractures may also be confused with calcific periarthritis. Expert review of radiographs or advanced imaging will typically aid in distinguishing a fracture from calcific periarthritis. (See "Forefoot pain in adults: Evaluation, diagnosis, and select management of common causes" and "Overview of finger, hand, and wrist fractures".)
●Sesamoiditis – Sesamoiditis, a tendinopathy, can also be confused with calcific periarthritis of the first metatarsal phalangeal joint, and advanced imaging may be required to distinguish between these two entities. (See "Forefoot pain in adults: Evaluation, diagnosis, and select management of common causes".)
●Synovial chondromatosis – Rarely, the calcifications of calcific periarthritis may resemble lesions of synovial chondromatosis. These appear as multiple intraarticular chondral bodies with "ring and arc" chondroid mineralization and extrinsic bony erosions. Symptoms are frequently chronic in synovial chondromatosis, and this may be more common in men. (See "Radiologic evaluation of knee tumors in adults", section on 'Synovial (osteo)chondromatosis' and "Imaging evaluation of the painful hip in adults", section on 'Pigmented villonodular synovitis and synovial osteochondromatosis' and "Radiologic evaluation of the painful shoulder in adults", section on 'Magnetic resonance imaging'.)
●Other conditions – Less commonly, calcific periarthritis can be confused with calcifications in the surrounding tissue outside of the joint, including skin, muscle, and vasculature (calcinosis cutis, myositis ossificans, or phleboliths). CT scanning should allow for accurate localization of the calcific density if these alternative diagnoses are entertained. Heterotopic ossification is often considered in the differential diagnosis but has a distinct radiographic appearance with a corticated rim of bone-like tissue around the density. Unusual ossicles can be confused with calcific periarthritis but should have visible trabeculae characteristic of bone. Tissue calcification can also occur after intralesional injections, including glucocorticoid injections [34]. These are typically asymptomatic, and a history of injections at the site of involvement would support this possibility. (See appropriate topic reviews.)
MANAGEMENT
Overall strategy — The goals of therapy are the elimination of pain, reduction of inflammation, and dissolution of the calcific deposit. Most patients do well with nonsteroidal antiinflammatory drug (NSAID) therapy alone or with the injection of intralesional glucocorticoids. Most symptoms resolve within four to eight weeks [24]. (See 'Initial therapy' below.)
In patients whose symptoms are refractory to NSAIDs and local glucocorticoid injection, percutaneous needling (barbotage) is generally both safe and well tolerated. We reserve extracorporeal shockwave therapy (ESWT) or arthroscopic or open surgical procedures for patients who continue to have symptoms despite treatment with NSAIDs, local glucocorticoid injection, and percutaneous needling. (See 'Resistant to initial therapy' below.)
Rarely, other types of systemic antiinflammatory therapy (specifically, systemic glucocorticoids or interleukin 1 [IL-1] inhibition) are used when patients are unable to use NSAIDs and have multiple affected sites or an affected site that is inaccessible to intralesional interventions. These approaches are also sometimes used to treat refractory symptoms. (See 'Other therapies for patients refractory to usual therapies' below.)
This approach is supported by case reports, case series, our personal experience, and by inference from the available, but somewhat limited, evidence regarding treatment of shoulder disease. There are few randomized trials of therapies in calcific periarthritis, but some systematic reviews have been performed in patients with shoulder involvement. These studies focus on ultrasound-guided needle lavage [35] and ESWT [36] and have uncertain applicability to calcific periarthritis in other sites. The management of calcific periarthritis of the shoulder is described in detail separately. (See "Calcific tendinopathy of the shoulder".)
Initial therapy — For initial therapy of calcific periarthritis, we use either NSAID therapy or an intralesional glucocorticoid injection.
●We use an NSAID (eg, naproxen 500 mg twice daily or ibuprofen 400 to 600 mg four times daily or 800 mg two to three times daily, with a maximum dose in young healthy individuals of 3200 mg daily) in patients with normal kidney function and without contraindications to NSAID use (eg, cardiovascular disease or risk factors for gastrointestinal disease). (See 'NSAIDs' below.)
●We use an intralesional glucocorticoid injection in patients in whom a local injection is feasible based upon the accessibility of the involved site; the availability of imaging guidance, where needed (eg, for deep sites); and the expertise of the treating clinician. An injection is also appropriate in patients unable to use NSAIDs (eg, due to contraindications) or who have experienced an inadequate response to NSAIDs after 48 to 72 hours of treatment. (See 'Intralesional glucocorticoids' below.)
NSAIDs — NSAIDs target both pain and inflammation and are the first-line therapy for many patients with calcific periarthritis. In patients with normal kidney function and no contraindications to NSAID use, we would begin with naproxen (500 mg twice daily). Alternatively, ibuprofen (eg, 400 to 600 mg four times daily or 800 mg two to three times daily, with a maximum dose in young healthy individuals of 3200 mg per day) could be used. For patients who do not tolerate relatively nonselective NSAIDs, a more cyclooxygenase 2 (COX-2)-specific NSAID may be substituted (eg, celecoxib 200 mg twice daily or meloxicam 7.5 mg daily). (See "Overview of COX-2 selective NSAIDs".)
Treatment should be given for the duration of symptoms. Significant reductions in pain levels and improvement of function after 48 to 72 hours of therapy should be used as indications of adequate response.
NSAIDs are generally be avoided in patients with certain conditions including active gastric or duodenal ulcers, cirrhosis, chronic kidney disease (especially with an estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m2), poorly controlled hypertension, moderate to severe or uncompensated heart failure, use of anticoagulants, and/or NSAID allergy. Contraindications to and adverse effects of NSAIDs are discussed in detail elsewhere. (See "Nonselective NSAIDs: Overview of adverse effects" and "Overview of COX-2 selective NSAIDs", section on 'Toxicities and possible toxicities'.)
Patients who are at high risk of gastrointestinal toxicity related to NSAIDs may need coadministration of a proton pump inhibitor (PPI; eg, omeprazole 20 mg orally twice daily). (See "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity" and "NSAIDs (including aspirin): Treatment and secondary prevention of gastroduodenal toxicity".)
This approach is supported by case reports and personal experience.
Intralesional glucocorticoids — Intralesional glucocorticoids may act more quickly to resolve symptoms and have fewer side effects compared with systemic medications. We use 10 to 40 mg of methylprednisolone acetate administered once. The dose should be based on the size of the area involved; areas around small joints typically have smaller calcifications and lower doses can be used. The use of shorter-acting glucocorticoids, such as methylprednisolone acetate, minimizes the risk of soft tissue atrophy that may occur with longer-acting glucocorticoids. Ultrasound or fluoroscopic guidance is warranted in situations where the calcification is not close to the skin surface, such as the hip; by contrast, calcific periarthritis around a finger or toe can often be injected without radiographic guidance.
We typically wait 48 to 72 hours to see an effect on pain and function.
This approach is supported by case reports and personal experience.
Resistant to initial therapy — In patients who do not respond NSAIDs or local glucocorticoid injection, there are several treatment options. Two of these are minimally invasive nonsurgical options (needle aspiration and ESWT) and the other is arthroscopic surgery to remove calcific deposits.
We use needle aspiration (eg, barbotage) in patients who are unresponsive to NSAIDs and/or glucocorticoid injection, and we reserve referral for arthroscopic or open surgery to patients who are refractory to NSAIDs, glucocorticoid injection, and needle aspiration. All three approaches have been reported as beneficial for calcific tendinopathy of the shoulder; most data are from case series, with only limited and heterogenous randomized trial data. (See "Calcific tendinopathy of the shoulder", section on 'Therapies for refractory cases'.)
●Needle aspiration (barbotage) — We generally reserve needle aspiration for patients who have not responded well to NSAIDs or intralesional glucocorticoids. The most commonly used procedure is also known as barbotage and involves repeated aspiration and injection of the calcific deposit.
Needle aspiration is typically performed under ultrasound guidance and in many centers is done by musculoskeletal radiologists. The skin is cleaned with betadine and the area is injected with 1% lidocaine after radiographic confirmation of the location of the deposit. Then a mixture of lidocaine and sterile saline is repeatedly injected and aspirated into the calcium deposit to break it up, typically using an 18 gauge needle attached to a 5 mL syringe. Small pieces of the deposit are often visible in the syringe. The addition of a subacromial glucocorticoid injection to this procedure may reduce pain and improve function in cases of calcific tendinitis in the shoulder. The use of this technique for calcific tendinopathy of the shoulder and a summary of the evidence is described in detail separately. (See "Calcific tendinopathy of the shoulder", section on 'Barbotage'.)
●Extracorporeal shockwave therapy – ESWT may be useful in patients who have not responded to initial therapy and have failed needle aspiration [36]. However, this procedure requires specially trained personnel and facilities, and although it has been studied in patients with shoulder involvement, its utility in calcific periarthritis in sites other than the shoulder remains unclear. (See "Calcific tendinopathy of the shoulder", section on 'Extracorporeal shock wave therapy'.)
●Surgical procedures – Arthroscopic or open surgical procedures to remove calcific deposits are generally safe and effective for patients with shoulder involvement, and referral for evaluation for one of these more invasive approaches is indicated in patients with involvement of other areas who are refractory to conservative treatments, including NSAIDS, intralesional glucocorticoids, and needle aspiration. (See "Calcific tendinopathy of the shoulder", section on 'Surgery'.)
Other therapies for patients refractory to usual therapies — Rarely, other treatments may be used for patients who are unable to tolerate or who do not respond to the therapies listed above. There is very limited information to support the use of other therapies.
●Systemic glucocorticoids – Systemic glucocorticoids are rarely used in this disorder. They might be most appropriate in patients who unable to use NSAIDs and have multiple affected sites, or an affected site that is inaccessible for intralesional interventions, as well as in patients with refractory symptoms despite the approaches listed above. Low to moderate doses of prednisone (10 to 30 mg daily) could be used initially until symptoms resolve. Very limited case reports support this approach [37].
●Interleukin 1 beta inhibition – IL-1 beta inhibitors can also be used for calcific periarthritis [38]. As with systemic glucocorticoids, these drugs may be suitable for patients who cannot use or do not respond to the above therapies, especially when there are multiple involved sites or areas that are inappropriate for intralesional interventions. We would use anakinra (100 mg subcutaneously for three days) in patients appropriate for this type of therapy, based upon case reports and a small pilot study [38].
●Other treatments – Other therapies have been tried in refractory disease. Intralesional platelet-rich plasma injection has been described in a case report but has not been tested in clinical trials [39]; these types of injections would be used for patients who failed or were intolerant of NSAIDs and more conservative intralesional therapies such as intralesional glucocorticoids. There is very little evidence for efficacy of bisphosphonates, such as clodronate, or for topical or intralesional applications of thiosulfate [40,41].
Adjunctive therapy for pain — Analgesic agents such as acetaminophen (500 to 1000 mg up to three times daily) can be used in calcific periarthritis in patients who are intolerant of or unable to use NSAIDs. Acetaminophen can be used alone or in combination with a local therapy such as intralesional glucocorticoids or needling. In patients with pain that is refractory to acetaminophen, other pain medications, including tramadol or opioids, may be necessary but should be used in the lowest dose and for the shortest time necessary. This approach is based upon our clinical experience, but there are no trials to document the benefit of these medications in this condition.
PROGNOSIS —
The natural history of calcific periarthritis is not well studied and may be site-dependent. For example, in small joints such as those in the foot, symptoms were present for a mean duration of 10 days with a range of 3 to 30 days [28], while in hip involvement, symptoms in treated patients resolved within four to eight weeks [24]. Recurrence rates are also not well documented.
More information is available with respect to shoulder involvement, which is discussed in detail separately. (See "Calcific tendinopathy of the shoulder", section on 'Prognosis and complications'.)
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: Gout and other crystal disorders".)
SUMMARY AND RECOMMENDATIONS
●Pathogenesis and risk factors – Basic calcium phosphate (BCP) mineral formation often occurs at sites of local tissue damage associated with injury or inflammation. BCP crystals can then produce symptoms and mediate tissue damage by several mechanisms, including the induction of an inflammatory response, biomechanical disruption, and direct tissue injury. Most patients are healthy and middle-aged, with females affected more often than males. Trauma, metabolic, and genetic factors may each be associated with increased risk of BCP-associated calcific periarthritis, although only a portion report recent trauma or overuse. (See 'Pathogenesis of BCP-associated musculoskeletal syndromes' above and 'Epidemiology and risk factors' above.)
●Clinical manifestations – Calcific periarthritis typically causes the acute onset of severe pain involving a single joint, tendon, or bursal area; there is focal tenderness and variable warmth and swelling, sometimes with erythema. It can occur around both large and small joints as well as in the spine. The area of tenderness may not correlate with the typical location of the joint line and a synovial effusion is usually not present. Patients sometimes report fever and chills. Attacks are usually self-limited, lasting a few weeks to several months. (See 'Clinical manifestations' above.)
●Imaging – Radiographs show extraarticular calcifications that are amorphous-appearing, especially when acute. Calcifications may be present in tendons, bursae, ligaments, or soft tissues; bone erosions may occur adjacent to the calcific density. Chronic calcifications may be denser and more homogeneous. Calcifications can also be visualized by ultrasound and by computed tomography (CT). (See 'Imaging' above.)
●Diagnosis – The diagnosis of calcific periarthritis is based upon a characteristic clinical presentation and typical findings on plain radiographs; with an acute onset of pain and swelling around a single joint, most often in a healthy young or middle-aged woman; no obvious joint effusion; and tenderness that may not be located at the joint line. The presence of periarticular calcifications on plain radiographs of symptomatic areas are usually sufficient to confirm the diagnosis. CT scanning may be necessary to visualize calcific deposits in deep structures. (See 'Diagnosis' above.)
●Differential diagnosis – The differential diagnosis includes acute gouty arthritis, acute calcium pyrophosphate (CPP) crystal arthritis infectious arthritis, and, less frequently, other conditions. (See 'Differential diagnosis' above.)
●Initial treatment – For initial therapy of calcific periarthritis, we suggest either nonsteroidal antiinflammatory drug (NSAID) therapy or an intralesional glucocorticoid injection rather than more invasive procedures. (See 'Initial therapy' above.)
•NSAIDs – In patients with normal kidney function and no contraindications to NSAID use, we give naproxen (500 mg twice daily). Alternatively, ibuprofen (eg, 400 to 600 mg four times daily or 800 mg two to three times daily, with a maximum dose in young healthy individuals of 3200 mg per day) could be used. (See 'NSAIDs' above.)
•Intralesional glucocorticoids – We use an intralesional glucocorticoid injection in patients in whom a local injection is feasible based upon the accessibility of the involved site; availability of imaging guidance, where needed (eg, for deep sites); and the expertise of the treating clinician. An injection is also appropriate in patients unable to use NSAIDs (eg, due to contraindications) or who have experienced an inadequate response to NSAIDs after 48 to 72 hours of treatment. (See 'Intralesional glucocorticoids' above.)
●Treatment of refectory symptoms – In patients who do not respond to NSAIDs or local glucocorticoid injection, we use needle aspiration (ie, "needling" or barbotage); we reserve referral for arthroscopic or open surgery for patients refractory to NSAIDs, injection, and needling. Extracorporeal shockwave therapy (ESWT) may be a useful alternative in patients who have not responded to initial therapy and have failed needle aspiration, where this technique is available. (See 'Resistant to initial therapy' above.)
