Calcium Hydroxyapatite Crystal Deposition Research Articles

Distinguishing erosive osteoarthritis and calcium pyrophosphate deposition disease

Erosive osteoarthritis is a term utilized to describe a specific inflammatory condition of the interphalangeal and first carpal metacarpal joints of the hands. The term has become a part of medical philosophical semantics and paradigms, but the issue is actually more complicated. Even the term osteoarthritis (non-erosive) has been controversial, with some suggesting osteoarthrosis to be more appropriate in view of the perspective that it is a non-inflammatory process undeserving of the "itis" suffix. The term "erosion" has also been a source of confusion in osteoarthritis, as it has been used to describe cartilage, not bone lesions. Inflammation in individuals with osteoarthritis actually appears to be related to complicating phenomena, such as calcium pyrophosphate and hydroxyapatite crystal deposition producing arthritis. Erosive osteoarthritis is the contentious term. It is used to describe a specific form of joint damage to specific joints. The damage has been termed erosions and the distribution of the damage is to the interphalangeal joints of the hand and first carpal metacarpal joint. Inflammation is recognized by joint redness and warmth, while X-rays reveal alteration of the articular surfaces, producing a smudged appearance. This ill-defined, joint damage has a crumbling appearance and is quite distinct from the sharply defined erosions of rheumatoid arthritis and spondyloarthropathy. The appearance is identical to those found with calcium pyrophosphate deposition disease, both in character and their unique responsiveness to hydroxychloroquine treatment. Low doses of the latter often resolve symptoms within weeks, in contrast to higher doses and the months required for response in other forms of inflammatory arthritis. Reconsidering erosive osteoarthritis as a form of calcium pyrophosphate deposition disease guides physicians to more effective therapeutic intervention.

Acute calcific tendinitis of tibialis posterior tendon (TPT): A rare site of involvement

Calcific tendinitis is a benign inflammatory disorder characterised by deposition of calcium hydroxyapatite crystals in tendons and is commonly seen in tendons around shoulder joint but can also sometimes be encountered in other sites including the hip, wrist, elbow, hand, neck and foot. Calcific tendinitis can clinically mimic many other pathologic entities like infection, gout, myositis ossificans or avulsion fracture which frequently leads to misdiagnosis and inappropriate management. Imaging plays an important role in recognizing and evaluating calcific tendinitis and in differentiating this entity from other pathologic conditions. Calcific tendinitis is largely a self-limiting process which usually responds to conservative treatment although in refractory cases invasive options like steroid injection, needle aspiration or surgery can be considered. Early and accurate diagnosis can prevent needless tests and interventions which the patient may be subjected. We report a case of acute calcific tendinitis involving a rare site (tibialis posterior tendon) with its multimodality imaging appearance.

Acute retropharyngeal calcific tendinitis: a case report with unusual location of calcification

Retropharyngeal calcific tendinitis is an inflammatory process caused by calcium hydroxyapatite crystal deposition in the longus colli tendon of the prevertebral space, and it may mimic a retropharyngeal infection or abscess. The diagnosis of retropharyngeal calcific tendinitis will be made radiologically by the detection of calcifications anterior to C1-C3 and prevertebral soft tissue swelling. We present a case of acute retropharyngeal calcific tendinitis with an unusual location of calcification anterior to the C5-C6 disc.

Extensive Calcinosis Cutis in Limited Cutaneous Scleroderma

The CREST syndrome is a subset of limited scleroderma characterized by calcinosis cutis, Raynaud’s phenomenon (RP), esophageal dysmotility, sclerodactyly, and telangiectasias. The calcinosis of skin and soft tissues results from deposition of calcium hydroxyapatite crystals and occurs to a different extent in 20%–40% of patients. The …

Calcific Tendinitis: A Pictorial Review

Calcific tendinitis is caused by the pathologic deposition of calcium hydroxyapatite crystals in tendons and is a common cause of joint pain. The disease typically affects the shoulder and hip, with characteristic imaging findings; however, any joint can be involved. Occasionally, calcific tendinitis can mimic aggressive disorders, such as infection and neoplasm, especially on magnetic resonance imaging. Radiologists should be familiar with the imaging findings to distinguish calcific tendinitis from more aggressive processes. Image-guided percutaneous needle aspiration and steroid injection of calcific tendinitis are useful techniques performed by the radiologist for the treatment of symptomatic cases. Familiarity with these procedures and their imaging appearance is an important aspect in the management of this common disease.

Calcific Tendinitis of Popliteus Tendon: Arthroscopic Excision and Biopsy

Calcific tendinitis results from the deposition of calcium hydroxyapatite crystals in periarticular muscular attachments. It is a rare cause of knee pain commonly affecting patients aged 40 to 70 years. Although commonly seen in the shoulder, it should be kept in mind in nontraumatic cases, particularly when the pain is severe and localized to the lateral aspect of the knee. The exact mechanism of hydroxyapatite deposition is unclear, although genetic and metabolic factors have been suspected. A 45-year-old man presented with severe pain in the lateral aspect of his knee with local tenderness over the lateral epicondyle. Radiographs revealed multiple calcific deposits just below the lateral epicondyle of the femur. Magnetic resonance imaging showed multiple areas of low-signal present intra-articularly near the popliteus tendon that was suspected to be calcification. Erythrocyte sedimentation rate and C-reactive protein were slightly raised and other blood investigations including uric acid were within normal limits. Due to failure of conservative treatment, arthroscopy was performed through standard anteromedial and anterolateral portals. Arthroscopy revealed reddish synovial congestion in the lateral gutter. Partial synovectomy was performed with a shaver through a superolateral portal and the calcific deposit was found to lie between the popliteus tendon and the lateral collateral ligament. This was excised and sent for biopsy. Histopathological evaluation revealed the presence of hydroxyapatite crystals within degenerated tendon thereby confirming the diagnosis of calcific tendinitis. Immediate resolution of symptoms following excision allowed the patient to perform activities of daily living immediately postoperatively without pain.

Retropharyngeal Calcific Tendonitis: Report of Two Cases

Retropharyngeal calcific tendonitis is an inflammatory process of the superior oblique tendons of the longus colli muscle, a neck flexor in the upper cervical spine, caused by deposition of calcium hydroxyapatite crystals; the definitive diagnostic test is computed tomography (CT). Presented in this article are two cases seen at our institution. Patients typically present with acute onset of neck pain/spasm, odynophagia, dysphagia, and/or low grade fevers. Leukocytosis and elevated erythrocyte sedimentation rate may be noted. It is important to understand this entity because its signs and symptoms are mimickers of those of the more serious condition of retropharyngeal space abscess. Calcific tendonitis is managed conservatively whereas retropharyngeal abscess requires incision and drainage. Some may argue that this entity is a zebra because its reported incidence in the literature is low. However, most of these studies were done in an era when CT was not yet in vogue. With today's widespread use of CT and its superb ability to visualize the calcification, the true incidence of this condition is probably higher and, thus, it is important for the family practitioner to be aware of this entity. The astute clinician may save the patient from unnecessary diagnostic workup, undue anxiety, and delays in hospital discharge.

Amplification of Atherosclerotic Calcification and Mönckeberg's Sclerosis: A Spectrum of the Same Disease Process

Autopsy studies have shown the near universal presence of fatty streaks and fibroatheromas in the general population from which chronic kidney disease (CKD) patients arise. The vast majority of CKD patients have multiple conventional cardiovascular risk factors. Atherosclerosis, once present, can predominantly manifest as medial calcification, which has been previously termed Mönckeberg's sclerosis. This term has also been used in rare cases to describe vascular calcinosis not related to CKD. This clarification is critical to advance the field in terms of pathological diagnosis and treatment of CKD bone and mineral disorder. Factors that appear to promote the osteoblastic transformation of vascular smooth muscle cells and enhance deposition of calcium hydroxyapatite crystals include phosphorus activation of the Pit-1 receptor, bone morphogenic proteins 2 and 4, leptin, endogenous 1,25 dihydroxy vitamin D, vascular calcification activating factor, and measures of oxidative stress. These entities work to accelerate the atherosclerotic process in CKD patients and may be future targets for diagnosis and treatment. Although conventional atherosclerotic risk factors should be optimally managed, it should be noted that trials of hydroxymethylglutaryl-CoA reductase inhibitors have failed to attenuate the rate of progressive vascular calcification as measured by computed tomography scans.

Accelerated Atherosclerotic Calcification and Mo[Combining Diaeresis]nckeberg's Sclerosis

Autopsy studies have demonstrated the near universal presence of fatty streaks and fibroatheromas in the general population from which patients with chronic kidney disease (CKD) arise. The vast majority of patients with CKD have multiple conventional cardiovascular risk factors. Vascular atherosclerotic calcification develops in most patients as they transition from the general population to significant CKD as part of cholesterol crystallization within atherosclerotic lesions. Once present, however, atherosclerotic medial calcification can become prominent and has been previously identified as Mönckeberg's sclerosis. A unifying concept supported by the preponderance of pathologic evidence contends that Mönckeberg's sclerosis is a manifestation of accelerated atherosclerosis in patients with CKD. The term has also been used in rare cases to describe vascular calcinosis not related to CKD. This clarification is critical to advance the field in terms of pathologic diagnosis and treatment of CKD bone and mineral disorder. Factors that seem to promote the osteoblastic transformation of vascular smooth muscle cells and enhance deposition of calcium hydroxyapatite crystals include phosphorus activation of the Pit-1 receptor, bone morphogenic proteins 2 and 4, leptin, endogenous 1,25 dihydroxyvitamin D, vascular calcification activating factor, and measures of oxidative stress. These entities work to accelerate the atherosclerotic process in patients with CKD and may be future targets for diagnosis and treatment because randomized trials with hydroxymethylglutaryl-CoA reductase inhibitors have failed to attenuate the rate of progressive vascular calcification.

Recurrent acute low back pain secondary to lumbar epidural calcification

Epidural calcification is a rare cause of back pain, and spontaneous epidural calcification has not been reported previously. We describe a patient with acute low back pain and signs of lumbar nerve root compression due to epidural calcification, as demonstrated by CT-scan and MRI. Radiological signs of spondylodiscitis led to a search for an infectious cause, which was negative, and her symptoms responded rapidly to NSAID treatment alone. Her symptoms recurred 18 months later, and further imaging studies again revealed epidural calcification, but with a changed distribution. Her symptoms were relieved once more by NSAID treatment alone. We propose that epidural calcification secondary to aseptic spondylodiscitis is the main cause of acute back pain in this patient. A possible mechanism may be the pro-inflammatory effects of calcium pyrophosphate or hydroxyapatite crystal deposition within the epidural space.

Calcium pyrophosphate dihydrate and hydroxyapatite crystal deposition in the joint: new developments relevant to the clinician.

The major types of crystals containing calcium, which causes arthropathy and periarticular disease, are calcium pyrophosphate dihydrate and basic calcium phosphates, including hydroxyapatite. Exciting advances include the identification of mutations in the gene ANKH associated with disordered inorganic pyrophosphate (PPi) transport in some kindred with familial chondrocalcinosis linked to chromosome 5p. In addition, central basic mechanisms governing cartilage calcification and their relationship to aging and osteoarthritis have now been elucidated. These include the role of plasma cell glycoprotein-1, the PPi-generating ecto-enzyme, in chondrocalcinosis and the linkage of low- grade inflammation to expression and activation of two cartilage-expressed transglutaminase isoenzymes with direct calcification-stimulating activity. This review discusses clinically pertinent new information on pathogenesis. The authors also address, in detail, current diagnostic and therapeutic issues pertaining to calcium pyrophosphate dihydrate and hydroxyapatite crystal deposition in the joint, as well as possible therapeutic directions for the future.

Endoscopic treatment of calcific tendinitis of gluteus medius and minimus

Calcific tendinitis results from deposition of calcium hydroxyapatite crystals in periarticular muscle attachments. Although involvement of tendons around the hip is not uncommon, gluteus medius and minimus tendons are rarely affected. We present endoscopic treatment of calcific tendonitis of gluteus medius and minimus and associated trochanteric bursitis in a patient with 2-year history of lateral hip pain. This is the first reported case treated using an endoscopic approach, which is effective and minimally invasive.

Calcific Tendinitis of the Shoulder

Calcific tendinitis of the shoulder is a self-limiting calcification of the rotator cuff (Figure 1). Radiologically evident calcification has been reported in 7.5 to 20 percent of adults with no symptoms1,2 and in 6.8 percent of those with shoulder pain.2 The disorder is most common among people between 30 and 60 years of age. Women are slightly more likely to be affected than men, and workers in sedentary jobs appear to be at higher risk than those in manual work. Bilateral involvement is not uncommon.The reason for the deposition of calcium hydroxyapatite crystals in the tendon is unclear. . . .

Light and Electron Microscopy of Hydroxyapatite Depositions in the Ligamentum Flavum

Ligamenta flava obtained from 24 patients who had undergone surgery for degenerative spinal diseases were investigated regarding the histopathology of hydroxyapatite crystal depositions. Light and electron microscopy and energy dispersive x-ray microanalysis were done to clarify the cause and process of hydroxyapatite crystal depositions in the ligament. No reports have been made regarding the cause of calcification in the ligamenta flava induced by hydroxyapatite crystal depositions. Samples were fixed in 10% formalin and 2.5% glutaraldehyde for light and electron microscopy. Energy dispersive x-ray microanalysis was done to detect calcium and phosphate hydroxyapatite crystal deposition areas. Hydroxyapatite crystals, which occasionally formed clusters, existed in the connective tissue of the dural side around abundant profiles of growing capillaries. Hydroxyapatite crystals showed needle shaped figures, and the x-ray microanalysis revealed that the ratio of calcium to phosphate was about 1.66:1. A decrease or loss of collagenous and elastic fibers was prominent in these hydroxyapatite deposition areas. Hydroxyapatite crystal depositions occur around the growing capillaries in the dural side of the ligamenta flava.

Idiopathic tumoral calcinosis.

A 22-year-old man had a recurrent mass in the sole of the right foot. Although he had been asymptomatic for approximately i5 years after a previous operation, he had noticed swelling and tendemess for several months. The patient was hyperphosphatemic, but renal function and serum calcium, alkaline phosphatase, and parathyroid hormone levels were normal. Plain films of the foot showed a 7-cm, multiglobular, calcified soft-tissue mass on the planter aspect of the forefoot (Fig. 1). CT showed discrete, rounded, 2to 20-mm CaICIfIC foci, some with homogeneous attenuation and some with sedimentation levels. The adjacent bones were normal. A local excision showed the lesion to consist of multiple calcific deposits surrounded by chronic foreign-body reaction and fibrosis. The calcareous material had the consistency of toothpaste. The final pathologic diagnosis was idiopathic tumoral calcinosis. Idiopathic tumoral calcinosis is thought to result from a heritable error in phosphorus metabolism that leads to extracellular deposition of calcium hydroxyapatite crystals [i , 2]. These are seen most frequently in the form of periarticular soft-tissue masses. Suspended calcium salts may layer out within cystic structures. The surrounding granulomatous foreign-body response to the deposits results in bright signal on T2-weighted MR images [1]. Because the deposits are active metabolically, radionuclide bone scans show abnormal accumulation. Idiopathic tumoral calcinosis is rare and appears to have autosomal dominant transmission and various clinical signs and symptoms. More common in blacks than in other racial groups, the most frequent age of presentation is during childhood or adolescence. The lesions enlarge slowly, may attain large size, and may become symptomatic by virtue of local mechanical effects. If incompletely resected, they may recur. Other manifestations include elevated i ,25-dihydroxyvitamin D3 levels (not measured in this case), calcific myelitis, and dental abnormalities. Dietary restriction of phosphorus may be beneficial in some patients; surgical excision is reserved for symptomatic lesions. The radiologically indistinguishable condition of secondary tumoral calcinosis may occur in association with such disorders as chronic renal failure or scleroderma.

Calcium hydroxyapatite deposition disease.

Calcium hydroxyapatite crystal deposition disease is characterized by the presence of basic calcium phosphate crystals--predominantly hydroxyapatite--in the periarticular soft tissues, especially the tendons. The entity is best recognized as "calcific tendinitis" at its most frequent site about the shoulder, but the disease involves numerous other sites and may be more appropriately termed calcific periarthritis. This article illustrates typical and atypical radiographic features of hydroxyapatite deposition, as well as some unusual manifestations of the disease. A brief review of various theories on the pathogenesis of the disease and a section on differential diagnosis is included.

Idiopathic familial chondrocalcinosis due to apatite crystal deposition

Idiopathic familial chondrocalcinosis was found in five members of a family. The clinical features of the disease were morning stiffness, pain and limitation of motion of the dorsolumbar spine in four of the five members, associated with arthritis of the small joints of the hands in three, shoulder periarthritis in two and costal cartilage pain in one. Radiologically, four of the five patients had multiple intervertebral disk calcifications, mainly located at the nucleus pulposus area. Three of them also had periarticular calcific deposits, associated with costal cartilage calcifications and degenerative changes in the small joints of the hands in two. None of these cases showed cartilage calcification in the knees, pubic symphysis or triangular ligament of carpus. In the propositus, optical microscopy of a specimen of the second proximal interphalangeal joint obtained by open biopsy showed the presence of multiple calcified areas in the intercellular matrix and chondroid metaplasia with calcification of the matrix in the synovial membrane and capsule. X-ray diffraction studies, energy dispersive analysis, and infrared spectrophotometry of a costal cartilage sample obtained by open biopsy demonstrated the presence of carbonate calcium hydroxyapatite. In this study, no relation was found between HLA antigens, loci A, B and C, and this syndrome due to calcium hydroxyapatite crystal deposition.