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PubMed2001

Induction of matrix metalloproteinase-8 in human fibroblasts by basic calcium phosphate and calcium pyrophosphate dihydrate crystals: effect of phosphocitrate.

Although matrix metalloproteinase-8 (MMP-8) was regarded as the exclusive product of the neutrophils, recent studies have shown that it is also expressed in articular chondrocytes, rheumatoid synovial fibroblasts and endothelial cells. Our aim was to determine the expression of MMP-8 in human fibroblasts (HF) by reverse transcription/polymerase chain reaction (RT/PCR). Northern and Western blotting methods and MMP-8 activity assay. We have shown the expression of MMP-8 in HF and its dose-dependent upregulation by basic calcium phosphate (BCP) and calcium pyrophosphate dihydrate (CPPD) crystals which are markers of severe joint degeneration in osteoarthritis. These effects require new protein synthesis and are reversed by phosphocitrate (PC). The results also show that this fibroblast MMP-8 is distinct from the neutrophil MMP-8 and from the fibroblast MMP-1. These results indicate that MMP-8 may play a significant role in the pathogenic effects of the crystals in osteoarthritis.

Anti-Bacterial Agents↗

PubMed1980

Cervical radiculomyelopathy caused by deposition of calcium pyrophosphate dihydrate crystals in the ligamenta flava. Case report.

A case of cervical radiculomyelopathy caused by multiple calcified nodules in the ligamenta flava is presented. Roentgenological examination of the cervical spine showed radiopaque nodular lesions, 7 x 7 x 5 mm in size, located in the paramedian portion of the posterior spinal canal. The nodules were removed surgically and they were confirmed to be calcifications of ligamenta flava. Microscopic examination of the nodules with the polarized light revealed extensive deposition of crystals. By x-ray diffraction study, the crystal was determined as calcium pyrophosphate dihydrate (CPPD: Ca2P2O7 . 2H2O). Although CPPD deposition in the cartilage has been known as pseudo-gout syndrome, deposition in the ligament has been reported only in a few cases. This is the first case with radiopaque calcified nodules in the ligamenta flava causing spinal cord compression, the composition of which proved to be CPPD.

Calcium Pyrophosphate↗

PubMedDate not supplied

Bartter's syndrome and chondrocalcinosis: a possible role for hypomagnesemia in the deposition of calcium pyrophosphate dihydrate (CPPD) crystals.

A new case of association between Bartter's syndrome and chondrocalcinosis is reported. The patient was shown to have marked hypomagnesemia. Indomethacin and magnesium therapy was started and resulted in increased magnesemia, even if it did not reach normal levels. There was complete remission of articular symptoms and no progression on the radiological picture after 2 years of continuous magnesium and indomethacin therapy. The 7 available family members were studied to assess the possible presence of a familial form of chondrocalcinosis and/or hypomagnesemia. The literature is reviewed and reports of previously described associations between Bartter's syndrome and chondrocalcinosis are summarized. The possible role of hypomagnesemia in predisposing to deposition of calcium pyrophosphate dihydrate crystal in cartilagine is also discussed.

Adult↗

PubMed1998

Activation of S6 kinase in human neutrophils by calcium pyrophosphate dihydrate crystals: protein kinase C-dependent and phosphatidylinositol-3-kinase-independent pathways.

Phosphatidylinositol 3-kinase (PI 3-kinase) has been shown previously to be a central enzyme in crystal-induced neutrophil activation. Since activation of the 70 kDa S6 kinase (p70S6K) has been shown to be dependent on PI 3-kinase activation in mammalian cells, and since the former is a key enzyme in the transmission of signals to the cell nucleus, activation of p70(S6K) was investigated in crystal-stimulated neutrophils. Cytosolic fractions from calcium pyrophosphate dihydrate (CPPD)-crystal-activated neutrophils were separated by Mono Q chromatography and analysed for phosphotransferase activity using a range of substrates and probed by Western analysis using antibodies to p70(S6K) and mitogen-activated protein kinase (MAP kinase). CPPD crystals induced a robust, transient activation (peak activity at 2 min) of p70(S6K) that was fully inhibited by pretreatment with rapamycin. This is the first report of the activation of p70(S6K) in neutrophil signal transduction pathways induced by an agonist. This crystal-induced activation of p70(S6K) could also be inhibited by a protein kinase C (PKC) inhibitor (Compound 3), but not by the PI 3-kinase inhibitor wortmannin. CPPD crystals also activated the ERK1 and ERK2 forms of MAP kinase (wortmannin insensitive), PKC (Compound 3 sensitive) and protein kinase B (wortmannin sensitive) in neutrophils. These data suggest that activation of p70(S6K) may proceed through a PI 3-kinase- and protein kinase B-independent but PKC-dependent pathway in crystal-activated neutrophils.

Androstadienes↗

PubMed1997

Monosodium urate, hydroxyapatite, and calcium pyrophosphate crystals induce tumor necrosis factor-alpha expression in a mononuclear cell line.

OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) is thought to be important in chronic inflammation of joints characteristic of crystal induced arthritis. Monocytes are instrumental in maintaining that inflammation. We investigated production of mRNA and protein for TNF-alpha in vitro in a murine mononuclear cell line, after exposure to relevant crystal types. METHODS: Using the cell line designated RAW 264.7, cells were grown in standard medium and exposed to varying amounts of monosodium urate (MSU), hydroxyapatite (HA), and calcium pyrophosphate dihydrate (CPPD) crystals for differing time periods. Analysis of TNF-alpha mRNA induced by such exposure was by Northern hybridization; analysis of TNF-alpha protein was by ELISA: RESULTS: RNA analyses of cells treated with various levels of MSU, HA, and CPPD crystals showed strong induction of TNF-alpha transcripts. ELISA on culture supernatants confirmed high level TNF-alpha peptide secretion resulting from that transcriptional upregulation. Time course studies showed peak accumulation of TNF-alpha mRNA 1-6 h post-treatment. Study of the signalling pathway involved in TNF-alpha transcriptional upregulation indicated that increased phospholipase A2 activity was required. CONCLUSION: These observations suggest that crystals in joints can directly stimulate production of TNF-alpha, and that the source of that cytokine may be the monocytes known to be present and playing an important role in chronic joint disease.

Acetophenones↗

PubMed2000

Density functional geometry optimization and energy calculations of calcium(II)-triphosphate complexes. Polyphosphates as possible dissolving agents for calcium pyrophosphate dihydrate crystals in chondrocalcinosis disease.

Geometry optimizations and energy calculations have been carried out via molecular orbital methods at the density functional B3LYP/LANL2DZ level on the molecules PO3-, OPO3(3-), HOPO3(2-), CH3OPO3(2-), H(CH3OPO3)-, O(PO3)2(4-), HO(PO3)2(3-), CH2(PO3)2(4-), (CH3OPO2)O(PO3)3-, O(PO3)3(5-), HO(PO3)3(4-), (PO3)3(3-), (CH3OPO2)O(PO3)2(4-), [Mg[O(PO3)2)]]2-, [Ca[O(PO3)2]]2-, [Ca[CH2(PO3)2]]2-, [Ca[CH3OPO2)O(PO3)]]-, [Ca(PO3)3]-, [Ca[O(PO3)3]]3-, and [Ca[CH3OPO2)O(PO3)2]]2- with the aim to find reliable and easily accessible computational methods to simulate some phosphate-containing molecules of importance for the living cells and to study the energetics for protonation and metal-complex formation reactions. The analysis is part of a general investigation on phosphate-containing molecules as potential dissolving agents for calcium pyrophosphate dihydrate (CPPD) crystals which deposit in certain articular diseases. The basis set was expanded to 6-31G** for the P atoms for all the molecules investigated and to 6-31G* for the O atoms for OPO3(3-). Calculations at the semiempirical MNDO/d level were also carried out for comparison purposes on the free ligand molecules and on [Mg[O(PO3)2]]2-. The density functional analysis reproduced well the geometry found at the solid state via X-ray diffraction. The analyses of the geometrical parameters and the total electronic energy of the molecules shows that O(PO3)2(4-) and other di- and tri-phosphates are versatile ligands for divalent metal ions like Ca2+. The computed P-O-P bond angle for free O(PO3)2(4-) is 180 degrees and the conformation of the two PO3- groupings is staggered along the P...P vector. The linear arrangement for P-O-P is assisted by P-O pi interactions. The bending of the P-O-P angle when accompanied by a slight P-O(b) elongation requires a very small amount of energy; 4.65 kcal/mol to pass from 180 to 140 degrees , as calculated at the DFT level. The computed Ca-O and Mg-O bond distances for [M[O(PO3)2]]2- are 2.378 and 2.079A, when the metal ions link two oxygen atoms from each PO3 group. The computed Ca-O bond lengths for [Ca[CH3OPO2)O(PO3)]]- are 2.482 (PalphaO2) and 2.358A (PbetaO2), showing a significant lengthening for Ca-OPalpha, when compared to the pyrophosphate derivative. The Ca-O bond lengths for [Ca[O(PO3)3]]3- and [Ca[CH3OPO2)O(PO3)2]]2- are 2.251A and 2.525 (PalphaO2), 2.407 and 2.338 (PbetaO2), and 2.251 and 2.228A (PgammaO2), showing a shortening for the Ca-OPgamma bond upon methylation. The (Pbeta)O-Pgamma bond length increases significantly (0.09 A) upon Ca(II) coordination to (CH3OPO2)O(PO3)2(4-) via all the three PO3 groups. This latter result suggests that metal complexes of linear organic-triphosphates have a larger tendency to release the PgammaO3 group when compared to the free ligand molecules. The electronic contribution to the energy of the complex formation reaction for [Ca[CH2(PO3)2]]2- is only slightly higher (some 1.8 kcal) than that for [Ca[O(PO3)2]]2-; but is much higher (some 63 kcal) than that relevant to the formation of [Ca[CH3OPO2)O(PO3)2]]2-. (ABSTRACT TRUNCATED)

Calcium Phosphates↗

PubMed1999

Further characterization of ATP-initiated calcification by matrix vesicles isolated from rachitic rat cartilage. Membrane perturbation by detergents and deposition of calcium pyrophosphate by rachitic matrix vesicles.

Although membrane associated enzymes such as ATPase, alkaline phosphatase, and NTP pyrophosphohydrolase in matrix vesicles (MVs) may underlie the mechanisms of ATP-promoted calcification, prior to the current investigation, the role of the MV membrane in calcification had not been addressed. In this study, various perturbations were introduced to the MV membrane in in vitro calcification systems to determine ideal conditions for ATP-initiated calcification by MVs isolated from rachitic rat epiphyseal cartilage. Membrane integrity appears to be required, since the rupture of the vesicular membrane by vigorously mixing with 10% butanol abolished calcification. In contrast, a mild treatment of MVs with low concentrations (e.g., 0.01%, which is much below the critical concentration for micelle formation) of either neutral Triton X-100 or anionic deoxycholate stimulated calcification by >2-fold, without inducing obvious changes in vesicular appearance. Fourier transform infrared spectroscopic studies were done to identify the mineral phase formed in these experiments. For the first time, rachitic MVs were shown to induce the formation of a calcium pyrophosphate dihydrate-like phase after their exposure to calcifying medium with 1 mM ATP. The integration of spectral areas indicated that calcification was enhanced by Triton X-100. The detergent effect was reversible and appeared to be not mediated through activation of ATPase, alkaline phosphatase, or ATP pyrophosphohydrolase. In contrast to neutral Triton X-100 and anionic deoxycholate, cationic cetyltrimethylammonium bromide inhibited both ATPase activity (I50=10 microM) and ATP-initiated calcification. These observations suggest that membrane perturbations can affect calcification and that the presence of NTP-pyrophosphohydrolase in MVs may play a role in the deposition of CaPPi in rachitic cartilage.

Adenosine Triphosphate↗

PubMed2001

[Compressive cervical myelopathy due to massive periodontoid calcium pyrophosphate crystal deposition]

A 77 year-old man suffering from psoriatic arthropathy presented with progressive myelopathy due to massive deposits of calcium pyrophosphate dihydrate crystals in peri-odontoid tissue. The magnetic resonance imaging and computer tomographic pictures of the involved site are shown and discussed. The clinical spectrum of crystal deposition disease involving the atlo-axial joint is briefly reviewed.

Journal Article↗

PubMed2000

Calcium pyrophosphate dihydrate crystal deposition disease of the wrist: trapezioscaphoid joint abnormality.

OBJECTIVE: To determine whether trapezioscaphoid (TS) joint alterations are associated with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease and, if so, to determine the nature of these alterations. METHODS: Radiographs of 160 wrists with evidence of chondrocalcinosis were evaluated with regard to TS joint abnormalities, and findings were compared with a similar number of radiographs in an age and sex matched control population in whom no evidence of chondrocalcinosis or other calcification in the wrist was seen. Two radiologists in consensus recorded radiographic findings in both groups, and a third radiologist blinded to the presence or absence of chondrocalcinosis reviewed wrist radiographs in both groups in a random order. Correlation of TS joint abnormalities with other changes in the wrist was also accomplished. RESULTS; TS arthropathy was found in 43.7% of CPPD wrists and in 14.4% of control wrists in the consensus evaluation. In the blind evaluation, 30% of CPPD wrists and 12.5% of control wrists had TS arthropathy. The degree of arthropathy was more extensive in the CPPD group than in the control group. Features associated with TS arthropathy in the patient population were first carpometacarpal arthropathy and subchondral cysts in the scaphoid or trapezium, or both bones. CONCLUSION: CPPD patients, compared to a control population, reveal frequent and significant radiographic abnormalities of the TS joint that may be suggestive of the diagnosis, even in patients in whom chondrocalcinosis is obscured or absent. The features associated with TS arthropathy are first carpometacarpal arthropathy and subchondral cysts in the scaphoid and trapezium.

Adult↗

PubMed2000

Familial osteoarthritis and Milwaukee shoulder associated with calcium pyrophosphate and apatite crystal deposition.

OBJECTIVE: To characterize and define the phenotypes observed in a large Italo-Argentinean kindred with osteoarthritis, chondrocalcinosis, and Milwaukee shoulder (MS). METHODS: Seventy-five members were evaluated with a history, examination, and radiographs of shoulders, spine, hands, and knees. Superior subluxation of the glenohumeral joint was graded using shoulder radiographs and tomography and nuclear magnetic resonance imaging and 3 dimensional computed tomography was performed on selected members. In 31 family members peripheral blood DNA was utilized for genetic linkage analysis of several candidate gene loci previously linked to chondrocalcinosis phenotypes, as well as those implicated in the proper patterning of skeletal elements and cartilage differentiation. In addition, direct sequence analysis of type II collagen gene (COL2A1), the gene that codes for the major structural protein of cartilage, was undertaken in 3 affected and 3 unaffected members of the family. RESULTS: MS was seen in one member of the first generation and 6 members of the 2nd generation, while 8 members of the 3rd generation showed an incomplete form of MS. Isolated superior subluxation of the shoulder was seen in 16 other family members of the 3rd and 4th generations. Osteoarthritis of the spine and peripheral joints was seen in 31 affected members, while chondrocalcinosis was observed in 6 members of the first generation. Shoulder synovial fluid from 2 patients showed the presence of both apatite and calcium pyrophosphate dihydrate crystals. Direct analysis of the COL2A1 gene indicated no known disease determining mutations in affected members, thus excluding this gene as a candidate gene in this family. Genetic linkage to several candidate loci, including the chondrocalcinosis loci on chromosomes 5p and 8q, as well as loci for HOX A and C were also excluded. Linkage analyses of other loci for the HOX B and D genes and the PAX 1 and 9 genes were uninformative in this kindred. CONCLUSION: This kindred illustrates an unusual type of osteoarthritis with secondary intraarticular and periarticular calcification and MS in the most severely affected elderly members. A search for linkage to some potential candidate genes was either excluded or uninformative. Further linkage analysis to identify potential candidate genes is in progress.

Adult↗

PubMed1999

Effects of the NSAIDs meloxicam and indomethacin on cartilage proteoglycan synthesis and joint responses to calcium pyrophosphate crystals in dogs.

NSAIDs are a major cause for concern for their propensity to cause joint deterioration in canine, as in human, patients receiving these drugs for treatment of pain in osteoarthritis and other acute and chronic painful conditions. To determine the potential effects of the new NSAID meloxicam on cartilage integrity, the effects of this drug on proteoglycan biosynthesis in vitro and ex vivo were compared with those of indomethacin, a known inhibitor of sulphated proteoglycans that accelerates joint injury in human osteoarthritis. In vitro cartilage proteoglycan synthesis from a radiosulphate precursor was unaffected by 0.5-10.0 micromol/L meloxicam but was significantly inhibited by 50 micromol/L indomethacin after 6 or 24 h incubation of femoral or tibial cartilage explants in organ culture. This is in accord with previous observations in human or porcine articular cartilage under the same culture conditions. Studies were performed in vivo to establish the effects of the NSAIDs on joint integrity. This involved determining cartilage proteoglycan synthesis ex vivo, leukocyte, fluid and protein accumulation, as well as pain relief. Thus, meloxicam (0.2 mg/kg i.v. x 3 doses) or indomethacin (0.5 mg/kg i.v. x 3 doses) was given for 26 h and the effects were compared with a control (1.0 ml saline i.v. x 3 doses) in dogs in which acute inflammation had been induced by intra-articular (i.a.) injection of calcium pyrophosphate dihydrate (CPPD) crystals into the right stifle joint, an equivalent volume of saline being injected into the left stifle joint as a control. No effects were observed of the treatment with the NSAIDs on ex vivo sulphated proteoglycan synthesis. The lack of the expected inhibitory effects of indomethacin may be related to the relatively low plasma concentrations of this drug obtained during the 26 h period of treatment. The pain response, which was elicited up to 6 h following i.a. injection of CPPD crystals, was totally prevented by the treatment with meloxicam and to a lesser extent with indomethacin. There were no effects from the drug treatment on synovial inflammatory reactions (fluid and cell accumulation), although the protein concentration of the exudate was reduced by meloxicam. This indicates that, at the doses given, it was possible to discriminate the analgesic action from the anti-inflammatory action of the two NSAIDs, this being achieved at relatively low plasma concentrations of these drugs. In conclusion, while relatively high therapeutic concentrations of indomethacin inhibit cartilage proteoglycan synthesis, this is not an effect seen even at high concentrations of meloxicam. Furthermore, the lack of effects on proteoglycan synthesis was evident when these two drugs were given in vivo to dogs. However, the signs of pain, but not the inflammation in the joint, were relieved by low plasma concentrations of the drugs. Meloxicam may thus be safely employed for acute analgesia without the potential risks of joint cartilage damage that occurs with indomethacin given at antiinflammatory doses for long periods of time.

Animals↗

PubMed2001

Osteoarthritis of the scaphoidtrapezium joint: an early sign of calcium pyrophosphate dihydrate disease.

The aim of this study was to determine the value of scaphoidtrapezium osteoarthritis (ST osteoarthritis) as an early sign of calcium pyrophosphate dihydrate disease (CPDD) in a cohort of patients undergoing surgery for osteoarthritis of the first carpometacarpal joint. We examined whether patients with cartilage calcification of the wrist at the time of operation had ST osteoarthritis, indicating CPDD at an earlier time (retrospective study), and whether patients with ST osteoarthritis but without cartilage calcification at the time of surgery develop radiological or clinical signs of CPDD at a later time (prospective study). From 1 January 1989 to 31 December 1995 a total of 169 patients (from an orthopaedic clinic) with a diagnosis of osteoarthritis of the first carpometacarpal joint were included in the study; 167 underwent surgery and two were treated without. Of the 16 patients showing calcification on surgery and therefore included in the retrospective study, 12 had prior radiographs, of which eight showed ST osteoarthritis. Among these, four had no concomitant cartilage calcification in the prior radiographs. Of the 32 patients in the prospective group having ST osteoarthritis but no calcifications at the time of surgery, 27 could be clinically examined. Of these, two showed cartilage calcifications on the follow-up radiographs of the hands. The presence of ST osteoarthritis is a helpful diagnostic finding for the diagnosis of CPDD, especially in cases without radiographic cartilage or fibrocartilage calcification of the wrist. ST osteoarthritis may then point to the correct diagnosis.

Aged↗

PubMed2005

A case of chronic calcium pyrophosphate dihydrate crystal disease (tophaceous pseudogout) in the temporomandibular joint.

Pseudogout is a rare joint disease which is characterized by the presence of calcium pyrophosphate dihydrate crystals in the intraarticular and periarticular tissue. The crystals tend to attach to fibrocartilage tissue. Pseudogout principally affects the knee and wrist joints. Involvement of the temporomandibular joint (TMJ) is very rare. There have been <20 cases reported world-wide. Both acute and chronic manifestations have been described. We present here an unusual case that necessitated a high condylectomy.

Chondrocalcinosis↗

PubMed1998

Calcium pyrophosphate dihydrate crystal deposition disease after anterior cruciate ligament reconstruction.

We report the case of a 34-year-old woman who presented with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease shortly after anterior cruciate ligament (ACL) reconstruction using a polyester artificial ligament (Leeds-Keio; Neoligaments, Leeds, England). The patient had earlier undergone a medial collateral ligament repair of a sprain to her right knee incurred while skiing. Nine years later, she underwent ACL reconstruction. Seventeen months after ACL reconstruction, calcification was observed on radiographs of the medial and lateral menisci. Based on these calcifications and polarized light microscopic findings of the joint fluid, the diagnosis was made of CPPD crystal deposition. CPPD deposition appeared to have resulted from intra-articular damage incurred during ACL reconstruction as well as prolonged anterior instability.

Adult↗

PubMed2001

[Diff-Quik(R) staining method for detection and identification of monosodium urate and calcium pyrophosphate crystals in synovial fluids]

The aim of this study was to evaluate whether DQ could prove useful to identify monosodium urate (MSU) and calcium pyrophosphate dehydrate (CPPD) crystals on permanent mounted stained slides. To this end, we studied 27 synovial fluid (SF) samples obtained from the knees of patients with the pseudogout (n=21) and acute gouty arthritis (n=6). Wet analysis for crystal detection and identification was performed within one hour of joint aspiration. In addition, we studied 16 inflammatory synovial effusions obtained from patients with knee arthritis not induced by crystals. For each SF, DQ stained slides were analyzed by 2 experienced doctors in SF analysis. The observers were blinded to the type of crystal present in the SF. Each slide was analyzed by compensated polarized and transmitted light microscopy. SF was considered positive if intracellular and/or extracellular crystals were clearly identified. In addition, the observers were asked to identify the type of the crystals using compensated polarized light microscopy. Sensitivity, specificity, accuracy, positive predictive value (PPV), and negative predictive value (NPV) of the DQ staining method were determined. 51 true positive and 28 true negative specimens were correctly classified (39 CPPD samples, 12 MSU samples, and 28 samples of crystals-unrelated arthropathies). All MSU specimens were correctly diagnosed.

Journal Article↗

PubMed1999

Calcium pyrophosphate dihydrate crystal deposition disease of the knee simulating spontaneous osteonecrosis.

A retrospective review of the frontal and lateral knee radiographs of 200 patients with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease was performed. Of these 200 patients, nine patients (four male, five female, mean age 74 years, age range 63-87 years) had radiographic findings simulating osteonecrosis of the knee. One patient also had magnetic resonance imaging of the involved knee. A total of 10 knee radiographs in nine patients showed articular and periarticular calcification diagnostic of CPPD crystal deposition of the knee. In addition, all 10 radiographs showed flattening of one femoral condyle. Four of the 10 cases demonstrated an area of radiolucency in the subchondral bone surrounded by a halo of sclerosis. Eight of the 10 cases had narrowing of the involved joint compartment and osteophytosis. These findings mimic the radiographic signs of spontaneous osteonecrosis of the knee. In conclusion, flattening of the femoral condyles in CPPD crystal deposition disease simulates that of spontaneous osteonecrosis and probably relates to articular cartilage and meniscal damage that subsequently leads to stress fracture of subchondral bone with bone collapse.

Aged↗

PubMed1998

Chondrocalcinosis is a feature of Gitelman's variant of Bartter's syndrome. A new look at the hypomagnesemia associated with calcium pyrophosphate dihydrate crystal deposition disease.

The occurrence of chondrocalcinosis in patients with Bartter's syndrome has been reported as a typical example of hypomagnesemia-associated calcium pyrophosphate dihydrate crystal (CPPD) deposition disease. However, hypomagnesemia is a feature of Gitelman's variant of Bartter's syndrome, whereas serum magnesium levels are normal in Bartter's syndrome strictly speaking. We managed four patients with chondrocalcinosis and hypomagnesemia who met criteria for Gitelman's disease, including hypomagnesemia, hypokalemia with normal or high urinary potassium excretion, hypocalciuria, and normal blood pressure. Based on our experience with these patients, we argue that many cases of chondrocalcinosis and hypomagnesemia ascribed in previously published articles to Bartter's syndrome were due to Gitelman's syndrome.

Adult↗

PubMed1997

Calcium pyrophosphate dihydrate crystal deposition disease presenting as a pseudotumor of the temporomandibular joint.

We report a case of a 66-year-old white woman with calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. The patient related a 2-month history of swelling with tenderness over the left pre-auricular region. A CT scan suggested a synovial chondromatosis. Surgical removal was done and histologic study showed CPPD crystals. This disease rarely involves the temporomandibular joint (TMJ) and is not usually considered in the differential diagnosis. To our knowledge, only 14 cases have been reported in the literature.

Aged↗