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PubMed2005

Adrenomedullin(27-52) inhibits vascular calcification in rats.

Adrenomedullin (ADM) has the vasodilatory properties and involves in the pathogenesis of vascular calcification. ADM could be degraded into more than six fragments in the body, including ADM(27-52), and we suppose the degrading fragments from ADM do the same bioactivities as derived peptides from pro-adrenomedullin. The present study carries forward by assessing the effects on vascular calcification of the systemic administration of ADM(27-52). The rat vascular calcific model was replicated with vitamin D3 and nicotine. ADM or/and ADM(27-52) were systemically administrated with mini-osmotic pump beginning at seventh day after the model replication for 25 days. Vascular calcific nodules histomorphometry, vascular calcium content, vascular calcium uptake, alkaline phosphatase activity, and osteopontin-mRNA quantification in aorta were assessed. ADM limited 40.2% vascular calcific nodules (P<0.01), did not effect on calcium content (P>0.05), reduced 44.4% calcium uptake (P<0.01), lowered 21.1% alkaline phosphatase activity (P<0.01), and regulated 40.9% downwards osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. ADM(27-52) receded 32.0% vascular calcific nodules (P<0.01), taken from 55.5% calcium content (P<0.01), did not affect calcium uptake (P>0.05), inhibited 22.5% alkaline phosphatase activity (P<0.01), and restrained 21.9% osteopontin-mRNA expression (P<0.01) in the aorta of rats with vascular calcification. Both of ADM and ADM(27-52) did interact on vascular calcification each other. ADM could partially antagonize the effects of ADM(27-52) in taking from calcium content (17.5%, P<0.01) and in receding vascular calcific nodules (18.6%, P<0.01). ADM could obviously enhance the action of ADM(27-52) in inhibiting alkaline phosphatase activity (14.4%, P<0.01) and in reducing calcium uptake (11.4%, P<0.01). ADM(27-52) could partially antagonize the effects of ADM on regulating downwards osteopontin-mRNA expression (17.0%, P<0.01). It is concluded that ADM(27-52) derived from ADM acts as an inhibitory agent on vascular calcification, with special mechanisms different from ADM derived from ADM progenitor molecule.

Adrenomedullin↗
PubMed2006

Correlation between carotid area calcifications and periodontitis: a retrospective study of digital panoramic radiographic findings in pretreatment cancer patients.

OBJECTIVES: The objective of this study was to examine the prevalence of carotid area calcifications retrospectively detected on digital panoramic radiographs of pretreatment cancer subjects, and to correlate the finding of such calcifications with radiographic evidence of periodontal bone loss in the same subjects. STUDY DESIGN: Digital panoramic radiographs of 201 subjects were evaluated for calcifications projected in the carotid artery bifurcation area as well as for alveolar bone loss as a result of periodontal disease. Inclusion criteria were unobscured carotid artery bifurcation regions bilaterally and sufficient index teeth present with a definable cemento-enamel junction and alveolar crest. Radiographs were independently observed for carotid area calcifications and for periodontal status. Image enhancements permitted for detection of calcifications projected in the carotid area included window/level, inverse, and emboss. Periodontal measurements were made on index teeth using proprietary imaging software and a mouse-driven measurement algorithm. A 3-factor analysis of variance was performed with 3 between-subjects comparisons. Percentage of bone loss was the dependent variable. Independent variables were age, subject sex, and the presence or absence of carotid area calcifications. RESULTS: Differences measured in percentage of bone loss between sexes were not statistically significant. While bone loss did increase with age, comparison of the mean bone loss of each age category revealed no statistical significance. There was a highly significant correlation between carotid artery area calcifications visible on panoramic radiographs and percent alveolar bone loss. Radiographs showing unilateral and bilateral calcifications had a mean percent bone loss of 24.2% +/- 12.6% and 25.7% +/- 13.0% respectively, compared to those with no calcification at 10.4% +/- 9.9%. CONCLUSIONS: Nearly 1 in 4 subjects in this study evidenced calcifications projected in the carotid bifurcation region. The finding of such calcifications was significantly related to the calculated percentage of alveolar bone loss.

Age Factors↗
PubMed2003

Progression of aortic valve stenosis: TGF-beta1 is present in calcified aortic valve cusps and promotes aortic valve interstitial cell calcification via apoptosis.

BACKGROUND: Aortic valve stenosis characteristically progresses due to cuspal calcification, often necessitating valve replacement surgery. The present study investigated the hypothesis that TGF-beta1, a cytokine that causes calcification of vascular smooth muscle cells in culture, initiates apoptosis of valvular interstitial cells as a mechanistic event in cuspal calcification. METHODS: Noncalcified and calcified human aortic valve cusps were obtained at autopsy or at the time of cardiac surgery. The distributions within cusps of TGF-beta1, latent-TGF-beta1-associated peptide, and TGF-beta receptors were studied using immunohistochemistry. The effects of TGF-beta1 on mechanistic events contributing to aortic valve calcification were also investigated using sheep aortic valve interstitial cell (SAVIC) cultures. RESULTS: Immunohistochemistry studies revealed that calcific aortic stenosis cusps characteristically contained within the extracellular matrix qualitatively higher levels of TGF-beta1 than noncalcified cusps. Noncalcified normal valves demonstrated only focal intracellular TGF-beta1. Addition of TGF-beta1 to SAVIC cultures led to a cascade of events, including: cellular migration, aggregation, formation of apoptotic-alkaline phosphatase enriched nodules, and calcification of these nodules. The time course of these events in the SAVIC culture system was rapid with nodule formation with apoptosis by 72 hours, and calcification after 7 days. Furthermore, ZVAD-FMK, an antiapoptosis agent (caspase inhibitor), significantly inhibited calcification and apoptosis induced by TGF-beta1, but had no effect on nodule formation. However, cytochalasin D, an actin-depolymerizing agent, inhibited nodule formation, but not calcification. CONCLUSIONS: TGF-beta1 is characteristically present within calcific aortic stenosis cusps, and mediates the calcification of aortic valve interstitial cells in culture through mechanisms involving apoptosis.

Aged↗
PubMed1997

Coronary calcification and coronary atherosclerosis: site by site comparative morphologic study of electron beam computed tomography and coronary angiography.

OBJECTIVES: We compared, on a site by site basis, the morphologic features of coronary calcifications determined by electron beam computed tomography (EBCT) and angiographically defined coronary atherosclerosis. BACKGROUND: Quantification of coronary calcification using EBCT is clinically useful for the prediction of coronary stenosis. However, the relation between calcification and angiographic findings has not been evaluated by site. METHODS: We studied 251 consecutive patients who underwent elective coronary angiography for suspected coronary artery disease by EBCT and analyzed findings by site. Coronary calcifications were classified according to their length and width versus the diameter of the coronary artery in which the calcification was observed as: none, spotty, long, wide and diffuse. RESULTS: Coronary calcifications were found in 666 (27%) of 2,470 segments. The positive predictive value (PPV) of coronary calcification for significant stenosis (> or = 75% densitometric narrowing) and for all angiographically detectable atherosclerotic lesions in a segment was 0.36 and 0.80, respectively. The PPV for significant stenosis and all atherosclerotic lesions was 0.04 and 0.17 in none, 0.18 and 0.59 in spotty, 0.32 and 0.87 in long, 0.40 and 0.84 in wide and 0.56 and 0.96 in diffuse calcifications, respectively. The PPV for both significant stenosis and all lesions differed significantly (p = 0.001) among the morphologic groups. Of the 105 eccentric significant stenoses, 54 (53%) were classified as long or diffuse calcifications. Of the 95 significant stenoses with multiple irregularities, 61 (64%) showed diffuse calcification. CONCLUSIONS: Morphologic evaluation of coronary calcifications using EBCT improved the prediction of coronary stenosis on a site by site basis and provided information related to angiographic morphology.

Adolescent↗
PubMed2006

Chemical and hormonal determinants of vascular calcification in vitro.

Vascular calcification is a complex process that is dependent not only on the physicochemical effects of Ca, PO(4), and pH, but also on smooth muscle factors that may be regulated by these ions as well as by 1,25-dihydroxyvitamin D(3) (calcitriol) and parathyroid hormone (PTH). These minerals and hormones were tested in a model of medial calcification in rat aorta maintained in culture for 9 days. Calcification was quantitated as incorporation of (45)Ca, alkaline phosphatase activity was measured in aortic homogenates, and osteopontin production was measured from immunoblots of culture medium. At 1.8 mM Ca (1.46 mM free), calcification occurred at or above 2.8 mM PO(4). At 3.8 mM PO(4), calcification occurred at or above 1.10 mM free [Ca]. At a constant [Ca] x [PO(4)], calcification varied directly with [Ca] and inversely with [PO(4)]. Calcification was directly related to pH between 7.19 and 7.50 but not altered by PTH or calcitriol. Alkaline phosphatase activity and osteopontin production were increased by Ca, PO(4), calcitriol, and PTH. We conclude that calcification of rat aorta in vitro requires elevation of both [Ca] and [PO(4)], and that [Ca] rather than [PO(4)] or the product of the two is the dominant determinant. The induction of alkaline phosphatase and osteopontin indicates that Ca and PO(4) have effects in addition to simple physicochemical actions. Although PTH and calcitriol did not increase calcification in vivo, they have effects on smooth muscle that could influence calcification in vivo. Calcification is enhanced by alkalinity within the range produced during hemodialysis.

Alkaline Phosphatase↗
PubMed1992

Mitral annular calcification and the risk of stroke in an elderly cohort.

BACKGROUND: Previous clinical studies have suggested that there is an association between mitral annular calcification and the risk of stroke, but it is unclear whether this association is independent of the traditional risk factors for stroke. We examined the relation between mitral annular calcification and the incidence of stroke in a population-based study. METHODS: Subjects in the Framingham Study receiving a routine examination underwent M-mode echocardiography to determine the presence and severity (thickness in millimeters) of mitral annular calcification. The incidence of stroke during eight years of follow-up was analyzed with a proportional-hazards model adjusting for the calcification, age, sex, systolic blood pressure, diabetes mellitus, cigarette smoking, atrial fibrillation, and coronary heart disease or congestive heart failure. RESULTS: Among 1159 subjects whose echocardiograms could be assessed for mitral annular calcification and who had no history or current evidence of stroke at the index examination (51 percent of all subjects), the prevalence of mitral annular calcification was 10.3 percent in the men and 15.8 percent in the women. Multivariate analysis demonstrated that the presence of mitral annular calcification was associated with a relative risk of stroke of 2.10 (95 percent confidence interval, 1.24 to 3.57; P = 0.006). There was a continuous relation between the incidence of stroke and the severity of mitral annular calcification; each millimeter of thickening as shown on the echocardiogram represented a relative risk of stroke of 1.24 (95 percent confidence interval, 1.12 to 1.37; P less than 0.001). Furthermore, even when subjects with coronary heart disease or congestive heart failure were excluded from the analysis, subjects with mitral annular calcification still had twice the risk of stroke. CONCLUSIONS: In an elderly, longitudinally followed population-based cohort, mitral annular calcification was associated with a doubled risk of stroke, independently of traditional risk factors for stroke. Whether such calcification contributes causally to the risk of stroke or is merely a marker of increased risk because of its association with other precursors of stroke remains unknown.

Adult↗
PubMedDate not supplied

Sonographic assessment of breast calcifications.

With widespread use of high-frequency sonography, breast imagers are beginning to commonly identify sonographic calcifications. The sonographic approach in assessing breast calcifications depends on whether the calcifications are initially identified sonographically or mammographically. If the calcifications are initially identified sonographically, a breast imager should first consider if the calcifications fit the characteristics of the American College of Radiology Breast Imaging Reporting and Data System Category 2--benign. If the calcifications are not benign, then one should assess the calcifications by their mammographic appearance. If the calcifications are initially identified mammographically, then the sonologist should be aware that one may not always visualize mammographic calcifications with sonography. Instead, if the radiologist seeks to localize mammographic calcifications with sonography, the imager should search for sonographic findings of invasive malignancy or ductal carcinoma in situ. These abnormalities include hypoechoic solid mass, focally dilated ducts, intraductal mass, or, rarely, isolated clustered calcifications.

Breast Diseases↗
PubMed2003

Calcification in large cell neuroendocrine carcinoma of the lung.

BACKGROUND: The aim was to investigate the prevalence of intratumoral calcification in large cell neuroendocrine carcinoma (LCNEC) and to review computed tomography (CT) and histological findings. PATIENTS AND METHODS: From August 1992 through March 2000, 35 out of 1183 surgically resected lung cancer patients were histologically diagnosed as having LCNEC at our institute. We reviewed the plain radiographs and CT scans of these 35 LCNEC patients. In LCNEC cases with intratumoral calcification, we examined the size, number, distribution and pattern of intratumoral calcifications visible on the CT scans and the histological features. RESULTS: Three cases (9%) exhibited calcification. The calcifications were recognized by CT scans alone. The CT scans showed punctate or eccentric intratumoral calcifications, which are considered to be a malignant feature, in all three cases. In two cases, the calcifications were histologically confirmed to be located within the necrotic areas of a tumor nest. CONCLUSION: We found three LCNEC cases with intratumoral calcification. The prevalence of LCNEC calcification was similar to that in previous reports on lung cancer. The mechanism of the intratumoral calcification in our LCNEC cases is speculated to be dystrophic calcification.

Aged↗
PubMed2000

Arterial stiffening and vascular calcifications in end-stage renal disease.

BACKGROUND: Epidemiological studies have identified aortic stiffness as an independent predictor of cardiovascular mortality in end-stage renal disease (ESRD) patients. In these patients, aortic pulse wave velocity (PWV) was associated with mediacalcosis, but the influence of arterial calcifications on the viscoelastic properties of large arteries was not well characterized. The purpose of the present study was to analyse the influence of arterial calcifications on arterial stiffness in stable haemodialysed patients. METHODS: We studied 120 stable ESRD patients on haemodialysis. All patients underwent B-mode ultrasonography of common carotid artery (CCA), aorta, and femoral arteries to determine CCA distensibility, the elastic incremental modulus (Einc), and the presence of vascular calcifications. All patients underwent measurement of aortic PWV and echocardiogram. The presence of calcifications was analysed semiquantitatively as a score (0 to 4) according to the number of arterial sites with calcifications. RESULTS: Our observations indicate that arterial and aortic stiffness is significantly influenced by the presence and extent of arterial calcifications. The extent of arterial calcifications is in part responsible for increased left ventricular afterload, and is inversely correlated with stroke volume. The influence of calcifications is independent of the role of ageing and blood pressure. Arterial calcifications density increases with age, duration of haemodialysis, the fibrinogen level, and the prescribed dose of calcium-based phosphate binders. CONCLUSIONS: The results of this study showed that the presence of vascular calcifications in ESRD patients was associated with increased stiffness of large capacity, elastic-type arteries, like the aorta and CCA. The extent of arterial calcifications increased with the use of calcium-based phosphate-binders.

Adult↗
PubMed2006

The natural history of coronary calcification progression in a cohort of nocturnal haemodialysis patients.

BACKGROUND: End-stage renal disease (ESRD) is associated with a markedly increased cardiac calcification burden, as reflected by computed tomography scans of the heart. Nocturnal haemodialysis (NHD) is a novel form of renal replacement therapy which has multiple physiologic effects that may affect vascular calcification, including improvements in phosphate and uraemia control. The objective of the present study is the determination of the natural history of coronary calcification progression in patients converted to NHD, and the examination of the relationships between calcification risk factors and calcification progression in these patients. METHODS: Thirty-eight ESRD patients were converted to NHD, and included in our observational cohort study. Coronary artery calcification scores (CACS) were documented at baseline and post-conversion (mean interscan duration 16+/-1 months). Other variables of interest included age, dialysis vintage, Framingham risk profile, phosphate binder and vitamin D usage, and plasma levels of calcium, phosphate and parathyroid hormone. RESULTS: Our cohort was stratified according to baseline calcification burden (minimal calcification: CACS < or = 10 vs significant calcification: CACS > 10). Twenty-four patients had baseline CACS < or = 10. These patients demonstrated no change in coronary calcification after 1 year of NHD (from 0.7+/-0.5 to 6+/-3, P = 0.1). Fourteen patients had higher initial CACS at baseline (1874+/-696), and demonstrated a non-significant 9% increase over 1 year to 2038+/-740 (P = 0.1). Plasma phosphate and calcium x phosphate product were significantly reduced, as were calcium-based phosphate binder and antihypertensive usage. CONCLUSIONS: Our study is the first to document CACS progression in a cohort of NHD patients. Further analysis of the effect of NHD on the physiology of cardiovascular calcification is required.

Adult↗
PubMed1996

Consistency of rotator-cuff calcifications. Observations on plain radiography, sonography, computed tomography, and at needle treatment.

RATIONALE AND OBJECTIVES: The author analyzes findings of consistency of rotator-cuff calcifications found at ultrasound (US)-guided needle treatment compared with findings of plain radiography, US, and computed tomography (CT). METHODS: Twenty patients had rotator-cuff calcifications (mean diameter, 1.5 cm; range, 1.1-2.6 cm) resistant to conservative therapy. At needle treatments, the consistency was assessed as hard or soft (slurry calcific deposit). In each imaging examination, the calcifications were divided into two groups. In radiographs, calcifications were divided into "well-defined" and "ill-defined." In US, they were divided into calcifications with acoustic shadow and calcifications with a faint shadow or no shadow. On CT, they were divided into homogeneous or nonhomogeneous calcifications. At CT, the density of the calcifications also was determined. The findings of consistency obtained at needle treatments were compared with the findings of plain radiography, US, and CT. RESULTS: At needle treatments, 45% (9 of 20) of the calcifications were soft or nearly liquid, and 55% (11 of 20) were hard. On plain radiographs, 67% (6 of 9) were as soft and 64% (7 of 11) as hard. On sonograms, 77% (7 of 9) were soft and 82% (9 of 11) were hard. On CT images, 77% (7 of 9) were soft and 91% (10 of 11) were hard; CT attenuation values were 77% (7 of 9) and 91% (10 of 11), respectively. CONCLUSIONS: Ultrasound and CT were reliable in predicting the consistency of rotator-cuff calcifications. Computed tomography attenuation values were the most accurate, and plain radiographs were the least accurate.

Acupuncture Therapy↗
PubMed2004

Aortic calcification is associated with age and sex but not left ventricular mass in essential hypertension.

The aim of this study was to investigate the prevalence of aortic calcification in patients with essential hypertension and its relationship with age, sex, and left ventricular hypertrophy. Two hundred ninety consecutive patients with essential hypertension were studied. A chest radiograph and an echocardiograph were performed. Aortic calcification was observed in 74/290 (25.5%) patients. Patients with calcification were mostly female (67.6%) and older (71.8+1.9 years), whereas patients without calcification were younger (59.0+0.79) and of both sexes (51.85% female). Left ventricular mass index in male patients with aortic calcification was 147.3+4.32 g/m(2) and without calcification was 132.7+2.28 g/(2) (p=0.023). Female patients' values were 131.9+4.32 g/m(2) with calcification and 121.2+2.85 g/m(2) without calcification (p=0.025). Left ventricular mass was independently associated with age and sex but not with aortic calcification. The prevalence of aortic calcification in essential hypertension is considerably higher compared to the general population. Essential hypertension and age seem to contribute to the concurrent appearance of aortic calcification and increased left ventricular mass.

Adult↗
PubMed1998

Calcification retrieval at stereotactic, 11-gauge, directional, vacuum-assisted breast biopsy.

PURPOSE: To determine the frequencies of calcification retrieval and histologic underestimates at stereotactic, 11-gauge, directional, vacuum-assisted breast biopsy. MATERIALS AND METHODS: Retrospective review of records revealed 112 calcific lesions in 80 women (aged 31-85 years) who underwent stereotactic, 11-gauge, directional, vacuum-assisted biopsy; a mean of 14 specimens per lesion were obtained. Calcification retrieval was defined as identification of calcifications on radiographs of specimens. Atypical ductal hyperplasia (ADH) underestimates were lesions that yielded ADH at stereotactic biopsy and carcinoma at surgery. Ductal carcinoma in situ (DCIS) underestimates were lesions that yielded DCIS at stereotactic biopsy and infiltrating carcinoma at surgery. Mammograms, stereotactic images, radiographs of specimens, and histologic findings were reviewed. RESULTS: Stereotactic, 11-gauge, directional, vacuum-assisted biopsy removed all calcifications in 51 (46%) lesions, some calcifications in 55 (49%) lesions, and no calcifications in six (5%) lesions. Failure to retrieve calcifications was significantly more likely in lesions 5 mm or smaller (12% [five of 43] vs 1% [one of 69], P = .03), in calcifications with amorphous morphology (21% [three of 14] vs 3% [three of 98], P < .03), or if the probe was fired outside the breast (12% [five of 40] vs 1% [one of 72], P = .02). Surgery revealed DCIS in one (10%) of 10 lesions that yielded ADH at stereotactic biopsy. Surgery revealed infiltrating carcinoma in one (5%) of 21 lesions that yielded DCIS at stereotactic biopsy. No underestimation occurred when all calcifications were removed. CONCLUSION: Stereotactic, 11-gauge, directional, vacuum-assisted biopsy resulted in successful calcification retrieval in 106 (95%) of 112 cases. Histologic underestimation was infrequent.

Adult↗
PubMed2004

Osteogenic regulation of vascular calcification: an early perspective.

Cardiovascular calcification is a common consequence of aging, diabetes, hypercholesterolemia, mechanically abnormal valve function, and chronic renal insufficiency. Although vascular calcification may appear to be a uniform response to vascular insult, it is a heterogenous disorder, with overlapping yet distinct mechanisms of initiation and progression. A minimum of four histoanatomic variants-atherosclerotic (fibrotic) calcification, cardiac valve calcification, medial artery calcification, and vascular calciphylaxis-arise in response to metabolic, mechanical, infectious, and inflammatory injuries. Common to the first three variants is a variable degree of vascular infiltration by T cells and macrophages. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clear; stroke, amputation, ischemic heart disease, and increased mortality are portended by the anatomy and extent of calcific vasculopathy. Along with dystrophic calcium deposition in dying cells and lipoprotein deposits, active endochondral and intramembranous (nonendochondral) ossification processes contribute to vascular calcium load. Thus vascular calcification is subject to regulation by osteotropic hormones and skeletal morphogens in addition to key inhibitors of passive tissue mineralization. In response to oxidized lipids, inflammation, and mechanical injury, the microvascular smooth muscle cell becomes activated. Orthotopically, proliferating stromal myofibroblasts provide osteoprogenitors for skeletal growth and fracture repair; however, in valves and arteries, vascular myofibroblasts contribute to cardiovascular ossification. Current data suggest that paracrine signals are provided by bone morphogenetic protein-2, Wnts, parathyroid hormone-related polypeptide, osteopontin, osteoprotegerin, and matrix Gla protein, all entrained to endocrine, metabolic, inflammatory, and mechanical cues. In end-stage renal disease, a "perfect storm" of vascular calcification often occurs, with hyperglycemia, hyperphosphatemia, hypercholesterolemia, hypertension, parathyroid hormone resistance, and iatrogenic calcitriol excess contributing to severe calcific vasculopathy. This brief review recounts emerging themes in the pathobiology of vascular calcification and highlights some fundamental deficiencies in our understanding of vascular endocrinology and metabolism that are immediately relevant to human health and health care.

Animals↗
PubMed2007

Calcifications, arterial stiffness and atherosclerosis.

UNLABELLED: Vascular calcification can occur in either the intimal or medial layers of the arterial wall. Intimal calcification is associated with atherosclerosis, which is characterized by lipid accumulation, inflammation, fibrosis and development of focal plaques. Medial calcification is associated with arterio sclerosis, i.e. age- and metabolic disease-related structural changes in the arterial wall which are related to increased arterial stiffness. It has been hypothesized that vascular calcification, either intimal or medial, may directly increase arterial stiffness. Alternatively, arterial stiffness may contribute to the development of calcification and focal plaque. Ample evidence (i.e. animal data and studies of diabetes and end-stage renal disease) has demonstrated that medial calcification of elastic fibers contributes to increased arterial stiffness. Evidence linking intimal calcification with arterial stiffness is less definitive, partly because it is very difficult to differentiate vascular calcification due to focal plaques (intimal) from medial calcification, and partly because the number of studies has been small. CONCLUSION: Current evidence supports that medial calcification is associated with increases in arterial stiffness. The association between intimal (atherosclerotic-associated) calcification and arterial stiffness is less definitive.

Aortic Diseases↗
PubMed1995

Beta-glycerophosphate accelerates calcification in cultured bovine vascular smooth muscle cells.

Calcification is a common feature of advanced atherosclerotic lesions and is being reemphasized as a clinically significant element of vascular disease. However, the scarcity of in vitro models of vascular calcification preclude studying its molecular and cellular mechanism. In the present study, we describe an in vitro calcification in which diffuse calcification can be induced by culturing bovine vascular smooth muscle cells (BVSMC) in the presence of beta-glycerophosphate, ascorbic acid, and insulin in a manner analogous to in vitro mineralization by osteoblasts. Calcification was confirmed by von Kossa staining and 45Ca accumulation. Factor analysis revealed that beta-glycerophosphate is the most important factor for this calcification process, suggesting that alkaline phosphatase (ALP) may be involved. As predicted, high levels of ALP expression were detected by ALP assay and Northern blot analysis. Functional significance of ALP was confirmed by demonstrating that levamisole, a specific inhibitor of ALP, inhibited BVSMC calcification in a dose-dependent manner. Bisphosphonates such as etidronate and pamidronate potently inhibited BVSMC calcification, suggesting that hydroxyapatite formation may be involved. Importantly, expression of osteopontin mRNA was dramatically increased in calcified BVSMC compared with uncalcified control cells. These data suggest that beta-glycerophosphate can induce diffuse calcification by an ALP-dependent mechanism and that this in vitro calcification system is useful for analyzing the molecular and cellular mechanisms of vascular calcification.

Alkaline Phosphatase↗
PubMed1979

Calcification of the basal ganglia: computerized tomography and clinical correlation.

During a 1-year period, 4219 consecutive computerized tomograms (CT) were reviewed for basal ganglia calcification; 14 patients with such calcification were identified. Calcifications on CT scan were bilateral in 12 of these cases and unilateral in 2. All bilateral calcifications were symmetric. The globus pallidus was the site of calcification in 13 of the 14 patients. Bilateral dentate nucleus calcification was seen in one patient. Skull radiograms were normal in all but one. Patients had diverse symptoms that were often explained by other findings, suggesting that calcifications may be coincidental and that basal ganglia calcification may not be a nosologic entity. Disturbances of calcium metabolism were not found in these patients, minimizing the pathophysiologic significance of altered calcium metabolism and the need for extensive endocrinologic evaluation. The finding of basal ganglia calcification alone does not justify invasive diagnostic procedures. Extrapyramidal signs may be associated with basal ganglia calcification; parkinsonism associated with basal ganglia calcification differs from idiopathic parkinsonism in being resistant to levodopa therapy.

Adult↗
PubMed2005

Calcifications in mucinous and serous cystic ovarian tumors.

Mucinous cystic ovarian tumors sometimes contain calcifications, but the frequency and significance of such calcifications in diagnostic radiology are not well understood. We therefore retrospectively investigated the radiological and histopathological evidence of calcifications in 44 cases of ovarian mucinous cystic tumors (22 benign, 13 borderline, and 9 malignant) and 21 cases of ovarian serous cystic tumors (6 benign and 15 malignant) in which a non-contrast CT scan was performed. The shape and distribution of the calcifications in the mass lesion were assessed both radiologically and histopathologically. Calcifications were noted in 34.1% of mucinous cystic tumors on CT scans and 56.8% in histopathological studies, and they were found in two locations, intramural and intra-cystic, according to the histopathological findings. Intramural calcifications were frequent in benign tumors, and intra-cystic calcifications were frequent in proliferating tumors. Calcifications (psammoma bodies) were noted in 4.7% of serous cystic tumors on CT scans and 14.3% in histopathological studies. CT was not sufficiently sensitive in the detection of intra-cystic calcification in mucinous tumors and psammoma bodies in serous tumors. However, the presence of intramural calcifications may be a good indicator of mucinous tumors. Understanding the frequency and morphology of the calcifications in these neoplasms is one of the keys to making a correct diagnosis.

Adult↗