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PubMed1979

Calcification of the mitral annulus: etiology, clinical associations, complications and therapy.

This report reviews the clinical features of 80 patients with roentgenographically proved mitral annular calcification. The mean age of the group was 73 years, and there was a 2.5 to 1 female to male ratio. Evaluation for underlying cardiovascular disease revealed six patients with severe calcific valvular aortic stenosis; five patients with hypertrophic cardiomyopathy, 11 with mitral prolapse and 33 with significant arterial hypertension (blood pressure greater or equal to 150/96 mm Hg). Eighty-five per cent of the group (68 of 80 patients) had an underlying cardiac disorder associated with either chronically increased left ventricular systolic pressure or abnormal leaflet motion. Other cardiovascular abnormalities occurring as complications secondary to the mitral ring calcification included subacute bacterial endocarditis (three cases), arterial emboli (five episodes) and high grade atrioventricular block (16 cases). Twelve patients had severe mitral regurgitation; successful mitral valve replacement was carried out in four patients (all with myxomatous mitral tissue). Evidence of diffuse conduction system disease, not limited to the area of the cardiac fibrous skeleton, was found frequently (44 patients). Nine patients had sinus node dysfunction and 35 patients had electrocardiographic evidence of distal intraventricular (fascicular) block. Twenty-one patients eventually required pacemakers for management of symptomatic bradyarrhythmias. Atrial fibrillation was present in 23 patients. In this review it was found that calcification of the mitral annulus is frequently associated with or induces serious cardiovascular disease. Since some of these disorders may be modified by appropriate therapy, calcification of the mitral annulus should no longer be ignored as a benign marker of the elderly heart.

Adult↗
PubMed1987

Association of Paget's disease of bone with calcific aortic valve disease.

To test the hypothesis that Paget's disease of bone is associated with a greater incidence of calcific aortic valve disease, a computer-generated list was obtained of all autopsy subjects from the Johns Hopkins Hospital in whom Paget's disease was diagnosed (n = 92). The severity of Paget's disease and cardiac valvular lesions was graded on a scale of 0 to 3, with 3 as the most severe. Two control cases were obtained for each case of Paget's disease. Each was the case either immediately before or after the Paget's case, and was matched for age, race, sex, and extent of autopsy. The incidences of moderate (10.9 percent) and severe (5.4 percent) calcific aortic valve disease were both fourfold greater than in the control group (chi-square analysis, p less than 0.01 and p less than 0.05, respectively). Additionally, the frequency of advancing grades of calcific aortic valve disease was greater in more advanced stages of Paget's disease. In fact, there was a dose-response effect of Paget's disease upon calcific aortic valve disease (trend analysis for proportion, p less than 0.01). These data therefore support the hypothesis that Paget's disease is associated with calcific aortic valve disease in a dose-response manner.

Aged↗
PubMed1990

Aortic calcification in chronic fluoride poisoning: biochemical and electronmicroscopic evidence.

Fluoride is known to cause ectopic calcification. The biochemical mechanism(s) involved in the initiation of calcification is not understood and the accompanying ultrastructural changes remain to be elucidated. Therefore, certain relevant parameters have been investigated in the aorta of rabbits administered fluoride, 10 mg NaF/kg body wt, every 24 hr for 17 and 24 months. The significant findings are: (i) degeneration of smooth muscle fibers in the tunica media of the aorta, (ii) presence of electron-dense granules in the mitochondria and on the inner surface of the plasma membrane of smooth muscle cells, (iii) presence of matrix vesicles with electron-dense deposits, (iv) enhanced calcium content and the Ca/P ratio, and (v) increased total glycosaminoglycan (GAG) content with reduced dermatan sulfate. The presence of electron-dense granules in the mitochondria, on the plasma membrane and matrix vesicles is suggestive of the process of calcification. The enhanced calcium content as well as the Ca/P ratio supports the view that the aorta is undergoing mineralization. The total GAG is enhanced, possibly due to an increase in the content of GAGs other than isomers of chondroitin. The observation that conveys an important message is that the dermatan sulfate normally known to exist in high concentrations in soft tissues begins to decrease as the process of calcification sets in. This perhaps would hold true and may serve as an index in the process of ectopic calcification.

Administration, Oral↗
PubMed1979

Low serum estradiol levels in subjects with arterial calcification.

The relationship between arterial calcification and serum estradiol levels was studied in 72 postmenopausal female and 59 male subjects. In both sexes, subjects with iliac artery calcification had rather lower serum estradiol levels (8.4 +/- 1.4 pg/ml in the females, and 19.2 +/- 2.5 pg/ml in the males) than controls (16.1 +/- 1.6 pg/ml in the females, and 29.7 +/- 2.4 pg/ml in the males). The bone mineral content of females with iliac artery calcification (0.44 +/- 0.02 g/cm2) was lower than controls (0.52 +/- 0.01 g/cm2); a positive correlation between serum estradiol levels and bone mineral content was found in the females. However, bone mineral content did not significantly differ between males with and without arterial calcification (0.67 +/- 0.03 g/cm2 in the former, and 0.65 +/- 0.02 g/cm2 in the latter). These results indicate that arterial calcification and increased bone resorption are both individual results of estrogen deficiency.

Adult↗
PubMed1984

Phosphocitrate and its analogue N-sulpho-2-amino tricarballylate inhibit aortic calcification.

This study reports the ability of phosphocitrate and its enzyme-resistant analogue N-sulpho-2-amino tricarballylate to inhibit aortic calcification. Dystrophic calcification of aorta was induced by transplanting fresh aortic segments in Millipore chambers to the peritoneal walls of recipient rats. Daily intraperitoneal injection of the new inhibitors remarkably reduced calcium accumulation by the aortae and prevented the appearance of hydroxyapatite-like crystalline structures. Phosphocitrate was the most effective of the anti-calcifying agents tested, preventing aortic calcification at 1 mumole/day/rat. N-sulpho-2-amino tricarballylate was less effective, reducing aortic calcification by 60% at 10 mumoles/day/rat. The new inhibitors might prove therapeutically useful in man to arrest soft tissue calcification.

Animals↗
PubMed1983

Soft-tissue calcifications of the dental follicle in regional odontodysplasia: a structural and ultrastructural study.

Soft-tissue calcifications of the dental follicle in regional odontodysplasia were studied via the correlated techniques of light microscopy, scanning electron microscopy (SEM), calcium x-ray cartography, and high-resolution transmission electron microscopy (TEM). The study revealed several types of calcification, mostly located within an area normally occupied by enamel formation. Some of them are produced without collagen being involved; others result from the mineralization of collagen fibers. Sometimes they were surrounded by a structureless homogeneous zone and resulted from the fusion of several smaller globules. High-resolution TEM revealed two different types of calcifications: a few composed of platelike crystallites, presenting a "sheath" characteristic of apatite formation, most of them poorly crystallized. The calcifications were in close contact with the cytoplasm of the neighboring connective tissue cells in which an abundance of microfilaments was found. It is suggested that these filaments might be involved in the formation of dystrophic soft-tissue calcifications.

Adolescent↗
PubMed1988

Inhibitory effects of cadmium on in vitro calcification of a clonal osteogenic cell, MC3T3-E1.

To examine an inhibitory mechanism of Cd on bone formation, the effects of Cd on calcification were investigated in a culture of a clonal osteogenic cell line, MC3T3-E1. At 3 days after inoculation, Cd was added to the medium containing 7 mM beta-glycerophosphate, and culture was continued for 8 days. Cd at 1.78 microM and above caused a significant decrease in 45Ca accumulation. The decrease in mineralization by Cd was similar to that in collagen content or alkaline phosphatase (ALP) activity. Histologically, the cell density and the mineralization degree were lower than those of the controls. Ultrastructurally, degenerated cells were observed with undifferentiated cells which had fewer rough-surfaced endoplasmic reticulum and many mitochondria. This suggests that Cd may inhibit the differentiation into osteoblasts as well as the cell function. On the other hand, calcification of cells at 8 days after inoculation was inhibited by Cd at 1.78 microM and above. The decrease in collagen content and ALP activity by Cd was much lower than that in calcification. Cd-treated cells were well differentiated into osteoblasts morphologically, but the mineralization degree was lower than that of the controls. Ultrastructurally, cell damage was not recognized so strongly compared with long-term Cd treatment. The mineralization of osteoblasts was also inhibited by Zn levels which left both collagen content and ALP activity unaffected. From these results, it was suggested that the inhibitory effect of Cd on in vitro calcification of MC3T3-E1 cells may be due to both a depression of cell-mediated calcification and a decrease in physiochemical mineral deposition.

Alkaline Phosphatase↗
PubMed1992

33-year follow-up after simple excision of a giant renal oncocytoma with calcifications: case report and review of the literature.

Renal oncocytoma can present with calcification seen on the plain roentgenogram. From a review of the literature (both before and after 1976, when the concept of oncocytoma was popularized in the English literature), 10 cases of calcification in association with renal oncocytoma were found. In three of these 10 cases, the calcifications could be grossly demonstrated on the plain roentgenogram; in the other seven cases, the calcifications were microscopic in nature. The presence of calcification in a renal tumor does not rule out the diagnosis of oncocytoma. Grossly, a renal oncocytoma has a brownish mahogany color. A case is presented in which simple excision of an oncocytoma resulted in a 33-year survival. In the future, excision instead of nephrectomy could become the standard treatment for these tumors.

Adenoma↗
PubMed1993

Synergistic inhibition of the calcification of glutaraldehyde pretreated bovine pericardium in a rat subdermal model by FeCl3 and ethanehydroxydiphosphonate: preincubation and polymeric controlled release studies.

Calcification is a frequent cause of the clinical failure of bioprosthetic heart valves fabricated from glutaraldehyde-pretreated porcine aortic valves or glutaraldehyde-pretreated bovine pericardium (GPBP). We investigated the hypothesis that ferric chloride (FeCl3) and sodium-ethanehydroxydiphosphonate (EHDP) may act synergistically to prevent bioprosthetic tissue calcification. Pre-incubations and controlled release systems were studied individually. FeCl3-EHDP polymeric controlled release matrices were formulated using silicone rubber and evaluated for in vitro release kinetics at pH 7.4 and 37 degrees C. The effects of Fe-EHDP synergism on GPBP calcification were investigated with 21 d subdermal implants in 3 wk-old male rats. Results demonstrated that levels of Fe3+ and EHDP uptake, measured in GPBP tissues pre-incubated first in an FeCl3 solution (10(-5) M) followed by an EHDP solution (0.1 M), were higher than in the reverse order of incubation. In the first series of rat implants, GPBP was pre-incubated in either FeCl3 or Na2EHDP solutions, or sequential pre-incubations of first FeCl3 and then Na2EHDP solutions, or the reverse. The inhibition of calcification was greatest when FeCl3 (first pre-incubation, 10(-5) M) was combined with Na2EHDP (second pre-incubation, 0.1 M) (1.78 +/- 0.2 micrograms of Ca2+/mg of dried tissue) compared with the other pre-incubation groups: EHDP (first pre-incubation) combined with FeCl3 (second pre-incubation) (21.7 +/- 6.4), FeCl3 solution alone at 10(-5) M (27.9 +/- 10.7), Na2EHDP solution alone at 0.1 M (52.3 +/- 11.9) and the control group (72.3 +/- 10.2). In a second series of implants, GPBP specimens were co-implanted with individual controlled release systems containing one of the following formulations (weight percentage in silicone rubber): 1% FeCl3, 20% CaEHDP, 20% protamine sulphate, 1% FeCl3-20% CaEHDP, and 1% FeCl3-20% protamine sulphate. The 1% FeCl3-20% CaEHDP silicone-rubber matrices were the most effective for inhibiting GPBP mineralization (13.7 +/- 3.0 micrograms Ca2+/mg of dried tissue) compared with non-drug silicone co-implant controls (74.7 +/- 5.58 micrograms Ca2+/mg of dried tissue) and other polymeric treatment groups (32.3 +/- 2.3-80.0 +/- 19.7). No adverse effects on bone or overall growth of any treatment protocols were noted. Thus, combinations of FeCl3 and EHDP, using either pre-incubations or polymeric controlled release, were synergistic for inhibiting GPBP calcification.

Animals↗
PubMed1996

Structural studies on bovine bioprosthetic tissues and their in vivo calcification: prevention via drug delivery.

Cardiovascular calcification, the formation of calcium phosphate deposits in cardiovascular tissue, is a common end-stage phenomenon affecting a wide variety of bioprostheses. To study the process of calcification in tissue prosthetics, glutaraldehyde-treated bovine pericardium, dura mater and fascialata were implanted subcutaneously in rats and retrieved 21 days later and thereby morphological findings were correlated with biochemically determined levels of calcium. Transmission electron microscopy showed that calcification primarily involved the surface of collagen fibrils and the interfibrillar spaces. The deposition of calcium was higher with dura and fascia prostheses compared to pericardium. However, the release of Fe3+ ions from chitosan matrix had substantially inhibited the deposits of calcium in all implanted tissues. It seems that the structural and anatomical features of the tissue is one of the important factors for tissue-associated calcification. It is also confirmed that glutaraldehyde-preserved pericardium is the most suitable material for the development of cardiac prosthesis, with an appropriate drug combination therapy for prevention of pathological calcification.

Animals↗
PubMed1992

Placental aryl hydrocarbon hydroxylase activity and placental calcifications.

Induction of aryl hydrocarbon hydroxylase (AHH) activity in the placenta as a result of maternal exposure to polycyclic aromatic hydrocarbons contained in cigarette smoke has been well documented. Furthermore, calcifications are more prevalent in the placentas of pregnant smokers than in those of non-smokers. The present study examines whether this latter relationship could be explained by the induction of AHH activity in the placenta. AHH levels were determined at birth in 141 unselected pregnant women admitted for delivery. Macroscopic placental examination was performed for vascular lesions, abnormalities of placental shape, of the cord and parameters of placental maturity such as basal and parenchymatous calcifications. Significant increases in the prevalence of calcifications of the placental basal plates and parenchyma with the induction of placental AHH were found. A similar significant association between smoking and AHH activation was also observed. These findings remained unchanged when controlling for smoking status assessed both by questionnaire and presence of cotinine in mother's urine. Moreover, the apparent association between smoking 'factor' and calcifications disappeared when controlling for AHH induction. Therefore, the association between smoking and placental calcifications previously related could be mediated by the AHH induction.

Aryl Hydrocarbon Hydroxylases↗
PubMed1992

Calcific aortic stenosis and autonomic dysfunction.

With an aging population, calcific aortic stenosis is becoming more important in medical practice. Its cause is unknown. This paper hypothesises autonomic dysfunction is the abnormality underlying the tendency of the aging aortic valve to calcify, a proposition based on 2 main lines of evidence: 1. the similarity between aortic valvular calcification and medial arterial calcification, the latter a condition in whose pathogenesis autonomic dysfunction is implicated; 2. the similarity between the changes of autonomic denervation and those of natural aging in the aortic valve, of which calcific aortic stenosis is an exaggerated form. Autonomic denervation leads to withdrawal of neurotrophic influences from cells and tissues. The resulting changes in function and in structure, it is proposed, give rise to a condition of vulnerability allowing other stresses, such as haemodynamic trauma, to result in calcification.

Aged↗
PubMed1992

Fluoroscopic coronary artery calcification and associated coronary disease in asymptomatic young men.

Little is known about the diagnostic significance of coronary artery calcification detected fluoroscopically in apparently healthy young men. This study compared the presence of fluoroscopically detected coronary artery calcification with angiographic coronary artery disease in asymptomatic male military aircrew undergoing noninvasive cardiac screening tests and coronary arteriography for occupational indications. Of 1,466 men screened with coronary fluoroscopy, 613 underwent coronary arteriography because of one or more abnormal noninvasive test results. The mean age (+/- SD) of all subjects screened was 40.2 +/- 5 years (range 26 to 65). Significant coronary artery disease (greater than or equal to 50% diameter stenosis) was found in 104 of the 613 subjects with arteriograms (16.9% disease prevalence). Overall sensitivity and specificity for coronary artery calcification detection of significant disease, based only on those subjects undergoing arteriography, were 66.3% and 77.6%, respectively. For measurable disease (mild plus significant), sensitivity was 60.6% and specificity 85.9%. Positive and negative predictive values were 37.7% and 91.9%, respectively, for significant disease. For measurable disease, positive and negative predictive values were 68.9% and 80.9%, respectively. In these asymptomatic young men, a fluoroscopic examination negative for coronary artery calcification indicated a low risk of significant coronary artery disease, whereas a positive test result (calcification present) substantially increased the likelihood of angiographically significant coronary artery disease.

Adult↗
PubMed2004

[Paediatric intervertebral calcifications: two cases report and review of the literature].

UNLABELLED: Discal calcification in childhood is rare. Calcifications are occasionally discovered during routine examinations. Generally, the calcification process is confined to the nucleus pulposus of the intervertebral disc. CASES REPORT: We describe the cases of two children, five and seven years old who presented with acute low back pain. The patients underwent a CT scan, which demonstrated a posterolateral calcified disc hernia. DISCUSSION: Only a few cases with evidence of calcification of the herniated portion of the disc have been previously described. The clinical picture is composed of pain and functional limitation. The radiographic picture consists of the association of morphological and structural alterations of vertebral bodies adjacent to one or more disc calcifications usually centrally sited, sometimes associated with anterior or posterior herniations. The surgical decompression of the nerve root could be necessary.

Back Pain↗
PubMed2004

Effects of periodate and chondroitin 4-sulfate on proteoglycan stabilization of ostrich pericardium. Inhibition of calcification in subcutaneous implants in rats.

Chemical modification of biological materials used in the manufacture of cardiac valves tends to reduce the relatively high degree of biodegradation and calcification of the implanted bioprostheses. The most widely used treatment to reduce biodegradability of the valves is glutaraldehyde fixation. However, this treatment is potentially toxic and induces tissue calcification. In order to minimize these undesirable effects, we have analyzed the effect of a pre-fixation of endogenous proteoglycans and exogenous glycosaminoglycans, as well as the borohydride reduction influence on the different modified ostrich pericardium implants after subcutaneous implantation in rats. The presence of calcific deposits was detected in all implanted GA-fixed samples; however, calcification was highly reduced in both groups of periodate-prefixed materials, which showed also a very low Ca/P molar ratio. Borohydride post-treatment of these biomaterials resulted in a significant increase in calcium phosphate precipitation, with the appearance of calcium deposits mainly in an amorphous form even though X-ray diffraction allowed the detection of brushite- and apatite-like crystals. Regarding tissue stability, no significant differences were found among the borohydride-untreated implants but higher levels of matrix metalloproteinases were observed by gelatin zymography in the periodate pre-fixed materials. This increase was partially reduced by pre-fixation of exogenous chondroitin 4-sulfate. On the other hand, borohydride post-treatment not only increased calcification, but also reduced tissue stability and increased the presence of matrix-degrading activities.

Animals↗
PubMed2005

Tissue response of defined collagen-elastin scaffolds in young and adult rats with special attention to calcification.

Collagen-elastin scaffolds may be valuable biomaterials for tissue engineering because they combine tensile strength with elasticity. In this study, the tissue response to and the calcification of these scaffolds were evaluated. In particular, the hypothesis was tested that calcification, a common phenomenon in biomaterials, may be due to microfibrils within the elastic fibre, and that these microfibrils might generate a tissue response. Four scaffolds were subcutaneously implanted, viz. collagen, collagen + pure elastin, collagen+microfibril-containing, and collagen + pulverised elastic ligament (the source for elastin). Explants were evaluated at day 3, 7 and 21. In young Sprague Dawley rats, collagen + ligament calcified substantially, whereas collagen + elastin (with and without microfibrils) calcified less, and collagen did not. Calcification started at elastic fibres. In both Sprague Dawley and Wistar adult rats, however, none of the scaffolds calcified. Mononuclear cell infiltration was prominent in young and adult Sprague Dawley rats. In adult Wistar rats, this infiltration was associated with the presence of microfibrils. Degradation of scaffolds and new matrix formation were related with cellular influx and degree of vascularisation. In conclusion, absence of microfibrils from the elastic fibre does not prevent calcification in young Sprague Dawley rats, but does reduce the tissue response in adult Wistar rats. Cellular response and calcification differs with age and strain and therefore the choice of animal model is of key importance in biomaterial evaluation.

Aging↗
PubMed2005

Calcifications in a clear cell mucoepidermoid carcinoma of the hard palate.

Although calcification is a common finding in inflammatory salivary gland disorders, salivary gland tumour rarely shows calcifications. A case of clear cell mucoepidermoid carcinoma (MEC) of the hard palate with extensive intratumoural calcifications visible on computed tomography (CT) scans and histologic sections is described. The calcification in the salivary gland tumour of the palate recognized by a CT scan should be considered in the differential diagnosis of a MEC. The mechanism of the intratumoural calcification in our case is speculated to be a result of a secretory function of the tumour cells.

Calcinosis↗
PubMed2005

Osteopontin expression and adventitial angiogenesis induced by local vascular endothelial growth factor 165 reduces experimental aortic calcification.

BACKGROUND: Vascular calcification is a common pathologic and precisely regulated process involving bone-associated proteins such as osteopontin. In this study, we investigated mechanisms by which recombinant human vascular endothelial growth factor 165 protects the arterial wall from severe vascular remodeling, including calcification, a newly discovered biologic action of vascular endothelial growth factor. METHODS: In a rabbit model of thoracic aortic end-to-end anastomosis that simulates cardiovascular intervention, recombinant human vascular endothelial growth factor 165 at a dose of 0.75 mug (n = 19) or albumin (control; n = 19) was delivered intraluminally and on the serosal surface. Animals were killed, and aortic tissue was evaluated by Western blotting, immunohistochemistry, and immunofluorescence at 4, 8, and 24 hours; 1 week; and 1 month after surgery. RESULTS: All controls revealed extensive aortic medial calcification at 1 month, whereas calcification was significantly reduced or absent with vascular endothelial growth factor treatment. Compared with controls, vascular endothelial growth factor treatment resulted in an earlier infiltration of macrophages in the vessel media (at 8 hours: 5.7 +/- 2.3 macrophages per high-power field in control vs 32.1 +/- 7.5 in vascular endothelial growth factor-treated aortas; P < .001), whereas controls showed an increase in macrophages starting at 1 week (24.1 +/- 6.9 vs 4.3 +/- 1.8; P < .001). Osteopontin expression was transiently increased and detected in macrophages and endothelial cells in vascular endothelial growth factor-treated vessels, and adventitial microvascular density was significantly increased by 1 week (9.5 +/- 0.43 vs 25.0 +/- 1.3; P < .001). CONCLUSIONS: Our data suggest that exogenous vascular endothelial growth factor is capable of increasing adventitial angiogenesis and shifting macrophage infiltration and osteopontin expression in the media to an earlier time point, thereby promoting prompt repair and diminishing vascular remodeling and calcification after acute vascular injury.

Animals↗