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PubMed1996

[Calcification of the pectineal ligament. An usual radiological imaging in pediatrics].

OBJECTIVES: Since its first description several years ago in the elderly subject, calcification of the Cooper ligament is often considered as a rare anecdotal phenomenon. We present the radiographic presentation which is often not well known. METHODS: Two experienced radiologists examined independently a series of 100 consecutive X-rays of the pelvis performed in a population of elderly subjects (mean age 84.4 +/- 9.2), looking for calcification of the Cooper ligament. RESULTS: Calcification of the Cooper ligament was observed on 7 of the 100 images of the pelvis. There was no significant difference in age, sex, or reason for ordering the examination between subjects with calcification and those without calcifications. Arterial calcifications were observed at an equal frequency. The usual aspect of the Cooper ligament was a fine opaque line following along the upper border of the iliopectinate crest. Oblique views visualized the calcification better. The line of calcification was either continuous of fragmented and was bilateral in all 7 cases. CONCLUSION: These images are apparently of no pathological significance. Clinicians should however be aware of the radiographic presentation in order to avoid confusion with visceral calcification or periosteal deposits.

Aged↗
PubMed2007

Chondrocyte apoptosis is not essential for cartilage calcification: evidence from an in vitro avian model.

The calcification of cartilage is an essential step in the process of normal bone growth through endochondral ossification. Chondrocyte apoptosis is generally observed prior to the transition of calcified cartilage to bone. There are, however, contradictory reports in the literature as to whether chondrocyte apoptosis is a precursor to cartilage calcification, a co-event, or occurs after calcification. The purpose of this study was to test the hypothesis that chondrocyte apoptosis is not a requirement for initial calcification using a cell culture system that mimics endochondral ossification. Mesenchymal stem cells harvested from Stages 21-23 chick limb buds were plated as micro-mass cultures in the presence of 4 mM inorganic phosphate (mineralizing conditions). The cultures were treated with either an apoptosis inhibitor or stimulator and compared to un-treated controls before the start of calcification on day 7. Inhibition of apoptosis with the caspase inhibitor Z-Val-Ala-Asp (O-Me)-fluoromethylketone (Z-VAD-fmk) caused no decreases in calcification as indicated by radioactive calcium uptake or Fourier transform infrared (FT-IR) analysis of mineral properties. When apoptosis was inhibited, the cultures showed more robust histological features (including more intense staining for proteoglycans, and more intact cells within the nodules as well as along the periphery of the cells as compared to untreated controls), more proliferation as noted by bromo-deoxyuridine (BrdU) labeling, decreases in terminal deoxynucleotidyl transferase (Tdt)-mediated dUTP nick-end labeling (TUNEL) staining, and fewer apoptotic bodies in electron microscopy. Stimulation of apoptosis with 40-120 nM staurosporine prior to the onset of calcification resulted in inhibition of calcium accretion, with the extent of total calcium uptake significantly decreased, the amount of matrix deposition impaired, and the formation of abnormal mineral crystals. These results indicate that chondrocyte apoptosis is not a pre-requisite for calcification in this culture system.

Amino Acid Chloromethyl Ketones↗
PubMed1994

Molecular weight dependence of calcification of polyethylene glycol hydrogels.

In vivo calcification of polyethylene glycol diacrylate (PEG DA) hydrogels of molecular weight (MW) 400, 1000, 4000, 6000 and 10,000 and polyethylene glycol tetraacrylate (PEG TA) of MW 18,500 was investigated using a rat subcutaneous model. This study was performed in 4-wk-old rats for durations of 1, 3, 6 and 8 wk. The results indicate a strong dependence of calcification upon the MW of the PEG precursor or the MW between crosslinks. Results for gels implanted for 6 wk show that calcification was maximal at a PEG MW of 1000 (224 mg/g +/- 12.8, n = 4) (mean +/- SEM) with less at MW = 400 (23.0 mg/g +/- 9.30, n = 4) and considerably less at higher MWs, e.g. for MW = 10,000 (0.23 mg/g +/- 0.01, n = 4). Results for other time periods indicate a similar calcification trend. The extent of calcification of gels from PEG TA (MW = 18,500) was intermediate (1.09 mg/g +/- 0.43, n = 3) between PEG DA (MW = 6000) (1.39 mg/g +/- 0.42, n = 6) and PEG DA (MW = 10,000) at 6 wk, i.e. calcification depended upon the PEG MW between crosslinks. When composite gels were implanted, such that a highly calcifying gel (MW = 400 or 1000) was encapsulated within a gel of low calcification (MW = 4000), the gel inside calcified to at least the same extent as if it had not been encapsulated. Thus, direct contact with tissues is apparently not necessary for calcification to occur. Energy dispersive X-ray spectroscopy was performed on the mineral deposits in the gels and a P:Ca ratio of 0.67 +/- 0.04 (95% confidence interval) for MW 1000 gels and 0.60 +/- 0.07 for MW 400 gels was found to be consistent with deposition of Ca3(PO4)2.

Animals↗
PubMed1988

Transmission electron microscopy of the morphological relationship between fibroblasts and pulp calcifications in temporary teeth.

Calcifications found in the coronal pulps of primary teeth extracted in an 8-year-old child were studied by TEM. Different types of relationship were observed between fibroblasts and pulp calcifications: extension of cell processes towards calcifications, modelling of the cells upon calcifications, internalizing process of calcifications. Fibroblasts proved to be able to enclose small pulp calcifications within intracytoplasmic vesicles. There was no evidence of any active role played by fibroblasts in the genesis of pulp calcifications. It was shown that collagen fibres could be involved or not in the mineralizing process. It is suggested that mitochondria might provide an adequate environment for initial mineralization. It is likely that the role played by the cytoskeleton in the internalizing process of calcifications is important.

Child↗
PubMed2006

Vascular calcification: pathobiological mechanisms and clinical implications.

Once thought to result from passive precipitation of calcium and phosphate, it now appears that vascular calcification is a consequence of tightly regulated processes that culminate in organized extracellular matrix deposition by osteoblast-like cells. These cells may be derived from stem cells (circulating or within the vessel wall) or differentiation of existing cells, such as smooth muscle cells (SMCs) or pericytes. Several factors induce this transition, including bone morphogenetic proteins, oxidant stress, high phosphate levels, parathyroid hormone fragments, and vitamin D. Once the osteogenic phenotype is induced, cells gain a distinctive molecular fingerprint, marked by the transcription factor core binding factor alpha1. Alternatively, loss of inhibitors of mineralization, such as matrix gamma-carboxyglutamic acid Gla protein, fetuin, and osteopontin, also contribute to vascular calcification. The normal balance between promotion and inhibition of calcification becomes dysregulated in chronic kidney disease, diabetes mellitus, atherosclerosis, and as a consequence of aging. Once the physiological determinants of calcification are perturbed, calcification may occur at several sites in the cardiovascular system, including the intima and media of vessels and cardiac valves. Here, calcification may occur through overlapping yet distinct molecular mechanisms, each with different clinical ramifications. A variety of imaging techniques are available to visualize vascular calcification, including fluoroscopy, echocardiography, intravascular ultrasound, and electron beam computed tomography. These imaging modalities vary in sensitivity and specificity, as well as clinical application. Through greater understanding of both the mechanism and clinical consequences of vascular calcification, future therapeutic strategies may be more effectively designed and applied.

Animals↗
PubMed2003

Endochondral bone formation in the heart: a possible mechanism of coronary calcification.

During the atherosclerotic process, calcification occurs and is associated with a high likelihood of adverse events. Coronary calcification has been perceived as a passive precipitation of mineral. Recently, calcification associated with atherosclerosis has been found to be the result of an organized, regulated process that is similar to the process of calcification in bone. Mineralization in skeletal tissue can form by endochondral ossification in which mesenchymal cells differentiate into chondroblasts and produce a cartilage matrix which then degenerates and is remodeled to form bone. In this study, hearts from oophorectomized, aged female Sprague Dawley rats were found to contain areas of cartilage. Micro-computerized tomography radiogrammetry provided quantitative images of the architecture and confirmed the calcified tissue. Histological analysis revealed staining for several markers consistent with cartilage and bone tissue: acid phosphatase and bone matrix proteins, osteocalcin, osteopontin, osteonectin, and bone sialoprotein. In addition, cartilage types II, X, and procollagen type I were present. The presence of chondrocytes in the aged rat heart provides insights into the process of calcification in coronary arteries. Many proteins associated with calcification in bone are present in the cartilage that is present in vascular tissue, suggesting that endochondral calcification is another possible mechanism by which calcification of vascular tissue may occur.

Aging↗
PubMed2002

Association between Chlamydia pneumoniae antibodies and intimal calcification in femoral arteries of nondiabetic patients.

BACKGROUND: Chlamydia pneumoniae, a gram-negative bacterium, has been suggested to be a risk factor for atherosclerosis. Calcium is a well-known component of atherosclerotic plaques, but it is uncertain whether infectious agents play a role in the calcification process of the arteries. PATIENTS: To address this issue we investigated the association of Chlamydia antibodies with intimal arterial calcification as assessed by soft tissue radiograms from the thigh region of 1373 nondiabetic Finnish individuals aged 45 to 64 years. RESULTS: At baseline, radiologically detectable intimal calcification in femoral arteries was found in 172 (27%) of 638 men and 43 (6%) of 735 women (P<.001). The presence of intimal artery calcifications was strongly related to conventional atherosclerotic risk factors and to Chlamydia antibodies. In Cox regression analysis, association of Chlamydia antibodies with intimal artery calcification persisted after extensive adjustment for other cardiovascular risk factors (P =.04). A dose-response relationship was observed between Chlamydia antibodies and intimal femoral artery calcification (P =.006). The presence of intimal artery calcification was strongly associated with an increased risk of future coronary heart disease mortality (P<.001). CONCLUSION: Chlamydia antibodies are strongly associated with intimal calcification of the femoral arteries.

Antibodies, Bacterial↗
PubMed2004

Alcohol consumption and coronary calcification in a general population.

BACKGROUND: A U- or J-shaped association exists between alcohol consumption and coronary heart disease. One of the proposed mechanisms for this association involves atherogenesis, but there are no data on the association between alcohol consumption and coronary atherosclerosis in asymptomatic subjects. Coronary calcification, a measure of coronary atherosclerosis, allows for the study of the association. METHODS: This cross-sectional study was performed using data from the population-based Rotterdam Coronary Calcification Study. Data on alcohol consumption were available for 1795 individuals without coronary heart disease. Mean +/- SD age of the participants was 71 +/- 5.7 years. Coronary calcification was detected on electron beam computed tomographic scans and quantified as a calcium score by the Agatston method. Extensive coronary calcification was defined as a calcium score above 400. RESULTS: In this population, 15.8% of individuals consumed no alcohol; 46.5% consumed 1 alcoholic drink or less per day; 16.9% consumed 1 to 2 drinks per day; and 20.9% consumed more than 2 drinks per day. A U-shaped association was found between alcohol consumption and coronary calcification. Compared with nondrinkers, the odds ratio of extensive coronary calcification was 0.60 (95% confidence interval [CI], 0.44-0.82) for those who consumed 1 drink or less daily; 0.51 (95% CI, 0.35-0.76) for those who consumed 1 to 2 drinks daily; and 0.90 (95% CI, 0.62-1.29) for those who consumed more than 2 drinks. The association remained after multivariate adjustment. CONCLUSIONS: The consumption of 2 alcoholic drinks or fewer per day was inversely associated with extensive coronary calcification. The risk of extensive coronary calcification was 50% lower in individuals who consumed 1 to 2 alcoholic drinks per day than in nondrinkers.

Aged↗
PubMed1997

Polyurethane heart valves: fatigue failure, calcification, and polyurethane structure.

Six flexible-leaflet prosthetic heart valves, fabricated from a polyetherurethaneurea (PEUE), underwent long-term fatigue and calcification testing. Three valves exceeded 800 million cycles without failure. Three valves failed at 775, 460, and 544 million cycles, respectively. Calcification was observed with and without associated failure in regions of high strain. Comparison with similar valves fabricated from a polyetherurethane (PEU) suggests that the PEU is likely to fail sooner as a valve leaflet. Localized calcification developed in PEUE leaflets at the primary failure site of PEU leaflets, close to the coaptation region of the three leaflets. The failure mode in PEU valves had the appearance of abrasion wear associated with calcification. High strains in the same area may render the PEUE leaflets vulnerable to calcification. Intrinsic calcification of this type, however, is a long-term phenomenon unlikely to cause early valve failure. Both polymers performed similarly during static in vitro and in vivo calcification testing and demonstrated a much lesser degree of calcification than bioprosthetic types of valve materials. Polyurethane valves can achieve the durabilities required of an implantable prosthetic valve, equaling the fatigue life of currently available bioprosthetic valves.

Animals↗
PubMed1999

Assessing the resistance to calcification of polyurethane membranes used in the manufacture of ventricles for a totally implantable artificial heart.

Ventricles made from segmented polyurethane membranes and used in the fabrication of a totally implantable artificial heart are known to undergo biomaterial-associated calcification. As there is no effective method currently available to prevent such biomaterials from calcifying, a practical solution is to use only materials with a relatively high resistance to calcification, to extend ventricular durability and ensure a longer functional life for the manufactured device. In the present study, an in vitro calcification protocol was used to determine the relative resistance to calcification of six different polyurethanes, namely, Carbothane PC3570A, Chronoflex AR, Corethane 80A, Corethane 55D, Tecoflex EG80A, and Tecothane TT1074A. The results demonstrated that all six polyurethanes did become calcified during the 60-day incubation period in the calcification solution. The degree of calcification was found to be associated with the surface chemistry of the particular polyurethane, with the Tecothane TT1074A exhibiting the highest level. The Corethane 80A and 55D polymers showed a relatively low propensity to calcify. These two membranes can, therefore, be considered as the most appropriate materials for the fabrication of ventricles for a totally implantable artificial heart. In addition, since the calcification occurred primarily at the surface of the membranes, without affecting the bulk microphase structure, the issue of modifying the surface chemistry to reduce the incidence of calcification is discussed.

Biocompatible Materials↗
PubMed1990

Calcific deposits in the heart.

Four case reports are presented which illustrate various patterns of calcific deposits in the heart. Valvular, myocardial, intracavitary, and coronary calcific deposits are illustrated, with emphasis on pathology and clinicopathologic-radiologic correlation. "Dystrophic" and "metastatic" calcifications are terms used to describe calcific deposits in abnormal and normal soft tissues, respectively. These terms are somewhat confusing in relation to the myocardium, however, as the chronologic sequence of cardiac injury is often uncertain. We suggest that these terms be avoided in relation to the heart, in favor of simple descriptive terms such as "myocardial calcific deposits." Many conditions, such as renal failure and hypercalcemia may contribute to the likelihood of soft tissue calcification, although a definite common etiology has not been identified. Likewise, soft tissue calcification has been difficult to diagnose premortem. The advent of ultrafast (cine) computed tomography may provide a quick, noninvasive, highly sensitive and specific method for diagnosis of soft tissue calcific deposits in the future.

Adult↗
PubMedDate not supplied

Calcification of the epididymis and the tunica albuginea of the corpora cavernosa in patients on maintenance hemodialysis.

The aims of this study were to determine the incidence rates of genital calcification in male hemodialysis patients based on ultrasonography findings and to identify risk factors for this condition. Twenty-three male end-stage renal disease (ESRD) patients (mean age, 51.4 +/- 12.1 years) who were on maintenance hemodialysis underwent penile and scrotal ultrasonography. For each case, we recorded the underlying renal disease and measured serum levels of phosphorus, intact parathormone, and calcium x phosphorus product. Patients were also questioned about erectile dysfunction. The control group consisted of 22 consecutive patients (mean age, 51 years) with type 2 diabetes mellitus with normal renal function who underwent penile and scrotal ultrasonography for various reasons. In the ESRD group, ultrasound revealed calcification of the tunica albuginea of the corpora cavernosa in 15 patients (65%) and calcification of the epididymis in 16 patients (70%; 14 bilateral and 2 unilateral cases). Twenty patients (87%) showed calcification of the epididymis and/or the tunica, and 10 (43%) showed calcification of both these tissues. The rates of epididymal and penile calcification in the ESRD patients and the controls were significantly different (P <.001 for both). There were no significant differences between patients with and without penile and epididymal calcification with respect to age, hemodialysis duration, frequencies of elevated serum phosphorus, elevated serum intact parathormone, elevated calcium x phosphorus product, and frequency of erectile dysfunction (ED) (P >.05 for all). Ultrasonography revealed high rates of penile (tunica albuginea of the corpora cavernosa) and epididymal calcification (65% and 70%, respectively) in the ESRD patients studied, but no association was found between risk factors such as age, underlying renal disease, hemodialysis duration, frequencies of elevated serum phosphorus, elevated serum intact parathormone, and elevated calcium x phosphorus product.

Adult↗
PubMed2003

Role of elastin in pathologic calcification of xenograft heart valves.

Bioprosthetic heart valves fabricated from glutaraldehyde crosslinked porcine aortic valves often fail because of calcific degeneration. Calcification occurs in both cusp and aortic wall portions of bioprosthetic heart valves. The purpose of this study was to discern the role of different aortic wall components in the calcification process. Thus, we selectively extracted cells and other extracellular matrix proteins from porcine aorta using trypsin/DNase/RNase, cyanogen bromide (CNBr), and sodium hydroxide (NaOH) treatments and subdermally implanted these pretreated aortas in young rats. Total DNA and phospholipid data showed complete removal of cells by CNBr and NaOH treatments, whereas trypsin/DNase/RNase treatment was effective in removing DNA but not phospholipids. As shown by amino acid data and Masson's trichrome staining, collagen was removed in CNBr and NaOH treatments. Control fresh porcine aorta calcified significantly after 21 days of implantation (Ca 26.4 +/- 2.4 microg/mg). Removal of cells and collagen from the aorta by CNBr treatment did not lead to a statistically significant reduction in aortic calcification (Ca 20.8 +/- 3.0 microg/mg). Moreover, partial degradation of elastin fibers caused by NaOH (during extraction) and trypsin treatment (after implantation) of the aorta significantly increased elastin-oriented calcification (Ca 94.4 +/- 9.3 and 58.4 +/- 4.6 microg/mg, respectively). Our results indicate that the elastin component of the aorta may undergo independent calcification irrespective of devitalized cell-mediated calcification observed in glutaraldehyde crosslinked aortas. Our results also demonstrate the importance of studying elastin-oriented calcification in decellularized elastin-rich aortic matrices currently used in tissue-engineering applications.

Amino Acids↗
PubMed2004

Statins inhibit in vitro calcification of human vascular smooth muscle cells induced by inflammatory mediators.

Although lipid-lowering therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) decreases the progression of coronary artery and aortic valve calcification, the mechanism of action of these drugs to inhibit the calcification process remains unclear. In this study, we investigated the effect of statins such as cerivastatin and atorvastatin on vascular calcification by utilizing an in vitro model of inflammatory vascular calcification. Cerivastatin and atorvastatin dose-dependently inhibited in vitro calcification of human vascular smooth muscle cells (HVSMCs) induced by the following inflammatory mediators (IM): interferon-gamma, 1alpha,25-dihydroxyvitamin D3, tumor necrosis factor-alpha, and oncostatin M. These statins also depressed expression of alkaline phosphatase (ALP) in HVSMCs induced by these factors. Mevalonate and geranylgeranylpyrophosphate reversed the inhibitory effect of cerivastatin on ALP expression in HVSMCs, while farnesylpyrophosphate showed no effect on the ALP activities inhibited by this drug, suggesting that inhibition of Rho and its downstream target, Rho kinase may mediate the inhibitory effect of cerivastatin. Cerivastatin prevented RhoA activation in HVSMCs induced by the IM. A specific inhibitor of Rho kinase (Y-27632) inhibited in vitro calcification and induction of ALP in HVSMCs. These findings provide a possible mechanism of statins to prevent the progression of calcification in inflammatory vascular diseases such as atherosclerosis and cardiac valvular calcification.

Alkaline Phosphatase↗
PubMed1987

Some rare causes of intracranial calcification in childhood: computed tomographic findings.

The CT findings in 36 cases of childhood intracranial calcification were analysed. Tuberous sclerosis was the commonest disease, predisposing to calcifications that were essentially nodular in type and bilaterally periventricular in distribution. Calcifications were also noted in other common diseases such as tuberculoma and osteopetrosis, and after meningitis. There were three cases of osteopetrosis with intracranial calcifications: one had calcifications in the peritentorial region and two in the junction regions between the grey and white matters with basal ganglia. These observations were previously unreported. The presence of basal ganglia calcification in Down syndrome is also reported. Most calcifications were not visualized on plain radiographs. Our study shows that if the CT attenuation values are less than 200 Hounsfield units (HU), the calcifications are not visualized on the plain radiographs.

Adolescent↗
PubMed2005

The relationship between coronary artery calcification detected by non-gated multi-detector CT in patients with suspected ischemic heart disease and myocardial ischemia detected by thallium exercise stress testing.

OBJECTIVE: To examine whether we could predict myocardial ischemia when coronary artery calcification is detected by non-gated multidetector CT in patients with suspected ischemic heart disease. METHODS: Eighty-three patients suspected of having ischemic heart disease (55 men, 28 women; age range 36-83 years; mean age 68 years) underwent multidetector CT and T1-201 single photon emission computed tomography. Prediction of myocardial ischemia by coronary arterial calcification detected on CT was evaluated by comparing the coronary artery territories that showed calcification with the area of myocardial ischemia determined by SPECT. The sensitivity, specificity, positive predictive value, and negative predictive value of multidetector CT for predicting myocardial ischemia were calculated. Coronary angiography was also examined and compared with multidetector CT. Risk factors, including hypertension, smoking, hyperlipidemia, diabetes, and family history, were compared for evidence of coronary artery calcification detected by multidetector CT and myocardial ischemia detected by thallium nuclear scans. RESULTS: For analysis by patients, the sensitivity, specificity, positive predictive value, and negative predictive value of coronary artery calcification for myocardial ischemia detection were 65, 63, 56, and 71%, respectively. Similarly, for analysis by coronary arterial territories, those values were 56, 77, 41 and 86%, respectively. Coronary stenosis on CAG was also related to the ischemia determined by SPECT and calcification on multidetector CT. Ischemia was better influenced by risk factors than was coronary arterial calcification. CONCLUSIONS: For analysis by coronary arterial territories, the specificity and negative predictive value of coronary arterial calcification seen by multidetector CT are relatively high.

Adult↗
PubMed2003

Increased bone resorption and failure to respond to antiresorptive therapy in progressive dystrophic calcification.

The aim of this study was to evaluate strategies to halt the progression of severe dystrophic calcification in a patient with progressive systemic sclerosis (PSS) and to monitor serial changes in biochemical markers of bone resorption and indices of calcium (Ca) metabolism in response to therapy. The relationship of bone turnover to the extent of dystrophic calcification was also investigated in a number of additional patients with varying degrees of calcinosis. Serial markers of bone turnover and indices of Ca metabolism were measured over a 3-year period in one patient with PSS and severe dystrophic calcification. Bone mineral density (BMD) was assessed by dual-energy x-ray absorptiometry (DXA). Bone turnover in this patient and two additional patients with PSS or dermatomyositis (DM) and severe dystrophic calcification (Group A, n = 3) was compared with that in patients with connective tissue disease with little or no evidence of dystrophic calcification (Group B, n = 13). Serial data on one patient with severe progressive calcinosis showed increased bone resorption markers, which remained high over a 3-year period despite antiresorptive therapy. BMD was low. Patients with PSS/DM with severe dystrophic calcification had higher bone resorption than those with minimal or no evidence of calcification. Mean serum ionized Ca and urinary Ca excretion were both lower in those with severe calcinosis. Bone resorption was increased in patients with connective tissue disease and severe dystrophic calcification. Several antiresorptive agents were shown to be ineffective in limiting either bone turnover or clinical progression in one patient.

Absorptiometry, Photon↗
PubMed2006

Incidental internal carotid artery calcifications on temporal bone CT in children.

BACKGROUND: Incidental internal carotid artery (ICA) calcifications are occasionally noted on CT images of the brain and temporal bone. In adults, incidental calcifications have been correlated with increased incidence of hypercholesterolemia, cardiac disease, diabetes and carotid stenosis. OBJECTIVE: To determine the incidence of incidental calcifications of the carotid siphon on temporal bone CT in children. MATERIALS AND METHODS: We retrospectively reviewed 24 months of consecutive temporal bone CT examinations in children aged 18 years and younger. CT examinations on 663 patients were reviewed and the presence or absence of ICA calcifications was ranked as absent, questionable or definitive. In patients in whom definitive calcifications were identified, hospital charts were reviewed for evidence of diabetes mellitus, hypercholesterolemia, hypertriglyceridemia, hyperlipidemia and chronic renal disease as potential causes of early atherosclerosis. RESULTS: Of the 663 patients, 25% had definitive calcifications within the wall of the ICA: 6% of children younger than 2 years and 28% of children 12-19 years of age. CONCLUSIONS: Incidentally noted ICA calcifications are a common finding on temporal bone CT in children, most likely a physiologic response to turbulent flow at natural bends in the artery rather than secondary to underlying disease predisposing to early atherosclerotic calcification.

Adolescent↗