Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CALCIFICATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMedDate not supplied

Processing factors as determinants of tissue valve calcification.

The effect of different processing factors on tissue valve calcification were studied in the subdermal rat model. Factors evaluated, were the influence of tissue ischaemia (4 degrees and 25 degrees C), different blocking reagents (KH2PO4, T6, MgCl2 and AlCl3), fixation pressures (0, 10 and 20 mmHg) and the pH (3.72 and 7.40) of the fixative. Tensile strength tests performed, showed that all blocking reagents tend to weaken valve tissue. Histologically calcification originated mainly in the spongiosa of the valve leaflets. Tissue ischaemia at 4 degrees C significantly (p less than 0.05) decreased the calcification potential of the valve tissue. Ischaemia at 25 degrees C significantly (p less than 0.05) increased this process. Blocking reagents KH2PO4, T6 and MgCl2 significantly (p less than 0.05) reduced calcification of valve tissue. AlCl3 pretreatment virtually prevented it to such an extend that the calcification process was down to 92% of the control group. Different fixation pressures had no influence on the calcification potential of the tissue. AlCl3 was dependent on a low pH (3.72) to act as a blocking reagent on tissue calcification. It is concluded that certain processing factors do influence the calcification potential of valve tissue. These factors should be considered when constructing bioprostheses with glutaraldehyde-treated porcine valves.

Abdominal Muscles↗
PubMed2005

[The role of calcium ions in the pathomechanism of the artery calcification accompanying atherosclerosis].

Artery calcification occurring in atherosclerosis is connected with a high risk of cardiovascular events. Quantitative calcification evaluation using electron beam tomography indicated a correlation between artery calcification and well-known cardiovascular risk factors, i.e. smoking, obesity, and hyperlipidemia. Elevated calcium scores are especially observed in diabetic patients, which may even explain the higher mortality in this group. Calcification leads to increased blood vessel rigidity and, consequently, elevated arterial vascular resistance and left ventricular hypertrophy. An increased risk of plaque rupture in relation to calcium-rich atherosclerotic lesions was not proved. Plaque rupture and thromboembolitic complications are probably higher in the case of lipid-rich lesions. Atherosclerotic calcification is an active process in which many cells (monocytes/macrophages, vascular smooth muscle cells, and endothelial cells) participate. Many substances and transcription factors normally participating in the bone remodeling process are found in calcified atherosclerotic lesions (e.g. Cbfa-1, osteocalcin, alkaline phosphatase, BMP-2, osteopontin, osteoprotegrin, and RANKL). On monocytes, cells playing an important role in atherosclerosis progression, the presence of a calcium-sensing receptor (CaR) has been demonstrated. Increase in monocyte chemotaxis and increased interleukin 6 secretion in response to extracellular calcium were observed. Monocytes also directly and indirectly enhance vascular calcification. Immune cells and cytokines participating in vascular calcification are connected in one pathogenetic mechanism, i.e. atherosclerosis as an inflammatory disease and calcification.

Animals↗
PubMed2005

Association of vascular 18F-FDG uptake with vascular calcification.

UNLABELLED: Both calcification and FDG uptake have been advocated as indicators of atheroma. Atheromas calcify as cells in the lesion undergo apoptosis and necrosis during evolution of the lesion and at the end stage of the lesion. FDG concentrates in lesions due to the relatively dense cellularity in regions of inflammation of active atheromas. This investigation examines the geographic relationship of focal vascular (18)F-FDG uptake, as a marker of atherosclerotic inflammation, to arterial calcification detected by contemporaneous CT. METHODS: We reviewed PET/CT images from 78 patients who were referred for tumor staging for the presence of vascular (18)F-FDG uptake and vascular calcification. Arterial wall (18)F-FDG accumulation greater than adjacent blood-pool activity was considered inflammation. Arterial attenuation of >130 Hounsfield units was considered calcification. Sites in the ascending and descending aorta, the carotid and iliac arteries, and the coronary territories were examined on the emission, CT, and fusion images on a point-by-point basis. When lesions were seen, we evaluated whether they were overlapping or discrete. RESULTS: The (18)F-FDG arterial distribution was consistent with established atherosclerotic topography, with increased uptake in the thoracic aorta, at the carotid bifurcation, and in the proximal coronary vessels. Arteries typically displayed a patchwork of normal vessel, focal inflammation, or calcification; inflammation and calcification overlapped in <2% of cases. Arterial inflammation preceded calcification, in terms of mean patient age. Coronary inflammation was more prevalent in patients with more cardiovascular risk factors. CONCLUSION: Vascular calcification and vascular metabolic activity rarely overlap, suggesting these findings represent different stages in the evolution of atheroma.

Adolescent↗
PubMed2006

Association between calcification of the cervical carotid artery bifurcation and white matter ischemia.

BACKGROUND AND PURPOSE: The association of cervical carotid artery bifurcation calcification to future stroke risk is unknown, though coronary artery calcification is a proven indicator of heart disease risk. Severity of white matter change has been correlated with future stroke risk. We sought to use white matter severity grade on CT as a surrogate predictor of relative future stroke risk and thus correlate white matter and future stroke risk with carotid calcification grade. METHODS: We retrospectively reviewed unenhanced neck and brain CTs in 209 patients. Carotid calcification degree was scored by the Agatston method, adapted from that commonly used to quantify coronary artery calcification. White matter change severity was scored by the European Task Force for Age-Related White Matter Change scale. Both scores were measured blinded to each other, and to age and sex covariables. Association was tested by univariate and multivariate analyses. RESULTS: Both carotid calcification and white matter scores were strongly, and independently, associated with increasing age (r = 0.61, P < .001; and r = 0.67, P < .001, respectively). Despite apparent association between carotid calcification and white matter scores on univariate analysis, there was no independent effect evident after adjusting for age as a covariant (r = 0.07, P = .14). Sex had no independent effect on white matter scores, though men had a marginally higher mean calcified carotid plaque load than women after controlling for age (P = .008). CONCLUSIONS: Carotid calcification scores do not independently predict severity of white matter ischemia. Future stroke risk, assessed by white matter severity scores, cannot be predicted from carotid calcium scores.

Adult↗
PubMed2006

[Calcification on the posterior surface of an implanted silicone intraocular lens in a patient with asteroid hyalosis].

BACKGROUND: Calcification on the surface of the hydrogel intraocular lens (IOL) has been reported, but the mechanism of the surface calcification is not fully understood. We report a case of surface calcification on an implanted silicone IOL. The purpose of our study was to examine the clinical and ultrastructural findings associated with the late surface calcification of a silicone IOL. CASE: A 70-year-old Japanese man had undergone cataract surgery in his left eye, with uneventful phacoemulsification and silicone IOL (Allergan SI-55 NB) implantation with the manufacturer's cartridge and injector. He was referred again 29 months later with blurred vision, glare sensitivity, and decreased vision in his left eye. He was diagnosed as having aftercataract. Although YAG laser capsulotomy was performed, the opacity on the posterior surface gradually increased. The opacity was located mainly within the capsulotomy window on the posterior surface of the lens, although the patient maintained good visual acuity. LV : 0.2 (1.0 x S-2.0 D). The lens was removed 46 months after the initial surgery. Scanning electron microscopy (SEM) showed membranous deposits on the posterior optical surface of the silicone lens. There were high levels of phosphoric acid (P) and calcium (C) confirming calcification of the silicone IOL. Asteroid hyalosis was observed in the fellow eye of the patient. CONCLUSION: This is the first report of surface calcification of a silicone IOL in Japan. Although the mechanism of the calcification has not been determined, careful clinical follow-up of patients implanted with silicone lenses is necessary to determine if this phenomenon is rare and sporadic or if it may be more widespread. Since 5 similar cases of calcification in silicone lenses with accompanying asteroid hyalosis have been reported in other countries, we can conclude that silicone lens implantation in eyes with asteroid hyalosis should be avoided.

Aged↗
PubMed2006

A multi-step approach in anti-calcification of glutaraldehyde-preserved bovine pericardium.

AIM: Bioprosthetic cardiovascular substitutes, manufactured from glutaraldehyde-preserved bovine or porcine tissues, are prone to calcification after implantation. The aim of the study was to evaluate the ultrastructure, material stability and calcification behaviour of glutaraldehyde-preserved bovine pericardium, treated with a multi-step anti-calcification process which addresses each of the major causes of calcification and tissue degeneration. METHODS: Bovine pericardium samples were divided into 2 groups. Group I (control) consisted of tissue fixed with 0.625% glutaraldehyde and Group II (study group) consisted of tissue fixed with 0.625% glutaraldehyde and exposed to a multi-step anti-calcification process. Ultrastructure was examined by scanning electron microscopy and material stability was assessed by mechanical testing, shrinkage temperature and enzymatic degradation. Calcification was assessed by histology (Von Kossa stain) and by atomic absorption spectrophotometry in the subcutaneous rat model. RESULTS: Bovine pericardium in the study group revealed less visible changes in the ultrastructure of the collagen matrix, improved material stability (P<0.05) and significantly (P<0.001) reduced calcification compared to control tissues (4.5+/-1.2 versus 136.03+/-11.39 ug/mg tissue). CONCLUSIONS: In conclusion, results demonstrate that the multi-step anticalcification process improved the material stability and reduced the calcification potential of bovine pericardial tissue. These improvements in the quality of the bovine pericardium should enhance the long-term durability of the tissue as a bioprosthetic substitute for cardiovascular application.

Animals↗
PubMed2006

[Basal ganglia calcification: clinical manifestations and diagnostic evaluation].

Physiological intracranial calcification occurs in about 0,3-1,5% of cases. It is asymptomatic and is detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases and other. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism doesn't respond to drugs containing levodopha. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders (blood calcium level and other), those are: Cockayne syndrome, tuberous sclerosis, Fahr's syndrome, Down syndrome and other. We observed some cases of basal ganglia calcification and studied clinical manifestations and treatment tolerance of this pathological condition. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyreoid hormone is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism. Basal ganglia calcification in young patient with acute hepatitis may be result of Wilson disease.

Adolescent↗
PubMed1986

Calcification in aging canine aortic valve.

Aging changes of aortic valves are thought to underlie the mechanism of calcification, which leads to calcific aortic stenosis in humans. The study of calcification in the aging valvular connective tissue has been hindered by the lack of a suitable animal model. In search of the model, canine aortic valves demonstrated age changes including calcification remarkably similar to those in humans. The mechanism of calcification was studied in the aortic valves of aged Beagles by electron microscopy. Fibroblasts in the canine aortic valves showed the most prominent age changes. The cells accumulated numerous residual bodies and appeared to disintegrate. The resultant membranous cellular degradation products which sequestered in the extracellular space were the nidi of calcification. It appeared that the membrane of cell debris played an important role in calcification. Canine aortic valve is an ideal model for the study of calcification in relation to aging of the valvular connective tissue.

Aging↗
PubMed1981

[Calcifications of the trunk of the left coronary artery in coronary disease. Anatomical study].

Calcification of the left main coronary artery (LCA) was found, with an equal sex distribution, in 30 out of 145 patients (21%) at autopsy. A series comprising 68 males and 77 females in whom death resulted from myocardial infarction (111 cases) or ischaemic heart disease (34 cases). The condition is rare before the sixth decade but becomes more frequent after the seventh decade of life. The incidence was the same in lethal anterior and posterior infarction (15% and 16% respectively). It was more common in ischaemic heart disease (38%, p less than 0,005). Significant narrowing of the LCA was found in 26 cases (87%) but this was only less than 70% in 11 cases. When the total number of LCA stenoses (calcified and non calcified: 39 cases) was considered, only two thirds had associated calcification. This was, therefore, only a moderately sensitive index of LCA stenosis. Calcification, nearly always circumferential, was usually situated on the second portion of the LCA. Its division was involved in all cases, the calcification extending to the initial segments of the left anterior descending artery (LAD) and left circumflex artery (CX). Calcification of the LCA was always associated with calcification of the LAD, 78% of which had stenotic lesions. Calcification of the CX and right coronary arteries was practically constant, the average percentages of occlusion being 72% and 68% respectively. On anatomical criteria, myocardial revascularisation surgery could only have been proposed in about 20% cases, and this would only rarely have been total. It is concluded that calcification of the LCA usually corresponds at least anatomically, to severe, diffuse multivessel coronary artery disease.

Aged↗
PubMed1995

[Evaluation of calcification in pulmonary nodules using bone images obtained with single exposure energy subtraction].

Bone images obtained by single exposure dual energy subtraction with computed radiography, a new image processing method, were evaluated for the detectability of calcification in lung nodules in both phantom and clinical studies. In the phantom study, five simulated nodules containing known and uniformly distributed amounts of calcium hydroxide were placed in a human chest phantom and images were obtained the following five techniques: 1) conventional radiography (CXR), 2) low kV conventional radiography (Low), 3) Fuji computed radiography (FCR), 4) bone images with conventional singles exposure energy subtraction (ES) and 5) bone image with fine single exposure energy subtraction (FES). The detectability of calcification in the simulated nodules was evaluated by six radiologists using ROC analysis and two-way analysis of variance. In the clinical study, images of 42 lung nodules (21 calcified lung nodules and 21 non-calcified nodules), in which calcification was diagnosed by computed tomography, were obtained with the following four techniques: 1) CXR, 2) FCR, 3) ES and 4) FES and the detectability of calcification in the lung nodules was evaluated by nine radiologists using ROC analysis. In the phantom study, FES was significantly superior to CXR, Low and ES, and equal to FCR in the detectability of calcification in the simulated nodules. Compared with ES, FES was especially superior in the underexposed portion of the chest radiograph. In terms of calcium content in the simulated nodules, FES and FCR were superior to CXR in detecting calcification when a lower calcium hydroxide content was present. In the clinical study, FES was significantly superior to CXR, FCR and ES in the diagnosis of calcification in lung nodules. These findings indicate the usefulness of FES in the detection of calcification in lung nodules, and suggests that it is promising for the diagnostic screening of lung nodules.

Calcinosis↗
PubMed1995

Soft-tissue calcifications: differential diagnosis and therapeutic approaches.

Calcification of soft tissue may be an unspecific local response or present as only a symptom of a complex underlying disease. Patient approach and treatment vary greatly depending on the cause of soft-tissue calcifications. The review of literature reveals multiple causes but also confusing nomenclature for similar clinical entities. Dystrophic and metastatic soft-tissue calcifications are discerned, but there is also contribution of both types of soft-tissue calcification to some syndromes. Six previously unpublished cases of soft-tissue calcification including Thibièrge-Weissenbach syndrome, scleroderma (progressive systemic sclerosis), calcifying cavernous hemangioma (2 patients), and heterotopic calcifications after burn injury (2 patients) are presented to discuss the differential diagnosis. The correct diagnosis is crucial for successful treatment. Resections of the lateral heads of the gastrocnemius muscles in 2 patients resulted in cure of the problem. The patient suffering from Thibièrge-Weissenbach syndrome had no recurrence during a 30-month postoperative follow-up period. Surgical treatment of scleroderma or soft-tissue calcification after burn injury is aimed toward relief of symptoms. A proposal for patient assessment and indications for surgical correction with regard to soft-tissue calcifications is presented and discussed.

Adolescent↗
PubMed1995

[Breast calcifications].

Calcifications are found in many women undergoing mammography. The majority of these calcifications are benign. Calcifications suggestive for malignancy prove to be cancer in about 30% of cases after biopsy. Study and personal experience should result in ready recognition of characteristically benign calcifications. Calcifications suggestive for malignancy should be biopsied and the ratio of malignant over benign biopsies should be as high as possible. The purpose of this paper is to present a practical approach to the evaluation of breast calcification, by means of a survey of the pattern of calcifications in breast pathology. We describe six types of typically benign calcifications and six criteria that entail an increased risk of malignancy.

Breast Diseases↗
PubMed1993

Role of ageing, chronic renal failure and dialysis in the calcification of mitral annulus.

Mitral annulus calcification, a common lesion of the elderly (over age 60 years), has been detected with increased frequency and at younger ages in patients with uraemia. To date a pathogenic role for dialysis and secondary hyperparathyroidism has been suggested only on the basis of older dialytic age and increased serum iPTH observed in the affected individuals. Because this is a potentially dangerous lesion we deemed it useful to evaluate more completely the respective roles of possible pathogenetic factors in uraemic individuals. Evaluation included echocardiography, ECG, limb radiography, and serum assays. A total of 225 dialysis (HD) patients, 67 chronic renal failure (CRF) patients on conservative treatment and 67 normal subjects were studied. Mitral annulus calcification was detected in 87 of 225 (38.6%) HD patients, 11 of 67 (16.4%) CRF and six of 67 (8.9%) normals. In HD, patients with calcification were older and on longer-term renal replacement therapy compared to those without calcification. They also had greater values of iPTH, BGP, AP, and Rx score of secondary hyperparathyroidism. Mitral annulus calcification was associated more frequently (chi 2 = 14.8; P < 0.0001) with rhythm and cardiac conduction defects, but not with ectopic calcifications. Multiple stepwise regression analysis, with mitral annulus calcification score as dependent variable, selected dialysis duration, age, and iPTH (rm = 0.368) as the most predictive parameters, with the first two carrying most of the information. The stratification of patients according with these two parameters showed a progressive increase in the frequency of calcification both with HD duration and age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Morphogenesis of calcification in porcine bioprosthesis: insight from high resolution electron microscopic investigation at molecular and atomic resolution.

High resolution electron microscopy (HREM) coupled with energy dispersive X-ray microanalysis were used to investigate the morphogenesis of calcification in 28 explanted porcine bioprosthetic heart valves. Different morphology and compositions of calcific deposits were consistently observed in various valvular structures of all explanted porcine bioprostheses. The most common forms of calcific deposits were present as spherical particles and needle-shaped structures. HREM investigation of spherical particles of calcium phosphate revealed very fine electron-dense dots about 0.3-1.0 nm in diameter which were packed to form sphere-like clusters of about 2.0-3.5 nm in diameter in the particles. HREM observations of the microneedle-shaped structures even as small as 1.9 nm in thickness could identify the lattice fringes with center-to-center spacings of about 0.8-0.9 nm. Energy dispersive X-ray microanalysis defined the components of needle-shaped calcification as calcium and phosphorus in a ratio typical of hydroxyapatite crystals. The calcific deposits in the collagen tissue have been shown to be at discrete sites on or in the collagen fibrils as the spherical particles or homogeneous electron-dense masses. Based on HREM observations of different types of morphogenesis of calcification it is suggested that chemical processes of calcification accompanying the deposition of calcium in the implanted bioprosthetic heart valves are specific to each substrate system. The formation of amorphous calcium phosphate precursors and direct deposition of microcrystalline hydroxyapatites are considered to be the primary mechanisms of calcification occurring in implanted porcine bioprostheses.

Animals↗
PubMed1995

Electron-beam computed tomographic detection of coronary calcification in patients undergoing percutaneous transluminal coronary angioplasty: predictability of restenosis. A preliminary report.

Coronary artery calcification is a recognized marker for coronary atherosclerosis; however, the relationship between calcification and the success of balloon angioplasty at a calcification site has not been determined. The purpose of this study was to evaluate whether the presence of coronary artery calcification, as detected by electron bean computed tomography (EBCT), was predictive of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Site- specific coronary calcification was determined by EBCT in 20 patients with 24 lesions before, immediately after, and 2 to 18 month after PTCA. Calcification was scored using >130 Hounsfield units and >1.02-mm2 area criteria. Coronary calcium at the PTCA site was significantly greater in restenosed versus nonrestenosed patients (109.16 +/- 198.16 mm2 v 4.39 +/- 9.50 mm2) (P < .025). The amount of coronary calcium did not change as a result of the PTCA procedure (+2.72 +/- 22.31 mm2 v -4.81 +/- 7.82 mm2) (P = NS). The rate of progression of calcification was not greater in restenosed versus nonrestenosed patients (1.78 +/- 3.32 mm2/month v 0.09 +/- 0.19 mm2/mo) (P = NS). Site-specific coronary calcification as determined by EBCT appeared to be predictive of patients with an increased likelihood to restenose after PTCA. Further studies are needed to verify these observations in a considerably larger patient population.

Angioplasty, Balloon, Coronary↗
PubMed1997

[A study of aortic calcification uremia].

For the purpose of clarifying the relationship between aortic calcification and several factors associated with uremia, aortic calcification was estimated in autopsied uremic patients as well as in uremic rats treated in 1, 25 dihydroxyvitamin D3 (1, 25D). Aortic calcification was evaluated by radiographic, pathologic and chemical studies in 28 patients on long-term homodialysis and in 11 non-uremic autopsied subjects as controls. Chest or abdominal X-ray showed the presence of aortic calcification in 48% of the hemodialyzed patients and 9% of the control subjects. Von Kossa staining of the aorta revealed positive tissue calcification in 43% of the hemodialyzed patients and in 18% of the control subjects. Calcium content of the aorta was increased in the hemodialyzed patients compared with the control subjects. Findings of aortic calcification in the hemodialyzed patients were correlated with their age and serum Ca x P products. In uremic rats, administration of 1, 25D increased serum Ca x P products and the calcium content of the aorta. On the other hand, treatment with Ca antagonist or magnesium inhibited elevation of the calcium content of the aorta induced by 1, 25D in the uremic rats. These results suggest that serum Ca x P product is a factor promoting aortic calcification and that calcium antagonist and magnesium may protect from the progression of aortic calcification in uremia.

Aged↗
PubMed1995

Calcification of valved aortic allografts in rats: effects of age, crosslinking, and inhibitors.

Experiments were carried out to investigate rat aortic allograft calcification using valved abdominal aortic allografts. Results indicated that this was a potentially useful model for investigating fresh allograft calcification, as well as mineralization of glutaraldehyde-crosslinked valved allografts. Valve cusp results, however, were not comparable to those noted in large animal or human studies, while aortic wall calcification was more comparable. Calcification inhibitor investigations demonstrated that nearly complete inhibition of the calcification of the aortic wall of glutaraldehyde-crosslinked allografts was achieved using a number of individual inhibitors, including controlled release diphosphonates, and pretreatment with either ferric chloride or aluminum chloride. However, aminopropanehydroxydiphosphonate pretreatment was not efficacious, and sodium dodecyl sulfate pretreatment was only partially effective for inhibiting the aortic wall calcification in the glutaraldehyde-crosslinked allografts. It is concluded that valved aortic allografts in rats provide a useful model for investigating aortic wall (but not valve cusp) calcification and its inhibition.

Aging↗
PubMed1988

The influence of vitamin D metabolites on the calcification of cartilage matrix and the C-propeptide of type II collagen (chondrocalcin).

The influence of vitamin D metabolites (at 1 X 10(-10) M) on the calcification of cartilage matrix (measured by 45Ca2+ uptake) and the C-propeptide of type II collagen (measured by radioimmunoassay) has been studied using organ cultures and chondrocytes isolated from growth plates of vitamin D-deficient and -sufficient 11-day-old rats. Vitamin D-deficient rats had reduced amounts of C-propeptide in their serum and freshly isolated growth plate chondrocytes. In all chondrocytes cultured from vitamin D-deficient animals, the C-propeptide content was maximal at 24 hr whereas calcification continued to increase for up to 72 hr. In organ and chondrocyte cultures of tissue from vitamin D-sufficient rats, both 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25(OH)2D3) were required for maximal stimulation of calcification and maximal increases in C-propeptide content. In these D-replete tissues, 24,25-(OH)2D3 had a less stimulatory effect on both calcification (organ and cell cultures) and C-propeptide (organ cultures only), while 1,25(OH)2D3 alone had no effect in cell cultures but an inhibitory effect in organ cultures. Studies of cells or tissue from growth plates of vitamin D-deficient rats demonstrated that 24,25(OH)2D3 alone produced maximal calcification and maximal increases in the C-propeptide content. 1,25(OH)2D3 generally had an inhibitory effect on both calcification and C-propeptide when used alone. In the presence of 1,25(OH)2D3, the stimulatory effect of 24,25(OH)2D3 was partly abrogated. Maximal stimulation of calcification and increases in C-propeptide by 24,25(OH)2D3 were observed at 1 X 10(-9) M and 1 X 10(-10) M. In none of these studies was there any effect on proteoglycan content.(ABSTRACT TRUNCATED AT 250 WORDS)

24,25-Dihydroxyvitamin D 3↗