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 991 records · Page 55Linked to original sources
PubMed1980

A study of the mineral phase of pulp calcification.

Physico-chemical properties of pulp calcification were studied by means of X-ray microbeam diffraction, electron spin resonance (ESR), X-ray energy-dispersive analysis, and chemical analysis. The material was obtained from the second molar of the right mandible of a 25-year-old woman. X-ray diffraction and ESR analyses showed that calcium salts of the calcification are deposited in the form of apatitie, possibly carbonate-containing apatite. Furthermore, the mineral phase of the calcification was found to be similar to that of bone rather than that of dentin with regard to crystallinity and inorganic content. An unexpected finding was that high concentrations of iron were detected in some areas near the surface of the calcification. The question remains open as to what role, if any, iron may play in the formation of pulp calcification.

Adult↗
PubMed1987

Age-related incidence of pineal gland calcification in children: a roentgenological study of 1,044 skull films and a review of the literature.

Anterior-posterior and lateral skull roentgenograms of 1,044 children aged 0-18 yr were examined for pineal gland calcification. Eighty children with pineal calcification were identified. Cranial computed tomograms (CCT) existing for half of the 80 cases provided confirmation. In contrast to existing reports on pineal calcification in the first decade of life, we found a significant percentage of "physiological" calcification even between 0 and 6 yr of age (range 2.9-4.2%). Contrary to current opinion we were not able to detect any signs of pineal gland tumors in these cases. We were able to confirm other reports which note a steep rise of the incidence of pineal calcification during the second decade of life.

Adolescent↗
PubMed2005

Novel conformation-specific antibodies against matrix gamma-carboxyglutamic acid (Gla) protein: undercarboxylated matrix Gla protein as marker for vascular calcification.

OBJECTIVE: Matrix gamma-carboxyglutamic acid (Gla) protein (MGP), a vitamin K-dependent protein, is a potent in vivo inhibitor of arterial calcification. We hypothesized that low endogenous production of MGP and impaired carboxylation of MGP may contribute to the development or the progression of vascular disease. METHODS AND RESULTS: Novel conformation-specific antibodies against MGP were used for immunohistochemistry of healthy and sclerotic arteries. In healthy arteries, MGP was mainly displayed around the elastin fibers in the tunica media. The staining colocalized with that for carboxylated MGP, whereas undercarboxylated MGP (ucMGP) was not detected. In atherosclerotic arteries, ucMGP was found in the intima, where it was associated with vesicular structures. In Mönckeberg's sclerosis of the media, ucMGP was localized around all areas of calcification. The results indicate that ucMGP is strongly associated with vascular calcification of different etiologies. In a separate study, serum MGP concentrations in a cohort of 172 subjects who had undergone percutaneous coronary intervention were significantly reduced compared with an apparently healthy population. CONCLUSIONS: These data show that impaired carboxylation of MGP is associated with intimal and medial vascular calcification and suggest the essentiality of the vitamin K modification to the function of MGP as an inhibitor of ectopic calcification.

Antibody Specificity↗
PubMed1993

Calcification of a cariogenic Streptococcus and of Corynebacterium (Bacterionema) matruchotii.

The main aim of this investigation was to challenge the idea that cariogenic streptococci do not calcify. Calcium uptake of calcification of Streptococcus mutans C180-2, proven to be an acidogenic and cariogenic strain, was compared with calcium uptake and calcification of Corynebacterium (Bacterionema) matruchotii, known as a ready calcifier. Bacteria were grown on Brain Heart Infusion Agar (BHIA) and on well-buffered semi-synthetic E-agar, both containing 1.4 mmol/L calcium, 2 g/L glucose, initial pH 7.4. Calcium uptake from BHIA by C. matruchotii (25 mmol Ca/kg wet bacterial cell mass), but not by S. mutans, was found. Grown as a plaque-like lawn on E-agar, the S. mutans cell mass concentrated calcium to 63 +/- 11 mmol/kg compared with 145 +/- 61 mmol/kg in C. matruchotii. X-ray diffraction confirmed the presence of crystalline apatite in the bacterial cell masses. Electron microscopy revealed crystals and mineralized deposits in both organisms. Heavy calcifications in some cells of S. mutans were seen. Calcification was partly inhibited by magnesium ion and by methanehydroxybisphosphonate. S. sobrinus 6715, as well as freshly isolated S. mutans and S. sobrinus from patients, concentrated very large quantities of calcium, up to 500-fold from the medium, when maintained for several weeks on E-agar of initial pH 7.6. Our observations widen the view on acidogenic bacteria as mineralization agents and support the notion that members of the mutans group of streptococci may be involved in events that trigger heavy intracellular calcifications and, possibly, dental calculus formation.

Agar↗
PubMed1983

Ultrastructural cytochemistry and immunocytochemistry of proteoglycans associated with epiphyseal cartilage calcification.

Proteoglycans (PGs) are closely associated with cartilage calcification. We have examined the hypertrophic zone of rat epiphyseal cartilage, in which calcification is occurring, using the high-iron diamine-thiocarbohydrazide-silver proteinate (HID-TCH-SP) method for sulfated glycosaminoglycans, an immunoferritin method specific for chondroitin sulfate A, and the tannic acid-ferric chloride (TA-Fe) method to stain cartilage matrix granules (MGs) presumed to be PG monomers. HID-TCH-SP produced stain deposits with a diameter of 11.2 +/- 3.2 nm (mean +/- SD; n = 200) in the MGs. However, HID-TCH-SP staining was not discernible in membrane-limited matrix vesicles (MVs). In areas of advanced calcification, partially disrupted MVs and globular bodies (GBs), derived in part from disrupted and/or degenerated MVs, contained a few too many small HID-TCH-SP stain deposits. Further down the epiphyseal cartilage, intact MVs markedly decreased and the GBs, containing many small HID-TCH-SP stain deposits, significantly increased in number. These GBs were found exclusively in the longitudinal septa rather than in the transverse septa. After enzyme digestion with testicular hyaluronidase, small (7.2 +/- 1.2 nm in diameter) stain deposits remained in the MGs and GBs, presumably localized to keratan sulfate. Immunoferritin localizing chondroitin sulfate strongly stained MGs, whereas MVs and GBs lacked staining. TA-Fe staining of glycoconjugates in the GBs demonstrated a striking decrease in the diameter of MGs associated with calcification in the GBs as compared with those in the noncalcifying area around the GBs. These results indicate that the GBs containing needle-like apatite crystals in morphologic preparations represent sites of chondroitin sulfate degradation. Testicular hyaluronidase-resistant sulfated glycosaminoglycans presumed to be keratan sulfate and partially degraded PGs selectively remain within the GBs as a probable requisite for expansion of the initial calcification in MVs.

Animals↗
PubMed1990

The impact of osteophytic and vascular calcifications on vertebral mineral density measurements in men.

To evaluate the influence of extravertebral calcification on spinal bone density determinations, we measured lumbar vertebral density in 71 hospitalized and 58 normal men using dual photon absorptiometry. The extent of vascular and osteophytic calcification was graded from lateral lumbar radiographs. Fifty-five (43%) of the subjects had identifiable osteophytes, and 86 (67%) had vascular calcifications. Despite similar ages and weights in subjects with and without ostephytes, those with osteophytes had greater spinal density (1.34 vs. 1.17 g/cm2; P less than 0.001), and there was a strong correlation between osteophyte severity and spinal density (r = 0.41; P less than 0.00001). Proximal femoral density was not different in those with and without osteophytes. The distribution of osteophytes in this population was not random, and as a result, the presence of osteophytes obscured the the relationship of bone density to age as well as the comparison of hospitalized to normal men. Vascular calcification had a minimal effect on vertebral density. In summary, osteophytic calcification exerted an important influence on the measurement of spinal bone density in men. This effect should be considered in both clinical and research applications of integral vertebral density measures.

Absorptiometry, Photon↗
PubMed2002

Effect of increased calcium concentration in sea water on calcification and photosynthesis in the scleractinian coral Galaxea fascicularis.

The relationship between calcification and photosynthesis in coral was investigated using standard sea water with enhanced calcium concentration. In standard sea water at 23 degrees C with the calcium concentration increased by 2.5 mmol l(-1), incorporation of calcium into the skeleton increased by 30-61 %, depending on the method of data normalisation, and photosynthesis, measured as (14)C incorporation into the tissues, also increased by 87 %. At 29 degrees C, calcium incorporation into the skeleton increased by 54-84 % and (14)C incorporation increased by 32 % when sea water calcium concentration was increased by 5 mmol l(-1). However, photosynthesis measured as net photosynthetic oxygen production did not increase. Similarly there was no change in respiration rate when coral polyps were incubated in high-calcium sea water. It is conjectured that an increase in photorespiration may be responsible for the latter observations. Bisphosphonate has been considered to inhibit calcification but not photosynthesis in corals. We show that bisphosphonate may not inhibit formation of amorphous calcium carbonate and that the inhibition of calcification is possibly illusory. The data are consistent with the trans-calcification model, which suggests that calcification is a source of CO(2) for photosynthesis in corals.

Animals↗
PubMed2003

Linked deficiencies in extracellular PP(i) and osteopontin mediate pathologic calcification associated with defective PC-1 and ANK expression.

Osteopontin and PP(i) both suppress hydroxyapatite deposition. Extracellular PP(i) deficiency causes spontaneous hypercalcification, yet unchallenged osteopontin knockout mice have only subtle mineralization abnormalities. We report that extracellular PP(i) deficiency promotes osteopontin deficiency and correction of osteopontin deficiency prevents hypercalcification, suggesting synergistic inhibition of hydroxyapatite deposition. Nucleotide pyrophosphatase phosphodiesterase (NPP) isozymes including PC-1 (NPP1) function partly to generate PP(i), a physiologic calcification inhibitor. PP(i) transport is modulated by the membrane channel protein ANK. Spontaneous articular cartilage calcification, increased vertebral cortical bone formation, and peripheral joint and intervertebral ossific ankylosis are associated with both PC-1 deficiency and expression of truncated ANK in ank/ank mice. To assess how PC-1, ANK, and PP(i) regulate both calcification and cell differentiation, we studied cultured PC-1 -/- and ank/ank mouse calvarial osteoblasts. PC-1 -/- osteoblasts demonstrated approximately 50% depressed NPP activity and markedly lowered extracellular PP(i) associated with hypercalcification. These abnormalities were rescued by transfection of PC-1 but not of the NPP isozyme B10/NPP3. PC-1 -/- and ank/ank cultured osteoblasts demonstrated not only comparable extracellular PP(i) depression and hypercalcification but also marked reduction in expression of osteopontin (OPN), another direct calcification inhibitor. Soluble PC-1 (which corrected extracellular PP(i) and OPN), and OPN itself (> or = 15 pg/ml), corrected hypercalcification by PC-1 -/- and ank/ank osteoblasts. Thus, linked regulatory effects on extracellular PP(i) and OPN expression mediate the ability of PC-1 and ANK to regulate calcification.

Alkaline Phosphatase↗
PubMed2006

Phytate (Myo-inositol hexakisphosphate) inhibits cardiovascular calcifications in rats.

Calcification is an undesirable disorder, which frequently occurs in the heart vessels. In general, the formation of calcific vascular lesions involves complex physicochemical and molecular events. Calcification (hydroxyapatite) is initiated by injury and is progressed by promoter factors and/or the deficit of inhibitory signals. Myo-inositol hexakisphosphate (phytate, InsP6) is found in organs, tissues and fluids of all mammals and exhibits an important capacity as a crystallization inhibitor of calcium salts in urine and soft tissues. The levels found clearly depend on the dietary intake but it can also be absorbed topically. In this paper, the capacity of InsP6 as a potential inhibitor of cardiovascular calcifications was assessed in Wistar rats. Three groups were included, a control group, an InsP6 treated group (subjected to calcinosis induction by Vitamin D and nicotine and treated with standard cream with a 2% of InsP6 as potassium salt) and an InsP6 non-treated group (only subjected to calcinosis induction). All rats were fed AIN 76-A diet (a purified diet in which InsP6 is undetectable). Animals were monitorized every 12 hours. After 60 hours of calcinosis treatment, all rats of the InsP6 non-treated group died and the rest were sacrificed. Aortas and hearts were removed. A highly significant increase in the calcium content of aorta and heart tissue was observed in the InsP6 non-treated rats (21 +/- 1 mg calcium/g dry aorta tissue, 10 +/- 1 mg calcium/g dry heart tissue) when compared with controls (1.3 +/- 0.1 mg calcium/g dry aorta tissue, 0.023 +/- 0.004 mg calcium/g heart dry tissue) and InsP6 treated (0.9 +/- 0.2 mg calcium/g dry aorta tissue, 0.30 +/- 0.03 mg calcium/g dry heart tissue) animals. Only InsP6 non-treated rats displayed important mineral deposits in aorta and heart. These findings are consistent with the action of InsP6, as an inhibitor of calcification of cardiovascular system.

Animals↗
PubMed2006

[Effects of IGF-I and BMP-2 combined application on promoting proliferation, differentiation and calcification of MC 3T3-E1 and NIH 3T3 cells].

OBJECTIVE: To demonstrate the effects of recombinant human insulin-like growth factor-I (rhIGF-I) and/or recombinant human bone morphogenetic protein-2 (rhBMP-2) on proliferation, differentiation and calcification of MC 3T3-E1 cells and NIH 3T3 cells. METHODS: Mouse osteoblast-like cell line MC 3T3-E1 and mouse fibroblast cell line NIH 3T3 were treated with different dosages of rhIGF-I or rhBMP-2 and rhIGF-I plus rhBMP-2. Cell proliferation was measured by methylthiazol tetrazolium (MTT)method and flow cytometry. Cell differentiation was examined by using alkaline phosphatase(ALP)measurement kit. Radioimmunoassay was applied to detect levels of osteocalcin (OC) secreted by cultured cells. Von kossa staining method was used to study the calcification effects. RESULTS: MC 3T3-E1 cells treated with 1-50 ng/ml rhIGF-I and NIH 3T3 cells treated with 5-75 ng/ml rhIGF-I showed marked effects of promoting proliferation (P<0.01), increasing the percentages of S-phase cells, decreasing the percentages of G1-phase cells and increasing activities of cellular ALP and percentages of calcification area (P<0.05). 10-100 ng/ml rhBMP-2 was also able to promote proliferation (P<0.01), increase the percentages of S-phase cells, decrease the percentages of G1-phase cells and enhancing cellular ALP activities and percentages of calcification area for both the two cells (P>0.05). CONCLUSION: rhIGF-I and rhBMP-2 have synergistical effects on promoting cell proliferation, early cell differentiation and calcification depending on the used dosages, but no significant effects on promoting advanced cell differentiation.

3T3 Cells↗
PubMed1999

Abnormal calcification on plain radiographs of the abdomen.

The purpose of this pictorial review is to facilitate recognition and understanding of calcifications seen on conventional radiographs of the abdomen. Calcifications can be categorized by organ system and location in the abdomen. Both common and rare calcifications in the urinary tract, liver, gallbladder, spleen, pancreas, adrenal glands, digestive tract, genital tract, peritoneal cavity, and retroperitoneum are illustrated. Abnormal calcifications in the urinary tract are subcategorized by kidneys, ureters, bladder, and urethra. The density, shape, size, margins, pattern, position, and mobility of calcifications are emphasized for differential diagnoses.

Adrenal Glands↗
PubMed2000

Ultrastructural, cytochemical, and biophysical aspects of mechanisms of bone matrix calcification.

Primary calcification in embryonic ossification occurs as follows: crystallization within matrix vesicles, formation of calcified nodules, and finally the establishment of expansive calcified matrix. However, the participation of the matrix vesicles in other types of bone calcification, such as bone formation during bone remodeling in adults has not been examined sufficiently. We introduce our recent observations on the presence of matrix vesicles in aged bones. In addition, although it is well known that the extracellular fluid supersaturates the calcification crystal, hydroxyapatite, the specific mechanisms by which bone matrix calcify remain unclear. In order to further approach the mechanisms of bone matrix calcification, we also review ultrastructural and localizational alterations of the matrix organics according to the progression of calcification, and an evaluation of mineral micro-environment in the calcifying sites by energy-filter transmission electron microscopy.

Animals↗
PubMedDate not supplied

Differentiation of breast calcifications.

Breast calcifications display a variety of characteristics, depending on the physiological process leading to their development. Because certain types of calcifications can be indicative of breast cancer, it is important that mammographers recognize which calcifications signify a benign or malignant process. In addition to discussing the causes of breast calcifications and describing ways to optimize their mammographic depiction, this article explains the differences in the mammographic appearances of various types of breast calcifications.

Adult↗
PubMed1976

Calcification of rachitic cartilage to study matrix vesicle function.

Growth plate cartilage from rachitic rats was studied to assess the role of extra-cellular matrix vesicles in the reinstitution of calcification during healing. The concentration and distribution of matrix vesicles was found to be normal in rachitic growth plate, and although the rachitic cartilage matrix was largely uncalcified, an occasional vesicle did contain internal mineral. Matrix vesicles served as initial loci for mineralization when healing was brought about either by in vivo injection of phosphate or in vitro incubation of growth plates in a metastable calcifying solution. During in vitro calcification a distinct line of mineralization developed in the upper growth plate which was shown by electron microscopy to reflect mineralization by the vesicles. The appearance of this vesicle-associated calcification line was inhibited by preheating or repeated freezing and thawing, and by 30 minutes preincubation in deoxycholate, ethane-1-hydroxy-1,1-diphosphonate, or beryllium sulfate. Our results suggest that vesicle calcification is dependent on the structural and enzymatic integrity of the vesicle membrane. Enzymes that may well play a role in vesicle calcification are phosphatases (e. g., alkaline phosphatase, pyrophosphatase and ATPase), which are known to be concentrated in vesicle membranes.

Animals↗
PubMed1991

[Sequence in calcification and eruption of second premolars and molars--a longitudinal study].

Investigation was done with the purpose of establishing frequency of eruption and calcification of P2 and M2 and to perform a longitudinal analysis of certain types, observing the changes during growth, character of these changes and their durability. Analysis was done on 354 orthopantomographic radiographs of orthodontic patients from Nis, aged 7 to 12 years. Eruption phase was determined on the bases of vertical relation to M1 Development phase was determined with the help of a table with 11 developmental phases. Depending on tooth in predominance, patients were divided into three groups: P2M2, (P2M2) and M2P2. All three types of eruption and calcification were recorded. (P2M2) eruption is dominant in maxilla, while M2 has some advantage in mandible. In calcification of both jaws, type P2M2 is predominant in both sexes. In later age, eruption shows changes of type-in 31% to 39% of cases, but this percentage is lower in calcification-from 22% to 25%. Relation of P2 and M2 in eruption is not permanent and changes with growth: in maxilla, P2 has synchronous position in relation to M2 until 8 years of age, to gain advantage in later years; in mandible, P2 has lower position until 10 years of age, to start quicker growth in eleventh year so that in 42% of cases it erupts before M2. In development phase, P2 has advantage in both jaws. P2M2 type shows least changes with age. Other two types change into type P2M2 in 40% of cases. Once set sequence of eruption and calcification cannot be a reliable indicator of later growth since considerable changes were observed in most patients.

Bicuspid↗
PubMed1987

Is there a calcification factor common to all calcifying matrices?

This paper reviews the principal morphological findings pertinent to the early phases of the calcification process and explores the possibility that there may be a calcification factor common to all calcifying matrices. Three structures have a main role in calcification: collagen fibrils, matrix vesicles, and crystal ghosts. Only crystal ghosts are present in all calcified tissues, so that only they can be taken into consideration as a common calcification factor. They are organic molecules which have the same morphology as that of the inorganic structures present in the calcified matrix, which means that they can be considered as templates for those structures. Early calcification might be initiated by the binding of calcium and phosphate ions to the unmasked reactive groups of the crystal ghosts which are probably contained not only in the matrix, but also in the "holes" of the collagen fibrils and in matrix vesicles. The available data suggest that crystal ghosts share many of the properties of "crystal bound proteins". The involvement of alkaline phosphatase in their composition may account for their calcium- and phosphate-binding activity.

Bone Matrix↗
PubMed1986

Calcification of the rabbit fetal skeleton.

The normal development of calcification in the fetal skeleton was studied in New Zealand White rabbits. The calcification process, confirmed by alizarin staining, was followed during days 16-30 of pregnancy. The process starts in the clavicle, most probably between day 15 and day 16. Simultaneously, calcification was observed in the mandible. In most of the bones of the skull, calcification starts during days 18-22. In the pectoral girdle and forelimbs the process starts in the diaphyses of the scapula, humerus, ulna and radius during days 16-19 and in the metacarpals and phalanges during days 21-26, the distal phalanges being the first to be calcified. The pelvic girdle and hindlimb follow a corresponding pattern. Calcification of the ribs commenced between days 18 and 20, and that of the vertebral column between days 19 (the atlas) and 28 (the last caudal vertebrae).

Animals↗
PubMed1982

Proteoglycans and calcification of cartilage in the femoral head epiphysis of the immature rat.

The femoral heads of young rats have been used to monitor changes in proteoglycan structure during growth and endochondral ossification. Proteoglycans were extracted in good yield. The tissue content of proteoglycans increased until the time of calcification and then decreased. In contrast, the collagen content increased over the period studied. On Day 20, just preceding the onset of calcification, the proteoglycans had a lower glycosaminoglycan content, were somewhat smaller, and contained a larger proportion of molecules that were not capable of interacting with hyaluronic acid. On Day 25, during ongoing calcification, the proportion of proteoglycans that were not capable of interacting with hyaluronic acid was low, while it again was high on Day 40, just preceding ossification. The relative glycosaminoglycan content of the proteoglycans was somewhat lower on Day 20 and Day 40. The results indicate that both at the time of calcification and at the time of ossification the proteoglycan structure changes, perhaps indicating a functional role for the proteoglycans in the calcification process.

Animals↗