[The mineral composition and structure of various physiological and pathological calcifications in the human body].
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Apatites↗
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Results for “Calcification, Physiologic”
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Calcification of the choroid plexus visualized by computed tomography.
Physiologic calcification of the choroid plexus increases in frequency and extent with age. As demonstrated in this report, it is visualized nine to 15 times more frequently with computed tomography (CT) than with plain skull radiography. Calcification involving the temporal horns is associated with neurofibromatosis. Young patients with exuberant calcification in the region of the glomerula, or with calcification extending into the bodies of the lateral ventricles should be evaluated for conditions associated with pathological calcification of the choroid plexus. This also applies to patients of any age in whom calcification of the choroid plexus in the roof of the third ventricle or in the region of the foramen of Monro can be visualized with routine CT center and window levels.
Adolescent↗
The presence of gamma-carboxyglutamic acid-containing protein in atheromatous aortae.
It has been established that a gamma-carboxyglutamic acid-containing protein is present in rat aortae after long term atherogenic diet administration. A similar protein was proven to be present in turkey tibial tendons that are predisposed to undergo physiological calcification. The molecular weight and amino acid composition of both proteins were identical. They contained six glutamic acid residues per molecule, three of which were gamma-carboxylated. The proteins studied were also identical in their N-terminal sequence over six residues. This sequence was fully coincident with that published for osteocalcin (Price, P.A., Poser, J.W. and Raman, N. (1976) Proc. Natl. Acad. Sci. U.S.A. 73, 3374--3375). In the region corresponding to residues 20--26 in osteocalcin, a single replacement of valine for isoleucine was found in turkey tendon protein. From the physiological point of view it should be mentioned that the level of the gamma-carboxyglutamic acid containing protein in atherogenic diet fet rat aortae exceeds that found normally in bone or in tissues predisposed for physiological calcification.
1-Carboxyglutamic Acid↗
Physiologic intracranial calcification with hyperintensity on MR imaging: case report and experimental model.
CT and MR imaging showed basal ganglia calcification that appeared as high signal intensity on T1-weighted images of a patient with pseudohypoparathyroidism. MR imaging of an experimental model of calcium phosphate suspensions showed a signal similar to that seen in the patient. Additionally, T1 and T2 relaxation times of the solutions were measured and showed decreases in both parameters with increasing calcium phosphate concentrations. Intracranial calcification can appear as high signal intensity on T1-weighted images. An experimental model shows that the calcium salt decreases the T1 of surrounding water. Therefore, calcium, and possibly other elements, may induce paramagnetic susceptibility effects.
Adolescent↗
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↗
Intracranial calcification in paediatric computed tomography.
An analysis of the computed tomograms of 18000 children examined consecutively form the basis of an assessment of the diagnostic significance of intracranial calcification. The low incidence of physiological calcification in the pineal and choroid of about 2% up to the age of 8 years, but increasing 5-fold by the age of 15 years, is confirmed. Pathological calcification occurred in 1.6%, the commonest causes being neoplasms (43%), neuroectodermal syndromes (20%) and infections (12%). Diffuse basal ganglia calcification (15%) bore little relation to the diverse clinical symptomatology, and routine biochemical studies showed a disorder of metabolism to be present in only 6 cases. Calcification has not been previously noted in acute haemorrhagic leukoencephalitis, Pertussis or Cocksackie encephalitis, infantile neuraxonal dystrophy, Marinesco-Sjögren syndrome or in the basal ganglia in neurofibromatosis.
Acute Disease↗
The morphology of the calcification front in articular cartilage. Its significance in joint function.
Biochemical and histochemical studies have indicated that there is specific cellular activity in the region of the calcification front of articular cartilage implying that a regulation process takes place there. Using scanning and transmission electron microscopy and light microscopy to examine tissue sections of both undecalcified and decalcified articular cartilage in the region of the calcification front, we have looked at its morphology with particular reference to its cellular control. Our observations show that physiological calcification is an active process under cellular control and is related to the presence of extracellular membrane-bound matrix vesicles.
Animals↗
Expression of the cadherin-11 gene is a discriminative factor between articular and growth plate chondrocytes.
OBJECTIVE: Calcification of hypertrophic chondrocytes is the final step in the differentiation of growth plates, although the precise mechanism is not known. We have established two growth plate-derived chondrocyte cell lines, MMR14 and MMR17, from p53-/- mice (Nakamata T, Aoyama T, Okamoto T, Hosaka T, Nishijo K, Nakayama T, et al. In vitro demonstration of cell-to-cell interaction in growth plate cartilage using chondrocytes established from p53-/- mice. J Bone Miner Res 2003;18:97-107). Prolonged in vitro culture produced calcified nodules in MMR14, but not in MMR17. Factors responsible for the difference in calcification between the two cell lines may also be involved in the physiological calcification in growth plate. DESIGN: Gene expression profiles of MMR14 and MMR17 were compared using a cDNA microarray to identify candidate genes involved in the calcification process. RESULTS: Forty-five genes were identified as upregulated in MMR14, including the cadherin-11 (Cdh-11) gene. The expression of Cdh-11 in MMR14 was detected in cell-cell junctions, while no expression was observed in MMR17. Primary cultured chondrocytes from growth plate (GC) also expressed the Cdh-11, and the staining of Cdh-11 was observed in the late hypertrophic zone of growth plate. Cell aggregation assays showed that chondrocytes required Ca2+ to form nodules, and knockdown of the Cdh-11 gene expression using short interfering RNA inhibited the formation of calcified nodules in MMR14. The introduction of Cdh-11 into MMR17 failed to produce calcified nodules indicating that Cdh-11 is one, but not the sole, factor responsible for the production of calcified nodules. CONCLUSION: Although the physiological role is still unclear, Cdh-11 is a discriminative factor between articular and growth plate chondrocytes.
Animals↗
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↗
Calcification of the basal ganglia as visualized by computed tomography.
Physiological calcification of the globus pallidus was visualized by computed tomography in 32 patients. The frequency of visualization increased with increasing age. Patients under the age of 40 with calcification of the globus pallidus should be evaluated for disorders associated with pathological calcification of the basal ganglia. Patients of any age with calcification in the lenticular nucleus and elsewhere in the basal ganglia, dentate nucleus, or multiple areas of the cortex should also be evaluated for these disorders.
Adolescent↗
Matrix proteins and mineralization: an overview.
There is a wealth of information on the mineral and matrix components in bones and teeth, in the exoskeletons of invertebrates, and in dystrophic calcific deposits. This information includes detailed characterization of their physical and chemical composition and details on the gene localization and regulation of gene expression for the major and minor protein constituents. The reason that mineral deposition occurs in some tissues and not in others remains unclear. In this review, studies in solution, cell culture studies, and investigations in mutant animals will be surveyed to indicate which matrix proteins may affect mineralization. Most of the molecules that appear to be involved in initiation and regulation of biological mineral formation are anionic; they have structural features that facilitate interaction with mineral, cells, and other matrix molecules, and they can have more than one function. Despite extensive data it is not yet clear which of these molecules is absolutely essential for physiologic calcification in each of the calcified tissues.
Animals↗
Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein.
Calcification of the extracellular matrix (ECM) can be physiological or pathological. Physiological calcification occurs in bone when the soft ECM is converted into a rigid material capable of sustaining mechanical force; pathological calcification can occur in arteries and cartilage and other soft tissues. No molecular determinant regulating ECM calcification has yet been identified. A candidate molecule is matrix GLA protein (Mgp), a mineral-binding ECM protein synthesized by vascular smooth-muscle cells and chondrocytes, two cell types that produce an uncalcified ECM. Mice that lack Mgp develop to term but die within two months as a result of arterial calcification which leads to blood-vessel rupture. Chondrocytes that elaborate a typical cartilage matrix can be seen in the affected arteries. Mgp-deficient mice additionally exhibit inappropriate calcification of various cartilages, including the growth plate, which eventually leads to short stature, osteopenia and fractures. These results indicate that ECM calcification must be actively inhibited in soft tissues. To our knowledge, Mgp is the first inhibitor of calcification of arteries and cartilage to be characterized in vivo.
Animals↗
Natural killer cell proliferation and circulating cytokines in patients with bilateral basal ganglia calcification.
Ten adult patients with symmetrical calcifications in the bilateral basal ganglia (diagnosed as physiological calcifications) were analyzed for lymphocyte subsets and cytokines. Increased number of natural killer (NK) cells were identified in the peripheral blood of seven patients by lymphocyte subset analysis. Tumor necrosis factor-alpha was detected in the sera of five patients and interferon-gamma was detected in one patient. In summary, NK cell propagation and circulating cytokines, particularly tumor necrosis factor-alpha, may be involved in the etiology of basal ganglia calcification.
Aged↗
Current concepts of the physiology and biochemistry of calcification.
The current picture of the process of biological calcifications portrays the cells within the calcifying tissues as central factors controlling the deposition of mineral crystals in the extracellular matrix. The cell responds to hormones and second messengers, and other changes in its environment, regulating the concentration of ions within the extracellular matrix and secreting macromolecules whose properties determine the ability of the matrix to be calcified. The mitochondria within the cells accumulate calcium and phosphate, releasing these ions into the matrix as calcification progresses. Extracellular matrix vesicles, derived from the cells of some, but not all, calcifying matrices, provide sites for initial mineral deposition in many tissues. Among the macromolecules secreted by the cell, collagen provides the support for the hydroxyapatite crystals; proteoglycans serve to control the extent and/or progress of mineralization. The proteoglycans, glycoproteins, enzymes and the collagen itself, along with the cells, determine the nature of the matrix, while phosphoproteins, proteolipids, and phospholipids may serve as hydroxyapatite nucleators or as surfaces upon which apatite is deposited. but it is the interaction of many or all of these factors that determines the process of biological calcification and controls the properties of the calcified matrices.
Bone and Bones↗
Molecular determinants of arterial calcification.
Calcification of extracellular matrix (ECM) can be either physiological or pathological. Physiological calcification (or mineralization) of ECM is restricted to bones, teeth and, to a lesser extent, growth plate cartilages. Pathological calcification appears often in the ECM of arteries where it is a frequent complication of atherosclerosis. However, calcification of the ECM of arteries is not restricted to atherosclerosis. Indeed, human diseases have been described that are characterized by calcification of the aortic media in the absence of any atherosclerotic lesions. The existence of these rare diseases, along with several mouse models recently generated and discussed below, indicates that the formation of atherosclerotic lesions and the calcification of the artery ECM are controlled by different genetic pathways. This emerging knowledge has implications for our understanding of ECM calcification beyond atherosclerosis.
Animals↗
Chondrogenesis mediated by PPi depletion promotes spontaneous aortic calcification in NPP1-/- mice.
OBJECTIVE: We recently linked human arterial media calcification of infancy to heritable PC-1/nucleotide pyrophosphatase phosphodiesterase 1 (NPP1) deficiency. NPP1 hydrolyzes ATP to generate PP(i), a physicochemical inhibitor of hydroxyapatite crystal growth. But pathologic calcification in NPP1 deficiency states is tissue-restricted and in perispinal ligaments is endochondral differentiation-mediated rather than simply a dystrophic process. Because ectopic chondro-osseous differentiation promotes artery calcification in atherosclerosis and other disorders, we tested the hypothesis that NPP1 and PP(i) deficiencies regulate cell phenotype plasticity to promote artery calcification. METHODS AND RESULTS: Using cultured multipotential NPP1-/- mouse bone marrow stromal cells, we demonstrated spontaneous chondrogenesis inhibitable by treatment with exogenous PP(i). We also demonstrated cartilage-specific gene expression, upregulated alkaline phosphatase, decreased expression of the physiological calcification inhibitor osteopontin, and increased calcification in NPP1-/- aortic smooth muscle cells (SMCs). Similar changes were demonstrated in aortic SMCs from ank/ank mice, which are extracellular PP(i)-depleted because of defective ANK transmembrane PP(i) transport activity. Moreover, NPP1-/- and ank/ank mice demonstrated aortic media calcification by von Kossa staining, and intra-aortic cartilage-specific collagen gene expression was demonstrated in situ in NPP1-/- mice. CONCLUSIONS: NPP1 and PP(i) deficiencies modulate phenotype plasticity in artery SMCs and chondrogenesis in mesenchymal precursors, thereby stimulating artery calcification by modulating cell differentiation.
Animals↗
HETEROTOPIC BONE FORMATION IN THE KIDNEY: CASE REPORT.
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Calcification, Physiologic↗
Osteoprotegerin reverses osteoporosis by inhibiting endosteal osteoclasts and prevents vascular calcification by blocking a process resembling osteoclastogenesis.
High systemic levels of osteoprotegerin (OPG) in OPG transgenic mice cause osteopetrosis with normal tooth eruption and bone elongation and inhibit the development and activity of endosteal, but not periosteal, osteoclasts. We demonstrate that both intravenous injection of recombinant OPG protein and transgenic overexpression of OPG in OPG(-/-) mice effectively rescue the osteoporotic bone phenotype observed in OPG-deficient mice. However, intravenous injection of recombinant OPG over a 4-wk period could not reverse the arterial calcification observed in OPG(-/-) mice. In contrast, transgenic OPG delivered from mid-gestation through adulthood does prevent the formation of arterial calcification in OPG(-/-) mice. Although OPG is normally expressed in arteries, OPG ligand (OPGL) and receptor activator of NF-kappaB (RANK) are not detected in the arterial walls of wild-type adult mice. Interestingly, OPGL and RANK transcripts are detected in the calcified arteries of OPG(-/-) mice. Furthermore, RANK transcript expression coincides with the presence of multinuclear osteoclast-like cells. These findings indicate that the OPG/OPGL/RANK signaling pathway may play an important role in both pathological and physiological calcification processes. Such findings may also explain the observed high clinical incidence of vascular calcification in the osteoporotic patient population.
Acid Phosphatase↗