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PubMed1985

Placental calcification: ultrastructural and X-ray microanalytic studies.

Calcification is common in human placentas and is widely recognized as a normal part of maturation and aging of this organ. Eleven human placentas were studied by light and electron microscopy to elucidate the mechanism of placental calcification. Earliest mineral deposits were seen along the trophoblastic basement membrane of the chorionic villi undergoing fibrinoid degeneration. Transmission electron microscopic examination revealed crystalline deposits within small membrane-bound vesicles; the latter appear to be derived from degenerating cells and were particularly numerous within the basement membrane. X-ray microanalysis of these deposits revealed calcium and phosphorus peaks and the pattern of calcium hydroxyapatite was noted by electron diffraction. This pattern of calcification, i.e., precipitation of calcium hydroxyapatite in association with extracellular membrane bound vesicles, is similar to that seen in physiologic and pathologic calcifications of other tissues.

Calcification, Physiologic↗

PubMed1987

The nature of the mineral component of bone and the mechanism of calcification.

From the physical chemical standpoint, the formation of a solid phase of Ca-P in bone represents a phase transformation, a process exemplified by the formation of ice from water. Considering the structural complexity and abundance of highly organized macromolecules in the cells and extracellular tissue spaces of mineralized tissues generally and in bone particularly, it is inconceivable that this phase transformation occurs by homogeneous nucleation, i.e., without the active participation of an organic component acting as a nucleator. This is almost surely true in biologic mineralization in general. Electron micrographs and low-angle neutron and X-ray diffraction studies clearly show that calcification of collagen fibrils occurs in an extremely intimate and highly organized fashion: initiation of crystal formation within the collagen fibrils in the hole zone region, with the long axes (c-axis) of the crystals aligned roughly parallel to the long axis of the fibril within which they are located. Crystals are initially formed in hole zone regions within individual fibrils separated by unmineralized regions. Calcification is initiated in spatially distinct nucleation sites. This indicates that such regions within a single, undirectional fibril represents independent sites for heterogeneous nucleation. Clearly, sites where mineralization is initiated in adjacent collagen fibrils are even further separated, emphasizing even more clearly that the process of progressive calcification of the collagen fibrils and therefore of the tissue is characterized principally by the presence of increasing numbers of independent nucleation sites within additional hole zone regions of the collagen fibrils. The increase in the mass of Ca-P apatite accrues principally by multiplication of more crystals, mostly by secondary nucleation from the crystals initially deposited in the hole zone region. Very little additional growth of the crystals occurs with time, the additional increase in mineral mass being principally the result of increase in the number of crystals (multiplication), not size of the crystals (crystal growth). The crystals within the collagen fibers grow in number and possibly in size to extend into the overlap zone of the collagen fibrils ("pores") so that all of the available space within the fibrils, which has possibly expanded in volume from its uncalcified level, is eventually occupied by the mineral crystals. It must be recognized that the calcification of separate tissue components and compartments (collagen, mitochondria, matrix vesicles) must be an independent physical chemical event.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1984

Microbial hydroxyapatite formation as a model of proteolipid-dependent membrane-mediated calcification.

The study of calcium hydroxyapatite (HA) formation in bacteria can be used as a model for membrane-associated normal and pathologic calcification in vertebrates. While the ability to deposit HA is common to a wide variety of microorganisms, the characteristic is not universal, even within closely related species (e.g., oral streptococci). Clues as to why some microorganisms can support HA formation while others cannot have been derived from analysis of calcification of Bacterionema matruchotii. These bacteria form intracellular HA which is crystallographically indistinguishable from bone mineral. Calcification is proteolipid (Pr)-dependent and involves Ca-phospholipid-Pi (CPLX) formation. Crystal deposition follows a defined series of events including changes in Ca:Mg:Pi ratios, membrane lipids, Pr concentration, protein and phospholipid composition, and mineral phase. Comparison with non-calcifiable Actinomyces naeslundii indicates that under appropriate conditions, most Pr-containing membranes can function as nucleating sites. Enrichment of Pr and CPLX in pathologic calcifications and matrix vesicle membranes suggests that similar mechanisms may operate in vertebrate HA formation.

Bacteria↗

PubMed1978

The role of mitochondria in growth plate calcification as demonstrated in a rachitic model.

In a phosphate-vitamin D-deficiency rachitic model in rats, potassium pyroantimonate was employed as a histochemical stain for calcium at the ultrastructural level in the costochondral growth plates. In the control plates, there was a shift of calcium from an intracellular, mainly mitochondrial location in the top part of the zone of hypertrophic cells to an extracellular, mainly matrix-vesicle location in the bottom part of the zone of hypertrophic cells. In the rachitic plates, mitochondria and cell membranes throughout the bottom of the hypertrophic zone remained heavily loaded with calcium. After treatment with phosphate was started, the mitochondria and cell membranes at the bottom of the hypertrophic zone rapidly lost calcium and matrix calcification began. Thus, in the normal growth plate, matrix calcification begins at the level in the plate where mitochondria lose calcium; in rickets, the matrix does not calcify and mitochondria do not lose calcium; and in healing rickets, calcification begins in the matrix at the bottom of the hypertrophic zone as the mitochondria at that level lose calcium. These findings support the hypothesis that mitochondria play an important role in matrix calcification.

Animals↗

PubMedDate not supplied

Morphological changes during survival, cellular transformation, and calcification of the embryonic mouse: Meckel's cartilage transplanted into heterotopic sites.

Meckel's cartilages obtained from 18-day-old embryonic mice were transplanted into heterotopic sites to examine their site-specific effects on cellular modification, calcification, and long-term survival. The explants were isografted into the liver, subcutaneous tissue, anterior chamber of the eye, kidney, peritoneal cavity, and intrafemoral muscle of mouse for up to 2 weeks. In addition, Meckel's cartilages were wrapped in a Nucleopore filter and transplanted into the spleen. Grafted Meckel's cartilages were observed by light and electron microscopy, including application of von Kossa's reaction and osmium-potassium ferrocyanide fixation. It was demonstrated by von Kossa's reaction that when Meckel's cartilage was grafted in liver parenchyma, initial calcification appeared on the territorial matrix as spotted deposits. The chondrocytes gradually transformed into small ovoidal cells and showed a morphology closely resembling that of osteocytes. Transplants in the kidney subcapsular site contained active surviving chondrocytes, and subcutaneously grafted Meckel's cartilage revealed three types of chondrocytes: nonhypertrophic and calcification-inducing hypertrophic chondrocytes, as well as cells showing osteocytelike phenotypes. Intraocular and Nucleopore filter-wrapped explants showed degenerative changes, and peritoneal-cavity transplants showed cellular hypertrophy, but calcified precipites were not observed. The present investigation demonstrated that in blood-rich tissues Meckel's cartilage showed long-term survival and could modulate calcified precipitation. Thus, this adaptation of Meckel's cartilage to the environment of various heterotopic sites suggests that it has the ability to induce calcification.

Animals↗

PubMed1997

Ultrastructural investigation of calcification and ossification in experimental fracture healing with special reference to osteogenic role of fibroblasts.

OBJECTIVE: To investigate ultrastructurally the process of calcification and ossification in experimental fracture healing. METHODS: A standardized fracture of the radius was made in rabbits. Undecalcified callus tissues from different fracture regions were subjected to ultrastructural observation under transmission electron microscope. RESULTS: In the mitochondria and membrane-bound vesicles of the fibroblasts, osteoblasts and chondrocytes, high electron density calcium granules were seen. These granules provided raw materials for the deposition of calcium salt crystals. Around these cells, round, oval or irregularly shaped matrix vesicles could also be discerned, and they became calcified and formed flocculent calcospherules. Then in the Type I collagen fibrils around the fibroblasts and osteoblasts, and in the Type II collagen fibrils around the chondrocytes, calcium salt crystals also appeared. Innumerable flocculent calcospherules and calcified collagen fibrils coalesced together, expanded and finally turned into pieces of bone tissues. The fibroblasts also possessed the indispensable prerequisites for calcification and ossification in fracture healing. They either transformed into osteocytes or degenerated, perished and eventually were replaced by bone tissues. CONCLUSIONS: Sequence of events taking place in calcification and ossification in experimental fracture healing was depicted. Calcification of matrix vesicles and collagen fibrils triggered these processes. Evidence of osteogenic role played by fibroblasts was provided.

Animals↗

PubMed2006

Cutaneous calcification in patients with end-stage renal disease: a regulated process associated with in situ osteopontin expression.

BACKGROUND: Cutaneous calcification, or calcinosis cutis (CC), is found in approximately 1% of patients with end-stage renal disease (ESRD) undergoing chronic dialysis. While the pathogenesis is not well understood, it may be similar to those for medial and intimal vascular calcifications, which are actively regulated processes. OBSERVATION: In a retrospective study of 9 patients, the role of an active calcification process leading to CC was assessed by the immunohistochemical detection of osteopontin, which is a regulator of osseous and extra-osseous calcification processes. Calcinosis cutis was associated with female sex, vascular comorbidity, inconstant secondary hyperparathyroidism, and elevated levels of plasma calcium-phosphorus product. Six patients had a favorable outcome after the lowering of plasma calcium levels during dialysis or after parathyroidectomy. CONCLUSIONS: Calcinosis of the vascular media of subcutaneous vessels was the most common histologic feature and was always associated with osteopontin staining, suggesting that CC is a regulated process. Moreover, to our knowledge, extravascular staining of osteopontin in sweat glands, nerves, and macrophages was demonstrated for the first time in this study.

Adult↗

PubMed1989

Symmetrical thalamic degeneration with calcifications of infancy.

We describe the clinical and radiographic features of three premature infants with symmetric thalamic calcification recognized by computed tomographic scan on days 6, 12, and 49 of life and contrast our findings with those reported in the literature. These lesions follow prepartum or intrapartum hypoxiaischemia and are clinically distinguished by prominent bulbar dysfunction, featuring weak or absent cry, poor feeding, and facial weakness. Neonatal thalamic calcification in premature infants may serve as a radiological marker of an acute, short-lived hypoxic-ischemic event. The presence of brain-stem dysfunction, particularly of lower cranial nerves in association with thalamic calcifications, constitutes a distinctive clinical-radiological entity and usually portends a poor outcome. The presence of these calcifications implies that injury was sustained to diencephalic and brain-stem structures at least 2 to 4 weeks prior to their appearance on computed tomographic scan.

Atrophy↗

PubMed1998

Calcification of the fetal heart--four case reports and a literature review.

Calcification of the heart and vessels in fetuses is a rare condition. It may be dystrophic or metastatic. An extremely rare form of vascular calcification has been termed 'idiopathic arterial calcification of infancy', which is inherited in an autosomal recessive pattern. We report four cases of myocardial calcifications of different origin diagnosed in utero. The correct diagnosis is very important in regard to genetic counselling.

Adult↗

PubMed1997

Effect of alternative crosslinking techniques on the enzymatic degradation of bovine pericardia and their calcification.

The in vitro calcification and enzymatic degradation of bovine pericardia (BP) after a series of surface treatments were studied as a function of exposure time. The degradation of these treated surfaces was monitored by scanning electron micrography and tensile strength measurements. Polyethylene glycol-(PEG) grafted BP and glutaraldehyde-(GA) treated BPs retained maximum stability in collagenase digestion compared with SDS-treated BP. The ability of alpha chymotrypsin, bromelain, esterase, trypsin, and collagenase to modulate the degradation of SDS-, GA-, PEG-, Carbodiimide-, and glycidylether-treated BPs also was investigated. Incubation of various enzymes to these crosslinked pericardia variably reduced the tensile strength of these tissues. It is conceivable that chemical treatments of pericardial tissues might have altered their physical and chemical configuration and the subsequent degradation properties. In vitro calcification studies showed a substantial reduction in the calcification profile of PEG-grafted bovine pericardia compared to other treated tissues. Furthermore, the biocompatibility aspects of pericardial tissues were established by platelet adhesion and octane contact angle. In conclusion, it seems that the surface modification of bovine pericardia via GA-PEG grafting may provide new ways of controlling biodegradation and calcification.

Animals↗

PubMed2001

Improved calcification resistance and biocompatibility of tissue patch grafted with sulfonated PEO or heparin after glutaraldehyde fixation.

A novel chemical modification of biological tissues was developed aimed at improving biocompatibility and calcification resistance. This method involved the additional grafting of sulfonated PEO (PEO-SO(3)) or heparin after conventional glutaraldehyde (GA) fixation of bovine pericardium (BP). The amino groups of PEO-SO(3) or heparin were utilized to react to the GA residues to block them. The PEO-SO(3) or heparin grafted tissues demonstrated a slightly higher shrinkage temperature and tensile strength, but greater resistance to collagenase digestion, than GA treated ones. These results suggest that modified tissues have improved durability due to the grafting and filling effect of PEO-SO(3) or heparin in addition to the GA cross-linking. At the direct contact cytotoxicity test in vitro, PEO-SO(3) or heparin grafted tissue was shown to be nontoxic, while relatively significant cytotoxicity was observed for the GA treated tissues, possibly due to the release of GA. From the in vivo calcification study, calcium contents deposited on the modified tissues were much less than those on GA treated tissues. Such a decreased calcification might be explained by the decrease of residual GA groups during the additional treatment, and the space-filling effect and the nonadhesive property and/or the blood compatibility of PEO-SO(3) or heparin grafted covalently. The newly modified tissue patch was observed to show improved pathological assessibility including less inflammation and tissue reactions. This simple modification method may be useful for calcification-resistant and blood-compatible tissue patches for cardiovascular implants.

Animals↗

PubMed2000

TNFalpha-308A allele in juvenile dermatomyositis: association with increased production of tumor necrosis factor alpha, disease duration, and pathologic calcifications.

OBJECTIVE: To characterize the association between the TNFalpha-308A allele and 1) duration of active disease, 2) peripheral blood mononuclear cell (PBMC) synthesis of tumor necrosis factor alpha (TNFalpha) in vitro, and 3) pathologic calcifications in patients with juvenile dermatomyositis (DM). METHODS: The TNFalpha-308 alleles were determined by polymerase chain reaction in 37 white patients with juvenile DM and in 29 control subjects. Patients were grouped according to duration of immunosuppressive therapy: long (> or =36 months) or short (<36 months). Unstimulated PBMC were examined by enzyme-linked immunosorbent assay for TNFalpha production in vitro. Sixty-five white patients with juvenile DM were examined for pathologic calcifications. RESULTS: TNFalpha-308A was identified in 18 of 37 patients with juvenile DM, in contrast with 5 of 29 controls (P = 0.009). Sixteen of the 18 patients with juvenile DM who had the TNFalpha-308A allele had a disease course > or =36 months, compared with 6 of 19 patients with TNFalpha-308G (P = 0.001). PBMC from 16 of the 18 juvenile DM patients with TNFalpha-308A synthesized more TNFalpha (median 53 pg/ml) compared with PBMC from 9 of 19 patients with TNFalpha-308G (median 19 pg/ml) (P = 0.007). Nineteen of 22 juvenile DM patients requiring therapy for > or =36 months produced more TNFalpha (median 20.5 pg/ml) in comparison with 6 of 15 juvenile DM patients with a <36-month treatment course (median TNFalpha 0.0 pg/ml) (P = 0.005). Detectable calcifications were present in 3 of 8 children with juvenile DM who had TNFalpha-308AA, compared with 2 of 21 children with TNFalpha-308AG and 1 of 36 children who had TNFalpha-308GG (P = 0.017). CONCLUSION: A long course of juvenile DM and the presence of pathologic calcifications were associated with the TNFalpha-308A allele and with the increased production of TNFalpha, which may perpetuate the inflammatory response.

Alleles↗

PubMed1994

Paradiaphyseal calcific tendinitis with cortical bone erosion.

OBJECTIVE: To determine the clinical, radiologic, and histologic features of calcific tendinitis with cortical bone erosion. METHODS: The records of 6 patients with paradiaphyseal calcific tendinitis and adjacent bone cortex erosion were reviewed. RESULTS: Calcific tendinitis involved the linea aspera in 4 patients, the bicipital groove in 1 patient, and the deltoid insertion in another. Calcium deposits were associated with cortical bone erosions, revealed on plain radiographs in 4 patients and computed tomography scans in 2. Bone scans were performed in 2 patients and showed local hyperfixation of the isotope. In 4 patients, suspicion of a neoplasm led to a biopsy. Calcium deposits appeared to be surrounded by a foreign body reaction with numerous giant cells. Apatite crystals were identified by transmission electron microscopy and elemental analysis in 1 surgical sample. CONCLUSION: Paradiaphyseal calcific tendinitis with cortical bone erosion is an uncommon presentation of apatite deposition disease.

Adult↗

PubMed2000

Phytate prevents tissue calcifications in female rats.

The AIN-76 A, a purified rodent diet, has a propensity to cause kidney calcifications in female rats which is not observed with non-purified rodent diets, suggesting a nutritional factor that avoids these calcifications. One candidate is phytate, which inhibits crystallisation of calcium salts and is practically absent in purified diets. Therefore, the effects on calcification of kidney tissue of phytate addition to the AIN-76 A diet using female Wistar rats were studied. The rats were assigned to three groups: AIN-76 A, AIN-76 A + 1% phytate and standard nonpurified chow. Urinary phytate of the AIN-76 A fed group was undetectable. Urinary phytate of AIN-76 A + 1% phytate and standard fed groups did not differ and was significantly higher than in the AIN-76 A group. The concentrations of calcium and phosphorus in kidneys were greater in the AIN-76 A group than in AIN-76 A + 1% phytate and standard groups. Only rats of the AIN-76 A group displayed mineral deposits at the corticomedullary junction. These findings demonstrated that the absence of phytate in the AIN-76 A diet is one of the causes of renal calcification in female rats.

Animal Feed↗

PubMed1980

Unusual echocardiographic appearances attributable to submitral calcification simulating left ventricular "masses".

Using M-mode and cross-sectional echocardiography, we visualized in five patients abnormal large echos attributable to anterior submitral calcification or sclerosis (on or near the ventricular aspect of the anterior mitral leaflet). Such abnormal echos on M-mode echocardiography could have been mistaken for a mass in the left ventricular chamber. Autopsy in two cases confirmed the presence of nonrheumatic anterior submitral calcification. Echocardiographic features of anterior submitral calcification which are helpful in differentiating it from neoplastic or thrombotic ventricular masses include (1) less diastolic mobility and more echo density; (2) continuity with the base of the anterior mitral leaflet and/or the posterior aortic root region, whereas tumors or thrombi are attached to the left ventricular wall; and (3) calcification in the region of posterior "mitral annulus." Cross-sectional long-axis views and M-mode scanning from the left ventricle to the aortic root were particularly helpful in making the differentiation.

Adult↗

PubMed1980

Severe mitral stenosis secondary to massive calcification of the mitral annulus with unusual echocardiographic manifestations.

In mitral annular calcifications, hemodynamic documentation of a significant diastolic gradient across the mitral valve has been rarely demonstrated, and then only with the associated finding of a small left ventricular cavity with hypertrophic left ventricular wall. We present a patient with severe mitral annular calcification, with a significant diastolic gradient and unusual echocardiographic manifestations which include a densely calcified mitral valve annulus with anterior mitral valve leaflets consistent with what is seen in patients with mitral stenosis. When recordings were made immediately below the mitral valve annulus at the free edge of the mitral valve, its leaflets were seen departing in opposite directions, certainly not suggestive of outflow obstruction of the left atrium. Although in previous studies it has been suggested that mitral stenosis does not exist in the presence of mitral annulus calcification, our present report indicates that significant diastolic gradients can be found in patients with mitral annular calcifications. Because of the predominance of this condition in the elderly population, it is suggested that a more aggressive approach be taken in those patients in whom it is warranted by clinical circumstance.

Calcinosis↗

PubMed1991

Prevention of bioprosthetic heart valve tissue calcification by charge modification: effects of protamine binding by formaldehyde.

Calcification is the principal cause of the clinical failure of bioprosthetic heart valves (BHV). Calcification occurs through an interaction of host and implant factors, mainly younger age and glutaraldehyde pretreatment, respectively. The hypothesis of this work was that an impaired balance between positively and negatively charged amino acids, due to the reaction with Lys and Hyl tissue-collagen residues, expose affinity sites to Ca++. We further hypothesized that regardless of the cause(s) of BHV calcification, positive charge modification of the tissues will prevent their propensity to calcify. Modification of BHV tissue was obtained by covalently binding protamine sulfate, a polybasic peptide, via formaldehyde and subsequent glutaraldehyde tissue crosslinking. Protamine-bound tissue exhibited stability properties (shrinkage temperature and resistance to collagenase digestion) similar to BHV tissue. Protamine-treated tissue was less permeable to Ca++, and reduced staining was observed with positively charged dyes, indicating the presence of positively charged functional groups in the modified tissue. Significant prevention of calcification was exhibited by the p-bound tissue in comparison to BHV tissue, 30.9 and 109 micrograms/mg calcium, respectively, after 30 days of subdermal implants in rats. The modification procedure resulted in stable, covalent links of approximately 10% w/w protamine with undiminished anticalcification properties, even after 1 year storage. The results support our hypotheses, and orthotopical heart valve replacements are required in order to completely evaluate the treatment efficacy and biocompatibility.

Biocompatible Materials↗

PubMed1993

Inhibition of calcification of glutaraldehyde pretreated porcine aortic valve cusps with sodium dodecyl sulfate: preincubation and controlled release studies.

Calcification of bioprosthetic heart valves fabricated from glutaraldehyde pretreated bovine pericardium or porcine aortic valves (PAV) is a frequent cause of the failure of these devices. Of all strategies considered thus far, only detergent preincubations using compounds such as sodium dodecyl sulfate (SDS) inhibited PAV bioprosthetic mineralization in circulatory sheep bioprosthetic valve replacements. The present study sought to characterize the mechanism of action of SDS preinicubation. Results of transport and material characterization studies showed that SDS had a relatively high affinity for PAV, with a maximum uptake of 167.1 +/- 6.8 micrograms SDS/mg tissue over 24 h at 37 degrees C with a partition coefficient of 19.3. The PAV diffusion of SDS was 1.95 +/- 0.35 10(-6) cm2/sec. The principal effect of SDS on PAV was phospholipid extraction. The residual organic phosphate in the SDS pretreated tissue was 2.22 +/- 0.72 nmol/mg tissue compared to the control untreated group with 18.52 +/- 2.1 nmol/mg tissue. Incubations of PAV specimens in a 1% SDS solution for 24 h significantly inhibited calcification after 21 days in subdermal implants in 3-week-old male rats (PAV Ca2+ = 18.0 +/- 11.8 micrograms/mg) compared to control (177.8 +/- 6.0 micrograms/mg). In contrast, coimplants of 30% SDS silicone rubber polymers, for regional sustained SDS administration, did not impede PAV calcification in 21 day implants Ca2+ = 166.0 +/- 14.0 micrograms/mg compared to the nondrug silicone matrix controls, Ca2+ = 173.0 +/- 6.6 micrograms/mg). Thus, we conclude that the mechanisms of SDS inhibition of PAV calcification is due to material effects which occur during preincubation, and is not facilitated by sustained SDS administration.

Animals↗