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PubMed1986

Calcification of subcutaneously implanted type I collagen sponges. Effects of formaldehyde and glutaraldehyde pretreatments.

Although collagen-containing implants are widely used in various surgical applications, there has been relatively little attention paid to the possibility that this type of biomaterial may undergo pathologic calcification which could compromise its function. The present study reports for the first time the calcification of a series of implants of purified collagen sponges prepared with graded degrees of aldehyde-induced cross-linkages (assessed by shrinkage-temperature, wetting time, and collagenase digestibility). Type I collagen sponges were pretreated with either glutaraldehyde (0.1% to 2.0% aqueous solution, for 5-180 minutes) or formaldehyde (as vapors for 15 minutes to 15 hours), and implanted subcutaneously for 21 days in weanling rats. Although specimens not pretreated with either aldehyde reagent and the formaldehyde sponges pretreated for 15 minutes were resorbed without evidence of calcification, all other aldehyde-pretreated implants mineralized. The degree of calcification did not correlate with extent of cross-linking. Formaldehyde-pretreated implants calcified more extensively (Ca2+ = 87.8 +/- 2.8 micrograms/mg, mean +/- standard error of the mean; n = 58) than did glutaraldehyde-pretreated implants (Ca2+ = 40.9 +/- 1.4 micrograms/mg; n = 52). It is concluded that both glutaraldehyde- and formaldehyde-pretreated Type I collagen sponges calcify after subdermal implantation in young rats. Although aldehyde pretreatment of Type I collagen sponge implants is a prerequisite for their eventual mineralization, the threshold level of aldehyde-induced cross-linking required to potentiate their maximal pathologic calcification is low.

Aldehydes↗
PubMed1988

[Calcification of the mitral ring and semilunar valves: clinico-instrumental aspects. Sensitivity and diagnostic specificity of M-mode echocardiography versus autopsy findings].

Mitral ring calcification is a frequent finding in geriatric patients. The aim of this study was: 1) to analyze clinical and instrumental features of patients with calcific mitral ring identified through M-mode echocardiography (group A: 96 pts) with respect to those observed in a control group (group B: 104 pts); 2) to define the sensitivity and specificity of M-mode echocardiography in the diagnosis of mitral ring and aortic valve calcification by means of comparison with autopsy findings. Data on arterial hypertension, previous myocardial infarction, heart failure, phosphoremia and calcemia values were similar in both groups. On the contrary, in group A, permanent or paroxysmal atrial fibrillation, aortic valve calcification and left atrial diameter was significantly higher then in group B (p less than 0.05; p less than 0.001; p less than 0.001 respectively). The prevalence of AV and IV cardiac blocks was similar in both groups. Twelve group A patients were restudied with M-mode echocardiography, after a variable period of time, to evaluate the velocity of calcification progression. An autopsy was carried out on the twenty-six pts who died within 3 months after the M-mode echocardiography study. The evaluation of the autoptic findings was performed with high resolution radiographic image, obtained from a heart transverse section containing mitral and aortic plane.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Biomaterial-associated calcification: pathology, mechanisms, and strategies for prevention.

Deposition of calcium-containing apatite mineral occurs widely in association with cardiovascular and noncardiovascular medical devices and biomaterials, is the leading cause of failure of contemporary bioprosthetic heart valves, and limits the functional lifetime of experimental (and potentially clinical) mechanical blood pumps and polymeric heart valves. Calcification of bioprosthetic tissue is primarily intrinsic, related to cuspal connective tissue cells and fragments, and collagen. In contrast, the predominant site of calcific crystals on flexing polymeric surfaces in blood pumps or valve prostheses is extrinsic, associated with adherent cells, thrombus, or pseudointima. Pathologic calcification shares key features with physiologic skeletal mineralization, including crystal initiation through the mediation of cell membranes, usually in the form of extracellular vesicles. This suggests a unified hypothesis for normal and abnormal mineralization. Several approaches are being studied experimentally for the inhibition of bioprosthetic heart valve calcification. Controlled-release diphosphonate therapy, perhaps in conjunction with an anticalcification cuspal pretreatment, appears most effective. Research objectives in biomaterial-associated calcification include (1) development of animal models, (2) determination of initial crystal nucleation events and sites, (3) elucidation of the relative roles of host, implant, and mechanical determinants, and (4) development of approaches for the inhibition of mineralization.

Assisted Circulation↗
PubMed1987

[Idiopathic nonatherosclerotic symmetrical calcification of the cerebral vessels].

A case of calcification of vessels of the basal ganglia in an 18-year-old girl is described. The authors consider the clinical and radiological picture, the differential diagnostic criteria, and modern methods of the diagnosis of the syndrome of idiopathic non-atherosclerotic symmetrical calcification of the cerebral vessels. A review of the modern notions about the etiology and pathogenesis of calcification of vessels of basal ganglia is presented. Conversely to calcification of the cerebral vessels related to dysfunction of the parathyroid glands, etiopathogenetic aspects of the syndrome of idiopathic non-atherosclerotic calcification of the basal ganglia still remain obscure.

Adolescent↗
PubMed1987

[Mitral annular calcification in dialysis patients].

Degenerative mitral anular calcifications (MAC) are most often found between the posterior mitral anulus and the left ventricular posterior wall. In advanced stages they may encircle the mitral valve and thus involve the insertion of the anterior mitral leaflet and the posterior part of the aortic root. They are usually found only after the age of 70. Among 33 patients on chronic dialysis for renal failure who were investigated by echocardiography (2-D and m-mode) we found an MAC incidence of 55% but no cases among a control population of the same age and sex (p less than 0.001). The diameter of the calcification exceeded 5 mm in 9 cases out of 18. Four of these calcifications extended in a circular fashion around the mitral valve. Additional significantly associated echocardiographic features included dilatation of the left atrium and sclerosis of the aortic root and valve. Furthermore, 12 patients with MAC had dysfunction of the mitral valve (p less than 0.05), viz. 10 isolated mitral valve regurgitations and 2 mitral stenosis, combined with regurgitation. The patients with MAC were older than those without MAC, their mean duration of dialysis was longer and parathormone level higher. The incidence of mitral anular calcifications is much higher among patients on chronic dialysis. The clinical significance of these calcifications lies primarily in the consequent dysfunction of the mitral valve.

Adult↗
PubMedDate not supplied

Brain calcification in Kallman's syndrome. Computed tomographic appearance.

We report a 21-year-old white male with Kallman's syndrome (gonadotropic hypogonadism, hyposmia and sensorineural hearing loss) with extensive brain calcification, demonstrated for the first time by computed tomography. The pattern and anatomic distribution of the extensive brain calcification is nonspecific, being indistinguishable from those seen in other causes of brain calcification (principally diseases related to a disturbance in calcium metabolism), despite the normal serum calcium levels found in this patient. This syndrome, therefore, should be considered along with Cockayne's, Kearns-Sayre and Down's syndromes, tuberous sclerosis, carbonic anhydrase II deficiency, congenital mental deficiency and idiopathic familial basal ganglia calcification as another developmental cause of brain calcification, which usually show no disturbance in serum calcium level.

Adult↗
PubMed1985

[Disk calcifications in children].

It is not unusual for intervertebral disk calcifications to be detected in pediatric practice, the 150 or so cases reported in the literature probably representing only a small proportion of lesions actually diagnosed. Case reports of 33 children with intervertebral disk calcifications were analyzed. In the majority of these patients (31 of 33) a diagnosis of "idiopathic" calcifications had been made, the cervical localization of the lesions being related to repeated ORL infections and/or trauma. A pre-existing pathologic factor was found in two cases (one child with juvenile rheumatoid arthritis treated by corticoids and one child with Williams and Van Beuren's syndrome). An uncomplicated course was noted in 31 cases, the symptomatology (pain, spinal stiffness and febricula) improving after several days. Complications developed in two cases: one child had very disabling dysphagia due to an anteriorly protruding cervical herniated disc and surgery was necessary; the other child developed cervicobrachial neuralgia due to herniated disc protrusion into the cervical spinal canal, but symptoms regressed within several days although calcifications persisted unaltered. These findings and the course of the rare complications documented in the literature suggest the need for the most conservative treatment possible in cases of disc calcifications in children.

Adolescent↗
PubMed1973

Experimental calcification of the myocardium. Ultrastructural and histochemical investigations.

Focal areas of calcification are frequent in rat myocardium 30 and 60 days after administration of dihydrotachysterol. These areas are PAS-positive, stain deeply with alcian blue and show high affinity for colloidal iron. Calcification is almost completely confined to intracellular structures. Small clusters of needle-shaped crystals are first found in apparently undamaged mitochondria in undamaged myocardial cells. When all the mitochondria are calcified, the cell degenerates, and inorganic crystals are laid down in relationship with its myofilaments. In other myocardial cells, clusters of amorphous or finely granular inorganic substance are found in both mitochondria and myofibrils. Both structures show signs of advanced degeneration. Inorganic substance has only occasionally been found within the structures of the sarcoplasmic reticulum. These structures do not seem to be involved in myocardial calcification under the present experimental conditions. Calcification of myocardial cells gives rise to a cellular reaction. Many macrophagic cells surround the calcified areas, which are rapidly reabsorbed. The present results show that myocardial mitochondria are actively engaged in controlling the intracellular concentration and movement of calcium ions. Their role in the myocardial contraction-relaxation cycle and the possible mechanism of myocardial calcification are discussed.

Animals↗
PubMedDate not supplied

Apatite-associated arthropathy: a clinical study of 14 cases and of 2 patients with calcific bursitis.

Fourteen cases of acute calcific periarthritis and 2 cases of acute calcific bursitis are described. All patients had radiologic periarticular calcific deposits. Synovial fluid was available from 8 patients. Hydroxyapatite crystals were positively identified in 1 by x-ray diffraction analysis and by scanning and transmission electron microscopy. Apatite-associated arthropathy likely represents a form of crystal-induced inflammation. Three articular syndromes can be recognized; acute calcific periarthritis, acute (calcific) arthritis and a subacute-to-chronic arthritis resembling osteoarthritis. To improve patient classification, diagnostic criteria are proposed.

Acute Disease↗
PubMed1979

Pulmonary calcification: scanning electron microscopic and X-ray energy-dispersive analysis.

Nine patients with chronic renal failure or neoplastic involvement of bone showed metastatic calcification in their lungs at autopsy. On light microscopy, the calcifications were shaped like threads, beads, elongated rods, or tablets, whereas on scanning electron microscopy they were either amorphous or irregularly crystalline. Energy-dispersive x-ray analysis of the calcification showed the presence of calcium and phosphorus in all cases and traces of magnesium, sulfur, and other elements in some. The calcium-to-phosphorus ratio, obtained using Hall's formula, varied from 1.406 to 2.145, which is quite similar to that of normal bone and dystrophic calcification. Calcium phosphates, therefore, seem to be the principal mineral salts in all three types of calcification. In certain diagnostic and investigative problems, a correlative analysis of structure and chemistry at the ultrastructural level, both qualitatively and quantitatively in terms of their element ratios, can be done on tissue routinely prepared for light microscopy.

Adolescent↗
PubMed1984

[Diagnosis of calcification of the patellar tendon. Echo-radiographic comparison].

Real-time sonography was compared to low-kilovoltage radiographs in the diagnosis of intra-tendinous calcifications in 10 patients with chronic patellar tendonitis. In these patients sonography demonstrated thickening (100% of cases) and hypoechogenicity (90% of cases) of the patellar tendon. Ultrasound disclosed all calcifications displayed on radiographs showing hyperechoic foci. The associated acoustic shadow was absent in one case of a calcification less than one millimeter in diameter. Real-time ultrasound appears highly reliable in the diagnosis of even minute intra-tendinous calcifications. It also provides an accurate three-dimensional localization of the calcific deposits in the tendons.

Calcinosis↗
PubMed1984

[Computer tomogram of changes in pancreatic calcification during pancreatitis].

In 3 patients an increase of pancreatic calcification was observed in the course of 2 months. The increase of the calcification was combined with an improvement of the patient and a decrease of pseudocysts. Therefore the increase of pancreatic calcification was considered as a good sign. After surgical drainage of a pseudocyst one patient showed a decrease of pancreatic calcification in the course of 1 year. In this patient the clinical picture indicated a favourable development. This observation demonstrates that a recovering pancreas may show diminishing calcifications.

Calcinosis↗
PubMed1983

Biologic determinants of dystrophic calcification and osteocalcin deposition in glutaraldehyde-preserved porcine aortic valve leaflets implanted subcutaneously in rats.

Bioprosthetic cardiac valve calcification is a frequent complication after long-term valve replacement. In this study the authors sought to examine the biologic determinants of this type of dystrophic calcification using subcutaneous implants of glutaraldehyde-preserved porcine aortic valve leaflets (GPVs) in rats. GPVs and clinical valvular bioprostheses were prepared identically. Retrieved implants were examined for calcification and the deposition of osteocalcin (OC), a vitamin K-dependent, bone-derived protein, that is found in other dystrophic and ectopic calcifications. GPVs implanted in 3-week-old rats calcified progressively (GPV Ca2+, 122.9 +/- 6.0 micrograms/mg) after 21 days, with mineral deposition occurring in a morphologic pattern comparable to that noted in clinical retrievals. Calcified GPVs accumulated osteocalcin (OC, 183.4 +/- 19.4 ng/mg); Nonpreserved porcine aortic leaflet implants did not calcify (Ca2+ + 5.6 +/- 1.0 micrograms/mg). Millipore diffusion chamber (0.45-mu pore size enclosed GPV implants accumulated calcium and adsorbed osteocalcin despite the absence of attached host cells. GPVs implanted for 21 days in 8-month-old rats calcified less (GPV Ca2+, 22.4 +/- 5.0 micrograms/mg) than did GPVs implanted in 3-week-old rats (see above). High-dose warfarin therapy (80 mg/kg) did not alter GPV calcification (GPV Ca2+, 39.6 +/- 2.9 micrograms/mg) in 72-hour subcutaneous implants in 3-week-old male rats, compared with control rats (GPV Ca2+, 40.8 +/- 4.8 micrograms/mg).

Age Factors↗
PubMed1995

Ultrafast computed tomography for detection of coronary artery calcification.

This review summarizes coronary artery calcification as a marker of coronary atherosclerosis as historically noted and detected with radiographic imaging modalities. This review concentrates on the use of ultrafast computed tomography (CT) for coronary artery calcification imaging. Ultrafast CT is uniquely qualified for imaging of the coronary arteries and calcific deposits in particular because of the x-ray attenuation characteristics of calcium. Current validation studies are summarized. In particular, the sensitivity of ultrafast CT coronary calcification in angiographically proven obstructive disease has been shown by many investigators to be above 90%, but with specificity on the order of 40% to 50%. These numbers may be different for younger men and women, where the detection of smaller calcific deposits is more difficult. The positive predictive value has been calculated as between 72% by angiographic validation and 40% in a population with a lower pretest bias.

Calcinosis↗
PubMed1995

[Calcific tendinitis of the shoulder].

Degenerative ossification is formed directly at the major tubercle. Like in any other gliding tendon, fibrocartilage cells lie on the articular side of the rotator tendon at the pivot of the humerus head. Typically, the calcific deposits of calcifying tendinitis are found between these two areas. At this site, hydroxyapatite is usually formed by fibrocartilage cells through an unknown stimulus. There is no ossification. This is a two-phase disease. During the chronic initial phase, a calcific deposit is formed in the tendon of the rotator cuff. In the X-ray, it is clearly circumscribed and has a dense appearance (type I). Pain is inconsistent and may exist for years. In the acute phase, the deposit undergoes spontaneous resolution. Now it takes on a translucent and cloudy appearance without clear circumscription (type III). Patients experience severe pain for 2-3 weeks. Finally, a normally functioning shoulder joint will result. The X-ray therefore allows a prognostic conclusion. In a study including 235 calcific deposits, it became clear that there are some cases where it is not possible to designate the specific X-ray morphology to a given deposit (type II). Irrespective of the phase of disease, the so-called calcific deposit is composed of poorly mineralized hydroxyapatite. For a diagnosis, we require: a typical history, clinical findings consistent with tendinitis of the rotator cuff, calcific deposits in the tendon associated with signs and symptoms of tendinitis. It is recommended that radiographs be taken at least in AP projections with the shoulder in internal and external rotation to demonstrate the deposits without super-imposition. Ultrasound shows concomitant bursitis and is useful for the differential diagnosis of rupture of the rotator cuff. Radiographic diagnosis is most difficult when there are small opacifications near the rotator attachment. In this case, allocation may become possible only later in the course of disease. Initial treatment should always be non-operative. Almost all therapeutic modalities are said to be quite successful. Needles under local anesthesia is recommended only for patients with marked pain who lack any signs of resolution in the X-ray. According to a prospective study, the success rates of needles depend on the roentgenologic findings: in type I deposits, resolution occurs in 33%, in typq II deposits in 71%. Freedom from pain is seen in about 50% of the patients. Type III deposits undergo resolution with and without therapy in about 2-3 weeks. Post-operative results are reported to lie between 77% and 96% irrespective of the method used.(ABSTRACT TRUNCATED AT 400 WORDS)

Calcinosis↗
PubMed1994

Effect of AOA on glutaraldehyde-fixed bioprosthetic heart valve cusps and walls: binding and calcification studies.

Alpha-aminooleic acid (AOA), a potent, non-toxic and biocompatible anticalcification agent, has been shown to be effective for glutaraldehyde-fixed valves in rat and juvenile sheep models, and is used for the treatment of Medtronic heart valve bioprostheses currently in clinical trials. In the pre-clinical sheep study of a stentless aortic root, the treatment with AOA prevented calcification of the cusps, but not of the wall. The experiments described in this manuscript were designed to investigate a possible relationship between the binding of AOA and the differential treatment efficacy in the cusp and the wall, and to improve the anticalcification effect of the AOA treatment in the wall. Glutaraldehyde-fixed porcine roots were treated with [14C]-AOA for binding studies, and with non-radioactive AOA for calcification studies for rat subdermal implants. The results indicate that a) the AOA treatment did reduce wall calcification, but only temporarily, b) the low efficacy of the AOA treatment on the wall was probably due to the limited penetration of AOA, and c) increasing the volume of the AOA solution during treatment significantly increased the content of AOA in the wall, and significantly decreased wall calcification. This study suggests that AOA efficacy in the wall may be hindered because of the physical characteristics of the wall, and that wall calcification may be prevented by developing methods aimed at increasing AOA penetration into the wall.

Animals↗
PubMed1993

Studies on the reduction of aortic calcification by alkali citrates in an ex vivo tissue preparation in the rat.

The effect of orally administered alkali citrates on the calcification of arterial vessel was studied in the rat. Freshly dissected aortic segments were placed in Millipore diffusion chambers and grafted intraperitoneally. Within 21 days calcification of the media had developed. Under treatment with 2.1 mmol citrate per animal and day a significant decrease in histologically detectable calcification areas occurred, as assessed by greatest thickness and longitudinal expansion. This effect was more pronounced with potassium citrate and potassium sodium citrate, and less marked with sodium citrate. The calcium and phosphorus content of aortic tissue remained unchanged, but magnesium increased significantly. The spheroid particles deposited in the media were characterized in more detail by electron microscopy and elemental microanalysis, X-ray diffraction, and determination of the molar calcium-phosphorus ratio. The combined data suggest that in the model selected for studying biocalcification not mature hydroxyapatite but some precursor of this substance is deposited, and that in animals receiving alkali citrate treatment deposition of amorphous calcium phosphate is likely. It is concluded that in the ex vivo aortic wall preparation oral alkali citrates a) bring about a reduction in calcification areas in the media layer, b) impair the maturation of hydroxyapatite and its deposition in the arterial tissue; c) promote the accumulation of magnesium. Whether these results are of significance for the calcification of arteries in situ and treatment regimens is unknown.

Animals↗
PubMed1993

Myocardial texture and cardiac calcification in uremia.

Seventy patients with advanced chronic renal failure were examined by 2D echocardiography in an effort to determine the prevalence of changes in myocardial texture and of valvular calcification. Changes in myocardial texture may be due to calcium deposition in the myocardium, the relationship between changes in myocardial texture and factors that may enhance myocardial calcification (blood levels of parathyroid hormone, PTH, and calcium-phosphorus product) were also evaluated. Myocardial texture was abnormal in 36 patients. In 68 patients, structural calcification could be assessed; a high degree of calcification was found. No correlation was found between either the echocardiographic parameter and blood levels of PTH or calcium-phosphorus product. We conclude that myocardial textural changes and intracardiac calcification are common in chronic renal failure and that these abnormalities do not correlate with blood PTH levels or calcium-phosphorus product.

Adult↗