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[Results of endoscopic treatment of non-broken tendinopathies of the rotator cuff. 2. Calcifications of the rotator cuff].

The authors studied the results of the arthroscopic treatment of the chronic calcifying tendinitis within a multi-center study of the French Society of Arthroscopy. 112 patients were available for the study. All shoulders had a preoperative radiographic clinical and radiographic evaluation. At follow up, functional results were assessed, using the Constant score, and X rays allowed to appreciate the acromial shape and the calcific deposit aspect. Several arthroscopic procedures were used on the calcification (respect or removal), and the coracoacromial arch (respect, ACL release or acromioplasty). This study found an objective success rate of 89 per cent and a patient subjective satisfaction rate of 82 per cent. Based on follow up radiographs, 88 per cent of the patients had a complete disappearance of the calcific deposit. There were no recurrence, no secondary rotator cuff tear. The results were not correlated with the age of the patients, or with the radiographic aspect (type, size, localization) of the calcification. The results were correlated with the arthroscopic procedure: they were better when the calcification had been removed (superior to deposit respect). Associated acromioplasty gave no better results: it was only considered as necessary when the calcification was not found (12 per cent). The greatest care must be taken in the surgical indication for this pathology because of a high rate of spontaneous resorption. The authors conclude that the arthroscopic surgery is a very effective method for chronic calcific tendinitis, compared to open procedure.

Adult↗

[Three cases of lung cancer with calcification--demonstration by chest CT].

We report three cases of lung cancer with calcification shown on chest CT scans. Case 1 was a 63-year-old man with well differentiated squamous cell carcinoma of the lung. Chest CT scan showed pronounced central calcification within the tumor. Case 2 was a 57-year-old woman with small cell carcinoma of the lung. Chest CT scan showed diffuse amorphous calcification within the tumor. Case 3 was a 70-year-old man with lung cancer for which pathologic data was not available. Chest CT scan showed punctate and linear calcification of the cavity wall within the tumor. Microscopic examinations revealed dystrophic calcification in cases 1 and 2. Calcification has long been recognized as a distinguishing radiologic feature of a benign pulmonary mass, however, the presence of calcification within a tumor on chest CT scan does not exclude the diagnosis of lung cancer.

Aged↗

Increased prevalence of aortic calcification in chronic pancreatitis.

OBJECTIVES: The seemingly frequent radiological observation of aortic calcification in patients with chronic pancreatitis seen in our clinic prompted us to assess the prevalence of this lesion in this disease. METHODS: Fifty-seven consecutive patients with chronic pancreatitis (52 male, five female; mean age 44.2 yr, range 26-59 yr), and 66 healthy controls, matched for sex and age, were studied. Of the 66 controls, 40 were both smokers and drinkers, as were most of the patients. The presence of aortic calcification was determined by performing anteroposterior and lateral radiograms of the prelumbar region. RESULTS: Radiological evidence of aortic calcification was found in 35 of the 57 patients with chronic pancreatitis (61.4%) and in 12 of the 40 smoker control (30.0%) (p < 0.005); none of the nonsmoker controls had aortic calcification. The increased frequency was more pronounced among the patients under 50 yr of age (40.0% vs. 0% and 70.4% vs. 35.3% in the 30-39 and 40-49 yr age groups, respectively). No significant differences in serum levels of cholesterol and triglycerides, blood pressure, alcohol, and smoking habits were observed between chronic pancreatitis patients with aortic calcification and those without, or between patients with aortic calcification and controls. CONCLUSIONS: The results indicate that patients with chronic pancreatitis have a significantly higher prevalence of aortic calcification than controls. The reason for the increased prevalence of this advanced atherosclerotic lesion is nuclear.

Adult↗

Isolated subacromial decompression for the treatment of chronic shoulder pain with rotator cuff calcification. A review of twenty-seven shoulders, including eighteen evaluated by magnetic resonance imaging after surgery.

We conducted a retrospective study of functional results and imaging study changes after isolated anterosuperior decompression of 27 chronically painful shoulders with calcification of the supraspinatus tendon at the time of surgery (n = 22) or at an earlier date (n = 5). Mean duration of pain at surgery was 4.5 years. Mean time between surgery and evaluation of results was three years. Absence of pain and full range of motion were noted in most cases (70%), usually after four to six months. There were no postoperative exacerbations of pain. The best results were obtained in those patients with a heterogeneous supraspinatus calcification. Most calcifications (18/22) disappeared within one year of surgery. Magnetic resonance imaging findings at last follow-up are reported for 18 shoulders. Functional results were nearly as good as those reported after calcification removal. In patients with shoulder pain and rotator cuff tendon calcifications who fail to respond to conservative therapy and aspiration with lavage, anterosuperior decompression may be the treatment of choice when the calcification is either heterogeneous and located within the tendon or no longer visible. In contrast, curettage may be the best treatment for superficial homogeneous calcifications that can be removed without damaging the rotator cuff.

Adult↗

Lung cancer associated with punctate calcification: CT and histological correlation.

The etiology of punctate calcifications in lung cancer was evaluated on the basis of CT and histological correlations. Seven cases of lung cancer with punctate calcifications were demonstrated on CT. The patients had undergone surgical resection (five men and two women, 60-70 years old; six adenocarcinomas and one squamous cell carcinoma), and each case was evaluated for its CT appearance and histological findings. The number of calcifications observed on CT varied from one to six. Most were eccentric, but some calcifications in four cases were within the more central portion of the nodules. Overall, in six of seven cases the calcifications were histologically estimated to be due to preexisting old granulomatous fibrotic changes or fragments of bronchial cartilage incorporated within the growing tumors. In only one case were the calcifications psammoma bodies within the tumor. We conclude that punctate calcifications in lung cancers correspond mostly to preexisting calcified granuloma or degenerated bronchial cartilage.

Adenocarcinoma↗

Endothelial alterations and senile calcific aortic stenosis: an electron microscopic observation.

Calcific degeneration of aortic valves were investigated in 10 patients with senile calcific aortic stenosis by means of high resolution scanning electron microscopy (HR-SEM) and transmission electron microscopy (TEM). All the specimens obtained during aortic valve surgery HR-SEM and TEM examinations consistently showed various degrees of pathological alterations and calcification involving surface endothelium, underlying basement membranes and deeper layers of interweaving networks of collagen fiber bundles in the pars fibrosa of the valve tissues. Calcific deposits in the valve tissues always occurred in the vicinity of the endothelial defects and in the subendothelial structures just beneath the defective endothelium. The amount of calcific deposits in the valve tissues increased in proportion to the severity of endothelial damage and gradually decreased from the defective endothelial surface to the deeper layer of collagen tissue. In addition, apoptotic cell death, particularly of the fibrocytes in the valve tissue, was closely related to the severity of endothelial injury. Cellular fragments derived from the apoptotic cells were always associated with calcium deposits. Based on the above findings, our results provide evidence that the alteration of endothelial integrity plays a contributory role in calcific degeneration in the aortic valve leading to the development of senile calcific aortic stenosis.

Aged↗

Evaluation of in vivo models for studying calcification behavior of commercially available bovine pericardium.

BACKGROUND AND AIM OF THE STUDY: A common frame of reference is essential when attempting to determine if new treatments intended to reduce calcification of bioprostheses are superior to existing processes and products. The aim of this study was to examine calcification behavior for a commercially available pericardial bioprosthesis in subcutaneous and sheep valve models, and to evaluate the importance of appropriate control treatments in comparative studies with proposed new treatments. METHODS: Samples of bovine pericardium were placed subcutaneously under the dorsal skin of weanling rats and juvenile rabbits for 30-, 60- and 90-day intervals. Samples were either commercially available pericardial tissue or tissue processed with phosphate-buffered glutaraldehyde alone. Commercially available pericardial valves were also implanted in the mitral position in juvenile sheep, with elective sacrifice at 20 weeks. Retrieved samples underwent X-ray, histologic and elemental analysis. RESULTS: Commercial samples retrieved from the subcutaneous and sheep models showed similar, minimal calcification behavior on X-ray and histologic slides, whereas pericardium exposed to glutaraldehyde alone demonstrated rapid calcification. CONCLUSIONS: The 90-day subcutaneous rabbit model produced patterns of calcification similar to those in valves explanted from juvenile sheep after 20 weeks. A statistically significant decrease (p < 10(-8)) in calcification was demonstrated for clinical pericardium when compared with pericardium exposed to glutaraldehyde alone in the subcutaneous model. This suggests that subcutaneous models may be a cost-effective, time-efficient means of evaluating and comparing various tissue treatment methods. The rabbit methodology may provide a more accurate prediction of clinical performance, offering a greater degree of sensitivity. These studies also indicate that the commercially available process shows minimal calcification in the commonly used 30-day weanling rat subcutaneous model, contradicting other reported studies that may not accurately represent commercially available processes.

Animals↗

Benign nodular calcification and calciphylaxis in a haemodialysed patient.

Several types of soft tissue calcification can be detected from radiographic evaluation of patients with end-stage renal failure. The factors that predispose to such calcification include an increase in CaxP product in serum, the degree of secondary hyperparathyroidism, the level of blood magnesium, the degree of alkalosis, and the presence of local tissue injury. Three major varieties include calcification of medium-sized arteries, periarticular or tumoral calcification and visceral calcification. Calciphylaxis is a phenomenon consisting of acute ischemic necrosis in presence of calcification of dermohypodermic arterioles. It occurs mostly in chronic renal failure patients with secondary or tertiary hyperparathyroidism with a persistently elevated calcium-phosphorus product. There are few options in treating calciphylaxis and the outcome is generally poor. The authors report the case of a haemodialised patient with benign nodular calcification and calciphylaxis. The coexistence of both entities in the same patient has never been described.

Calcinosis↗

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↗

Ultrastructural cytochemistry of proteoglycans associated with calcification of shark cartilage.

Proteoglycans (PGs) as well as sulfated glycosaminoglycans (GAGs) are closely associated with cartilage calcification. An inner zone of endoskeletal tesserae of sharks is composed of a unique calcified hyaline cartilage. Initial calcification can be seen in the cartilage close to the inner zone. We have ultrastructurally examined shark, Triakis scyllia, noncalcifying, calcifying, and calcified cartilage using the tannic acid-ferric chloride (TA-Fe), the high iron diamine (HID), and the HID-thiocarbohydrazide-silver proteinate (HID-TCH-SP) methods for localization of sulfated complex carbohydrates. In noncalcifying cartilage, TA-Fe and HID strongly stained matrix granules which were round, ovoid, elongated, or irregularly shaped and presumably represented PG monomers. The size and staining intensity of the reactive matrix granules progressively decreased in calcifying cartilage toward the calcification front of the calcified cartilage. Similarly, a progressive decrease in the size of the HID-TCH-SP stain deposits in the matrix granules was observed in the calcifying cartilage close to the calcification front and was interpreted as a decrease in length of sulfate containing GAG chains. In the calcified cartilage, the highly calcified areas were often localized in the calcification front and contained few or no small HID-TCH-SP stain deposits, whereas the weakly calcified regions contained more stain deposits. These results indicate that partial and complete degradation of sulfated GAGs and/or PGs may be a requisite for calcification of shark cartilage.

Animals↗

Relationship between toluidine blue-stained calcification fronts and tetracycline-labeled surfaces in normal human iliac crest biopsies.

The relationship between toluidine blue-stained calcification fronts and tetracycline labeling was examined in iliac crest biopsies from 56 normal subjects aged 19-80 years, all of whom had received double tetracycline labeling. Sections were quantitated using an eye-piece graticule and all values were expressed as a percentage of osteoid surface. Values for double plus single tetracycline-labeled surfaces were lower than those obtained for toluidine blue-stained calcification fronts in 66% of subjects, although the difference between the two measurements was not statistically significant. Values obtained for calcification fronts demonstrated by toluidine blue staining were significantly greater than those obtained for single, double, and double plus half single tetracycline-labeled surfaces. No significant correlation could be demonstrated between toluidine blue-stained calcification and tetracycline-labeled surfaces. In conclusion, the fraction of osteoid bearing a tetracycline label differed from that showing a toluidine blue-stained calcification front and no correlation could be demonstrated between the two measurements. These differences may arise from methodological problems associated with their demonstration and identification; alternatively their lack of similarity might reflect uptake of stain and tetracycline at different sites within the calcification front. Which of the two parameters most accurately represents the active mineralizing surface is unknown.

Adult↗

Growth cartilage calcification and formation of bone trabeculae are late and dissociated events in the endochondral ossification of Rana catesbeiana.

Endochondral ossification in the growth cartilage of long bones from the bullfrog Rana catesbeiana was examined. In stage-46 tadpoles and 1-year-old animals, the hypertrophic cartilage had a smooth contact with the bone marrow and the matrix showed no calcification or endochondral bone formation. In spite of showing no aspects of calcification, the chondrocytes exhibited alkaline phosphatase activity and some of them died by apoptosis. However, matrix calcification and endochondral ossification were observed in 2-year-old bullfrogs. Calcium deposits appeared as isolated or coalesced spherical structures in the extracellular matrix of hypertrophic cartilage. Bone trabeculae were restricted to the central area at the sites where the hypertrophic cartilage surface was exposed to the bone marrow. Cartilage matrix calcification and the formation of bone trabeculae were not dependent on each other. Osteoclasts were involved in calcified matrix resorption. These results demonstrate that the calcification of hypertrophic cartilage and the deposition of bone trabeculae are late events in R. catesbeiana and do not contribute to the development and growth of long bones in adults. These processes may play a role in reinforcing bony structures as the bullfrog gains weight in adulthood. In addition, the deposition of bone trabeculae is not dependent on cartilage matrix calcification.

Alkaline Phosphatase↗

Hypertrophy and calcification of rabbit permanent chondrocytes in pelleted cultures: synthesis of alkaline phosphatase and 1,25-dihydroxycholecalciferol receptor.

Cartilage calcification at specific sites is a key event that leads to skeletal development and growth. To obtain insights into the control of cartilage calcification, we examined whether cells distributed in permanent cartilage regions might have the ability to express the calcification-related phenotype in a permissive environment. Chondrocytes were isolated from the permanent and growth plate cartilages of 4-week-old rabbit ribs. They were seeded as a pelleted mass in a centrifuge tube and cultured in Eagle's minimum essential medium supplemented with 10% fetal bovine serum. These cells proliferated for several generations, and then synthesized large amounts of proteoglycans, yielding a cartilage-like tissue in 16 days. Cultures from the permanent and growth plate cartilages showed similar time courses for increases in DNA synthesis and proteoglycan production that reached similar maximal levels. Thereafter, they initiated the syntheses of alkaline phosphatase and 1,25-dihydroxycholecalciferol receptor and induced matrix calcification without additional phosphate. The increases in alkaline phosphatase, 1,25-dihydroxycholecalciferol receptor, and calcium contents in cultures from the permanent cartilage were consistently delayed for 4-7 days relative to the growth plate-derived cells, but caught up by Day 28. The maximal levels of alkaline phosphatase and 1,25-dihydroxycholecalciferol receptor in the cultures from the permanent cartilage were 40- to 100-fold higher than that of the in vivo permanent cartilage. These results provide evidence that permanent cartilage cells in postnatal young rabbit ribs have the capacity to express alkaline phosphatase and 1,25-dihydroxycholecalciferol receptor and induce calcification in a permissive environment, although they never express these calcification-related phenotypes in vivo.

Alkaline Phosphatase↗

Alkaline phosphatase and calcification, correlated or not?

The effects of alkaline phosphatase inhibitors (levamisole, L-bromotetramisole) on the activity of the enzyme and on calcification in vitro were studied, to find out whether there is a relationship between alkaline phosphatase and calcification. Metatarsal bones of 15 1/4-day-old embryonic mice were dissected and cultured for 40 hours in the presence and absence of inhibitor. Levamisole and L-bromotetramisole fully inhibited calcification in vitro when present in concentrations which almost totally inhibited alkaline phosphatase activity, as measured biochemically or histochemically. However, incorporation of 3H-thymidine and 35S-sulphate was also inhibited. Furthermore, D-bromotetramisole, the dextroform of bromotetramisole which has no effect on alkaline phosphatase, inhibited calcification and 3H-thymidine and 35S-sulphate incorporation as well. The results of this study show that these inhibitors cannot be used to study the relationship between alkaline phosphatase and calcification. In addition, they suggest that although alkaline phosphatase may be important for the process of calcification, it is probably not a critical factor.

Alkaline Phosphatase↗

Cloning and expression of a cDNA encoding a matrix peptide associated with calcification in the exoskeleton of the crayfish.

Calcification-associated peptide (CAP)-1 isolated from the exoskeleton of the crayfish, Procambarus clarkii, has anti-calcification activity and chitin-binding ability and is, therefore, considered to be associated with calcification. In this study, a cDNA encoding CAP-1 was cloned and characterized. An open reading frame encoded a pre-propeptide of 99 amino acid residues, which was composed of a signal peptide, a CAP-1 precursor and two-basic amino acid residues at the C-terminus. The dibasic residues were not observed in the natural CAP-1. Expression analyses using Northern blot and RT-PCR revealed that the mRNA encoding CAP-1 was strongly expressed in the epidermal tissue during the postmolt stage, where and when the calcification takes place. These results support that CAP-1 may play an important role in the calcification of the exoskeleton. Based on the nucleotide sequence of the cDNA encoding CAP-1, a recombinant CAP-1 and that carrying the basic residues at the C-terminus were expressed in Escherichia coli. Anti-calcification assay showed that these recombinant peptides were less active than natural CAP-1, indicating that the phosphate group at the 70th residue, Ser, in natural CAP-1 is important for inhibitory activity and that the paired basic residues have some contribution to the elevation of inhibitory activity.

Amino Acid Sequence↗

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↗

Increased cellular expression of matrix proteins that regulate mineralization is associated with calcification of native human and porcine xenograft bioprosthetic heart valves.

Dystrophic mineralization remains the leading cause of stenotic or regurgitant failure in native human and porcine bioprosthetic heart valves. We hypothesized that cellular expression of noncollagenous matrix proteins (osteopontin, osteocalcin, and osteonectin) that regulate skeletal mineralization may orchestrate valvular calcification. Porcine bioprosthetic heart valves and native human heart valves obtained during replacement surgery were analyzed for cells, matrix proteins that regulate mineralization, and vessels. Cell accumulation and calcification were correlated for both valve types (rho = 0.75, P = 0.01, native; rho = 0.42, P = 0.08, bioprosthetic). Osteopontin expression correlated with cell accumulation (rho = 0.58, P = 0.04) and calcification (rho = 0.52, P = 0.06) for bioprosthetic valves. Osteocalcin expression correlated with calcification (rho = 0.77, P = 0.04) and cell accumulation (rho = 0.69, P = 0.07) in native valves. Comparisons of calcified versus noncalcified native and bioprosthetic valves for averaged total matrix protein mRNA signal score revealed increased noncollagenous proteins mRNA levels in calcified valves (P = 0.07, group I vs. group II; P = 0.02, group III vs. group IV). When stratified according to positive versus negative mRNA signal status, both calcified bioprosthetic valves (P = 0.03) and calcified native valves (P = 0.01) were significantly more positive for noncollagenous proteins mRNA than their noncalcified counterparts. Local cell-associated expression of proteins regulating mineralization suggests a highly coordinated mechanism of bioprosthetic and native valve calcification analogous to physiologic bone mineralization. Modulation of cellular infiltration or cellular expression of matrix proteins that regulate mineralization, may offer an effective therapeutic approach to the prevention of valve failure secondary to calcification.

Aged↗

Calcification preceding new bone formation induced by demineralized bone matrix gelatin.

Demineralized bone matrix gelatin (BMG) was implanted into the skeletal muscle of Sprague-Dawley (S.D.) rats, and histological changes were examined 3, 5, 7, 10 and 15 days later. Before bone formation, a specific calcification process was found in most of the BMG from day 5 and 7 after implantation. The heterotopic calcified sites were not always consistent with the sites of the alkaline phosphatase activity. It was considered that this calcification progresses without any cellular components, and we distinguished this type of calcification as "acellular mineral deposition" from the calcification which occurs in new bone formation. This "acellular mineral deposition" was first observed as small spherical calcified deposits in the BMG on day 7 after implantation; these deposits then gradually grew and fused with each other. Some multinucleated cells appeared near the site of calcification on day 7 after implantation, but osteoblasts or osteoblast-like cells were scarcely observed around the calcified deposits in BMG until day 7. Vascularization was often observed near the "acellular mineral deposition" and the new bone formation. Fourier transform infrared spectroscopy showed that the calcified deposits in BMG were composed of hydroxyapatite, carbonateapatite and other calcium phosphate components, and that the first two components became prominent with time. It is believed that the "acellular mineral deposition" is due to the deposition of calcium and phosphate into the BMG by a process of heterogenic nucleation that does not involve osteoblasts or matrix vesicles. Bone formation induced by the BMG occurred after the "acellular mineral deposition." The experimental calcification shown in this paper seems a useful model for the study of biocalcification.

Alkaline Phosphatase↗