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PubMed1995

Sonographic findings of rotator cuff calcifications.

We studied the findings and value of sonography in the diagnosis of rotator cuff calcifications in comparison to plain radiographs. Sonograms were correlated with plain radiographs in 951 patients. The diagnosis of rotator cuff calcifications was made by ultrasonography in 87 and with plain films in 93 of 951 patients. Sonography displayed two additional bursal slurry calcifications were found on plain films. Three types of calcifications were found with ultrasonography: (1) a hyperechoic focus with a well-defined shadow (79%); (2) a hyperechoic focus with a faint shadow (14%); and, (3) a hyperechoic focus with no shadow (7%). Large and slurry calcifications and bursal calcifications were better seen with ultrasonography, but small and more scattered deposits were better found on plain radiographs. Sonography proved to be reliable in the detection and localization of rotator cuff calcifications, but classification into a formative or resorptive phase could not be done. Because of this and the possibility of pathologic conditions of bone, plain radiographs should always be obtained prior to doing sonography.

Adult↗
PubMedDate not supplied

Calcification in mucinous cholangiocellular carcinoma.

Calcification is rarely seen in cholangiocellular carcinoma. We herein report the case of a 53 year-old man with calcification in a cholangiocellular carcinoma. Because imaging studies had revealed coarse calcified foci, hepatolithiasis was suspected pre-operatively. The patient underwent a laparotomy in which intra-operative cholangioscopy revealed no gallstones but did reveal an unsuspected tumor with abundant mucin. A left hepatic lobectomy with resection of the extrahepatic bile duct was performed. The tumor histology was mucinous adenocarcinoma with calcification. In the English language literature, we found 9 cases of cholangiocellular carcinoma with macroscopic calcification. Six of these cases were mucinous adenocarcinomas. Roentgenologic examination revealed coarse calcification in 7 cases and fine calcification in 2 cases. Clinicians should note that cholangiocellular carcinoma, especially the mucinous variant, may be accompanied by coarse calcification.

Adenocarcinoma, Mucinous↗
PubMed2000

Glutaraldehyde detoxification in addition to enhanced amine cross-linking dramatically reduces bioprosthetic tissue calcification in the rat model.

BACKGROUND AND AIM OF THE STUDY: Enhanced fixation of bioprosthetic tissue by both increased concentrations of glutaraldehyde (GA) and the introduction of additional cross-links with L-lysine significantly reduces calcification. We have previously reported that prolonged exposure to high-volume amino-compounds under warm, acidic conditions leads to thorough, non-rebounding GA detoxification. The aim of the present study was to prove that removal of excess GA can amplify the benefits of enhanced GA cross-linking with regard to bioprosthetic tissue calcification. METHODS: Porcine ascending aortas and leaflet tissue, and bovine pericardium were immediately fixed using three GA concentrations (0.2%, 1.0%, 3.0% (v/v)) for seven days at 4 degrees C. Samples were allocated to nine groups. Groups I to III received no further treatment (one at each GA concentration); groups IV to IX underwent an additional L-lysine interim step (48 h/37 degrees C/0.1 M) two days before completion of standard seven-day GA fixation; and groups VII to IX were additionally treated with a GA extraction process using high-volume urazole solution (acetic acid buffer, pH 4.5, 37 degrees C, one week) followed by NaBH4 reduction (2 days, 37 degrees C). Samples were implanted subcutaneously in rats (six per group) for six weeks. Tissue calcium was measured by atomic absorption spectrophotometry and examined histologically after von Kossa staining. RESULTS: Calcification was reduced in all three tissue types by enhanced cross-linking and by extraction of excess GA. Increasing the GA concentration from 0.2% to 3.0% led to a reduction in calcification of 11.5% (p = 0.074; Student's t-test) in leaflets; 63.6% (p <0.0001) in pericardium; and 17.5% (p = 0.034) in aortic wall tissue. The introduction of additional cross-links with L-lysine resulted in a significant reduction of calcium in all tissues (maximally 42.5%, p = 0.0003 in leaflets; 79.3%, p = 0.005 in pericardium; and 49.6%, p <0.0001 in aortic wall; Student's t-test). Optimal reduction in calcification could be achieved with the combined effect of 3.0% GA fixation, L-lysine enhancement and urazole detoxification. When compared with 0.2% GA-fixed tissue, calcification could be reduced by 99.1% in leaflets, 95.9% in pericardium, and 90.8% in aortic wall tissue (p <0.0001 for all tissue types; Student's t-test). CONCLUSION: Removal of excess GA from fixed bioprosthetic tissue was capable of markedly improving the anti-calcific effect of enhanced GA cross-linking.

Animals↗
PubMed2003

Media calcification, low erythrocyte magnesium, altered plasma magnesium, and calcium homeostasis following grafting of the thoracic aorta to the infrarenal aorta in the rat--differential preventive effects of long-term oral magnesium supplementation alone and in combination with alkali.

Calcifications in arterial media are clinically well documented, but the role played by magnesium in pathophysiology and therapy is uncertain. To clarify this, an animal model in which the juxtacardial aorta was grafted to the infrarenal aorta, and the subsequent calcifications in the media of the graft and their response to oral supplementation with three magnesium-containing and alkalinizing preparations was investigated. Groups of highly inbred rats were formed as follows: sham-operation (Sham, n = 12), aorta transplantation (ATx, n = 12), ATx + magnesium citrate (MgC, n = 12), ATx + MgC + potassium citrate (MgCPC, n = 12), ATx + MgC + MgCPC (MgCPCSB, n = 12). At 84 (+/-2) days after ATx with or without treatment the following observations were made: (1) weight gain and general status were normal; (2) ATx rats developed massive media calcification, mineral accumulation in the graft, decreased erythrocyte magnesium and plasma parathyroid hormone, and increased plasma ionized magnesium and calcium, and uric acid; (3) Mg-treated rats developed variable degrees of metabolic alkalosis, but only MgCPCSB supplementation prevented calcifications. Additional findings after ATx alone were: imbalance in endothelin and nitric oxide production, the mineral deposited in media was poorly crystallized calcium phosphate, calcium exchange between plasma and graft, and bone resorption were unchanged. The superior anti-calcification effect of MgCPCSB was characterized by complete restoration of normal extracellular mineral homeostasis and uric acid, but sub-optimal normalization of erythrocyte magnesium. It was concluded that in the rat: (1) ATx causes loss of cellular magnesium, excess of extracellular magnesium and calcium in the presence of apparently unchanged bone resorption, and increased uricemia; (2) ATx facilitates enhanced influx of calcium into vascular tissue, leading to calcium phosphate deposition in the media; (3) ATx-induced calcification is prevented by dietary supplementation with a combination of magnesium, alkali citrate and bases. Although the described circulatory model of media calcification in the rat requires further investigation, the data allow ascribing a fundamental role to magnesium and acid-base metabolism.

Animals↗
PubMed2002

Non-tumoral non-infectious intracranial calcifications.

Intracranial calcifications are often an accidental finding on conventional radiograms or computed tomography (CT) scans. They can be physiologic or pathologic, accompanying various diseases of the central nervous system. Pathologic calcifications can be found in tumors as well as in other non-neoplastic diseases. In differential diagnosis of intracranial calcifications there should be mentioned two groups: infectious and non-infectious calcifications. In the paper there were discussed non-tumoral non-infectious intracranial calcifications. Although more sporadic than tumoral or infectious calcifications, calcified lesions in non-infectious diseases should also be taken into account in differential diagnosis of intracranial calcifications.

Brain Diseases↗
PubMed2004

Medial arterial calcification mimicking temporal arteritis.

Medial arterial calcification, which has been increasingly recognized in end-stage renal disease (ESRD) patients, has been associated with acutely symptomatic vascular complications including calcific uremic arteriolopathy (calciphylaxis) and ischemic changes in the extremities. This report describes a 50-year-old ESRD patient on maintenance hemodialysis in whom medial arterial calcification developed with features mimicking the findings of temporal arteritis. He complained of persistent bilateral temporal area headaches with associated symptoms of blurred vision; pain in his shoulders, hips, and knees; and intermittent symptoms consistent with jaw claudication. He was not receiving calcium or vitamin D supplements. Superficial temporal arteries were dilated, tortuous, nodular, and tender to palpation. Ophthalmologic examination was unremarkable, except for the presence of peripapillary atrophy. Temporal artery biopsy results showed medial arterial calcification with mild inflammatory changes. No giant cells were identified. Additional long-term complications of medial arterial calcification have included the development of painful ischemic ulceration of the glans penis and extensive mitral annulus calcification detected by echocardiography. The findings in this patient show that clinical manifestations of medial artery calcification associated with ESRD can mimic those seen with other vascular diseases.

Arteriosclerosis↗
PubMed2004

Evaluation of 18F-FDG uptake and arterial wall calcifications using 18F-FDG PET/CT.

UNLABELLED: Glucose metabolic activity expressed as (18)F-FDG uptake may be increased in active atherosclerotic plaque. Calcium depositions are often increased in mature atherosclerotic plaque. The purpose of the present study was to assess the patterns of vascular-wall (18)F-FDG uptake and CT calcifications using combined PET/CT. METHODS: One hundred twenty-two consecutive patients over the age of 50 (47 women and 75 men; mean age, 66 +/- 9 y) undergoing whole-body (18)F-FDG PET/CT for tumor assessment were retrospectively evaluated. PET, CT, and PET/CT slices were generated for review. Abnormal vascular findings in major arteries in the chest and abdomen were categorized as PET positive (PET+), PET negative (PET-), CT positive (CT+), or CT negative (CT-). The topographic relationship between increased vascular-wall (18)F-FDG uptake on PET and the presence of calcifications on CT was assessed on PET/CT fused images, with abnormal sites further classified as PET+/CT+, PET+/CT-, or PET-/CT+. The presence of CT calcifications and increased vascular-wall (18)F-FDG uptake was correlated with age, sex, presence of cardiovascular risk factors, and cardiovascular disease. RESULTS: Abnormal findings were identified at 349 sites. CT calcifications (CT+) were observed at 320 sites (92%) of 100 patients (82%), more commonly in men (P < 0.03), in older patients (P < 0.0001), in patients with hypertension (P < 0.003) or hyperlipidemia (P < 0.04), and in smokers (P < 0.008). Increased vascular-wall (18)F-FDG uptake (PET+) was observed at 52 sites (15%) of 38 patients (31%), more commonly in men (P < 0.02), in older patients (P < 0.0001), and in patients with hypertension (P < 0.02), and was borderline in patients with cardiovascular disease (P = 0.057). PET+ and CT+ findings correlated in 12 patients, a PET+/CT- pattern was found in 18 patients, and 8 patients had increased vascular-wall (18)F-FDG uptake in sites with and without calcifications (PET+/CT+, CT-). Twenty-two patients (18%) had a PET-/CT- pattern. CONCLUSION: Hybrid PET/CT can be used to identify and to correctly localize vascular-wall (18)F-FDG activity. Increased vascular-wall (18)F-FDG activity was found in 15% of sites and CT calcifications were noted in 92% of sites, with congruent findings in 7%. The clinical significance of the relationship between vascular-wall (18)F-FDG uptake and CT calcifications needs to be assessed by further prospective studies with long-term follow up.

Adult↗
PubMed2004

[Atherosclerosis and vascular calcification in hemodialysis patients].

Cardiovascular disease is the largest cause of mortality in hemodialysis patients. Cardiovascular mortality is fivefold to twentyfold higher in hemodialysis patients than in the general population. Atherosclerosis and vascular calcification are the characteristic complications in hemodialysis patients. Hemodialysis patients have traditional risk factors such as abnormal lipid metabolism and uremia-related risk factors such as oxidative stress and hyperphosphatemia. Oxidative stress takes place by increased production of oxidants by leukocytes and antioxidant loss of vitamin C and E. Oxidatively modified LDL exist in the circulation by excess of oxidative stress in hemodialysis patients. Oxidative stress is a major contributor to accelerated development atherosclerosis. Oxidative stress and hyperphosphatemia also influence vascular calcification. The pattern of vascular calcification in hemodialysis patient is characterized by mineral deposition in the tunica media. It is reported that the obvious calcification in aorta and artery of the MGP knockout mouse is recognized. It is indicated that MGP has the inhibitory effect of the calcification of vessel wall. Vitamin E protects atherosclerosis and vascular calcification in hemodialysis patients. It is also important to control hyperphosphatemia for vascular calcification.

Animals↗
PubMed2004

Transcription factor Egr-1 in calcific aortic valve disease.

BACKGROUND AND AIM OF THE STUDY: Previous immunohistochemistry studies have shown that the transcription factor, Egr-1, is increased in human atherosclerotic lesions but is absent from the normal adjacent aortic wall. The hypothesis was investigated that Egr-1 is also increased in calcified heart valve cusps because of the unique presence in these tissues of proteins known to be regulated by Egr-1, such as tenascin C (TN-C). METHODS: Non-calcified and calcified human aortic valves were obtained at autopsy or from cardiac surgery. Egr-1 immunohistochemical studies were performed. The effects of Egr-1 on cellular proliferation and on mechanisms of calcification were also investigated using sheep aortic valve interstitial cell (SAVIC) cultures. Signal transduction pathways involving Egr-1 were studied with specific inhibitors. RESULTS: Immunohistochemical studies revealed that calcific aortic stenosis cusps contained a significantly higher level of Egr-1 in the spindle-shaped interstitial cells of calcified human aortic valves, but not white blood cells. By comparison, Egr-1 was detected at very low levels in the interstitial cells of non-calcified human aortic valve cusps. SAVIC cultivated on denatured versus native collagen substrates demonstrated a marked increase in Egr-1 levels (by Western blotting), and an absence of calcification in these cultures, compared to SAVIC grown on native collagen which calcified severely with little Egr-1 expression. Parallel increases in TN-C and osteopontin (OPN), both of which are proteins associated with heart valve calcification, were observed (by Western blotting) in SAVIC grown on denatured collagen. Furthermore, a protein kinase-C (PKC) inhibitor blocked the up-regulation of Egr-1 and TN-C, implicating PKC-dependent signaling control of Egr-1 and TN-C up-regulation. CONCLUSION: Egr-1 is up-regulated in human calcific aortic stenosis cusps compared to non-calcified normal cusps. Egr-1 up-regulation involves a PKC-dependent signaling pathway. TN-C and OPN appear to be co-regulated with Egr-1. Furthermore, in SAVIC cultures on denatured collagen, Egr-1 up-regulation was associated with inhibition of calcification. Taken together, these results suggest that complex Egr-1 mechanisms may be operative in calcific aortic stenosis.

Aged↗
PubMed2002

[Vascular calcification and phosphate metabolism].

Vascular calcification is often encountered in the development of atherosclerotic intimal lesions. In chronic renal failure patients, vascular calcification contributes to both the morbidity and mortality. Although the molecular mechanisms regulating vascular calcification remain obscure, recent studies suggest that vascular calcification may be an actively regulated process in which vascular cells may acquire osteoblast-like functions. Several clinical studies indicate that a high serum phosphate level is highly correlated with the extent of vascular calcification and vascular disease. In vitro studies demonstrated that inorganic phosphate regulates the expression of bone matrix proteins, and that calcification is regulated by inorganic phosphate through a sodium dependent phosphate transport system. These findings suggest that inorganic phosphate may play an important role in the development of vascular calcification.

English Abstract↗
PubMed2002

[Diabetes mellitus and vascular calcification].

Two types of arterial calcification are well recognized:intimal (atherosclerotic) and medial (Monckeberg type). These two calcifications are considered different in pathogenesis. Arterial calcification has recently been reported to be an organized, regulated process similar to bone formation. The relation of calcification to diabetes mellitus remains still unclear. EBCT can noninvasively and accurately detect coronary artery calcification. Diabetic patients seem to have increased prevalence of coronary calcification when compared with non-diabetic patients. Medial artery calcification is an independent predictor of cardiovascular mortality in diabetic patients.

English Abstract↗
PubMed2005

Prevention of porcine aortic wall calcification by acellularization: necessity for a non-glutaraldehyde-based fixation treatment.

BACKGROUND AND AIM OF THE STUDY: Acellularization prevents cell-mediated calcification of the aortic wall, but the inflammatory response towards the unfixed tissue is problematic. Two additional fixation methods, applied after tissue acellularization, were studied. METHODS: Porcine aortic wall samples were randomized into four groups: (1) Standard fixation with glutaraldehyde (GA); (2) acellularization by a combined method of enzymes (DNase, RNase) and a detergent (Triton X-100); (3) acellularization followed by standard GA fixation; (4) acellularization followed by photo-oxidation. Samples were implanted into the wall of both jugular veins of six juvenile sheep. Tissue was explanted after three months and evaluated by X-radiography, light and electron microscopy, and calcium content (cc) measurement (atomic absorption spectrometry). Auto-fluorescence of elastic fibers was used to identify the relationship between calcific deposits and elastin. RESULTS: GA-fixed aortic wall samples showed clear mineralization (cc 41.6 +/- 17.8 microg/mg), occurring predominantly at the level of cell remnants, as confirmed by electron- and fluorescence microscopy, locating calcific deposits in between elastic fibers. Acellularized aortic wall fragments were calcified significantly less, but an important (non-infectious) inflammatory response caused elastolysis and subsequent calcification of the elastic fibers (cc 5.6 +/- 2.8 microg/mg). Acellularized and GA-fixed fragments revealed important, inhomogeneously spread calcific deposits (cc 24.7 +/- 10.0 pg/mg). Photo-oxidized samples remained free from calcification (cc 0.82 +/- 1.6 microg/mg). CONCLUSION: Acellularization is a promising tool in the prevention of porcine aortic wall calcification, but additional tissue fixation is necessary to prevent structural degeneration. GA fixation after acellularization causes important inhomogeneous tissue mineralization. Photo-oxidation combines optimal tissue fixation with superior anticalcification characteristics.

Animals↗
PubMed2005

[Pathogenesis and therapy for vascular calcification in patients on chronic hemodialysis].

Vascular calcification is a common complication of end-stage renal disease (ESRD) and is likely related to the high incidence of cardiovascular disease in patients with ESRD. Vascular calcification occurs both in the vascular intima and in the tunica media. Intimal calcification is disseminated and is associated with damaged endothelium and macrophage. On the contrary, medial calcification occurs in patchy distribution and the most frequent cells types found in its vicinity are smooth muscle cells (SMC). The uremic state is associated with numerous metabolic abnormalities and endocrine disturbances primarily involving calcium and phosphorus metabolism. In addition, ESRD is considered state of active inflammatory response. These dysfunctions likely contribute to the development and progression of vascular calcification. Recent reports have shown that this is a highly regulated process governed by factors that closely resemble calcium deposition in bone tissue. Vascular calcification requires changes in the phenotype of SMC and the expression of several bone-associated proteins normally involved in bone metabolism. This review is focused on the role of phosphorus in the pathogenesis of vascular calcification and the therapeutic approaches currently available to slow its progression in patients with ESRD.

Calcinosis↗
PubMed2005

Diamine-extended glutaraldehyde- and carbodiimide crosslinks act synergistically in mitigating bioprosthetic aortic wall calcification.

BACKGROUND AND AIM OF THE STUDY: The extension of glutaraldehyde (GA) crosslinks with diamine bridges was shown previously to reduce bioprosthetic heart valve calcification to a significant degree. The aim of the present study was to investigate whether the additional crosslinking of functional carboxyl groups could augment this anticalcific effect at the low glutaraldehyde concentrations typically used in commercial heart valve production. METHODS: Entire aortic roots of medium-sized pigs were fixed after 48 h of cold storage. Crosslinking of amino-functional groups was achieved either by GA fixation alone (0.2% or 0.7%) or with an interim treatment with the diamine L-lysine (25, 50 or 100 mM; 37 degrees C; 2 days). Carboxyl groups were activated with carbodiimide (N'-{3-dimethylaminopropyl}-N-ethyl carbodiimide hydrochloride (EDC), 240 mM) and crosslinked with an oligomeric diamine (polypropylene glycol-bis-aminopropyl ether (Jeffamine), 60 mM, 230D). By permutation of treatments and combinations thereof, a total of 17 groups was compared. Aortic wall discs (12 mm diameter) were implanted subcutaneously into seven-week-old Long-Evans rats for 60 days. Tissue calcification was determined by histology and atomic absorption spectrophotometry. RESULTS: There was no significant difference in tissue calcification if either GA or carbodiimide fixation was used alone. Equally, the combined crosslinking with GA and EDC/Jeffamine did not achieve a mitigation of tissue calcification below levels seen in at least one of the two treatments alone. When commercial GA fixation was mildly diamine-enhanced with L-lysine (25 mM), additional EDC/Jeffamine crosslinking of carboxyl groups resulted in a distinct additive effect in both 0.2% (-31%; p < 0.0002) and 0.7% (-36%; p = 0.0073) GA-fixed tissue. Relative to conventional GA fixation, this combination mitigated aortic wall calcification by 43% (p < 0.0001) and 34% (p = 0.0014) in 0.2% and 0.7% GA-fixed tissue, respectively. An increase in L-lysine concentration to 100 mM further reduced calcification of 0.7% GA-fixed tissue (18.5%; p = 0.016), but had no additional effect on 0.2% GA-fixed tissue (0.6%; p = 0.463). CONCLUSION: A distinct reduction in bioprosthetic aortic wall calcification can be achieved by combining diamine-extended conventional GA fixation with a diamine-extended carbodiimide based crosslinking step.

Animals↗
PubMed2005

[Diffuse muscular calcification with subcutaneous cysts].

OBJECTIVE: Diffuse muscular calcification was rare myopathological change due to abnormal metabolism of calcium, which was mainly found in dermatomyositis and myositis ossificans progressiva. Here we reported a case of diffuse muscular calcification that clinically mimicked myositis ossificans progressiva. The disease might be a new type of congenital calcium metabolic disease. METHODS: A 15-year-old girl developed subcutaneous cysts in the wrist and ankle when she was 1 year old. At the age of 9, she developed recurrent fever with myalgia, fatigue and diffuse muscular calcification. It was difficult for her to squat, run or walk. Protuberance presented in the subcutaneous tissue of her trunk. Some nodules ruptured with outflow of chalky material. ESR, ENA, RF, CRP, PTH, CK were in normal limits. EMG was unremarkable. X-ray confirmed diffuse calcification in the muscle and subcutaneous tissues. Biceps muscle biopsy was performed. RESULTS: Numerous inflammatory cells infiltrated around vessels in the perimyosium with perifascicular muscle fiber atrophy and degeneration. Many RRF and SDH positive fibers were also observed. EM showed tubular reticular inclusions in vascular endothelium. CONCLUSION: Diffuse muscular calcification indicated existence of systemic calcium metabolic abnormality. As the clinical symptoms and distribution pattern of calcification were different from dermatomyositis with subcutaneous calcification and myositis ossificans progressiva, our case might be a new type of disease. The microvascular changes might result in the lesion of muscle fibers.

Adolescent↗
PubMed2006

Reduction of calcification of carbodiimide-processed heart valve tissue by prior blocking of amine groups with monoaldehydes.

BACKGROUND AND AIM OF THE STUDY: Failure of implanted bioprostheses due to calcification is a commonly occurring phenomenon. In order to prevent calcification, many alternative cross-linking methods to glutaraldehyde (GA) have been developed and evaluated. METHODS: In a novel approach an improved carbodiimide (EDC) cross-linking method that comprises a two-step process was developed. First, the available amine groups in (tissue) collagen were blocked with a monoaldehyde, followed by an EDC-activated cross-linking reaction of the carboxyl groups in the tissue with a poly (propylene glycol) bis 2-(amino-propyl) ether (Jeffamine). RESULTS: Samples processed via this method have shown a significantly reduced calcification in a subdermal juvenile rat model compared to samples with standard GA treatment. In the present study, heart valve tissue was blocked with various monoaldehydes, followed by reaction with Jeffamine using carbodiimide cross-linking chemistry. Leaflet calcification was almost eliminated using different aldehydes, whereas wall calcification was maximally 95% reduced when propionaldehyde was used as blocking agent, as compared to a carbodiimide cross-linked control without Jeffamine and blocked amine groups. CONCLUSION: Amine blocking and cross-linking technology appears promising in the design of the next generation of tissue valves. Calcification was significantly reduced compared to GA cross-linking. The mechanistic insight of decreased wall calcification is still unknown, and research investigations are ongoing.

Animals↗
PubMed1991

Treatment of soft tissue calcifications with magnesium.

80 patients with soft tissue calcifications were treated. 24 patients suffered from myositis ossificans traumatica, 23 from calcific bursitis (Duplay's disease), 6 from osteoarthropathy of elbow joint after severe craniocerebral trauma, 9 from calcifications round elbow joint after local trauma, 13 from calcifications round hip joint, 5 from calcifications in ligaments and tendons. About 75 per cent patients were cured. Calcifications disappeared or substantially diminished. Very good functional improvement followed in affected joints. Patients were treated with new method: local application of MgSO4 into calcification area was used for 2-20 weeks, peroral administration of Mg lactate was given for 4-6 months. There were neither complications nor side effects of this treatment.

Adolescent↗
PubMed1991

Juvenile intervertebral disc calcification: recognition, management, and pathogenesis.

Juvenile intervertebral disc calcification is an uncommon disorder of childhood, characterized by calcification of the nucleus pulposus of one or more intervertebral discs. Calcification may remain dormant or subsequently become symptomatic. The symptoms include fever, malaise, and neck pain and are associated with an elevated erythrocyte sedimentation rate and, occasionally, leukocytosis. Although disc protrusion occurs in 38% of patients, neurological signs are distinctly uncommon. We report the case of a patient with a herniated T2-T3 calcified intervertebral disc and compressive myelopathy. Juvenile intervertebral disc calcification is generally a self-limiting disease that seldom requires an operation. The symptoms are transient, and resorption of the disc calcification is the rule once symptoms occur. Neither the cause of the disc calcification nor the trigger for the onset of symptoms is known. An inflammatory response within the disc appears to give rise to clinical symptoms and is associated with eventual resorption of the disc calcification.

Calcinosis↗