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Calcifications of the disc of the temporomandibular joint.

Calcified lesions of the temporomandibular joint discs obtained from 135 human cadavers were studied. Calcifications were observed in 92 of 250 discs by soft x-ray radiography. Studies by light and electron microscopy and x-ray diffraction revealed that there were two different types of calcification in the discs: apatite crystal deposition with or without ossification, and calcium pyrophosphate dehydrate (CPPD) crystal deposition. Calcifications were recognized more frequently posteriorly than anteriorly, and were related to disc perforation. The results of this investigation suggest that disc degeneration, which may occur as a result of aging or mechanical stress, causes calcifications.

Aged↗

Clinicostatistical study of carotid calcification on panoramic radiographs.

OBJECTIVE: The purpose was to evaluate carotid calcifications on panoramic radiographs, and relate to risk factors for vascular diseases. METHOD: Between 1997 and 2001, 2568 radiographs were retrospectively collected from new patients at Mie University Hospital whose ages ranged from 50 to 70 years. The mean age of the subjects was 62.2 years (men 61.9 years, women 62.3 years). Medical and social data were collected from case notes, and body weight, height, and age of menopause confirmed by telephone interviews. RESULT: About 106 carotid calcifications were found on the panoramic radiographs of 26 males and 80 females. The ratio of males to females was 1:3.07. The subjects with carotid calcifications had medical histories that included hypertension (27.6%), obesity (21.1%), hyperlipidemia (14.5%), and cardiovascular diseases (13.2%), all with recognized risk factors for atheromas. Of 76 patients who responded to follow up interviews, two (2.63%) died from cardiovascular stroke during an average follow up of 2.43 years. CONCLUSIONS: The results show carotid calcifications detected on panoramic radiographs can be used to help predict vascular strokes in patients. In cases where calcified carotid artery atheromas are detected, the dentist or oral and maxillofacial surgeon should refer the patient to a specialized physician.

Aged↗

Peters' anomaly with bilateral perisylvian polymicrogyria and abdominal calcification.

We report a neonatal case of Peters' anomaly with bilateral perisylvian polymicrogyria and abdominal calcification. The male infant was born after a normal labor. Bilateral central corneal opacities with iridocorneal strands indicated Peters' anomaly. The X-ray and abdominal computed tomography demonstrated multiple calcifications beneath the diaphragma around the liver and the spleen. TORCH serology was negative. Intracranial calcification was not detected. Brain magnetic resonance imaging demonstrated bilateral perisylvian polymicrogyria. Abdominal calcification was suspected to be related to vascular disruption. Bilateral perisylvian polymicrogyria has been thought to result from ischemic events such as intrauterine hypotension or vascular occlusions. Based on these considerations, we conclude that a vascular disruption sequence may an important pathogenetic mechanism of Peters' anomaly.

Abdomen↗

Cardiovascular calcification in patients with end-stage renal disease.

Vascular calcifications are very frequent extraosseous calcifications in patients with chronic renal disease. They occur in the intima and in the media. They are associated with decreased arterial elasticity and increased mortality. The risk factors are: advanced age, duration of dialysis treatment, diabetes, increased phosphate concentration, the dose of Ca-containing phosphate binders and inflammation. It is now well established that vascular smooth muscle cells actively take up phosphate to form bioapatite. This process is associated with a phenotypic transformation of vascular smooth muscle cells during which they express osteoblast markers. Lipids and inflammatory cytokines also increase bioapatite formation. Calcification inhibitors are matrix Gla protein and fetuin-A. Decreased serum fetuin-A concentration is associated with a higher mortality rate in dialysis patients. An important preventive measure for vascular calcification is the substitution of Ca-containing by non-Ca-containing phosphate binders.

Calcinosis↗

Computed tomography detection of a cerebral calcific embolus following coronary catheterization.

A 77-year-old man underwent coronary artery angiography quite well. However, several attempts were required to pass the pigtail catheter across a calcified stenotic aortic valve. On return to the floor, motor aphasia and right hemiparesis developed and improved steadily within a few days. Computed tomography (CT) of the head revealed a calcific density in the left middle cerebral artery. The authors believe the calcific plaque originated from the calcified aorta and aortic valve. The patient was discharged within 48 hours with minimal neurological signs. Spontaneous calcified emboli to cranial vessels from calcific aortic stenosis or other sources are rare. CT detection of a calcific plaque in a cranial vessel following coronary vessel catheterization is well documented in this patient.

Aged↗

Calcific shoulder periarthritis (tendinitis) in adult onset diabetes mellitus: a controlled study.

Two groups, one of 824 adult diabetics and one of 320 age and sex matched non-diabetics, were examined for abnormal glucose metabolism and calcifications on anteroposterior shoulder x rays. Two hundred and sixty two (31.8%) of the diabetics had shoulder calcification compared with 33 (10.3%) of the control group, with a preponderant localisation in the right shoulder. Diabetes of long duration treated with insulin for a long time was associated with a larger percentage of shoulder calcifications. These data and previous laboratory findings suggest a possible pathogenetic correlation between the prevalence of calcific shoulder tendinitis and diabetes.

Adult↗

Scleral and choroidal calcifications in a patient with pseudohypoparathyroidism.

This case report suggests that calcifications in the sclera and choroid may be a feature of pseudohypoparathyroidism and shows a calcium distribution more extensive and severe than that characteristically seen in other metabolic conditions associated with calcium deposits in the eye. Ocular ectopic calcification is a part of the more generalised ectopic soft tissue calcification seen with pseudohypoparathyroidism. Evaluation of the contribution of the terminal renal failure and uraemia to the ectopic ocular calcification would require sequential evaluation of eyes with pseudohypoparathyroidism, but without the added complication of uraemia.

Adult↗

Medial arterial calcification and diabetic neuropathy.

X-ray examinations of the feet, knees, and hands were performed on 20 diabetics with severe neuropathy and 20 diabetics with no evidence of neuropathy but with a similar mean age and duration of diabetes. All were under 53 years old with no clinical evidence of peripheral vascular disease. Medial arterial calcification was much more common and extensive in the patients with neuropathy, occurring in the feet in 15 and in the hands in eight compared with in four (p less than 0.001) and none (p less than 0.001) of the controls respectively. Although there was some correlation between calcification and both proteinuria (p less than 0.05) and proliferative retinopathy (p less than 0.02), the association between calcification and neuropathy (p less than 0.001) was much stronger. Neuropathy, with sympathetic denervation of the smooth muscle of the tunica media, may be important in the aetiology of medial arterial calcification.

Adult↗

Renal calcification in preterm infants: follow up at 4-5 years.

AIM: To determine the consequences of renal calcification in preterm infants. METHODS: A cohort of 11 preterm babies was studied at the age of 4 to 5 years. They had had renal calcification as neonates. Seventeen matched controls were also studied. Each child had a renal ultrasound scan, a calcium load test, and a desmopressin test for renal concentrating ability (RCA). The study group also had glomerular filtration rate (GFR) estimated, using the height:creatinine ratio, and tubular phosphate reabsorption, without phosphate load, per glomerular filtration rate (Tp/GFR) calculated, RESULTS: In the study group the median GFR was 61 ml/min/1.73m2 (range 46-79 ml/min/1.73m2) and the median calculated Tp/GFR SD score was -0.94 (range -2.8-0.68). Five children out of the study group had ultrasonic evidence of renal calcification. There was no significant difference between the two groups in renal size, calciuria, before or after calcium load, or RCA. Eight children (three patients, five controls) had an abnormal calcium load test. The RCA of the children in the study and control groups combined was below that of published values, with a median calculated SD score -0.71 (95% CI -1.21 to -0.23). CONCLUSIONS: There was evidence of renal dysfunction in children who had been born preterm. Renal calcification detected in the neonatal period does not seem to be a major predisposing factor for the abnormalities of renal function subsequently observed in these infants.

Calcinosis↗

Papillary muscle calcification after inferoposterior myocardial infarction.

Extensive papillary muscle calcification is quite a rare finding in echocardiographic examinations. A case of a 71 year old man with isolated calcification of the papillary muscles, detected by fluoroscopy and confirmed by echocardiography, is presented. Intracardiac calcifications in patients with prior right coronary artery occlusion and mitral regurgitation should suggest the possibility of posteromedial papillary muscle calcification and dysfunction.

Aged↗

Coronary calcifications in young patients with first, unheralded myocardial infarction: a risk factor matched analysis by electron beam tomography.

OBJECTIVE: To compare the presence and extent of coronary calcifications in young patients with first, unheralded acute myocardial infarction with matched controls without a history of coronary artery disease. METHODS: In 102 patients under 60 years of age (19-59 years, mean 41 years; 88% male), electron beam tomography was done 1-14 days after acute myocardial infarction, before any coronary intervention. Coronary calcifications were quantified using the Agatston score. Age related calcium centiles were determined based on the Mayo Clinic "epidemiology of coronary calcification" study, and results were compared with a group of 102 controls without coronary artery disease, matched for sex, age, and risk factors. RESULTS: Calcifications were present in 95.1% of patients with acute myocardial infarction and in 59.1% of controls (p = 0.008). The mean (SD) Agatston score was 529 (901) in the infarct patients versus 119 (213) in the controls (p < 0.001). An Agatston score above the 50th centile was present in 87.2% of infarct patients and 47.0% of controls (p = 0.006), and above the 90th centile in 60.7% of infarct patients and only 5.8% of controls (p = 0.001). CONCLUSIONS: In young patients with their first, unheralded acute myocardial infarction, the presence and extent of coronary calcium are significantly greater than in matched controls.

Adult↗

Calcific retinal embolism as an indicator of severe unrecognised cardiovascular disease.

OBJECTIVE: To describe the association between calcific retinal embolism (CRE) and cardiac valve stenosis. DESIGN AND SETTING: Retrospective chart review of patients with clinical criteria for CRE. PATIENTS: 24 patients with CRE who underwent two dimensional echocardiography between 1976 and 1998. RESULTS: Nine patients (38%) had calcific valve stenosis, which was haemodynamically severe in five patients (four aortic and one mitral), four of whom had no cardiac symptoms. Six patients underwent surgical intervention (aortic valve replacement in three patients, mitral and aortic valve replacement in one patient, removal of calcific cardiac pseudotumour in one patient, and carotid endarterectomy in one patient). CONCLUSIONS: CRE may be the presenting feature of otherwise asymptomatic, clinically important underlying cardiovascular disease and, in particular, haemodynamically severe calcific valve stenosis.

Adult↗

Visual disturbances representing occipital lobe epilepsy in patients with cerebral calcifications and coeliac disease: a case series.

Paroxysmal visual manifestations may represent epileptic seizures arising from the occipital lobe. In coeliac disease (CD) bilateral occipital calcifications and seizure semiology consistent with an occipital origin have been described, primarily in Mediterranean countries. By reporting three adult patients from an Australian outpatient clinic with visual disturbances, occipital cerebral calcifications, and CD, this study seeks to emphasise that CD should be considered even when patients of non-Mediterranean origin present with these symptoms. Seizure types included simple partial, complex-partial, and secondarily generalised seizures. The seizure semiology consisted of visual disturbances such as: blurred vision, loss of focus, seeing coloured dots, and brief stereotyped complex visual hallucinations like seeing unfamiliar faces or scenes. Symptoms of malabsorption were not always present. Neurological examination was unremarkable in two patients, impaired dexterity and mild hemiatrophy on the left was noted in one. Routine electroencephalography was unremarkable. In all cases, computed tomography demonstrated bilateral cortical calcification of the occipital-parietal regions. Magnetic resonance imaging showed no additional lesion. All patients had biopsy confirmed CD. Seizure control improved after treatment with gluten free diet and anticonvulsants. This report illustrates the association between seizures of occipital origin, cerebral calcifications, and CD even in patients not of Mediterranean origin.

Adult↗

Bilateral basal ganglia calcifications visualised on CT scan.

Thirty-eight cases of basal ganglia calcification imaged on computed axial tomography were reviewed. Most cases were felt to represent senescent calcification. The possibility of a vascular aetiology in this group is discussed. A less common group of patients was identified with calcification secondary to abnormalities in calcium metabolism or radiation therapy. Three cases of basal ganglia calcifications were detected in juvenile epileptic patients receiving chronic anticonvulsants. These cases may be related to abnormalities in calcium metabolism and alkaline phosphatase activity. Clinical evidence of basal ganglia abnormality was generally absent demonstrating the preservation of neuronal pathways in most cases.

Adolescent↗

The significance of the incidental finding of basal ganglia calcification on computed tomography.

Basal ganglia calcification was found as an incidental finding in 42 out of 7000 patients who underwent computed tomography. The calcification showed on plain skull radiography when the maximum density on computed tomography exceeded 100 Hounsfield units. The 26 patients with basal ganglia calcification detected on computed tomography who were available for follow-up, were investigated with matched controls. No clinical features of basal ganglia calcification were noted. Twenty-four patients had no significant metabolic abnormality and two patients had parathyroid disorder identified.

Basal Ganglia Diseases↗

Basal ganglia calcification in Down's syndrome.

The basal ganglia from 33 patients (all over one year of age) with Down's syndrome were examined pathologically. Forty-five per cent had calcification. Basal ganglia calcification was localised to a constant area of globus pallidus and became more prominent with increased age. Calcification and amyloid degeneration of the adjacent blood vessels were present. The proximity of abnormal blood vessels to basal ganglia calcification suggests a pathogenetic relationship.

Adolescent↗

Calcification in polycystic disease.

Two patients with polycystic disease demonstrated extensive calcification in the kidneys, liver, and spleen. Though flecks of calcium have been noted in the walls of such cysts, to the authors' knowledge, curvillinear, arcuate, and central amorphous calcifications have not been previously reported. Dystrophic calcifications may be diagnosed solely on the basis on polycystic disease with superimposed hemorrhage and infection. Polycystic disease should be included in the differential diagnosis of abdominal calcifications.

Calcinosis↗

Pancreatic calcifications in malignant islet cell tumors.

Of 623 cases of malignant pancreatic tumor seen at University of Chicago hospitals over the last 30 years, 23 cases of malignant islet cell tumor were found (8 additional cases were found in the literature). Calcification, found in 2 of these cases, was characteristically discrete and nodular (calcifications found in chronic pancreatitis are typically diffuse, multiple, and punctuate). At least 7 of the 10 cases of islet cell tumor with calcification were malignant. Slow growth of the tumor, with calcified metastases, strongly suggests the diagnosis of malignancy; this combination of findings has been established in 3 cases. In 73 cases of benign islet cell tumor, no calcifications were found.

Adenoma, Islet Cell↗