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Biomedical subjects

M C Faugere

Publications and source records attributed to M C Faugere.

14 recordsLinked to original sources
PubMed1990

Bone changes occurring early after cessation of ovarian function in beagle dogs: a histomorphometric study employing sequential biopsies.

The beagle dog model has been established by our laboratory as a useful animal model to study bone loss after cessation of ovarian function. Previously we demonstrated bone loss associated with an osteoblastic insufficiency at 4 months after ovariohysterectomy (OHX). This study was designed to evaluate by four sequential monthly bone biopsies the development and course of the histologic bone abnormalities after OHX. We found cancellous bone volume, trabecular density, and wall thickness to be decreased (p less than 0.05) and trabecular separation increased (p less than 0.05) as early as 1 month after OHX. After 2 months, there was a decrease in mineralizing surface and mineral apposition rate (p less than 0.05). Volume and surface of osteoid were increased after 3 months (p less than 0.05), and there was an increase in the number of osteoblasts (p less than 0.01). No histologic signs of increased resorption were observed during the experiment. However, the findings of low bone volume with decreased trabecular density and increased separation without a change in trabecular plate thickness 4 weeks after OHX suggest that a dramatic increase in resorption must have taken place soon after OHX. These results point to an early phase of initiation of bone loss related to hyperresorption followed by a maintenance phase of low bone mass ascriblastic insufficiency. The events that stimulate the early initiating phase after cessation of ovarian function, the factors contributing to it, and the direct demonstration of hyperresorption await further studies.

Animals↗
PubMed1990

Role of calcitriol in the management of osteoporosis.

Ovariohysterectomized Beagle dogs provide a useful model for the study of bone loss following cessation of ovarian function. Data obtained in our laboratory suggest that the sequence of events occurring after cessation of such function proceeds in two phases. The first, or "initiation," phase begins within 1 month after ovariohysterectomy (OHX). Although the number of osteoclasts is unchanged, there is an increase in trabecular separation, accompanied by a dramatic decrease in cancellous bone volume, which suggests an apparent dramatic hyperresorption. This early phase is followed by a "maintenance" phase, which commences in the second month and is related to an osteoblastic insufficiency. In another experiment, administration of 1,25(OH)2D3 corrected bone loss occurring after OHX in Beagle dogs. However, a positive balance between increased bone cell activity and decreased bone cell number was not maintained. This calls for new strategies to separate the positive effect of 1,25(OH)2D3 on bone cell activity from the negative effect on bone cell number.

Animals↗
PubMed1990

Five-year postoperative results of cemented femoral arthroplasty in patients with systemic bone disease.

To determine whether bone cellular abnormality affects the results of cemented femoral arthroplasty, 21 patients had biopsies of the iliac crest and femoral cortex at the time of surgery. Roentgenographic and histomorphometric studies were used to characterize fibrous membrane formation, cancellous bone, calcar resorption, and bone turnover. Patients with high bone turnover and decreased femoral thickness and density before surgery were at risk of developing calcar resorption and cancellous diaphyses, conditions that weaken proximal stem support and lead to early failure. These findings suggest that noncemented stems may be indicated in this group. Another group, osteoporotic patients, suffered from osteoblastic insufficiency, which may be the indication for the use of cemented stems rather than noncemented stems, which require bony ingrowth.

Aged↗
PubMed1989

1,25(OH)2D3 administration in moderate renal failure: a prospective double-blind trial.

This study represents the first randomized prospective, double-blind, placebo-controlled trial of the efficacy of 1,25(OH)2D3 on bone histology and serum biochemistry in patients with mild to moderate renal failure. Sixteen patients with chronic renal impairment (creatinine clearance 20 to 59 ml per min) received either 1,25(OH)2D3, at a dose of 0.25 to 0.5 microgram daily (eight patients), or placebo. Transiliac crest bone biopsies were performed before entrance into the study and after 12 months of experimental observation. None of the patients were symptomatic or had radiological evidence of bone disease. Of the thirteen patients who completed the study, initial serum 1,25(OH)2D levels were low in seven patients and parathyroid hormone levels were elevated in seven patients. Bone histology was abnormal in all patients. 1,25(OH)2D3 treatment was associated with a significant fall in serum phosphorus and alkaline phosphatase concentrations as well as with histological evidence of an amelioration of hyperparathyroid changes. In contrast to previous reports, no deterioration of renal function attributable to the treatment occurred, perhaps because a modest dose of 1,25(OH)2D3 was employed combined with meticulous monitoring. Further investigation is required to determine whether alternative therapeutic strategies (smaller doses or intermittent therapy) may avoid the potential for suppressing bone turnover to abnormally low levels in the long term.

Adult↗
PubMed1989

Early therapy of renal bone disease with calcitriol: a prospective double-blind study.

The value of calcitriol administration in the management and prevention of renal bone disease was studied in a prospective double-blind manner in 16 patients with chronic renal impairment (creatinine clearance 20 to 59 ml per min). They were given either calcitriol at a dose of 0.25 to 0.5 micrograms daily (eight patients), or placebo. Transiliac crest bone biopsies were performed before entrance into the study and after 12 months of experimental observation. None of the patients were symptomatic or had biochemical or radiological evidence of bone disease. Of the thirteen patients who completed the study, initial serum 1,25(OH)2D levels were low in seven patients and parathyroid hormone levels were elevated in seven patients. Bone histology was abnormal in all patients. Calcitriol treatment was associated with a significant fall in serum phosphorus concentrations and alkaline phosphatase levels as well as with histological evidence of an amelioration of hyperparathyroid changes. In contrast to previous reports, no deterioration of renal function attributable to the treatment occurred, perhaps because a modest dose of calcitriol was employed combined with meticulous monitoring. Further investigation is required to determine whether alternative therapeutic strategies (smaller doses or intermittent therapy) may avoid the potential for suppressing bone turnover to abnormally low levels in the long term.

Bone Diseases↗
PubMed1987

Oxalosis in bone causing a radiographical mimicry of renal osteodystrophy.

We report a patient on maintenance dialysis with oxalosis and radiographical signs typical of hyperparathyroid bone disease in patients with end-stage renal insufficiency. The patient underwent a subtotal parathyroidectomy. Because his bone pain worsened during long-term dialytic therapy, a bone biopsy was performed and revealed crystalline deposits in trabecules and the bone marrow characteristic of oxalate. Trabecular destruction and signs of defective mineralization of bone were also found. When the diagnosis was made, the patient had become addicted to narcotic analgesics; he died from an overdose. The case underscores the limits of skeletal radiographs for the diagnosis of oxalosis in bone. Furthermore, the radiographic findings may lead to erroneous conclusions in patients with renal osteodystrophy because the radiographic signs of oxalosis can mimic those of hyperparathyroid bone disease.

Adult↗
PubMed1986

Stainable aluminum and not aluminum content reflects bone histology in dialyzed patients.

Quantitative evaluation of stainable bone aluminum and measurement of bone aluminum content were done in 55 patients on chronic maintenance dialysis. All patients underwent bone biopsies. Histomorphometry of static and dynamic parameters of bone structure, bone formation and resorption, and quantitation of stainable bone aluminum at the osteoid-bone interface were performed. In addition, bone aluminum content was measured by atomic absorption spectrophotometry. Bone aluminum content was elevated in all patients (81 +/- 9.6 vs. 18 +/- 6 micrograms/g dry wt) and stainable aluminum was found in 47% of them. All patients with predominant low-turnover osteomalacia or adynamic bone disease displayed stainable bone aluminum. In contrast, stainable bone aluminum was not present in individuals with predominant-hyperparathyroid bone disease. Patients with stainable aluminum had lower bone mass (P less than 0.05), higher volume and surface of lamellar osteoid (P less than 0.01), less volume and surface of woven osteoid (P less than 0.05 and P less than 0.01), lower osteoblastic and osteoclastic indices (P less than 0.01), less doubly labelled osteoid seams, lower mineral apposition rate and lower bone formation rates (P less than 0.05 to P less than 0.01). Stainable aluminum correlated with volume of lamellar osteoid and cellular parameters of bone formation and resorption, mineral apposition rate, and bone formation rates (P less than 0.05 to P less than 0.001). In contrast, bone aluminum content correlated with volume of lamellar osteoid only (P less than 0.001). These findings indicate that stainable aluminum at the mineralization front and not aluminum content of bone reflects the histopathologic changes found in bone of dialyzed patients.

Adult↗
PubMed1985

Infant formula as a cause of aluminium toxicity in neonatal uraemia.

Aluminium toxicity occurred in two infants with congenital uraemia who had never received phosphate binders or other aluminium-containing agents or intravenous fluids. One patient was treated by peritoneal dialysis from the age of two weeks and died at three months after the sudden onset of neurological symptoms; the other died after one month of conservative management without dialysis. Brain aluminium concentration was high in both infants (6.4 and 47 micrograms/g, respectively) whereas bone aluminium content was normal and there were no histological changes or stainable aluminium on bone biopsy specimens. Both infants were fed with 'Similac PM 60/40'. To investigate possible sources of aluminium, powdered milk formula, sterilised water used for preparation of the feed, and dialysate concentrate (first patient) were analysed. Aluminium concentration was high (232 +/- 60 ng/ml) in powdered milk but negligible in sterilised water and dialysate concentrate (4 ng/ml and 3.4 +/- 2.4 ng/ml, respectively). These findings indicate that proprietary infant milk formula is another source of aluminium. Aluminium-free milk should contribute to the prevention of aluminium toxicity in infants with renal failure.

Aluminum↗
PubMedDate not supplied

Centronuclear myopathy: possible central nervous system origin.

The authors describe a case of myopathy characterized physically by limb weakness, eyelid ptosis, voluntary and reflex paralysis of vertical movements of gaze, and loss of deep tendon reflexes; and morphologically by the abnormal presence of centrally located nuclei in muscle fibers and type 1 fiber hypotrophy. The establishment in this case study of two particular findings--the probably nuclear or supranuclear ophthalmoplegia and the apparently impaired nuclear migration from the center of the muscle fiber toward its periphery--supports the hypothesis of a neuromuscular disorder whose level of severity depends on the degree of difficulty in the nuclear migration itself. This would be linked to a reduction in central nervous system influence.

Adolescent↗
PubMedDate not supplied

Type III glycogenosis with multicore structures.

A case of an infantile type III glycogenosis (Forbes disease), confirmed by morphologic and biochemical studies, had light-microscopic, histochemical, and electron-microscopic evidence of multicore structures and type 1 fiber predominance with hypotrophy. This association is discussed with relation to the unusual clinical findings. The authors conclude that two distinct disease entities--Forbes disease and multicore myopathy--may coexist.

Adenosine Triphosphatases↗