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Biomedical subjects

M Silbermann

Publications and source records attributed to M Silbermann.

At least 163 records · Page 9Linked to original sources
PubMed1978

Mechanisms involved in mandibular condylopathy secondary to intraarticular injections of glucocorticoids.

Pharmacologic doses of triamcinolone hexacetonide were injected intramuscularly or intraarticularly in immature Papio papio baboons. The mandibular condyle served as a model for histologic examinations concerning the effect of glucocorticoid hormone on cartilage and bone. Biochemical examinations of blood and urine indicated the development of distinct hypophosphatemia, hypercalcemia followed by hyperphosphaturia, and hypocalciuria. Serum alkaline phosphatase activity rose during the initial phases of the experiment but decreased considerably after the sixth injection of the hormone. Hyperglycemia and an increase in serum amylase were noticed along with signs of moderate metabolic acidosis. Histologic examinations disclosed signs of severe destruction of cartilage and bone. By the sixth intraarticular injection, definite fibrillation was noted in the articular cartilage, followed by complete disappearance of cartilage. The subchondral bone appeared to be adversely affected by the hormone as it lost its typical lamellar organization and attained the characteristics of woven bone. The condyle showed clear signs of fibro-osseous transformation, with fibrosis as the dominant structural feature. The preceding biochemical and morphologic findings are indicative of parathyroid hyperactivity.

Animals↗
PubMed1978

An electron microscopic study of the premineralizing zone of the condylar cartilage of the mouse mandible.

The mandibular condylar cartilage of young ICR mice was used for ultrastructural studies with special emphasis on the cells and matrix in the premineralizing zone. It became evident that cytodifferentiation of chondroblasts was accompanied by deposition of intracellular lakes of glycogen, followed within the premineralizing hypertrophic chondrocytes by a gradual reduction in the glycogen content of the lakes and its replacement by lipid-like droplets. The premineralizing condylar cartilage, like that of other cartilage involved in mineralization, showed numerous matrix vesicles (Types I and II) unassociated with appreciable amounts of collagen.

Animals↗
PubMed1978

Ultrastructure of parathyroid glands in triamcinolone-treated mice.

6 weeks old ICR strain mice were given 21 daily injections of the synthetic glucocorticoid, triamcinolone diacetate (8 mg/kg body weight) and their parathyroid glands were examined by light and electron microscopy and compared with untreated litter-mate controls. Parathyroid glands are composed of a single basic cell type, but some cells are electron-dense ('dark' cells) and some less dense ('light' cells). There is considerable variability in numbers of light and dark cells from gland to gland. Following triamcinolone treatment the cells are arranged more in whorls, and there is a relative increase in the numbers of 'light' cells, which become more elongated, with pronounced nucleoli, and develop in many cases marked cytoplamsic vacuolation. Some cells show accumulations of lipid droplets. Interdigitations between adjacent cells become more complex, and the numbers of atrophic cells increase. The significance of the various cell conditions is considered. The ultrastructural appearances suggest that parathyroid gland cellular activity is stimulated in response to the drug-induced hypercorticoidism, but no overall glandular hypertrophy is found.

Animals↗
PubMed1977

Corticosteroid-induced changes in glucose metabolism of chondrocytes.

Immature mice were treated for up to 12 weeks with daily doses of triamcinolone diacetate. Using quantitative histochemical methods, the proximal epiphyseal plate of the humerus was studied at regular intervals. By the tenth injection significant decrease was noted in the acid glycosaminoglycans content (25%) and in the neutral mucopolysaccharides (30%). Concomitantly, a marked increase was noted in the intracellular depots of glycogen (70%). It is suggested that the hormone's antiglycolytic effect in cartilage caused the glucose metabolic pathway to divert in the direction of glycogen synthesis, and thereby interfered with the normal synthetic pathway of the chondrocytes. The hormone's primary effect on the cells' hexose metabolism could be responsible, at least in part, for its inhibitory influence on bone growth.

Animals↗
PubMed1977

Triamcinolone-induced wasting disease in young mice.

Young mice were treated for up to 8 weeks with daily graded doses of triamcinolone diacetate. The body weights of treated, placebo and nontreated animals were measured daily throughout the experimental period, calculated and analysed. By the first injections, significant decrease was noted in the body weight of all experimental mice regardless of their sex or initial bodyweight. The latter was followed by a so-called 'steady state' which longed for approximately 4 weeks. Marked deterioration and mortality also occurred but became severe from the fifth week of triamcinolone administration. Possible explanations for the above findings are discussed.

Animals↗
PubMed1977

Age-related changes in the cellular population of the growth plate of normal mouse.

Age-related changes in the number of cartilage cells within the proximal growth plate of the humerus were determined in normal ICR male mice. The rates of reduction in the number of proliferative and hypertrophic chondrocytes were calculated and compared during the animals' first 6 months of life. It was found that during the period of highest growth activity, between weanling and sexual maturation, the rate of cell production is hardly decreased, thus maintaining the thickness of the cartilaginous growth plate and thereby enabling an extensive bone growth. A close correlation was found between the following skeletal activities: decrease in longitudinal bone growth, narrowing of the epiphyseal growth plate and a decrease in the proliferative activity of young chondrocytes.

Age Factors↗
PubMed1977

Observations on the growth of the normal male mouse.

The pattern of body weight gain, the longitudinal growth of the humerus and the changes in the width of its proximal growth plate were determined in normal ICR male mice. The respective growth rates were calculated and compared throughout the animals' first year of life. It was found that the overall growth period can be divided into four phases which differ markedly in their growth rate. Whereas skeletal maturation is reached at the age of 20 weeks, the animals' body weight continues to increase up to the end of the 52nd week. The humeral growth plate retains its existence and function until old age is reached, i.e. 15 months. During the period of highest growth activity extending between weanling and sexual maturation, the growth velocities of the various parameters do no coincide.

Age Factors↗
PubMed1977

Quantitative changes in the cellular population of the growth plate of triamcinolone-treated mice.

Triamcinolone-induced changes in the number of cartilage within the proximal growth plate of the humerus were determined in ICR male mice. It was found that pharmacological doses of corticosteroid hormone possess a direct inhibitory effect upon the proliferative activity of young cartilage cells and thereby adversely affect the growth potential of this growth center. Concomitantly, the activity of chondroclasts also appears to be depressed, thus resulting in a decreased rate of cartilage reorption followed by a slight increase in the number of hypertrophic chondrocytes. It therefore appears that systemic treatment with corticosteroid hormones inhibits the renewal of cartilage cells in the epiphyseal plate, leading to an accelerated 'aging' of this growth center with subsequent impairment of long bone growth.

Animals↗
PubMed1977

Effects of corticosteroid hormone on the epiphyseal growth center of immature pregnant mice.

Immature pregnant mice treated with glucocorticoid hormone (triamcinolone hexacetonide) were killed 1 week following delivery. The epiphyseal growth plates of the humerus and their cellular constituents were analyzed quantitatively. It became evident that pregnancy per se evokes a marked suppressive effect upon young cartilage cells, thus interfering with the normal process of endochondral bone formation. Pregnant mice treated with glucocorticoid hormone experienced an even higher degree of chondrocytic derangement, however, to a lesser extent than chondroxytes of nonpregnant mice treated with the hormone. It therefore appears that pregnancy-induced elevation of systemic estrogens and progesterone provides some kind of a protection against the antianabolic activity of glucocorticoids upon chondrocytes.

Adrenal Cortex Hormones↗
PubMed1977

Cortical bone loss in triamcinolone-treated mice.

Immature mice were treated for up to 8 weeks with daily doses of triamcinolone diacetate. The humerus was studied radiographically at regular intervals. Roentgenographic measurements included midshaft width, medullary width, cortical thickness and total length. By the time of the tenth injection significant cortical bone loss was noted, followed by increased width of the medullary cavity and osteoporosis. An initial phase of active endosteal bone resorption was replaced by a prolonged steady state which extended throughout the experimental period. Possible explanations for the above findings are discussed.

Animals↗
PubMed1976

Triamcinolone-induced systemic infections in female mice.

Six-week-old female mice were injected for prolonged periods of time with a synthetic glucocorticoid (triamcinolone diacetate). With the progression of the experiment the mortality rate increased significantly. Tissue samples were obtained from the surviving animals after 10, 22, 35 and 45 consecutive daily injections. Cultures were obtained from kidney and liver homogenates as well as from blood samples. Quantitative measurements indicated severe renal and hepatic infections which were followed by bactoeremia. The prevalent organisms in all cultures were enterobacteriae such as E. coli, Klebsiella, Pseudomonas and Streptococcus fecalis. Placebo-control animals which received daily injections of the vehicle revealed a moderate, transient infection.

Animals↗
PubMed1976

Experimentally induced osteoarthrosis in the temporomandibular joint of the mouse.

(1) 6-week-old ICR mice were injected daily with pharmacologic doses of triamcinolone diacetate (1.5 mg/kg body weight) for 8 consecutive weeks. (2) The temporomandibular joint served as a model for histological and histochemical examinations concerning the effect of glucocorticoid hormone upon bone and cartilage. (3) Histochemical reactions indicated a large number of lipid droplets within the peripheral vasculature. (4) Histological examinations revealed pathologic features, indicative of primary osteoarthrosis.

Animals↗
PubMed1976

Effect of triamcinolone on the ultrastructure of mouse hepatocytes.

Premature female mice were injected daily with 1.5 mg/kg body weight of triamcinolone diacetate for 10 and 21 consecutive days. Electron-microscopic study of hepatocytes indicated the formation of 'giant' mitochondria concomitant with a marked increase in the number and size of lipid droplets. Hypertrophied mitochondria and enlarged lipid droplets were found to be in a close topographical association. The mechanism of mitochondrial enlargement is discussed as well as the latters' role in the hepatocytes' lipid metabolism.

Animals↗
PubMed1976

Effect of long-term hyperglucocorticoidism on the neuronal morphology of the trigeminal ganglion of the mouse.

Immature mice were treated for up to 12 weeks with daily doses of triamcinolone diacetate. The trigeminal ganglion was studied histologically at regular intervals. By the tenth injection significant morphological changes were noted in the various nerve cells, followed by marked cellular deterioration in the form of lysis or pyknosis. A possible explanation for the above findings is discussed.

Animals↗
PubMed1976

Retardation of bone growth in triamcinolone-treated mice.

Immature mice were treated for up to 8 weeks with daily doses of triamcinolone diacetate. The epiphyseal cartilage plate and its surrounding bone from the humeral head were studied histologically at regular intervals. Concomitantly, roentgenographic measurements were performed on the humeri in toto. By the tenth injection significant morphological changes were noted in the cartilaginous plate, followed by complete cessation of bone growth. Severe triglyceride accumulation appeared in the experimental livers and humeral bone marrow. Osteoporosis also occurred and became severe from the fifth week of triamcinolone administration. Possible explanations for the above findings are discussed.

Animals↗
PubMed1975

Mandibular actinomycosis: report of case.

A case of mandibular actinomycosis, secondary to a compound fracture in an alcoholic patient, is described. The factors that apparently enhance the development of this disease are discussed.

Actinomyces↗