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Biomedical subjects

M Silbermann

Publications and source records attributed to M Silbermann.

At least 145 records · Page 8Linked to original sources
PubMed1981

Retardative effects of a corticosteroid hormone upon chondrocyte growth in the mandibular condyle of neonatal mice.

This study examined the influence of triamcinolone hexacetonide, a long-acting synthetic analog of cortisol on the proliferative activity and subsequent development of chondroprogenitor cells in condylar cartilage of neonatal mice. It became evident that a single injection of relatively low doses of the hormone significantly reduced the uptake and incorporation of [3H]thymidine followed by a significant decrease in the number of young cartilage cells. A unique feature was the fact that at the same time condyles of triamcinolone-treated mice revealed an increase in the number of mesenchyme-like cells within the condylar chondroprogenitor zone. High values of correlation were noted between the inhibitory effects of the hormone upon the incorporation of [3H]thymidine, the number of mitotic figures (within the chondroprogenitor zone), and the dimension of the chondroblastic zone. This study indicates that in young animals fluorinated corticosteroid hormones possess a significant bivalent inhibitory effect upon both the proliferative activity of chondroprogenitor cells as well as upon capacity of the latter cells to differentiate into chondroblasts. In so doing, corticosteroids adversely affect the normal process of endochondral bone formation in one of the prominent growth centers within the craniofacial skeleton. Thus, in the developing animal, corticosteroids impair the growing mandible from expressing its inherent morphogenetic pattern.

Adrenal Cortex Hormones↗
PubMed1980

Masseter myopathy following systemic corticosteroid administration: an experimental study.

Immature A/J mice were treated with a series of alternate (every 4 days) doses of triamcinolone hexacetonide, a long-acting synthetic analogue of cortisol, and their masseter muscles were studied ultrastructurally. Various degrees of degenerative changes were found in most myofibers of triamcinolone-treated animals. These changes ranged from local alterations in the configuration of the Z discs to a complete disarray of the myofibrilar architecture. Severely affected myofibers revealed areas with total disintegration of myofilaments, loss of mitochondria, and an almost total depletion of glycogen. In addition, some nuclei were centrally located and an obvious enhancement of collagen fibrillogenesis was found in the endomysial spaces. The latter comprised a mixture of banded collagen fibrils and slender filaments which lacked any specific orientation of organization. Endothelial cells of intramuscular capillaries were hypertrophic, thus evoking a marked occlusion of the vascular lumen. Ultrastructural changes were also noted in axon terminals and in the sole-plate sarcoplasm: loss of synaptic vesicles along with shrinkage of axon terminals, partial loss of postsynaptic folds, and a decrease in the number of mitochondria within the sole-plate sarcoplasm. It is proposed that triamcinolone, even if administered on an alternate schedule, promotes myopathic changes in the masseter muscles of immature mice which, in turn, might possibly contribute to the hormone-retardive effect upon the growth potential of the developing mandible.

Animals↗
PubMed1980

Fine structure of the parathyroid glands in baboons, Papio hamadryas in response to experimental hypercorticoidism.

Female baboons maintained under laboratory conditions were subjected to a series of 10 weekly injections (4 mg/kg body weight) of the synthetic glucocorticoid, triamcinolone hexacetonide. In response to the treatment, serum immunoreactive parathyroid hormone (PTH) levels were raised, though blood calcium levels remained within normal physiological limits. Light and electron-microscopic studies were made on the parathyroid glands at the end of the experimental period. The baboon parathyroid glands were composed of 'light' and 'dark' forms of the chief cells in varying ratios from gland to gland even within a single animal. Glucocorticoid-induced parathyroid hyperactivity as measured by circulating PTH levels was not accompanied by cellular hypertrophy, though there was an increase in the relative number of 'light' cells. At the ultrastructural level, after treatment, many of the 'light' cells were found to contain more free ribosomes, larger profiles of granular endoplasmic reticulum and had better developed mitochondria. Interdigitations between adjacent chief cells were more complex in treated glands. Apart from these features, chief cells of treated glands were basically similar to those of untreated controls. Our study showed that functional parathyroid hyperactivity in baboons is not necessarily accompanied by significant ultrastructural changes in chief cells.

Animals↗
PubMed1980

Reversibility of systemic corticosteroid-induced mandibular osteoarthritis: an experimental study in A/J mice.

Immature A/J mice were treated for up to seven weeks with intermittent systemic doses of triamcinolone hexacetonide (4 mg/kg body weight) and were than allowed to recover for seven weeks. Morphological studies were performed on the mandibular condylar cortilage of treated and control animals. By the third dose, obvious structural changes were seen within the cartilaginous matrix. The latter appeared first in the midst of the condylar cartilage and, in the more severe cases, also involved the articular surface. The hormonal catabolic influence intensified progessively so that by the end of the experimental period, most condyles had undergone severe degenerative changes in the form of cartilage fibrillation and ulceration. After the recovery period, experimental condyles had regained their normal appearance. Thus, although intermittent systemic administration of corticosteroid hormone tends to induce osteoarthritic changes in the mandibular joint of the mouse, the mice possess the capacity to undergo full recovery shortly after the termination of the hormonal treatment.

Animals↗
PubMed1980

Steroid-induced ultrastructural changes in the proximal convoluted tubule cells of baboon kidneys with special reference to peroxisomes.

An electron microscopic study was performed on kidneys of immature female baboons, Papio hamadryas, that received a series of 10 consecutive weekly injections of the synthetic glucocorticoid, Triamcinolone hexacetonide (4 mg/kg body wt). In the steroid-treated kidneys the most distinctive change found is a significant increase in the number and a marked change in the form of peroxisomes (microbodies) in proximal convoluted tubule cells. These cells also develop hypertrophic mitochondria and in some instances mitochondrial hyperplasia is present to such a degree as to lead to the formation of "oxyphil-like" mitochondrion-rich cells, containing degenerating nuclei. Many proximal cells also develop large secondary lysosomes packed with fibrous contents. Our results indicate a morphological response in proximal tubule cells caused by the corticosteroid-treatment, though the responses seen may possibly be also due to the development of a secondary hyperparathyroidism.

Animals↗
PubMed1979

Long bone growth during prolonged intermittent corticosteroid treatment and subsequent rehabilitation.

Immature A/J mice were treated for up to 7 weeks intermittent doses of triamcinolone hexacetonide and were thereafter allowed to recover for 7 weeks. Qualitative and quantitative morphological measurements were performed on the epiphyseal cartilage plate and diaphyseal bone of the humerus. By the third injection significant structural changes were noted in the cartilaginous tissue followed by a complete cessation of bone growth. The hormonal inhibitory effect on long bone growth lasted throughout the experimental period. However, at the end of the recovery period the length of the humerus was 96% of the normal. In contrast, the humeral width at midshaft and the width of its medullary cavity revealed slower recovery, achieving only 80% of the control values. Following rehabilitation, the growth of experimental epiphyseal plates exceeded that of nontreated animals as their width and the number of hypertrophic chondrocytes were 131% and 125% of their controls respectively. Thus, in A/J mice (a highly susceptible inbred strain of mice) intermittent (every four days) administration of a long-acting corticosteroid hormone arrested endochondral and periosteal bone formation; the former, however, underwent full recovery following the termination of the hormonal treatment.

Animals↗
PubMed1979

Mandibular growth retardation in corticosteroid-treated juvenile mice.

Juvenile mice were treated for up to eight weeks with weekly doses of a synthetic analogue of cortisol:triamcinolone hexacetonide. The mandibular condylar cartilage was studied histologically and histochemically at regular intervals. Morphometric measurements were performed along the mandibular posterior vertical dimension (condylar process and ramus). By the second injection significant morphological changes were noted in the condylar cartilage, followed by retardation of bone growth. The most distinctive feature in the cartilage of triamcinolone-treated mice was a marked increase in the dimension of its mineralized zone concomitant with a significant increase in the number of hypertrophic chondrocytes. The role of condylar cartilage in mandibular growth is discussed.

Animals↗
PubMed1979

Skeletal changes in the condylar cartilage of the neonate mouse mandible.

Histological and histochemical qualitative and quantitative determinations are provided concerning the skeletal changes taking place in the growth center of the mandibular condyle in the neonatal ICR mouse. This study followed the changes in both the major matrical components (collagen, acidic glycosaminoglycans and glycolipids) as well as in the various cartilage cells throughout the maturational period of the neonatal condyle. It was found that the transformation of neonatal condylar cartilage to its mature form involved a significant decrease in its acid glycosaminoglycan content concomitant with a rapid increase in its collagen content. In addition, significant quantitative changes were found within the zone of hypertrophic chondrocytes. The period of highest growth activity along the mandibular posterior vertical dimension (ramus) was between birth and weanling 3rd postnatal week). At this time interval, the adaptive abilities of the growing condyle appeared maximal. A high degree of correlation was noted between the overall reduction in the height of the condylar cartilage and that of its hypertrophic zone. Further, the increase in the ramal height was highly correlated with the structural changes characteristic of the neonatal condyle.

Age Factors↗
PubMed1979

Late effects of corticosteroid treatment on condylar regeneration in the monkey.

The mandibular condyles of immature baboons were used to study the late effects of intraarticular administration of glucocorticoid hormone on the regeneration of cartilage and bone. Analyses of blood and urine showed a distinct increase in the level of parathyroid hormone along with hyperphosphaturia. Regenerated condyles of animals treated with steroid showed lack of de novo formation of cartilage and severe changes in the newly formed bone. Fibrosis became the dominant feature in the newly formed bone marrow. The initial catabolic effect of glucocorticoid hormone was augmented by steroid-induced secondary hyperparathyroidism.

Animals↗
PubMed1979

Corticosteroid-induced mandibular growth retardation and palatal malformation in the ICR mouse fetus.

Pregnant ICR mice were treated with triamcinolone hexacetonide at various stages of gestation. The mandibular ramus and its condylar cartilage were studied histologically in both viable and non-viable offspring. In addition, measurements were made of the overall height of the posterior vertical dimension of the mandible and of condylar height and width. Significant changes were noted in these parameters. Concomitantly, marked changes were observed in the various zones of the condylar cartilage. A very high incidence of cleft palate was noted in newborn and stillborn mice previously treated with triamcinolone. A possible correlation between mandibular growth retardation and palatal clefting is discussed.

Abnormalities, Drug-Induced↗
PubMed1979

Age-related degenerative changes in the mouse mandibular joint.

The mandibular joints of ageing male ICR mice were studied by light and electron microscopy. A high incidence of degenerative joint disease was found relatively early in adult life, osteoarthrosis being evident by the seventh month. Initially the pathological changes were those of chondromalacia confined to isolated foci on the articular surface of the condylar cartilage. Later, characteristic signs of osteoarthrosis were noted, namely fibrillation, fibrous ankylosis, lipping and subchondral osteosclerosis. Ultrastructural examination indicated a marked heterogeneity in the articular lesions. Deep fissures and extensive cracks spread to the underlying matrix, and these were associated with severe alterations in its macromolecular structure. It is proposed that ageing chondrocytes produce a matrix which is increasingly incapable of withstanding normal mechanical forces, and this leads to the morphological changes recognized first as chondromalacia and then as osteoarthrosis.

Aging↗
PubMed1979

Effect of glucocorticoid hormone on the content and synthesis of nucleic acids in cartilage of growing mice.

Glucocorticoid hormones are known to exert distinct inhibitory effects upon skeletal growth. This study examined the influence of triamcinolone hexacetonide, a long-acting synthetic analogue of cortisol, on nucleic acid synthesis in condylar cartilage of neonatal mice. It became evident that following a single injection of the hormone the DNA, RNA and protein contents were significantly reduced. The hormone inhibited both the uptake and incorporation of 3H-thymidine and 3H-uridine into DNA and RNA. Significant changes became apparent by 24 hours and persisted for 72 hours after administering the hormone. Thereafter full recovery was noted. Correlative relationship was noted between the inhibitory effects on the uptake and the subsequent incorporation of the above precursors into their respective nucleic acids. This study clearly indicates that corticosteroid hormones possess a significant inhibitory effect on the proliferative activity of neonatal chondrocytes and upon the latter's protein synthetic pathways, thereby affecting the normal process of endochondral bone growth.

Animals↗
PubMed1978

Erythrocytes within pancreatic B-cells of corticosteroid-treated mice.

An ultrastructural study of the endocrine pancreas of female ICR mice that received 21 daily injections of the synthetic glucocorticoid, Triamcinolone diacetate (8 mg/kg b.wt) revealed some examples of microhaemorrhage within islets of Langerhans, extravasation of erythrocytes, and the presence of erythrocytes within B-cells, where they undergo degradation to form myelin-like configurations.

Animals↗
PubMed1978

Glucocorticoid-induced alterations in collagen of neonatal mouse condylar cartilage.

Neonatal mice were treated with a single dose of triamcinolone hexacetonide, a long-acting synthetic analogue of cortisol, and their mandibular condyles were studied ultrastructurally ten days thereafter. A pronounced decrease in the number and size of matrix granules (proteoglycans) was found in the cartilaginous matrix of triamcinolone-treated condyles. In contrast, a marked increase concomitant with significant structural changes was noted in collagen fibrils. An obvious enhancement of collagen fibrillogenesis was noticed in the pre-mineralizing extracellular matrix. Atypical, wider than normal, banded collagen fibrils were found to form dense meshworks which appeared to lack any specific orientation or organization. It is proposed that glucocorticoid hormones, given systemically to neonatal mice, interfere with regulatory mechanisms involved with the biosynthesis of cartilaginous matrical macromolecules, i.e., proteoglycans and collagen and thereby promote certain aging processes within active growth centers.

Animals↗
PubMed1978

Activity of phosphatases and succinic dehydrogenase in the trigeminal ganglion of the corticosteroid-treated mouse.

Immature mice were treated for 21 days with daily doses of triamcinolone diacetate. The trigeminal ganglion was studied enzymatically for the activity of alkaline phosphatase, acid phosphatase, ATPase and succinic dehydrogenase. It became apparent that the prolonged treatment with a potent corticosteroid hormone did not affect significantly the in vivo activity of the above enzymes. Some enzymes even appeared to have increased their intracellular activity. The heterogeneous effect of corticosteroid upon their peripheral target organs is discussed.

Acid Phosphatase↗
PubMed1978

Mechanisms of glucocorticoid-induced growth retardation: impairment of cartilage mineralization.

Immature female mice were treated with daily doses of triamcinolone diacetate. Using histochemical and fluorescent methods, the mineralization pattern of the proximal epiphyseal plate of the humerus was studied at various intervals. Following 1 injection, a noticeable decrease was noted in the oxytetracycline incorporation at the mineralizing zone of the growth plate. By the 10th injection, the mineralization process was almost totally arrested. Marked accumulation of phospholipids appeared in experimental plates concomitantly with a lack of acidic glycosaminoglycans' synthesis as well as degradation. Chondroclastic activity was also inhibited resulting in an increased number of hypertrophic chondrocytes at the mineralization zone. It is suggested that the hormone's antianabolic effect led to an impairment in the activity of the chondrocytes' hydrolytic enzymes and thereby interfered with the maturation of the matrix, a prerequisite phase for normal mineralization.

Animals↗
PubMed1978

The exocrine pancreas in triamcinolone-treated mice. A light and electron microscopy study.

6-week-old ICR strain female mice were given between 16 and 21 daily injections of the synthetic glucocorticoid, triamcinolone diacetate (8 mg/kg body weight). Portions of their pancreas were examined by light and electron microscopy and compared with untreated littermate controls. Despite marked variability from animal to animal and lobule to lobule, triamcinolone treatment induced increased zymogen depletion and also the development of large basal vacuoles in many acinar cells. At the ultrastructural level, acinar cells show pronounced mitochondrial swelling, which in many instances is accompanied by the development of myelin whorls. The number of cells with distended granular endoplasmic reticulum is increased as is the number of atrophying cells and cells apparently undergoing disintegration. In addition, there are indications of marked activation of interlobular perivascular macrophages which show marked vacuolation. Our observations suggest that pancreatic acinar cells show cytological changes as a result of experimental hypercorticoidism.

Animals↗