Glucocorticoid-induced changes in the activity of cartilage alkaline phosphatase.

Glucocorticoid hormones are known to exert distinct inhibitory effects upon cartilage metabolism and endochondral bone growth. This study examined the influence of triamcinolone hexacetonide, a long-acting synthetic analogue off cortisol, on the activity of non-specific alkaline phosphatase i condylar cartilage of neonatal mice. Four-day-old mice received a single dose (10 mg/kg) of the hormone and the activity of beta-glycerophosphatase was assayed 3 and 6 days thereafter. Whereas no significant changes were noted in the enzyme's specific activity, distinct alterations were observed in the latter's distributional pattern. By 48 hours cells along both the proliferative and chondroblastic zones exhibited a significant enhancement of alkaline phosphatase activity. This increase in enzyme activity was most prominent along the cells' plasmalemma and within their adjacent matrix. Thus, glucocorticoid hormones possess a significant stimulatory effect upon alkaline phosphatase activity in very young cartilage cells which in turn might affect the mineralization process.

Combined effect of calcitonin and glucocorticoid hormone on calcium content of cultured bone cells.

The combined effect of calcitonin and triamcinolone acetonide on Ca2+ content in cultured bone cells was studied. Cultures were first preincubated with 45Ca for 24 hrs thus achieving a steady state between the extracellular and intracellular 45Ca2+. Calcitonin was added for 24 hrs and subsequently, triamcinolone acetonide was added for time intervals ranging from 1 to 24 hrs. Calcitonin induced a significant increase in the content of cellular exchangeable Ca2+. When triamcinolone was added to cultures pretreated with calcitonin a marked efflux activity was noted. Concomitant ultrastructural histochemical examinations, using the K-pyroenthymonate fixation method, further substantiated the above finding: calcitonin treated cells revealed increased number of Ca-pyroenthymonate precipitates, whereas the combined treatment led to the disappearance of such Ca-aggregates.

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.

Corticosteroid-induced enhanced mineralization in neonatal condylar cartilage.

Neonatal mice were treated with triamcinolone hexacetonide and the cartilage of their mandibular condyle was studied biochemically and histochemically. Three days following the hormonal treatment the condylar protein content decreased significantly but a marked increase was noted in the tissue's calcium and phosphate. The condylar mineralization front extended up to the chondroblastic and proliferative zones. Triamcinolone arrest cartilage cell proliferation and enhanced an atypical hypertrophy of chondroblasts. One week following the hormonal treatment the condyle revealed clear signs of weight loss and changes in its size and form. Glucocorticoids enhance the mineralization of neonatal cartilage via: a direct effect upon chondrocytic metabolic and control systems (genom) and possibly also through an indirect adverse effect upon other organ systems.

Fusion of intact human erythrocytes and erythrocyte ghosts.

Sendai virus is able to induce the fusion of human erythrocytes. Bivalent cations or ATP are not essential for polyerythrocyte formation. High fusion indices were obtained when Sendai virus was added to cells incubated in the presence of both EDTA and iodoacetic acid. Human erythrocyte ghosts prepared by gradual hemolysis still retain the potential to undergo virus-induced fusion. Fusion of human red blood cells without the addition of viruses was obtained by incubation of erythrocytes at pH 10.5 in the presence of Ca(++) (40 mM) or by addition of phospholipase C Clostridium perfringens preparations to cells previously agglutinated or polylysine.