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The stimulation of bone resorption, assessed by the release ofCa from prelabeled bones, was associated with an increase in number of osteoclasts per bone section in parathyroid hormone (PTH)-treated bones, but not in lipopolysaccharide (LPS)-treated bones. By contrast the number of nuclei per osteoclast increased following LPS treatment, but was not affected by PTH. LPS-treated bones had more multinucleated cells, some having as many as 27 nuclei per osteoclast. More osteoclasts were adjacent to the bone collar in bones treated with LPS or PTH than in control bones. In LPS-treated bones this area also contained the largest osteoclasts, as determined by the greatest number of nuclei per osteoclast. The results suggest that LPS and PTH stimulate osteoclastic resorption by different mechanisms. [ABSTRACT FROM AUTHOR]

Two diphosphonates alter the morphology of the osteoclast, as they inhibit the calcium release from bones stimulated to resorb by lipopolysaccharide. Disodium dichloromethylene diphosphonate was more potent than disodium ethane-1-hydroxy-1,1-diphosphonate in both inhibitingcalcium release and altering osteoclast morphology. Alteration in the morphology of osteoclasts is associated with little or no change in the morphology of the surrounding non-osteoclast cells. These results indicate a specific morphological effect of diphosphonates on osteoclasts. [ABSTRACT FROM AUTHOR]

Gingival fragments from monkeys have been found to release a factor in vitro into incubation medium which stimulates bone resorption in organ culture. Indomethacin effectively blocks the occurrence of this stimulatory factor in the gingival incubation medium. All of this bone resorptive activity can be accounted for by prostaglandin-like material. The prostaglandins contributing to the bone resorptive activity have been found to be prostaglandins E and E. [ABSTRACT FROM AUTHOR]

The binding of prostaglandin E (PGE) to bone cells was studied to provide direct evidence for the existence of specific receptors in bone. Bone cells were isolated by collagenase digestion of fetal and newborn rat calvaria. Isolated cells were incubated withH-PGE and collected on Millipore filters. Specific binding was determined by subtracting the binding that occurred with 10 M non-radioactive PGE andH-PGE from that withH-PGE alone. With heterogeneous cell preparations and at PGE concentrations from 10 − 1.7 × 10 M at 37°C, specific binding reached steady state within 10 min. BoundH-PGE was displaced by the addition of increasing amounts of unlabeled PGE. Inhibition of PGE binding was observed with PGE and the endoperoxide analog, U44069, but not with PGE, a lipopolysaccharide, or 13,14-dihydro 15-keto PGE. Studies with bone cell populations, obtained by sequential digestions, indicated that an osteoclastic population binds 30-fold more PGE than osteoblastic cells. Scatchard analyses revealed that the osteoclastic cells have an affinity constant for PGE binding similar to that obtained with heterogeneous populations. However, the PGE binding capacity in this osteoclastic population was fivefold greater than in the heterogeneous population. The osteoclastic population responded with an increase in cyclic AMP to lower concentrations of PGE than the osteoblastic populations. These studies suggest that differences in the binding capacity of PGE receptors exist among bone celltypes and that these differences are reflected in the cellular cyclic AMP response. [ABSTRACT FROM AUTHOR]

The bone resorptive factor and amphipathic antigen (AcA) previously identified by us in preparations from Actinomyces viscosus have been partially purified, characterized chemically, and compared. They elute at the same location on chromatography with Ac 22. The fatty acid composition of AcA and the bone resorptive factor is the same. Some differences in carbohydrate composition are observed. The Actinomyces factor does not affect calcium influx or cyclic AMP in isolated bone cells. Therefore it is concluded that AcA stimulates resorption either by gaining entrance into bone cells or by way of a yet undetermined second messenger. [ABSTRACT FROM AUTHOR]

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Copyright of Calcified Tissue Research is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Calcified Tissue Research is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Zeitschrift für Anatomie und Entwicklungsgeschichte is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A 22-year-old man attempted to commit suicide by swallowing an unknown amount of barium carbonate dissolved in hydrochloric acid. Shortly after ingestion, he developed crampy abdominal pain and generalized muscle weakness. About 2 h later, respiratory failure ensued necessitating orotracheal intubation and mechanical ventilation. Concomitantly, life-threatening arrhythmias including ventricular fibrillation occurred, and he had to be resuscitated for 45 min. After correction of severe hypokalemia (serum potassium 1.5 mmol/l), cardiac rhythm stabilized. In an attempt to accelerate removal of barium from the circulation hemodialysis was begun. During hemodialysis muscle strength returned. Pharmacokinetic analysis of serum barium levels suggest that hemodialysis shortened the serum half-life of barium. Subsequently, the patient made a complete and uneventful recovery. Our case demonstrates that severe barium poisoning can be survived provided that early aggressive therapeutic measures are undertaken. Hemodialysis seems to be efficacious in the therapy of barium intoxication. [ABSTRACT FROM AUTHOR]