|Reinhardt, Timothy - Tim|
Submitted to: Journal of Dairy Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/14/1995
Publication Date: N/A
Citation: N/A Interpretive Summary: Calcium is important for the maintenance of strong bones. The general importance of calcium, in the maintenance of life itself, is not as well recognized. Blood calcium must be tightly regulated at all times. The inability of an animal to regulate blood calcium is life- threatening. Approximately 8 to 10% of dairy cows are unable to regulate their blood calcium when giving birth to a calf. These cows lapse into a coma, and would die if not treated promptly. Treated cows recover quickly; however, they have been stressed to the point that they develop other metabolic and infectious diseases. This results in reduced productivity and necessitates treatment of these animals with antibiotics and drugs, which can be food safety concerns. One hypothesis for the inability of cows to regulate their blood calcium at calving is an inability to mobilize calcium from bone. Recent evidence suggests that cells responsible for fighting infectious disease (monocytes) are precursors for cells that mobilize calcium from bone. We examined the monocytes' ability to degrade bone in vitro following treatment of cattle with bone mobilization agents. The data collected suggest that monocytes are important for calcium mobilization. Furthermore, we now have a model to effectively study factors affecting monocyte-mediated bone calcium resorption in milk fever cows.
Technical Abstract: Cells of the monocyte-macrophage lineage have been proposed to play a role in bone resorption. We examined the effects of in vivo administration of parathyroid hormone and 1,25-dihydroxyvitamin D3 on in vitro monocyte bone degrading activity. Administration of parathyroid hormone for 4 d resulted in a sustained hypercalcemia and a transient 1-d increase in plasma 1,25-dihydroxyvitamin D3. Parathyroid hormone significantly stimulated monocyte bone degrading activity to 2.6 times that observed in pretreatment controls. Parathyroid hormone treatment resulted in a significant 3-fold enhancement in phorbol 12-myristate, 13-acetate-mediated release of superoxide anion by isolated monocytes and a pronounced increase in migration of monocytes to bone particles in vitro. Continuous 7-d infusion of 1,25-dihydroxyvitamin D3 (50 ug/d) elevated plasma 1,25- dihydroxyvitamin D3 until infusions were discontinued. Increased 1,25- dihydroxyvitamin D3 was associated with hypercalcemia that continued for several days postinfusion. In vivo administration of 1,25- dihydroxyvitamin D3 did not affect in vitro monocyte-mediated bone degrading activity. We conclude that in vivo administration of parathyroid hormone enhances in vitro responsiveness of isolated monocytes in a manner consistent with a role for monocytes in bone remodeling.