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The Role of Phospholipase A2 in Interleukin-1-mediated Inhibition of Mineralization of the Osteoid Formed by Fetal Rat Calvaria Cells in vitro

MRC Group in Periodontal Physiology, Faculty of Dentistry, 4384 Medical Sciences Building, University of Toronto, Toronto, Ontario, Canada M5S 1A8

J.N.M. Heersche

MRC Group in Periodontal Physiology, Faculty of Dentistry, 4384 Medical Sciences Building, University of Toronto, Toronto, Ontario, Canada M5S 1A8

W. Pruzanski

The Inflammation Research Group, The Wellesley Hospital, Toronto, Ontario, Canada M4Y 1Z3

P. Vadas

The Inflammation Research Group, The Wellesley Hospital, Toronto, Ontario, Canada M4Y 1Z3

J.E. Aubin

MRC Group in Periodontal Physiology, Faculty of Dentistry, 4384 Medical Sciences Building, University of Toronto, Toronto, Ontario, Canada M5S 1A8

Interleukin-1 (IL-1) may be an important mediator of bone remodeling, since it is a potent stimulator of bone resorption and has biphasic effects on bone formation. Continuous exposure of fetal rat calvaria (RC) cells to IL-la or IL-1β results in a dose-dependent inhibition of both bone nodule formation and mineralization of the organic matrix. In this study, the effects of recombinant human IL-1 on the mineralization process were examined by the addition of IL-la late in the culture period, after osteoid nodules had formed and when they were induced to mineralize by the addition of organic phosphate. By means of a quantitative 45calcium radiolabeling assay, it was shown that short-duration exposures of fully-formed bone nodules to IL-la also inhibited mineralization, and that the duration of treatment directly correlated with the degree of inhibition. Because our earlier studies had demonstrated that IL-1 stimulated the release of PLA₂ and PGE₂ from RC cells, the effects of PLA₂ and of inhibition of PGE2 synthesis on mineralization were investigated. Exogenous Naja naja group I PLA₂ had little effect on the mineralization of bone nodules; however, Crotalus adamanteus group II PLA₂ inhibited mineralization at concentrations similar to those found in the media from IL-la-treated cultures. Although PLA₂ is thought to stimulate PGE2 synthesis by releasing arachidonic acid from membrane phospholipids, PGE₂ release by RC cells accounted for only part of the IL-la-mediated inhibition, suggesting the presence of other mechanisms of exogenous PLA₂ action in inhibiting mineralization. These results suggest that the IL-1-induced synthesis and release of PLA ₂ from RC cells is primarily responsible for the inhibition ofmineralization seen in vitro with exposure to IL-1. Thus, the presence of IL-la in vivo at sites of chronic inflammation or infection may compromise tissue repair by inhibiting bone formation and mineralization as well as stimulating bone resorption.

Journal of Dental Research, Vol. 72, No. 1, 18-24 (1993)
DOI: 10.1177/00220345930720010101


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