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Assessment of the Influence of NaF or 1,25-(OH)₂ Vitamin D₃ on the Proliferative Bone Effect of an Avian Osteopetrosis Virus, MAV-2(O)

Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523

James K. Maurer

The Procter & Gamble Company, P.O. Box 398707, Cincinnati, Ohio 45239-8707

Phil H. Long

The Procter & Gamble Company, P.O. Box 398707, Cincinnati, Ohio 45239-8707

James E. Proctor

Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523

Jofrid L. Torgersen

Department of Microbiology, Colorado State University, Fort Collins, Colorado 80523

1,25-(OH)₂ vitamin D₃ (D₃) and sodium fluoride (NaF) were given to chicken embryos and newly hatched chickens infected with a slow onset strain of avian osteopetrosis-inducing virus [MAV-2(O)] to determine if either agent influenced MAV-2(O)-induced proliferation of bone. Embryos were administered MAV-2(O) and treated with: 1) up to 240 Mg NaF or up to 100 ng D₃ as embryos; 2) up to 1.8 g NaF/kg or up to 9.5 µg D₃/kg after hatching; or 3) 240 µg NaF as embryos and up to 1.8 g NaF/kg after hatching. Administration of MAV-2(O) alone resulted in expansion of the cortical diameter of bone. Coadministration of NaF or D₃ with MAV-2(O) did not influence the change in cortical diameter seen with MAV-2(O) alone at 18 days of incubation, and 3 and 6 weeks after hatching. Increased osteoid relative to bone (hyperosteoidosis), with NaF and MAV-2(O) compared to MAV-2(O) alone, and NaF compared to untreated controls reflected delayed mineralization of osteoid, a known fluoride effect. We conclude that the administration of NaF or D₃ did not influence the incidence, severity or time of onset of the MAV-2(O)-induced proliferative changes of bone.

Key Words: Sodium fluoride • retrovirus • chicken • chemical-virus interaction

• 1. Baylink DJ, Duane PB, Farley SM, and Farley JR (1983). Monoflurophosphate physiology: The effects of fluoride on bone. Caries Res. 17(Suppl. 1): 56–76.[Web of Science][Medline] [Order article via Infotrieve]
• 2. Farley JR, Wergedal JE, and Baylink DJ (1983). Fluoride directly stimulates proliferation and alkaline phosphatase activity of bone-forming cells. Science 222: 330–332.[Abstract/Free Full Text]
• 3. Hock JM, Gunneso-Hus M, Poser J, Olson H, Bell NH, and Raisz LG (1986). Stimulation of undermi-neralized matrix formation 1,25 dihydroxyvitamin D3 in long bones of rats. Calcif. Tissue Int. 38: 79–86.[Web of Science][Medline] [Order article via Infotrieve]
• 4. Larsson SE, Lorcntzon R, and Boquist L (1977). Low doses of 1,25-dihydroxycholecalciferol increase nature bone mass in adult normal rats. Clin. Orthop. 127: 228–235.[Medline] [Order article via Infotrieve]
• 5. Lundy MW, Farley JR, and Baylink DJ (1986). Characterization of a rapidly responding animal model for fluoride-stimulated bone formation. Bone 7: 289–293.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
• 6. Powers BE, Norrdin RW, Snyder SP, and Smith RE (1987). A sequential study of bone lesions caused by isolates of avian osteopetrosis virus, MAV-2(O). Bone 8: 231–240.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
• 7. Powers BE, Norrdin RW, Snyder SP, and Smith RE (1988). Sequential study of visceral lesions caused by isolates of avian osteopetrosis virus (myeloblastosis-associated virus). Am. J. Vet. Res. 49: 1589–1597.[Web of Science][Medline] [Order article via Infotrieve]
• 8. Rapp, F (1984). Appendix B. Current knowledge of mechanisms of viral carcinogenesis. CRC Crit. Rev. Toxicol. 13: 197–204.[CrossRef]
• 9. Rodan GA and Rodan SB (1984). Expression of the osteoblastic phenotype. In: Bone and Mineral Research Annual, WA Peck (ed). Elsevier Science Publishers B.V., New York, NY, pp. 244–285.
• 10. Sanger VL, Fredrickson TN, Morrill CC, and Burmester BR (1966). Pathogenesis of osteopetrosis in chickens. Am. J. Vet. Res. 27: 1735–1744.[Web of Science][Medline] [Order article via Infotrieve]
• 11. Schmidt EV, Crapo JD, Harrelson JM, and Smith RE (1981). A quantitative histologic study of avian os-teopetrotic bone demonstrating normal osteoclast numbers and increased osteoblastic activity. Lab. Invest. 44: 164–173.[Web of Science][Medline] [Order article via Infotrieve]
• 12. Smith RE (1982). Avian Osteopetrosis. Curr. Top. Microbiol. Immunol. 101: 75–94.[Web of Science][Medline] [Order article via Infotrieve]
• 13. Smith RE and Morgan JH (1982). Identification of rapid and slow onset plaque isolates of avian osteopetrosis virus. Virology 119: 488–499.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
• 14. Smith RE and Morgan JH (1984). Pathogenesis of osteopetrosis induced by rapid and slow onset plaque isolates of avian osteopetrosis virus. Metab. Bone Dis. Rel. Res. 5: 289–298.[CrossRef]
• 15. Smith RE (1987). Immunology of ALV Infection. In: Avian Leukosis, GF DeBoer (ed). Martinus Nijhoff, Boston, MA, pp. 121–129.
• 16. Smith RE, Torgersen J, Long PH, and Maurer JK (1988). Lethality and bone alterations in chicken embryos and newly hatched chickens given bone-active agents. Am. J. Vet. Res. 49: 1376–1381.[Web of Science][Medline] [Order article via Infotrieve]
• 17. Wronki TJ, Hallgrhan BP, Bikle DD, Globus RK, and Morey-Holton ER (1986). Chronic administration of 1,25-dihydroxyvitamin D3: Increased bone but impaired mineralization. Endocrinology 119: 2580–2585.[Abstract/Free Full Text]

Toxicologic Pathology, Vol. 18, No. 3, 380-386 (1990)
DOI: 10.1177/019262339001800304


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This Article Abstract Free Full Text (Free PDF) Free Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Smith, R. E. Articles by Torgersen, J. L. Search for Related Content PubMed PubMed Citation Articles by Smith, R. E. Articles by Torgersen, J. L. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB 1,25-DIHYDROXYCHOLECALCIFEROL SODIUM FLUORIDE Social Bookmarking                         What's this?