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The Biological Study of Bisphosphonate Drug treatment in Periodontal and Periapical Diesease.

Research Project

Project/Area Number 09671969
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Conservative dentistry
Research InstitutionKanagawa Dental College

Principal Investigator

TANI-ISHII Nobuyuki  Kanagawa dental College, Associate Professor, 歯学部, 講師 (20163610)

Co-Investigator(Kenkyū-buntansha) MINAMIDA Genshi  Kanagawa dental College, Assistant Professor, 歯学部, 助手 (70288083)
TSUNODA Akira  Kanagawa dental College, Assistant Professor, 歯学部, 助手 (70236933)
Project Period (FY) 1997 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
KeywordsBisphosphonates / Incadronate / apoptosis / osteoclasts / ビスフォスフォネート / 根尖病変 / アポトーシス
Research Abstract

Bisphosphonates inhibit bone resorption, though there is disagreement about their effects on osteoblastic cells. They are used as therapeutic agents in hyper-resorptive bone diseases such as Paget's disease, malignant hypercalcaemia, and osteoporosis. In the present study we observed the effects of Incadronate (a third-generation bisphosphonate) on osteoclast formation, cytotoxicity of osteoclast supporting cells, and apoptosis of osteoclasts. Osteoclast formation was examined bty addition of incadronate to co-cultures of C57BL/6N mouse bone-marrow cells and MC3T3-G2/PA6 cells on dentin slices in the presence of 1α, 25(OH)2D3 and dexamethasone. At the end of the culture period, we found that the number of TRAP-positive cells was significantly lower for treated cultures than that of the control culture. We also found that the fraction of pitted surface on dentin from treated cultures was lower than that on dentin from untreated control cultures. Incadronate cytotoxicity of osteoclasts was greater than osteoblastic/stromal cells and osteoblasts. The proportion of a apoptotic osteoclasts was increased by Incadronate. Incadronate caused a dose-dependent increase in the death rate of osteoblastic/stromal cells and osteoclasts. These results suggested that incadronate inhibits osteoclastogenesis by inhibiting the proliferation or fusion of pre-osteoclasts through its action on osteoblastic/stromal cells.

Report

(4 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • 1997 Annual Research Report

URL: 

Published: 1997-04-01   Modified: 2016-04-21  

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