OPN deficiency suppresses appearance of odontoclastic cells and resorption of the tooth root induced by experimental force application

Chooryung J. Chung, Kunimichi Soma, Susan R. Rittling, David T. Denhardt, Tadayoshi Hayata, Kazuhisa Nakashima, Yoichi Ezura, Masaki Noda

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Osteopontin (OPN) is a major non-collagenous bone matrix protein implicated in the regulation of cell function. Although OPN is rich in the cementum of the tooth, the significance of OPN in this tissue is not understood. Tooth root resorption is the most frequent complication of orthodontic tooth movement (TM). The objective of this study was to examine the pathophysiological role of OPN in cementum of the tooth root. For this purpose, the upper right first molar (M1) in OPN-deficient and wild-type (WT) mice was subjected to mechanical force via 10 gf NiTi coil spring while the left side molar was kept intact to serve as an internal control. Micro-CT section and the level of tartrate resistant acid phosphatase (TRAP)-positive cells on the tooth root surface defined as odontoclasts were quantified at the end of the force application. In WT mice, force application to the tooth caused appearance of odontoclasts around the mesial surface of the tooth root resulting in tooth root resorption. In contrast, OPN deficiency significantly suppressed the force-induced increase in the number of odontoclasts and suppressed root resorption. This force application also induced increase in the number of TRAP-positive cells in the alveolar bone on the pressure side defined as osteoclasts, while the levels of the increase in osteoclastic cell number in such alveolar bone were similar between the OPN-deficient and WT mice. These observations indicate that OPN deficiency suppresses specifically tooth root resorption in case of experimental force application.

Original languageEnglish
Pages (from-to)614-620
Number of pages7
JournalJournal of Cellular Physiology
Volume214
Issue number3
DOIs
Publication statusPublished - 2008 Mar

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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