MISC

2003年4月

The regulation of bone resorption in tooth formation and eruption processes in mouse alveolar crest devoid of cathepsin K

JOURNAL OF PHARMACOLOGICAL SCIENCES
  • M Okaji
  • ,
  • H Sakai
  • ,
  • E Sakai
  • ,
  • M Shibata
  • ,
  • F Hashimoto
  • ,
  • Y Kobayashi
  • ,
  • N Yoshida
  • ,
  • K Okamoto
  • ,
  • K Yamamoto
  • ,
  • Y Kato

91
4
開始ページ
285
終了ページ
294
記述言語
英語
掲載種別
DOI
10.1254/jphs.91.285
出版者・発行元
JAPANESE PHARMACOLOGICAL SOC

Osteoclastic bone resorption has recently been implicated in the tooth formation and eruption in alveolar bone. Cathepsin K (CK) is a cysteine proteinase expressed predominantly in osteoclasts and is believed to play a critical role in degradation of bone matrix proteins. Here we present evidence that the alveolar bone resorption is essential for the tooth formation and that eruption proceeds normally in CK-deficient (CK-/-) mice. Radiographic and histological analyses revealed that the alveolar bone from these animals had no significant abnormalities during the tooth development between 5 and 28 days after birth. The tooth crown was normally erupted through the alveolar bone layer at 28 days after birth. The number of tartrate-resistant acid phosphatase-positive multinuclear cells in the alveolar bone around the tooth germ was apparently increased in 5-day-old CK-/- mice compared with age-matched littermates. More important, however, the immunohistochemical localization of matrix metalloproteinase-9 (MMP-9) was clearly increased in the CK-/- osteoclasts. In contrast, no significant difference in the immunoreactivity for cathepsin D was observed between the CK-/- osteoclasts and the wild-type ones. These results indicate that CK-/- osteoclasts are fully differentiated and are capable of degrading the organic phase of alveolar bone during the tooth formation and eruption, which may result from the compensatory action by MMP-9 increasingly expressed in the osteoclasts.

Web of Science ® 被引用回数 : 14

リンク情報
DOI
https://doi.org/10.1254/jphs.91.285
CiNii Articles
http://ci.nii.ac.jp/naid/30003472503
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/12719657
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000182602200004&DestApp=WOS_CPL
ID情報
  • DOI : 10.1254/jphs.91.285
  • ISSN : 1347-8613
  • CiNii Articles ID : 30003472503
  • PubMed ID : 12719657
  • Web of Science ID : WOS:000182602200004

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