RANKL, osteopontin, and osteoclast homeostasis in a hyperocclusion mouse model.

RANKL, osteopontin, and osteoclast homeostasis in a hyperocclusion mouse model.
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DOI:
10.1111/j.1600-0722.2008.00545.x
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发表时间:
2008-08
影响因子:
1.9
通讯作者:
Diekwisch TG
Diekwisch TG
中科院分区:
医学4区
文献类型:
--
作者:
Walker CG;Ito Y;Dangaria S;Luan X;Diekwisch TG

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The biological mechanisms that maintain the position of teeth in their sockets establish a dynamic equilibrium between bone resorption and apposition. In order to reveal some of the dynamics involved in the tissue responses toward occlusal forces on periodontal ligament and alveolar bone homeostasis, we have developed the first mouse model of hyper-occlusion. Swiss Webster mice were kept in hyper-occlusion for 0, 3, 6, and 9 d. Morphological and histological changes in the periodontium were assessed using micro CT and ground sections with fluorescent detection of vital dye labels. Sections were stained for tartrate-resistant acid phosphatase (TRAP), and expression of RANKL and OPN was analyzed by immunohistochemistry and real-time PCR. Traumatic occlusion resulted in enamel surface abrasion, inhibition of alveolar bone apposition, significant formation of osteoclasts at 3 d, 6 d, and 9 d, and upregulation of OPN and RANKL. Data from this study suggest that both OPN and RANKL contribute to the stimulation of bone resorption in the hyperocclusive state. In addition, we propose that the inhibition of alveolar bone apposition by occlusal forces is an important mechanism for the control of occlusal height that might work in synergy with RANKL induced bone resorption to maintain normal occlusion.
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