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Stimulation of bone formation in the expanding premaxillary suture with a GSK‐3β inhibitor
Author(s) -
Jiang Y,
Liu HX,
Guo JJ,
Tang GH,
Qian YF
Publication year - 2013
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2012.01957.x
Subject(s) - gsk 3 , fibrous joint , catenin , glycogen synthase , medicine , gsk3b , stimulation , chemistry , endocrinology , signal transduction , wnt signaling pathway , dentistry , glycogen , biochemistry
Oral Diseases (2012) 19 , 73–79 Objectives: Glycogen synthase kinase‐3β (GSK‐3β)/β‐catenin signaling mediates osteogenesis in response to mechanical loading. We tested the hypothesis that local administration of a GSK‐3β inhibitor could stimulate new bone formation in the expanding premaxillary suture. Materials and methods: Thirty‐five Sprague–Dawley rats were subjected to premaxillary suture expansion using a helix spring. The experimental rats were given one or two local injections of SB‐415286, a small‐molecule GSK‐3β inhibitor. Animals were administered calcein and sacrificed on day 7 to quantify new bone formation. To evaluate the proliferation and differentiation of osteoblasts, rats were labeled with bromodeoxyuridine on day 1 and sacrificed on day 2 or 4. β‐catenin expression was evaluated by immunohistochemical staining. Results: Two injections of SB‐415286 led to an elevation of β‐catenin expression and an increase in the number of proliferating osteoblasts in expanding sutures on day 2 and day 4. Consequently, new bone formation in the suture increased significantly on day 7. Conclusions: These results suggest that local delivery of a GSK‐3β inhibitor could stimulate bone formation in the expanding premaxillary suture by eliciting β‐catenin signaling. GSK‐3β could be a pharmaceutical target for improving the effect of orthodontic treatments such as rapid palatal expansion.