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Chronology and regulation of gene expression of RANKL in the rat dental follicle
Author(s) -
Liu D.,
Yao S.,
Pan F.,
Wise G. E.
Publication year - 2005
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2005.00245.x
Subject(s) - rankl , osteoprotegerin , dental follicle , medicine , endocrinology , bone resorption , gene expression , rank ligand , dental alveolus , biology , activator (genetics) , chemistry , microbiology and biotechnology , receptor , dentistry , gene , genetics , stem cell
Tooth eruption in the rat requires bone resorption resulting from a major burst of osteoclastogenesis on postnatal day 3 and a minor burst of osteoclastogenesis on postnatal day 10 in the alveolar bone of the first mandibular molar. The dental follicle regulates the major burst on postnatal day 3 by down‐regulating its osteoprotegerin (OPG) gene expression to enable osteoclastogenesis to occur. To determine the role of receptor activator of nuclear factor‐kappa B ligand (RANKL) in tooth eruption, its gene expression was measured on postnatal days 1–11 in the dental follicle. The results show that RANKL expression was significantly elevated on postnatal days 9–11 in comparison to low expression levels at earlier time‐points. As OPG expression is high at this latter time‐point, this increase in RANKL expression would be needed for stimulating the minor burst of osteoclastogenesis. Tumor necrosis factor‐ α enhances RANKL gene expression in vitro and it may be responsible for up‐regulating RANKL in vivo . Transforming growth factor‐ β 1 and interleukin‐1 α also enhance RANKL gene expression in vitro but probably have no effect in vivo because they are maximally expressed early. Bone morphogenetic protein‐2 acts to down‐regulate RANKL expression in vitro and, in vivo , may promote alveolar bone growth in the basal region of the tooth.