A requirement for tooth eruption is the resorption of alveolar bone. Becaus
e bone resorption is stimulated by dexamethasone both in vivo and in vitro,
dexamethasone 21-phosphate, a soluble form of dexamethasone, was injected
into rats to determine its effect on tooth eruption. Such dexamethasone inj
ections accelerate the time of intra-osseous eruption in rat incisors but d
o not accelerate the eruption time of rat molars when injected into rats. T
he injections of dexamethasone 21-phosphate also accelerate the time of eye
lid opening in the postnatal rats, as well as retarding growth, as measured
by body weight. These effects of dexamethasone 21-phosphate parallel the e
ffects of epidermal growth factor injections, including the absence of an e
ffect on molar eruption. This suggests that the molecular signals for the i
nitiation of tooth eruption (i.e., onset of bone resorption) differ between
rat incisors and molars. Given that rat incisors are teeth of continuous e
ruption whereas rat molars are teeth of limited eruption, as are human teet
h, care must be taken in extrapolating results derived from rat incisors to
human dentition. In vitro, dexamethasone has no effect on the gene express
ion of either osteoprotegerin or epidermal growth factor in dental follicle
cells derived from molars. Because osteoprotegerin expression during norma
l tooth eruption is transitorily inhibited early postnatally in the molar d
ental follicle to allow osteoclast formation, the absence of inhibition of
its expression by dexamethasone could explain why dexamethasone does not ac
celerate eruption in molars. (C) 2001 Wiley-Liss. Inc.