title: Osteopontin deficiency enhances parathyroid hormone/ parathyroid hormone related peptide receptor (PPR) signaling-induced alteration in tooth formation and odontoblastic morphology.
abstract: Parathyroid hormone/parathyroid hormone-related protein receptor (PPR) signaling is known to be involved in tooth development. In bone, extracellular matrix protein osteopontin (OPN) is a negative regulator of PPR signaling in bone formation. However, the role of OPN in modulation of PPR action in tooth development is not understood. Therefore, we examined the tooth in double mutant mice. Constitutively active PPR was expressed specifically in the odontoblasts and osteoblasts (caPPR-tg) in the presence or absence of OPN. Radiographic analysis indicated that the length of the third molar (M3) and the incisor was decreased in the caPPR-tg mice compared to wild type, and such reduction in molar and incisor length was further enhanced in the absence of OPN (caPPR-tg OPN-KO). With respect to histology of incisors, caPPR-tg induced high cellularity and irregularity in odontoblastic shape and this was enhanced by the absence of OPN. These morphological observations suggest that OPN modulates PPR signaling that are involved in tooth formation.
authors.affiliation: Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, 113-8510, Tokyo, Japan.
authors.forename: Maki
authors.initials: M
authors.lastname: Morishita
authors.forename: Noriaki
authors.initials: N
authors.lastname: Ono
authors.forename: Kentano
authors.initials: K
authors.lastname: Miyai
authors.forename: Tomomi
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Ryo
authors.initials: R
authors.lastname: Hanyu
authors.forename: Masashi
authors.initials: M
authors.lastname: Nagao
authors.forename: Paksinee
authors.initials: P
authors.lastname: Kamolratanakul
authors.forename: Takuya
authors.initials: T
authors.lastname: Notomi
authors.forename: Susan R
authors.initials: SR
authors.lastname: Rittling
authors.forename: David T
authors.initials: DT
authors.lastname: Denhardt
authors.forename: Henry M
authors.initials: HM
authors.lastname: Kronenberg
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Ezura
authors.forename: Tadayoshi
authors.initials: T
authors.lastname: Hayata
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Nakamoto
authors.forename: Masaki
authors.initials: M
authors.lastname: Noda
mesh_terms: D000818:Animals; D007180:Incisor / Q000254:growth & development; D051379:Mice; D018345:Mice, Knockout; D009804:Odontoblasts / Q000378:metabolism*; D010006:Osteoblasts / Q000378:metabolism*; D053495:Osteopontin / Q000172:deficiency*; D010281:Parathyroid Hormone; D044168:Receptor, Parathyroid Hormone, Type 1 / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D014070:Tooth / Q000254:growth & development*
chemical_list: D010281:Parathyroid Hormone; D044168:Receptor, Parathyroid Hormone, Type 1; D053495:Osteopontin