title: Sex hormones receptors play a crucial role in the control of femoral and mandibular growth in newborn mice.
abstract: Sex hormones are important for bone growth. However, the mechanism by which sex hormone receptors influence bone growth remains unclear. In orthodontic treatment, there is a need to develop an indicator of bone maturity to accurately predict the beginning and end of growth. This indicator might be developed from the screening of sex hormones. The purpose of this study was to investigate the role of each sex hormone receptor on bone growth in newborn mice. Five-day-old C57BL/6J mice were used in this experiment. Forty mice underwent an orchiectomy (ORX), ovariectomy (OVX), or sham surgery. One week after surgery, the femur and the mandible were resected for immunohistochemical staining. Alternatively, 80 mice were daily injected with antagonist against receptors oestrogen alpha (ERα), beta (ERβ), or androgen receptor (AR). One week after the first injection, radiographs of the femur and mandible were taken and then measured. Analysis of variance and pairwise comparisons (Fisher) were performed to examine the differences in values measured among the groups In the sham-operated male and female mice, ERβ was found to be more prominent than ERα and AR during all experimental periods. In the ORX and OVX groups, the expressions of all receptors were significantly reduced in comparison with the sham-operated control group throughout the experiment. Moreover, femur and mandibular growth were significantly affected in the group injected with ERβ antagonist. The deficiency of any sex hormone leads to reduced bone growth. In particular, a disturbance in ERβ produces a greater aberrance in both male and female mice immediately after birth.
authors.affiliation: Department of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical Sciences, Japan. ranaa2@hotmail.com
authors.forename: R A
authors.initials: RA
authors.lastname: Márquez Hernández
authors.forename: J
authors.initials: J
authors.lastname: Ohtani
authors.forename: T
authors.initials: T
authors.lastname: Fujita
authors.forename: H
authors.initials: H
authors.lastname: Sunagawa
authors.forename: T
authors.initials: T
authors.lastname: Kawata
authors.forename: M
authors.initials: M
authors.lastname: Kaku
authors.forename: M
authors.initials: M
authors.lastname: Motokawa
authors.forename: K
authors.initials: K
authors.lastname: Tanne
mesh_terms: D000704:Analysis of Variance; D059002:Androgen Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D005269:Femur / Q000187:drug effects / Q000254:growth & development*; D012739:Gonadal Steroid Hormones / Q000502:physiology; D008297:Male; D008334:Mandible / Q000187:drug effects / Q000254:growth & development*; D051379:Mice; D008810:Mice, Inbred C57BL; D010012:Osteogenesis / Q000187:drug effects / Q000502:physiology*; D011944:Receptors, Androgen / Q000502:physiology*; D011960:Receptors, Estrogen / Q000037:antagonists & inhibitors / Q000502:physiology*
chemical_list: D059002:Androgen Receptor Antagonists; D004967:Estrogens; D012739:Gonadal Steroid Hormones; D011944:Receptors, Androgen; D011960:Receptors, Estrogen