Selective ß2-adrenergic Antagonist Butoxamine Reduces Orthodontic Tooth Movement.
J Dent Res
; 93(8): 807-12, 2014 Aug.
Article
en En
| MEDLINE
| ID: mdl-24868013
Recently, involvement of the sympathetic nervous system in bone metabolism has attracted attention. ß2-Adrenergic receptor (ß2-AR) is presented on osteoblastic and osteoclastic cells. We previously demonstrated that ß-AR blockers at low dose improve osteoporosis with hyperactivity of the sympathetic nervous system via ß2-AR blocking, while they may have a somewhat inhibitory effect on osteoblastic activity at high doses. In this study, the effects of butoxamine (BUT), a specific ß2-AR antagonist, on tooth movement were examined in spontaneously hypertensive rats (SHR) showing osteoporosis with hyperactivity of the sympathetic nervous system. We administered BUT (1 mg/kg) orally, and closed-coil springs were inserted into the upper-left first molar. After sacrifice, we calculated the amount of tooth movement and analyzed the trabecular microarchitecture and histomorphometry. The distance in the SHR control was greater than that in the Wistar-Kyoto rat group, but no significant difference was found in the SHR treated with BUT compared with the Wistar-Kyoto rat control. Analysis of bone volume per tissue volume, trabecular number, and osteoclast surface per bone surface in the alveolar bone showed clear bone loss by an increase of bone resorption in SHR. In addition, BUT treatment resulted in a recovery of alveolar bone loss. Furthermore, TH-immunoreactive nerves in the periodontal ligament were increased by tooth movement, and BUT administration decreased TH-immunoreactive nerves. These results suggest that BUT prevents alveolar bone loss and orthodontic tooth movement via ß2-AR blocking.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Técnicas de Movimiento Dental
/
Butoxamina
/
Proceso Alveolar
/
Antagonistas de Receptores Adrenérgicos beta 2
Límite:
Animals
Idioma:
En
Revista:
J Dent Res
Año:
2014
Tipo del documento:
Article
País de afiliación:
Japón
Pais de publicación:
Estados Unidos