DIKUL - logo
E-viri
Celotno besedilo
Recenzirano
  • PTH [1-34] enhances bone re...
    Almagro, M. Isabel; Roman-Blas, Jorge A.; Bellido, Miriam; Castañeda, Santos; Cortez, Raul; Herrero-Beaumont, Gabriel

    Clinical oral implants research, September 2013, Letnik: 24, Številka: 9
    Journal Article

    Introduction Dental implant osseointegration can be impaired in medical conditions with low bone mass, such as glucocorticoid‐induced osteoporosis. Intermittent human parathyroid hormone (PTH) 1‐34 administration has shown relevant anabolic bone activity in various animal models of osteoporosis. Therefore, we studied the effects of intermittent PTH 1‐34 on bone response around titanium implants in experimental osteoporosis induced by ovariectomy and glucocorticoid administration. Methods Titanium dental implants were placed in the proximal tibia metaphysis in 38 animals. Twenty‐eight rabbits had undergone bilateral ovariectomy and further methylprednisolone administration for 4 weeks to induce osteoporosis. Ten healthy rabbits were used as controls. At week 8, osteoporotic rabbits started saline vehicle or intermittent PTH administration for 12 weeks. Bone mineral density (BMD) was assessed in peri‐implant area, lumbar spine, and global and subchondral knee bone at baseline, and weeks 6 and 20. Animal sacrifice was carried out at week 21. Afterward, tibiae were removed for μCT morphometry and undecalcified sections were evaluated by light and scanning electron microscopy. Results PTH increased bone‐to‐implant contact compared with control rabbits or vehicle administration in osteoporotic rabbits (P < 0.005). PTH‐induced new bone formation around external and internal surfaces of titanium implants led to a significant increase of BMD at peri‐implant area in osteoporotic rabbits at week 20, when compared with vehicle (P < 0.005). Likewise, PTH increased BMD in other analysed regions. Conclusions Intermittent administration of PTH 1‐34 enhances the bone response around titanium implants in a rabbit model of ovariectomy and glucocorticoid‐induced osteoporosis.