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<p>Inositol 1,4,5-trisphosphate receptors (IP3Rs) function as fundamental calcium channels, with calcium ions acting as crucial second messengers that stimulate various cellular signaling pathways, including osteoprotein expression. Given alendronate’s established role as a pharmacological agent influencing bone remodeling, this study aimed to evaluate its effect on the presence of IP3Rs, as well as on osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANK-L), concurrently with a histomorphometric analysis of bone tissue. A standardized transosseous defect, 8.7&#xa0;mm in diameter, was surgically created in the calvaria of each of 40 ovariectomized female rats. All defects received autogenous bone grafts. Twenty of these rats were randomly assigned to receive alendronate administration at a dose of 1.0&#xa0;mg/kg, three times per week, until euthanasia on either the second or sixth post-surgical week. The findings of this study demonstrated increased bone quantification and accelerated maturation in specimens treated with alendronate. This positive outcome was associated with a significantly higher expression of IP3Rs, which in turn correlated with an increase in the OPG-to-RANK-L ratio. It is concluded that alendronate administration enhances osteogenesis and promotes rapid bone maturation. This accelerated bone formation coincides with a heightened expression of IP3Rs, suggesting a potential mechanistic link between alendronate’s action and IP3R-mediated signaling in bone remodeling.</p>

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Alendronate Enhances Osteoconduction and Bone Maturation in Ovariectomized Rats: Implications for Craniofacial Bone Regeneration Via IP3R Upregulation

  • 期刊论文

  • 发表日期：

    2025年12月4日

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  • Renan Dainez Sant’Ana,
  • Mariana Verona Camargo,
  • Fernando Issamu Tabushi,
  • Marcos Fabiano Sigwalt,
  • Allan Fernando Giovanini

摘要

Inositol 1,4,5-trisphosphate receptors (IP3Rs) function as fundamental calcium channels, with calcium ions acting as crucial second messengers that stimulate various cellular signaling pathways, including osteoprotein expression. Given alendronate’s established role as a pharmacological agent influencing bone remodeling, this study aimed to evaluate its effect on the presence of IP3Rs, as well as on osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANK-L), concurrently with a histomorphometric analysis of bone tissue. A standardized transosseous defect, 8.7 mm in diameter, was surgically created in the calvaria of each of 40 ovariectomized female rats. All defects received autogenous bone grafts. Twenty of these rats were randomly assigned to receive alendronate administration at a dose of 1.0 mg/kg, three times per week, until euthanasia on either the second or sixth post-surgical week. The findings of this study demonstrated increased bone quantification and accelerated maturation in specimens treated with alendronate. This positive outcome was associated with a significantly higher expression of IP3Rs, which in turn correlated with an increase in the OPG-to-RANK-L ratio. It is concluded that alendronate administration enhances osteogenesis and promotes rapid bone maturation. This accelerated bone formation coincides with a heightened expression of IP3Rs, suggesting a potential mechanistic link between alendronate’s action and IP3R-mediated signaling in bone remodeling.