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<p>Long-term proton pump inhibitor (PPI) use is associated with increased risks of osteoporosis and fractures. To investigate strategies for mitigating PPI-induced bone loss, this study evaluated the preventive effects of calcium carbonate or sodium bicarbonate on bone alterations in a 12-week esomeprazole-treated Wistar rat model. Esomeprazole monotherapy exhibited compromised trabecular microarchitecture, as evidenced by a decrease in bone volume fraction and trabecular number, alongside an increase in trabecular separation. Conversely, co-administration of esomeprazole with either sodium bicarbonate or calcium carbonate preserved trabecular microarchitecture and attenuated bone resorption of osteoclast. Histological and in vitro assays showed that esomeprazole enhanced osteoclastogenesis by upregulating integrin subunit beta 3 and <i>cathepsin K</i>, which were significantly suppressed by the buffering agents. Consistently, serum levels of C-terminal cross-linked telopeptides of type I collagen were significantly lower in both combination groups. These results indicate that long-term esomeprazole administration induced bone loss, primarily by enhancing osteoclast-mediated resorption. The co-administration of calcium carbonate and sodium bicarbonate effectively attenuated these deleterious effects. Notably, the comparable efficacy of sodium bicarbonate suggests that buffering systemic acidity may be a viable strategy for mitigating PPI-induced osteoporosis.</p>

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Co-administration of calcium carbonate or sodium bicarbonate prevents esomeprazole-induced osteoporosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月20日

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  • Dae Hyun Lim,
  • Seung Hoon Lee,
  • Dongju Kim,
  • Chanhyeok Jeon,
  • Da Bhin Kim,
  • Hye-Ryeong Jo,
  • Jin Ah Shin,
  • Sungsin Jo,
  • Hang Lak Lee,
  • Tae-Hwan Kim

摘要

Long-term proton pump inhibitor (PPI) use is associated with increased risks of osteoporosis and fractures. To investigate strategies for mitigating PPI-induced bone loss, this study evaluated the preventive effects of calcium carbonate or sodium bicarbonate on bone alterations in a 12-week esomeprazole-treated Wistar rat model. Esomeprazole monotherapy exhibited compromised trabecular microarchitecture, as evidenced by a decrease in bone volume fraction and trabecular number, alongside an increase in trabecular separation. Conversely, co-administration of esomeprazole with either sodium bicarbonate or calcium carbonate preserved trabecular microarchitecture and attenuated bone resorption of osteoclast. Histological and in vitro assays showed that esomeprazole enhanced osteoclastogenesis by upregulating integrin subunit beta 3 and cathepsin K, which were significantly suppressed by the buffering agents. Consistently, serum levels of C-terminal cross-linked telopeptides of type I collagen were significantly lower in both combination groups. These results indicate that long-term esomeprazole administration induced bone loss, primarily by enhancing osteoclast-mediated resorption. The co-administration of calcium carbonate and sodium bicarbonate effectively attenuated these deleterious effects. Notably, the comparable efficacy of sodium bicarbonate suggests that buffering systemic acidity may be a viable strategy for mitigating PPI-induced osteoporosis.