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Purpose <p>This review aims to comprehensively integrate and qualitatively synthesize the current evidence on fluoride-induced cardiotoxicity. Specifically, it evaluates in vitro, animal, and human studies to examine mechanistic pathways including oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis and associated structural and functional cardiac alterations. By integrating findings from experimental and observational research, this review assesses the extent to which existing data support fluoride-related cardiac effects and highlights areas requiring deeper mechanistic and clinical investigation.</p> Methods <p>A systematic literature search was conducted using PubMed, Google Scholar to identify studies between 1957 and 2024 on fluoride-induced cardiovascular outcomes. Predefined inclusion and exclusion criteria were applied to select the relevant in vitro, animal, and human studies. Data were extracted and qualitatively synthesized. Keywords included “fluoride,” “cardiotoxicity,” “oxidative stress,” “apoptosis,” and “histological alterations,” with a focus on both in vivo and in vitro models.</p> Results <p>Reviewed studies reveal that fluoride exposure report myocardial necrosis, edema, vacuolization, and fiber disorganization. Biochemical data show elevated oxidative stress (MDA), reduced antioxidants (SOD, CAT, GSH), dyslipidaemia, and increased inflammatory and cardiac injury markers (TNF-α, IL-1β, CK-MB, cTnI). The in vitro findings further demonstrate mitochondrial-mediated apoptosis including cytochrome c and caspase-9 activation, supporting fluoride’s cardiotoxic mechanisms at both tissue and cellular levels.</p> Conclusion <p>Fluoride exposure is associated with histological alterations, oxidative stress, dyslipidaemia, inflammation, and mitochondrial-mediated apoptosis in experimental models. These outcomes support the biological plausibility of fluoride-induced cardiac dysfunction. However, available human evidence remains limited, precluding definitive conclusions. Further longitudinal and mechanistic studies are needed to clarify the cardiovascular implications of chronic fluoride exposure and potential mitigation strategies.</p> Graphical Abstract <p></p>

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Cardiovascular Health and Fluoride Toxicity: A Qualitative Systematic Review

  • 期刊论文

  • 发表日期：

    2026年4月13日

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  • Rashi Baltoo,
  • Ruhi Thakur,
  • Srishti Rana

摘要

Purpose

This review aims to comprehensively integrate and qualitatively synthesize the current evidence on fluoride-induced cardiotoxicity. Specifically, it evaluates in vitro, animal, and human studies to examine mechanistic pathways including oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis and associated structural and functional cardiac alterations. By integrating findings from experimental and observational research, this review assesses the extent to which existing data support fluoride-related cardiac effects and highlights areas requiring deeper mechanistic and clinical investigation.

Methods

A systematic literature search was conducted using PubMed, Google Scholar to identify studies between 1957 and 2024 on fluoride-induced cardiovascular outcomes. Predefined inclusion and exclusion criteria were applied to select the relevant in vitro, animal, and human studies. Data were extracted and qualitatively synthesized. Keywords included “fluoride,” “cardiotoxicity,” “oxidative stress,” “apoptosis,” and “histological alterations,” with a focus on both in vivo and in vitro models.

Results

Reviewed studies reveal that fluoride exposure report myocardial necrosis, edema, vacuolization, and fiber disorganization. Biochemical data show elevated oxidative stress (MDA), reduced antioxidants (SOD, CAT, GSH), dyslipidaemia, and increased inflammatory and cardiac injury markers (TNF-α, IL-1β, CK-MB, cTnI). The in vitro findings further demonstrate mitochondrial-mediated apoptosis including cytochrome c and caspase-9 activation, supporting fluoride’s cardiotoxic mechanisms at both tissue and cellular levels.

Conclusion

Fluoride exposure is associated with histological alterations, oxidative stress, dyslipidaemia, inflammation, and mitochondrial-mediated apoptosis in experimental models. These outcomes support the biological plausibility of fluoride-induced cardiac dysfunction. However, available human evidence remains limited, precluding definitive conclusions. Further longitudinal and mechanistic studies are needed to clarify the cardiovascular implications of chronic fluoride exposure and potential mitigation strategies.

Graphical Abstract