Oral microenvironmental dysregulation and female reproductive health: clinical evidence, immunological mechanisms, and bidirectional crosstalk
Abstract
Oral microenvironmental dysregulation, particularly at the periodontal interface, represents a potential source of microbial and host-derived signals that may influence female reproductive health through host–microbiome interactions and immune-mediated inflammatory pathways. Clinical and epidemiological studies have reported associations between oral or periodontal conditions and bacterial vaginosis, fecundability, time to conception, polycystic ovary syndrome, and other gynaecological conditions; however, the evidence remains heterogeneous and causal relationships are not established. Most available clinical evidence is observational, while many of the proposed molecular and tissue-level mechanisms are supported by experimental or indirect evidence, with the strength of support varying across reproductive outcomes and biological pathways. This review synthesises current clinical evidence and discusses the biological and immunological mechanisms potentially linking oral and periodontal dysregulation with female reproductive health. At the periodontal interface, community-level microbial dysbiosis, altered physicochemical conditions, non-resolving inflammation, and epithelial barrier impairment may disrupt mucosal homeostasis and permit microbial products and host-derived inflammatory signals to access systemic circulation. These signals may subsequently be amplified through innate immune activation, altered myeloid-cell responses, endothelial dysfunction, oxidative stress, and metabolic pathways, thereby modifying tissue-specific responses in the cervicovaginal mucosa, endometrium, ovary, and gestational tissues. Direct haematogenous dissemination of oral microorganisms appears biologically plausible in selected intrauterine infections, whereas systemic host-mediated mechanisms may better explain the broader spectrum of reported oral–reproductive associations. Conversely, hormonal fluctuations and endocrine-metabolic disturbances may alter periodontal susceptibility and inflammatory responses to dental biofilm. Current evidence supports biologically plausible and potentially bidirectional interactions between oral mucosal dysregulation and female reproductive health, although their direction, magnitude, disease specificity, and clinical significance remain incompletely defined. Future longitudinal and interventional studies integrating periodontal phenotyping, microbiome profiling, immune-metabolic assessment, and reproductive evaluation are required to clarify temporal relationships and biological mediation.
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BibTeX
@article{yu2026oral,
title = {{Oral microenvironmental dysregulation and female reproductive health: clinical evidence, immunological mechanisms, and bidirectional crosstalk}},
author = {Jie Yu and Bo Lei and Ming Zhang and Lin Sun and Chang-Feng Qu and Matthias Hannig and Yong Liu},
journal = {Frontiers in Immunology},
year = {2026},
month = nov,
doi = {10.3389/fimmu.2026.2000537},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.2000537},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Oral microenvironmental dysregulation and female reproductive health: clinical evidence, immunological mechanisms, and bidirectional crosstalk
AU - Jie Yu
AU - Bo Lei
AU - Ming Zhang
AU - Lin Sun
AU - Chang-Feng Qu
AU - Matthias Hannig
AU - Yong Liu
PY - 2026
DA - 2026/11/02
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.2000537
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.2000537
AB - Oral microenvironmental dysregulation, particularly at the periodontal interface, represents a potential source of microbial and host-derived signals that may influence female reproductive health through host–microbiome interactions and immune-mediated inflammatory pathways. Clinical and epidemiological studies have reported associations between oral or periodontal conditions and bacterial vaginosis, fecundability, time to conception, polycystic ovary syndrome, and other gynaecological conditions; however, the evidence remains heterogeneous and causal relationships are not established. Most available clinical evidence is observational, while many of the proposed molecular and tissue-level mechanisms are supported by experimental or indirect evidence, with the strength of support varying across reproductive outcomes and biological pathways. This review synthesises current clinical evidence and discusses the biological and immunological mechanisms potentially linking oral and periodontal dysregulation with female reproductive health. At the periodontal interface, community-level microbial dysbiosis, altered physicochemical conditions, non-resolving inflammation, and epithelial barrier impairment may disrupt mucosal homeostasis and permit microbial products and host-derived inflammatory signals to access systemic circulation. These signals may subsequently be amplified through innate immune activation, altered myeloid-cell responses, endothelial dysfunction, oxidative stress, and metabolic pathways, thereby modifying tissue-specific responses in the cervicovaginal mucosa, endometrium, ovary, and gestational tissues. Direct haematogenous dissemination of oral microorganisms appears biologically plausible in selected intrauterine infections, whereas systemic host-mediated mechanisms may better explain the broader spectrum of reported oral–reproductive associations. Conversely, hormonal fluctuations and endocrine-metabolic disturbances may alter periodontal susceptibility and inflammatory responses to dental biofilm. Current evidence supports biologically plausible and potentially bidirectional interactions between oral mucosal dysregulation and female reproductive health, although their direction, magnitude, disease specificity, and clinical significance remain incompletely defined. Future longitudinal and interventional studies integrating periodontal phenotyping, microbiome profiling, immune-metabolic assessment, and reproductive evaluation are required to clarify temporal relationships and biological mediation.
SN - 1664-3224
ER -