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<p>Autoimmune rheumatic diseases (ARDs) are chronic disorders driven by impaired immune tolerance. They often develop through a preclinical phase in which early immune dysregulation occurs before clinical symptoms emerge. Identifying markers during this stage is critical for preventive strategies. Periodontitis, a chronic inflammatory disease linked to oral dysbiosis, shares key immunopathological features with ARDs, including microbial translocation, molecular mimicry, autoantibody production, and T-cell imbalance. Alterations in the oral microbiome—particularly involving <i>Porphyromonas gingivalis</i> and <i>Aggregatibacter actinomycetemcomitans</i>—have been associated with increased risk of RA. Furthermore, the Th17/Treg imbalance commonly observed in periodontitis mirrors immune dysfunctions in autoimmune conditions and contributes to systemic inflammation. Accumulating evidence suggests that periodontitis may serve as an early indicator of immune dysregulation, particularly in genetically predisposed individuals. Recognizing this connection could refine risk assessment, support early detection, and promote interdisciplinary strategies for prevention.</p>

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Periodontitis as a predictive marker in the preclinical phase of autoimmune rheumatic diseases

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月15日

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  • Hamidreza Bashiri,
  • Fahimeh Rashidi Maybodi

摘要

Autoimmune rheumatic diseases (ARDs) are chronic disorders driven by impaired immune tolerance. They often develop through a preclinical phase in which early immune dysregulation occurs before clinical symptoms emerge. Identifying markers during this stage is critical for preventive strategies. Periodontitis, a chronic inflammatory disease linked to oral dysbiosis, shares key immunopathological features with ARDs, including microbial translocation, molecular mimicry, autoantibody production, and T-cell imbalance. Alterations in the oral microbiome—particularly involving Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans—have been associated with increased risk of RA. Furthermore, the Th17/Treg imbalance commonly observed in periodontitis mirrors immune dysfunctions in autoimmune conditions and contributes to systemic inflammation. Accumulating evidence suggests that periodontitis may serve as an early indicator of immune dysregulation, particularly in genetically predisposed individuals. Recognizing this connection could refine risk assessment, support early detection, and promote interdisciplinary strategies for prevention.