Oral diseases · 2026
From Mood to Mouth: Unraveling the Impact of Emotional Dysregulation on Periodontitis.
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Li Siyao, Zhang Shuang, Liu Yitong, Liu Yi
Аннотация
OBJECTIVES: Periodontitis is a chronic infectious disease which is recognized as a major cause of periodontal tissue destruction. Negative emotional states have been associated with periodontitis, although causal inference remains constrained by heterogeneous exposure and outcome measures. This narrative review critically examines the evidence linking emotional dysregulation with periodontitis and summarizes plausible psychoneuroimmunological pathways.
SUBJECTS: This review focuses on the association between psychological stress and periodontitis, including the psychoneuroimmunological pathways mediated by the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. Current experimental models and clinical epidemiological evidence support this psychophysiological interconnection.
RESULTS: Psychological stress may influence periodontal inflammation through HPA axis and SNS/SAM-mediated changes in immune regulation and, potentially, alterations in oral microbial ecology. Converging experimental and clinical evidence supports the biological plausibility of this psychophysiological link, although heterogeneity in exposure assessment, periodontal outcome definitions, and study design limits causal inference.
CONCLUSIONS: Further understanding of stress-periodontitis interactions provides insights into an emerging oral-brain crosstalk mechanism, which may help identify prospective therapeutic targets for interceptive periodontal management.
SUBJECTS: This review focuses on the association between psychological stress and periodontitis, including the psychoneuroimmunological pathways mediated by the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. Current experimental models and clinical epidemiological evidence support this psychophysiological interconnection.
RESULTS: Psychological stress may influence periodontal inflammation through HPA axis and SNS/SAM-mediated changes in immune regulation and, potentially, alterations in oral microbial ecology. Converging experimental and clinical evidence supports the biological plausibility of this psychophysiological link, although heterogeneity in exposure assessment, periodontal outcome definitions, and study design limits causal inference.
CONCLUSIONS: Further understanding of stress-periodontitis interactions provides insights into an emerging oral-brain crosstalk mechanism, which may help identify prospective therapeutic targets for interceptive periodontal management.