# Oral Cellular Homeostasis and Occupational Wellbeing in Healthcare Professionals Under the Lens of Salivary, Immune, and Microbiome Mechanisms

**Authors:** Maria Antoniadou, Theodoros Varzakas

PMC · DOI: 10.3390/cells15050406 · 2026-02-26

## TL;DR

This paper explores how oral health reflects and responds to occupational stress in healthcare workers, suggesting saliva and microbiome markers could help detect and manage stress.

## Contribution

The paper introduces oral cellular homeostasis as a novel biological interface linking occupational stress, immunity, and the microbiome.

## Key findings

- Chronic occupational stress increases salivary cortisol and inflammation markers like IL-6 and TNF-α.
- Reduced salivary immunoglobulin A and microbiome diversity are linked to occupational stress.
- Balanced oral immune and microbial profiles correlate with better psychological adaptation and lower fatigue.

## Abstract

Positions oral cellular homeostasis as a biological interface linking occupational stress, immunity, and the oral microbiome.

Integrates evidence from oral biology, nutrition, and occupational health.

What are the main findings?
Occupational stress is associated with dysregulation of salivary biomarkers and oral immune–microbial balance.

Occupational stress is associated with dysregulation of salivary biomarkers and oral immune–microbial balance.

What are the implications of the main findings?
Oral biomarkers may support early detection of occupational strain.Integrated stress and diet-based interventions may enhance professional wellbeing.

Oral biomarkers may support early detection of occupational strain.

Integrated stress and diet-based interventions may enhance professional wellbeing.

Background: Healthcare professionals experience continuous biological and psychosocial stressors that may disturb oral and systemic homeostasis. Alterations in salivary secretion, mucosal immunity, and microbiome composition reflect adaptive cellular responses to chronic occupational stress. Understanding these mechanisms may provide a biological framework for resilience and wellbeing in everyday clinical practice. Objective: To narratively review the evidence linking oral cellular and molecular mechanisms—salivary biomarkers, epithelial and immune cell activity, and microbiome dynamics—with stress, fatigue, burnout, and wellbeing outcomes among healthcare professionals. Methods: This narrative review employed a PRISMA-guided literature search of PubMed, Scopus, Web of Science, and Cochrane Oral Health to enhance transparency and coverage across databases. Given the heterogeneity of study designs and outcomes, data were synthesized thematically without quantitative pooling or formal meta-analysis. Methodological strength was evaluated qualitatively, focusing on biomarker validity, sampling conditions, and conceptual relevance. Eligible designs included observational, experimental, and interventional studies. Results: Evidence from 99 studies suggests that chronic occupational stress elevates salivary cortisol, oxidative stress markers, and pro-inflammatory cytokines (IL-6, TNF-α), while reducing protective salivary immunoglobulin A and microbiome diversity. Balanced oral immune and microbial profiles were associated with better psychological adaptation and lower fatigue indices. Conclusions: Oral cellular homeostasis offers a promising window into the biological underpinnings of occupational stress and resilience in healthcare professionals. Systematic integration of salivary and mucosal biomarkers into workplace wellbeing programs could enhance early detection of dysregulated stress physiology. Future interdisciplinary research should bridge oral biology, occupational medicine, and mental health to strengthen sustainable wellbeing strategies across the health workforce.

## Linked entities

- **Proteins:** IL6 (interleukin 6), TNF (tumor necrosis factor)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** burnout (MESH:D002055), fatigue (MESH:D005221), inflammatory (MESH:D007249)
- **Chemicals:** cortisol (MESH:D006854)

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12984415/full.md

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Source: https://tomesphere.com/paper/PMC12984415