Mouth Breathing, Sleep Disorders, and the Risk of Early Childhood Caries: A Contemporary Interdisciplinary Review
DOI:
https://doi.org/10.33295/1992-576X-2026-4-PDEN-1Keywords:
early childhood caries, mouth breathing, pediatric obstructive sleep apnea, salivary biomarkers, oral microbiome, sleep-disordered breathing, interdisciplinary approach, caries risk, screening, causalityAbstract
Background. Early childhood caries (ECC) remains a leading chronic disease, affecting up to 70% of preschoolers in some regions, with a substantial burden in Europe. Meanwhile, mouth breathing (often due to adenoid hypertrophy or allergic rhinitis) affects ~21% of children, and pediatric obstructive sleep apnea (OSA) prevalence has risen to 10–20% over the past decade. Despite frequent coexistence, pathophysiological links are underexplored, and evidence remains fragmented, warranting a critical interdisciplinary synthesis.
Objective. To synthesize contemporary (2016–2026) evidence on biological, microbiological, and clinical associations between mouth breathing, sleep-disordered breathing, and ECC risk in children, focusing on interdisciplinary diagnostic and preventive strategies, with critical appraisal of evidence quality.
Methods. A systematized search was conducted in PubMed, Scopus, Web of Science, Embase, and Cochrane Library following a PROSPERO-registered protocol. We included systematic reviews, meta-analyses, cohort, cross-sectional, and case-control studies in children aged 0–12 years. Study quality was assessed using Newcastle-Ottawa Scale (NOS) and GRADE tools.
Results. Evidence supports a pathogenic cascade: nasal obstruction → mouth breathing → salivary dysfunction (xerostomia, reduced buffering, altered pH and ionic content) → microbiome dysbiosis (overgrowth of Streptococcus mutans, Lactobacillus spp., Scardovia wiggsiae) and elevated inflammatory biomarkers (IL-6, TNF-α, lactoferrin). Nocturnal dehydration and intermittent hypoxia in OSA amplify oxidative stress. Most studies are cross-sectional, precluding causal inference; some show contradictory associations (e.g., lower caries in OSA children, potentially due to heightened parental care). Orthodontic sequelae (maxillary constriction, high palate) perpetuate the cycle. Salivary biomarkers (lysozyme, sIgA, β-defensin-2, histatin-5) are promising but require prospective validation.
Conclusions. Mouth breathing and pediatric OSA are modifiable ECC risk factors mediated by salivary dysfunction, dysbiosis, and inflammation, but evidence is largely correlational. Structured interdisciplinary screening algorithms (incorporating PSQ, mouth breathing assessment, and caries risk tools) in dental and primary care are essential. Long-term cohort studies are urgently needed to establish causality and evaluate intervention efficacy.
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