Journal of dentistry · 2026
Multiomics analyses in young grade C molar incisor pattern periodontitis.
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Alamri Meaad M, Proctor Gordon, Garcia-Guevara Fernando, Guennec Adrien Le, Mainas Giuseppe, Shoaie Saeed, Nibali Luigi
Аннотация
OBJECTIVE: To explore the microbial profiles in plaque and saliva and metabolic profiles in saliva and serum collected from young patients (≤25 years old) with grade C molar incisor pattern periodontitis (C/MIP), to compare them to age-matched controls and integrate both omics to elucidate C/MIP pathogenesis.
MATERIAL AND METHOD: Thirty-one young patients with C/MIP and 31 periodontally healthy age-matched controls were recruited. Bacterial profiles were investigated in unstimulated saliva and subgingival plaque using shotgun sequencing metagenomics while metabolic profiles were assessed in saliva using nuclear magnetic resonance and serum using mass spectrometry. Data from both omics analyses were integrated and visualised as interaction networks using Cytoscape software.
RESULTS: C/MIP showed significantly lower levels of several salivary (e.g., dimethylamine, proline, glycine) and serum metabolites, and higher levels of others including methyl indole-3-acetate and sulfosalicylic acid, compared to controls (P < 0.001). Fifteen bacteria, of which twelve were associated with C/MIP, were differentially prevalent between groups. The plaque microbiome in C/MIP was enriched with pathogenic species such as D. oralis, C. rectus, T. denticola, and P. endodontalis, while health-associated bacteria like R. mucilaginosa and L. hongkongensis were more prevalent in controls. D. oralis and GGB10485-SGB49305 emerged as potential microbial biomarkers. Notably, metabolites such as DL-glutamine and taurine were significantly associated with periodontal pathogens.
CONCLUSION: C/MIP is marked by a distinct dysbiotic microbiome and altered metabolic profile. While key pathogens and metabolites likely contribute to disease progression, the underlying mechanisms remain only partially understood due to the complexity and incomplete characterisation of many associated factors.
CLINICAL SIGNIFICANCE: This study highlighted the multifactorial nature of C/MIP, driven by microbial dysbiosis, immune disturbances, and metabolic alterations. A comprehensive multi-omics approach offered a foundation for understanding microbial-metabolite dynamics in young patients, and highlighted candidate biomarkers for future diagnostics and therapeutics.
MATERIAL AND METHOD: Thirty-one young patients with C/MIP and 31 periodontally healthy age-matched controls were recruited. Bacterial profiles were investigated in unstimulated saliva and subgingival plaque using shotgun sequencing metagenomics while metabolic profiles were assessed in saliva using nuclear magnetic resonance and serum using mass spectrometry. Data from both omics analyses were integrated and visualised as interaction networks using Cytoscape software.
RESULTS: C/MIP showed significantly lower levels of several salivary (e.g., dimethylamine, proline, glycine) and serum metabolites, and higher levels of others including methyl indole-3-acetate and sulfosalicylic acid, compared to controls (P < 0.001). Fifteen bacteria, of which twelve were associated with C/MIP, were differentially prevalent between groups. The plaque microbiome in C/MIP was enriched with pathogenic species such as D. oralis, C. rectus, T. denticola, and P. endodontalis, while health-associated bacteria like R. mucilaginosa and L. hongkongensis were more prevalent in controls. D. oralis and GGB10485-SGB49305 emerged as potential microbial biomarkers. Notably, metabolites such as DL-glutamine and taurine were significantly associated with periodontal pathogens.
CONCLUSION: C/MIP is marked by a distinct dysbiotic microbiome and altered metabolic profile. While key pathogens and metabolites likely contribute to disease progression, the underlying mechanisms remain only partially understood due to the complexity and incomplete characterisation of many associated factors.
CLINICAL SIGNIFICANCE: This study highlighted the multifactorial nature of C/MIP, driven by microbial dysbiosis, immune disturbances, and metabolic alterations. A comprehensive multi-omics approach offered a foundation for understanding microbial-metabolite dynamics in young patients, and highlighted candidate biomarkers for future diagnostics and therapeutics.