Background: To date, several studies have confirmed the fact that over 700 species of microbiota interacts with host, modulating immunity, controlling the homeostasis environment, and thus maintaining systemic condition. Dysbiosis in the subgingival biofilm can initiate chronic inflammation of the gingiva, potentially progressing to periodontitis. Advances in DNA sequencing analysis of the subgingival microbial community have shown that periodontal treatment causes a microbial shift in subgingival plaque, affecting the taxonomic composition (disease- and health-associated taxa). Yet, none of these have been investigated in Indonesia.
Objective: The objective was to profile the composition of oral microbiome in Indonesian population with healthy, gingivitis, and periodontitis status. Further, we analyzed the subgingival bacterial alteration following the therapy in periodontitis group.
Methods: Twelve subjects consisting of healthy, gingivitis, and periodontitis patients were included. Additionally, the periodontitis group was observed at baseline, 1-month, and 3-month. Subgingival dental plaque were sampled and 16S rRNA NGS analysis was performed. Alpha (Chao1, Shannon, and Simpson indices) and beta diversity (PCoA plots based on Bray–Curtis dissimilarity) were observed. Microbiota composition at the genus and species levels was analyzed.
Results: No statistically significant differences (
p > 0.05) were found for Chao1, Shannon, and Simpson indices amongst groups and in periodontitis patients across the observation. At the genus level, PCoA plots based on Bray–Curtis dissimilarity revealed that the clinical status accounted for 21.9% of the total variation (R
2 = 0.219,
p = 0.197), while at the species level, it accounted for 19.8% (R
2= 0.198,
p = 0.281). Periodontitis samples across all timepoints showed no distinct clustering at either the genus 7.6% (R
2 = 0.076
p = 0.097) or species levels 9.7% (R
2 = 0.097
p = 0.995). Top five subgingival microbiota at the genus and species levels in all groups showed definite pattern of composition. Although no significant association was found (
p > 0.05), it described that
Veillonella parvula,
Campylobacter gracilis, and
Capnocytophaga granulosa were more abundant in healthy subjects than in gingivitis and periodontitis.
Prevotella oris and
Selenomonas noxia were less abundant in healthy subject than in gingivitis and periodontitis. In periodontitis subjects,
Prevotella intermedia was increased by the therapy at 1 month and reduced again at 3 months. On the other hand,
Capnocytophaga granulosa was increased by the therapy at 1 and 3 months.
Hoylesella loescheii was reduced by the time.
Porphyromonas gingivalis was reduced at 1 month and increased again at 3 months.
Discussion: The result showed that the number of alpha diversity was notably higher in the gingivitis and periodontitis groups compared to health group, supporting a trend toward increased community richness and evenness in diseases states. The microbial richness and evenness remained relatively stable across the evaluated periods within periodontitis cohort. Oral microbial composition defines the periodontal status and disease. More abundance of Red Complex bacteria is associated with disease-associated condition. Pathogen re-colonization may occur 3 months after the therapy.
Conclusions: These findings suggest that maintaining health-associated microbiome may be beneficial to the clinical status. Periodontal recall may be addressed from 1 to 3 months after the therapy to avoid bacterial re-colonization. Suppressing bacterial dysbiosis and regulating periodontal homeostasis are the main key in managing periodontal treatment.
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