Abstract
Periodontitis is a kind of infectious disease initiated by colonization of subgingival periodontal pathogens, which cause destruction of tooth-supporting tissues, and is a predominant threat to oral health as the most common cause of loss of teeth. The aim of this pilot study was to characterize the subgingival bacterial biodiversity of periodontal pockets with different probing depths in patients with different forms of periodontitis. Twenty-one subgingival plaque samples were collected from three patients with chronic periodontitis (ChP), three patients with aggressive periodontitis (AgP) and three periodontally healthy subjects (PH). Each patient with periodontitis was sampled at three sites, at different probing depths (PDs, one each at 4 mm, 5–6 mm, and ≥ 7 mm). Using 16S rRNA gene high-throughput sequencing and bioinformatic analysis, we found that subgingival communities in health and periodontitis samples largely differed. Meanwhile, Acholeplasma, Fretibacterium, Porphyromonas, Peptococcus, Treponema_2, Defluviitaleaceae_UCG_011, Filifactor, and Mycoplasma increased with the deepening of the pockets in ChP, whilst only Corynebacterium was negatively associated with PD. In AgP, Corynebacterium and Klebsiella were positively associated with PD, while Serratia, Pseudoramibacter, Defluviitaleaceae_UCG_011, and Desulfobulbus were negatively associated with PD. And among these two groups, Corynebacterium shifted differently. Moreover, in subgingival plaque, the unweighted UniFrac distances between samples from pockets with different PD in the same patients were significantly lower than those from pockets within the same PD category from different patients. This study demonstrated the shift of the subgingival microbiome in individual teeth sites during disease development. Within the limitation of the relative small sample size, this pilot study shed new light on the dynamic relationship between the extent of periodontal destruction and the subgingival microbiome.
Highlights
Periodontitis is a kind of infectious disease initiated by the colonization of subgingival periodontal pathogens, which cause destruction of the ligament and alveolar bone supporting the teeth and, results in the loss of the affected teeth and with the resultant loss of quality of life (Newman et al, 2011; Al-Harthi et al, 2013)
The results indicated that along with the changes of probing depth (PD), the relative abundance of several bacteria changed in Chronic periodontitis (ChP) and aggressive periodontitis (AgP), and some among them showed significant linear correlation
The results indicated that, along with the changes of PD of the periodontal pockets in the same periodontitis patient, the relative abundance of several bacteria changed in both ChP and AgP, and some among the genus showed significant liner correlation
Summary
Periodontitis is a kind of infectious disease initiated by the colonization of subgingival periodontal pathogens, which cause destruction of the ligament and alveolar bone supporting the teeth and, results in the loss of the affected teeth and with the resultant loss of quality of life (Newman et al, 2011; Al-Harthi et al, 2013). According to the latest official classification system for periodontal diseases from the American Academy of Periodontology, periodontitis can be classified into two main types: chronic and aggressive. Chronic periodontitis (ChP) is a slowly progressive disease, most prevalent in adults and usually associated with marked accumulation of biofilm and calculus. Aggressive periodontitis (AgP) belongs to a group of rare periodontal diseases initiated at a young age with rapid attachment loss, which is not necessarily correlated with high levels of biofilm and calculus (Armitage, 1999). The microorganisms in a dental biofilm are believed to be involved in the pathogenesis of periodontitis; in particular, subgingival bacteria plays an important role in its initiation and progression. Decades of investigations have tried to identify a microbiological element of AgP to help in the differential diagnosis from ChP, the notion that AgP has a distinct microbiological pathogenesis from ChP has still not been confirmed (Armitage and Cullinan, 2010; Heller et al, 2012)
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