Aim To investigate the effects of sodium butyrate (NaB) and lipopolysaccharide (LPS) on gingival epithelial barrier. Material and methods We cultured human primary gingival epithelial cells and investigated the effects of NaB and LPS on gingival epithelial barrier and involved mechanisms at in vitro and in vivo levels by immunostaining, confocal microscopy, field emission scanning electron microscopy (FE‐SEM), transmission electronic microscopy (TEM), transepithelial electrical resistance (TEER), FTIC‐dextran flux, flow cytometry, real‐time PCR and Western blot assays. Results Our results showed that NaB, rather than LPS, destroyed the epithelial barrier by breaking down cell–cell junctions and triggering gingival epithelial cell pyroptosis with characteristic morphological changes, including swollen cells, large bubbles, pore formation in the plasma membrane and subcellular organelles changes. The upregulated expression of pyroptosis‐related markers, caspase‐3 and gasdermin‐E (GSDME) contributed to this effect. Pyroptosis aroused by NaB is a pro‐inflammatory cell death. Pyroptotic cell death provoked inflammatory responses by upregulation of IL‐8 and MCP‐1, and releasing intracellular contents into the extracellular microenvironment after pyroptotic rupture of the plasma membrane. Conclusions Our new findings indicate that butyrate is a potent destructive factor of gingival epithelial barrier and pro‐inflammatory mediator, which shed a new light on our understanding of periodontitis initiation.

BackgroundGlycine air polishing has been proved to be safe, comfortable and time-saving. Whether it could substitute ultrasonic scaling to remove dental plaque biofilm during periodontal maintenance remains unclear. The purposes of this study were to evaluate the effect of supragingival glycine air polishing (SGAP) on the subgingival periodontal pathogens during maintenance therapy and to check the association of periodontal pathogens and clinical parameters.MethodsTwenty-three chronic periodontitis patients during their maintenance therapy were enrolled in the 12-week study. According to randomized split-mouth design, the test side was treated with SGAP (65 μm), while the control side was treated with supragingival ultrasonic scaling and polishing (SUSP) with rubber cup. Clinical examination including plaque index (PLI), probing depth (PD), bleeding index (BI) were performed at baseline and 12 weeks post-treatment. Sampling of the subgingival plaque at each investigational site (mesiobuccal site of the mandibular first molar) was performed at baseline and 2, 4, 8, 12 weeks after maintenance treatment. Four periodontal pathogens including Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola and Fusobacterium nucleatum were detected by 16S rDNA polymerase chain reaction.ResultsClinical status generally improved after treatment in both groups. PLI in both groups, PD in SGAP group and bleeding on probing (%) in SUSP group significantly decreased after treatment (p < 0.05). There was no significant difference of clinical parameters between two groups before and after treatment. The detection rates of P. gingivalis, T. denticola in both groups, T. forsythia in SUSP group and F. nucleatum in SGAP group decreased after maintenance treatment in both groups, although no significant difference was found, and it rebound to baseline level at 12 weeks after maintenance treatment. There was no significant difference between SGAP group and SUSP group at any time point. T. denticola-positive sites had significantly greater BI than T. denticola-negative sites (p < 0.05).DiscussionSupragingival glycine air polishing had a reliable effect in removing subgingival dental plaque biofilm during maintenance period, and three months may be a proper maintenance interval for pockets not more than 5 mm.

Aim To assess the subgingival microbial shift of maintained periodontitis treated by ultrasonic scaling (US) or air polishing (AP) during a 3‐month maintenance interval. Materials and methods We conducted a 12‐week randomized split‐mouth controlled trial with US and AP in 17 maintained subjects (bleeding on probing [BOP%] ≤25%, probing depth [PD] ≤5 mm). They were monitored at baseline, week 2, week 8 and week 12. The V3‐V4 region of the 16S rDNA from 136 subgingival plaque samples was sequenced and analysed. Results Treatment by US or AP could effectively reduce the PD, microbial richness, diversity, periodontitis‐associated microbiota and pathogenic metabolism in maintained periodontitis. Bacteria recolonized after treatment and returned to the pre‐treatment level 12 weeks after treatment. Ultrasonic scaling group demonstrated slight advantage in reducing BOP (%), pathogenic bacteria and metabolism than AP group. Pathogenic microbiota and commensal microbiota kept a balance in subgingival community of maintained patients during the 3‐month interval. Conclusions Treatment by US or AP effectively reduced the pathogenicity of subgingival microbiome by reducing microbial diversity, proportion of periodontitis‐associated microbiota and pathogenic metabolism. It helped to keep a balanced subgingival community and stable periodontal condition over a single maintenance interval of 3 months.