Journal of periodontal research最新文献

Aims

This study aimed to elucidate the alterations in Follistatin-like protein 1 (FSTL1) and its association with the pathological process of periodontitis.

Methods

This study included 48 patients with periodontitis and 42 healthy controls. The expression level of FSTL1 in the gingiva was determined by RT-qPCR, validated using the dataset GSE16134, and subsequently examined by western blotting. Bioinformatics analysis revealed a single-cell distribution of FSTL1, characteristic of angiogenesis and immune cell infiltration. The expression and distribution of FSTL1, vascular endothelial marker protein CD31 and myeloperoxidase (MPO), the indicator of neutrophil activity, were determined by immunohistochemistry (IHC). A series of correlation analyses was performed to determine the associations between FSTL1 and clinical parameters, including probing depth (PD) and clinical attachment loss (CAL), and their potential role in angiogenesis (CD31) and neutrophil infiltration (MPO).

Results

FSTL1 was significantly upregulated in the gingiva of patients with periodontitis compared to their healthy counterparts. In addition, FSTL1 was positively correlated with the clinical parameters PD (r = .5971, p = .0005) and CAL (r = .6078, p = .0004). Bioinformatic analysis and IHC indicated that high FSTL1 expression was significantly correlated with angiogenesis and neutrophil infiltration in periodontitis. Moreover, receiver operating characteristic (ROC) analysis demonstrated that FSTL1 could serve as an independent indicator for evaluating the severity of periodontitis (area under the curve [AUC] = 0.9011, p < .0001).

Conclusion

This study demonstrated FSTL1 upregulation in periodontitis and its potential contribution to the disease via angiogenesis and neutrophil infiltration.

Aims

This study sought to explore the impact of Fusobacterium nucleatum on hepatic steatosis in apolipoprotein E (ApoE) knockout (KO) mice induced by a high-fat diet (HFD) and elucidate the underlying mechanism.

Methods

ApoE KO mice, on a HFD, received F. nucleatum oral inoculation every other day. After 24 weeks, body weight, liver weight, and liver index were assessed. Serum biochemistry and pro-inflammatory factors in serum and liver were analyzed. The histopathology of right maxilla and live were performed. Oil red O, immunohistochemistry, and immunofluorescence staining for the liver were conducted. Myeloperoxidase (MPO) activity, apoptosis, lipid reactive oxygen species (ROS), ROS, lipid peroxides, and hepatic lipids were also evaluated. Liver inflammation, fibrosis, de novo lipogenesis (DNL)-related molecule, and Nrf2/Keap1-related signaling molecule gene/protein expression were determined by real-time PCR (RT-PCR) and/or Western blot (WB) analysis.

Results

HFD-fed ApoE KO mice infected by F. nucleatum demonstrated significant changes, including increased body and liver weight, elevated proinflammatory factors and lipids in serum and liver, as well as neutrophil infiltration, fibrosis, apoptosis, oxidative stress, and lipid peroxidation in the liver. Additionally, F. nucleatum stimulates hepatic lipid accumulation and activates de novo lipogenesis (DNL), while simultaneously suppressing the Nrf2/Keap1 antioxidant pathway.

Conclusion

In conclusion, our study reveals that oral inoculation of F. nucleatum might promote hepatic steatosis by inhibiting Nrf2/Keap1 pathway.

The aim of this systematic review (SR) was to assess whether tooth mobility (TM) increases the risk of tooth extraction/loss. The protocol was registered in PROSPERO database (CRD42023485425). The focused PECO questions were as follows: (1) “In patients with periodontitis, undergoing periodontal treatment, are teeth affected by mobility at higher risk of being extracted/lost compared to non-mobile teeth, with a minimum follow-up of 10 years?” and (2) “In these patients, does varying degrees of tooth mobility increase the risk of tooth extraction/loss, with a minimum follow-up of 10 years?”. Results were reported according to PRISMA statement. Electronic and manual searches were conducted to identify longitudinal studies. The different assessments of tooth mobility were pooled into three groups: TM0: Undetectable tooth mobility, TM1: Horizontal/Mesio-distal mobility ≤1 mm, TM2: Horizontal/Mesio-distal mobility >1 mm or vertical tooth mobility. Tooth loss was the primary outcome. Various meta-analyses were conducted, including subgroup analyses considering different follow-up lengths and the timing of TM assessment, along with sensitivity analyses. A trial sequential analysis was also performed. Eleven studies were included (1883 patients). The mean follow-up range was 10–25 years. The weighted total of included teeth, based on the sample size, was 18 918, with a total of 1604 (8.47%) extracted/lost teeth. The overall rate of tooth extraction/loss increased with increasing mobility: TM0 was associated with a 5.85% rate (866/14822), TM1 with the 11.8% (384/3255), TM2 with the 40.3% (339/841). Mobile teeth (TM1/TM2) were at an increased risk for tooth extraction/loss, compared to TM0 (HR: 2.85; [95% CI 1.88–4.32]; p < .00001). TM1 had a higher risk than TM0 (HR: 1.96; [95% CI 1.09–3.53]; p < .00001). TM2 had a higher risk than TM1 (HR: 2.85; [95% CI 2.19–3.70]; p < .00001) and TM0 (HR: 7.12; [95% CI 3.27–15.51]; p < .00001). The results of the tests for subgroup differences were not significant. Sensitivity meta-analyses yielded consistent results with other meta-analyses. Within the limits of the quality of the studies included in the meta-analyses, mobile teeth were at higher risk of being extracted/lost in the long-term and higher degrees of TM significantly influenced clinicians‘ decision to extract a tooth. However, most teeth can be retained in the long-term and thus TM should not be considered a reason for extraction or a risk factor for tooth loss, regardless of the degree of TM.

Aim

We investigated the in vitro effect of Limosilactobacillus reuteri DSM 17938 supernatant on the inflammatory response of human gingival fibroblasts (HGF) challenged by lipopolysaccharide (LPS) or elevated glucose levels.

Methods

HGF were exposed to LPS (1 μg/mL), glucose (5, 12 mM or 25 mM), and dilutions of supernatant prepared from L. reuteri DSM 17938 (0.5 × 10⁷, 1.0 × 10⁷, 2.5 × 10⁷, and 5.0 × 10⁷ CFU/mL). After 24 h cell viability and levels of cytokines (IL-1β, IL-6 and IL-8) and TLR-2 were determined.

Results

None of the tested L. reuteri (DSM 17938) supernatant concentrations reduced the viability of HGF. Supernatant concentrations (2.5 × 10⁷ and 5 × 10⁷ CFU/mL) significantly (p < .05) decreased the production of IL-1β, IL-6, IL-8, and TLR-2 in the presence of LPS. In contrast, inflammatory markers were not reduced by L. reuteri supernatant in the presence of glucose. Glucose concentrations of 12 mM and 24 mM still lead to an elevated production of the investigated biochemical mediators.

Conclusion

While L. reuteri (DSM 17938) supernatant attenuates the inflammatory response of HGF to LPS in a dose-dependent manner, elevated glucose levels suppress this action. These in vitro results support the overall anti-inflammatory efficacy of L. reuteri supplementation in plaque-associated periodontal inflammations.

Aims

To histologically compare osseointegration and crestal bone healing between newly introduced tapered, self-cutting bone-level test implants and tapered bone-level control implants in sites with fully healed sites.

Methods

Sixty-six implants (33 test, 33 control) were placed 1 mm subcrestally in a minipig model and underwent qualitative histologic and quantitative histometric analyses after 3, 6 and 12 weeks of submerged healing. The primary and secondary outcomes were the bone-to-implant contact (BIC) and first bone-to-implant contact (fBIC). Outcomes between the test and control implants were statistically compared.

Results

The BIC values of the test implants were comparable and non-inferior over the time points studied, except for the 12 weeks time point which showed statistically significantly higher BIC values of the test (88.07 ± 5.35%) compared to the control implants (80.88 ± 7.51%) (p = .010). Similarly comparable and non-inferior were the fBIC values, except for the 6-week outcome, which showed statistically higher values for the test (−546.5 ± 450.80 μm) compared to the control implants (−75.7 ± 100.59 μm). fBIC results for the test implants were qualitatively more stable and consistent between test time points.

Conclusion

Novel self-cutting bone-level test implants demonstrated superior osseointegration and similar bone levels compared to conventional bone-level implants after a healing period of 12 weeks in healed ridges.

Aim

The present systematic review with meta-analysis aimed to investigate the global association between smokeless tobacco (SLT) use and periodontitis, considering significant effect size variation based on the income levels of countries.

Methods

We searched seven databases to identify studies that assessed the prevalence of periodontitis in adult SLT users compared to non-users. The quality of studies was evaluated using the 10-item risk-of-bias tool, and publication bias was addressed through the trim-and-fill method. Sensitivity analysis utilized the leave-one-out approach. Meta-analysis and meta-regression, stratified by country income, SLT type, and smoking status, employed robust variance estimation.

Results

From an initial pool of 484 studies, 29 studies met the selection criteria and were subjected to qualitative synthesis. Subsequently, data from 19 studies were included in the meta-analysis. SLT users exhibited a nearly threefold greater likelihood of periodontitis compared to non-users (OR = 2.99; 95% CI: 2.10, 4.27; p < .01). The pooled estimate did not vary significantly based on the type of SLT used or concurrent smoking. However, the odds of periodontitis varied according to the economic level of the country; the pooled estimate was higher in high-income countries (OR = 1.69; 95% CI: 1.20, 2.37; p < .01) and even higher in lower-middle-income and lower-income countries (OR = 3.91; 95% CI: 2.66, 5.77; p < .01).

Conclusions

Smokeless tobacco users have a higher likelihood of developing periodontitis. This study underscores global disparities in the SLT–periodontitis relationship, highlighting the need for targeted interventions, particularly in economically challenged areas where SLT use is largely unregulated.

Aim

Evidence suggests that translocation of oral pathogens through the oral–gut axis may induce intestinal dysbiosis. This study aimed to evaluate the impact of a highly leukotoxic Aggregatibacter actinomycetemcomitans (Aa) strain on the gut microbiota, intestinal mucosal integrity and immune system in healthy mice.

Methods

Eight-week-old male C57BL6 mice were divided into control (n = 16) and JP2 groups (n = 19), which received intragastric gavage with PBS and with a suspension of Aa JP2 (HK921), respectively, twice a week for 4 weeks. Colonic lamina propria, fecal material, serum, gingival tissues, and mandibles were obtained for analyses of leukocyte populations, inflammatory mediators, mucosal integrity, alveolar bone loss, and gut microbiota. Differences between groups for these parameters were examined by non-parametric tests.

Results

The gut microbial richness and the number of colonic macrophages, neutrophils, and monocytes were significantly lower in Aa JP2-infected mice than in controls (p < .05). In contrast, infected animals showed higher abundance of Clostridiaceae, Lactobacillus taiwanensis, Helicobacter rodentium, higher levels of IL-6 expression in colonic tissues, and higher splenic MPO activity than controls (p < .05). No differences in tight junction expression, serum endotoxin levels, and colonic inflammatory cytokines were observed between groups. Infected animals presented also slightly more alveolar bone loss and gingival IL-6 levels than controls (p < .05).

Conclusion

Based on this model, intragastric administration of Aa JP2 is associated with changes in the gut ecosystem of healthy hosts, characterized by less live/recruited myeloid cells, enrichment of the gut microbiota with pathobionts and decrease in commensals. Negligible levels of colonic pro-inflammatory cytokines, and no signs of mucosal barrier disruption were related to these changes.