Antibiofilm activity of ultra-small gold nanoclusters against Fusobacterium nucleatum in dental plaque biofilms.

Pathogenic dental plaque biofilms are universal and harmful, which can result in oral infections and systemic diseases. Many conventional therapeutic methods have proven insufficient or ineffective against plaque biofilms. Therefore, new strategies are urgently needed. Fusobacterium nucleatum (F. nucleatum), a periodontal pathogen associated with a variety of oral and systemic diseases, is thought to be central to the development and structure of dental plaques. Here, ultra-small gold nanoclusters (AuNCs) were prepared. They exhibited potent antibacterial activity against F. nucleatum through enhanced destruction of bacterial membranes and generation of reactive oxygen species. Furthermore, due to their excellent penetration, the AuNCs could inhibit biofilm formation and destroy mature biofilms in vitro. Their antibiofilm efficacy was further confirmed in a mouse model, where they reduced biofilm accumulation and ameliorated inflammation. Meanwhile, the disruption of oral and gut microbiota caused by colonization of oral F. nucleatum could be partially restored through AuNCs treatment. Therefore, AuNCs could be considered as promising antibiofilm agents and have great potential in the clinical treatment of dental plaque.

Accelerated alveolar bone loss in a mouse model of inflammatory bowel disease and its relationship with intestinal inflammation.

BACKGROUND: Bone loss is a common complication of inflammatory bowel disease (IBD); however, few studies have focused on alveolar bone loss (ABL) in IBD. Herein, we systematically observed ABL in an interleukin (IL)-10 knockout (IL-10-/- ) mouse model of IBD and explored the possible mechanisms. METHODS: IL-10-/- and age-matched wild-type (WT) male mice were sacrificed every 2 weeks from 12 to 24 weeks of age. ABL was determined by microcomputed tomography. Periodontal and intestinal inflammation were evaluated using histological grading and inflammatory factor expression levels. Intestinal barrier integrity and cytokine levels in serum were examined by immunofluorescence and enzyme-linked immunosorbent assays, respectively. The expression of macrophage phenotype markers, including inducible nitric oxide synthase (iNOS), arginase-1 (Arg-1), and bone metabolic markers, including osteoprotegerin, receptor activator of nuclear factor-κB ligand (RANKL), were measured by immunohistochemistry. The macrophage phenotype in the periodontium was also examined by real-time quantitative polymerase chain reaction. RESULTS: Compared with WT mice, IL-10-/- mice exhibited significant ABL from 18 weeks of age. However, no significant differences were observed in the periodontium between the two groups in either histopathological scores or inflammatory factor levels. In the colon and ileum, these measurements significantly increased in IL-10-/- mice from 12 and 14 weeks, respectively. Correlation analysis also revealed that ABL in IL-10-/- mice was positively correlated with intestinal inflammation. Furthermore, IL-10-/- mice showed a destroyed intestinal barrier and higher serum levels of inflammatory factors. In both the intestine and periodontium, higher iNOS and lower Arg-1 levels, along with an increase in RANKL expression in the periodontium, were examined in IL-10-/- mice. CONCLUSIONS: An accelerated ABL spontaneously occurred in IL-10-/- mice and was correlated more with inflammation of the intestine than periodontium. Immunopathological changes may be the potential cause of abnormal alveolar bone metabolism.

The Association between Periodontitis and Inflammatory Bowel Disease: A Systematic Review and Meta-analysis.

BACKGROUND: It has been reported that patients with inflammatory bowel disease (IBD) are more susceptible to periodontitis. However, data regarding the risk of periodontitis in IBD patients are scarce, and results from individual studies remain controversial. The aim of this study is to investigate the risk of periodontitis in IBD patients. METHODS: Web of Science, PubMed, and Embase were searched for studies investigating the risk of periodontitis in the IBD patient population from Jan. 2000 to Nov. 2020. Articles were included if they contained the number of people with IBD diagnosed with periodontitis (or periodontal disease parameters) compared with a control group. Case reports, reviews, animal studies, and articles without available abstracts were excluded. A pooled odds ratio (OR) and 95% confidence interval (CI) were calculated to assess the association between periodontitis and IBD. RESULTS: Six studies were included in the meta-analysis. The overall risk of periodontitis was significantly higher in IBD patients than controls (OR: 2.10, 95% CI: 1.60-2.74; I 2 = 27%). In particular, Crohn's disease (CD) and ulcerative colitis (UC) were both linked to an increased risk of periodontitis (OR: 1.72, 95% CI: 1.36-2.19; I 2 = 0% for CD vs. OR:2.39, 95% CI: 1.19-4.80; I 2 = 85% for UC). CONCLUSIONS: IBD patients are at higher risk of periodontitis than controls. After subgroup analysis, the elevated risk remained significant when analyzing CD or UC alone. UC patients were at higher risk of developing periodontitis than CD patients.

Human ß-defensin 3 gene modification promotes the osteogenic differentiation of human periodontal ligament cells and bone repair in periodontitis.

Efforts to control inflammation and achieve better tissue repair in the treatment of periodontitis have been ongoing for years. Human ß-defensin 3, a broad-spectrum antimicrobial peptide has been proven to have a variety of biological functions in periodontitis; however, relatively few reports have addressed the effects of human periodontal ligament cells (hPDLCs) on osteogenic differentiation. In this study, we evaluated the osteogenic effects of hPDLCs with an adenoviral vector encoding human ß-defensin 3 in an inflammatory microenvironment. Then human ß-defensin 3 gene-modified rat periodontal ligament cells were transplanted into rats with experimental periodontitis to observe their effects on periodontal bone repair. We found that the human ß-defensin 3 gene-modified hPDLCs presented with high levels of osteogenesis-related gene expression and calcium deposition. Furthermore, the p38 MAPK pathway was activated in this process. In vivo, human ß-defensin 3 gene-transfected rat PDLCs promoted bone repair in SD rats with periodontitis, and the p38 mitogen-activated protein kinase (MAPK) pathway might also have been involved. These findings demonstrate that human ß-defensin 3 accelerates osteogenesis and that human ß-defensin 3 gene modification may offer a potential approach to promote bone repair in patients with periodontitis.

[Relationship between patients' sensitivity to moxibustion stimulation and clinical effect in the treatment of peripheral facial palsy].

OBJECTIVE: To compare the outcome difference between the heat-sensitive and non-sensitive moxibustion stimulation of Yifeng (TE 17) in the treatment of peripheral facial palsy. METHODS: A total of 43 patients with peripheral facial paralysis were divided into heat-sensitive moxibustion (n = 21) and non-sensitive moxibustion (n = 22) groups in accordance with their reactions to moxa-heat stimulation. Mild moxibustion was applied to bilateral Yifeng (TE 17) for 45 minutes, followed by mild acupuncture stimulation of Cuanzhu (BL 2), Yangbai (GB 14), Sibai (ST 2), Hegu (LI 4), etc. Moxibustion treatment was conducted once daily for 10 days, and acupuncture treatment given once daily for 20 days (with 2 days interval between every 10 days). Following moxibustion, if the patient felt regional heat penetrating to the deep tissue, extending peripherally, or propagating to other part of the body, or felt mild warm in the stimulated region but warmer in the slightly distant part, or felt mild warm on the skin surface but warmer in the deep tissue, it was considered to be heat-sensitivity. Patients with occurrence of heat-sensitivity being equal to and more than 3 times during the 10 sessions of treatment were assigned to heat-sensitive group, and those with occurrence of heat-sensitivity being equal to or less than 2 times assigned to non-sensitive moxibustion group. According to Portmann Scale (including movement and resting posture) for the voluntary movement state of the face, forehead, winkles eye closure, open mouth smile, snarl, and pucker; points 0, 1, 2 and 3 indicate no muscular movement, marked asynersis, asynersis and normal, respectively. In the light of resting posture of the eye, the nasolabial fold and mouth corner, 0, 1, and 2 points indicate severe, mild dissymmetry and normal, separately. In evaluation of the therapeutic effect, twenty points (at most) indicate cured, 17-19 points marked improvement; 14- 16 points improved, and < or = 13 points failure. RESULTS: Compared with pre-treatment, Portmann scores of both heat-sensitive moxibustion and non-sensitive moxibustion groups were significantly increased after the treatment (P < 0.001), and the score of the heat-sensitive moxibustion group was markedly higher than that of the non-sensitive moxibustion group (P < 0.05). Of the 21 and 22 facial palsy patients in the heat-sensitive moxibustion and non-sensitive moxibustion groups, 8 and 5 cases were cured, 10 and 7 were markedly effective, 3 and 10 were improved, with the markedly effective rates being 85.71% and 54.55%, respectively. The therapeutic effect of the heat-sensitive moxibustion group was statistically better (P < 0.05). CONCLUSION: Heat-sensitive moxibustion is significantly superior to non-sensitive moxibustion in improving symptoms of peripheral facial palsy patients, suggesting a necessity for paying attention to patients' reactions during moxibustion treatment.