Poor periodontal health, dental care, and oral health knowledge were significantly associated with an increased risk of COPD. Our findings indicate the importance of promoting dental care and oral health knowledge that can be integrated into the prevention and treatment of COPD.

Effects of periodontal treatment on lung function and exacerbation frequency in patients with chronic obstructive pulmonary disease and chronic periodontitis: A 2-year pilot randomized controlled trial. J Clin Periodontol 2014; 41: 564-572. doi: 10.1111/jcpe.12247. AbstractAim: To evaluate the direct effects of periodontal therapy in Chronic Obstructive Pulmonary Disease (COPD) patients with chronic periodontitis (CP). Materials and Methods: In a pilot randomized controlled trial, 60 COPD patients with CP were randomly assigned to receive scaling and root planing (SRP) treatment, supragingival scaling treatment, or oral hygiene instructions only with no periodontal treatment. We evaluated their periodontal indexes, respiratory function, and COPD exacerbations at baseline, 6 months, 1, and 2 years. Results: Compared with the control group, measurements of periodontal indexes were significantly improved in patients in two treatment groups at 6-month, 1-year, and 2-year follow-up (all p < 0.05). Overall, the means of forced expiratory volume in the first second/forced vital capacity (FEV1/FVC) and FEV1 were significantly higher in the two therapy groups compared with the control group during the follow-up (p < 0.05). In addition, the frequencies of COPD exacerbation were significantly lower in the two therapy groups than in the control group at 2-year follow-up (p < 0.05). Conclusions: Our preliminary results from this pilot trial suggest that periodontal therapy in COPD patients with CP may improve lung function and decrease the frequency of COPD exacerbation.

Fewer remaining teeth, high PLI scores, and low tooth brushing times are significant correlates of COPD exacerbations, indicating that improving periodontal health and oral hygiene may be a potentially preventive strategy against COPD exacerbations.

Probiotic bacteria are known to harbor intrinsic and mobile genetic elements that confer resistance to a wide variety of antibiotics. Their high amounts in dietary supplements can establish a reservoir of antibiotic resistant genes in the human gut. These resistant genes can be transferred to pathogens that share the same intestinal habitat thus resulting in serious clinical ramifications. While antibiotic resistance of probiotic bacteria from food, human and animal sources have been well-documented, the resistant profiles of probiotics from dietary supplements have only been recently studied. These products are consumed with increasing regularity due to their health claims that include the improvement of intestinal health and immune response as well as prevention of acute and antibiotic-associated diarrhea and cancer; but, a comprehensive risk assessment on the spread of resistant genes to human health is lacking. Here, we highlight recent reports of antibiotic resistance of probiotic bacteria isolated from dietary supplements, and propose complementary strategies that can shed light on the risks of consuming such products in the context of a global widespread of antibiotic resistance. In concomitant with a broader screening of antibiotic resistance in probiotic supplements is the use of computational simulations, live imaging and functional genomics to harvest knowledge on the evolutionary behavior, adaptations and dynamics of probiotics studied in conditions that best represent the human gut including in the presence of antibiotics. The underlying goal is to enable the health benefits of probiotics to be exploited in a responsible manner and with minimal risk to human health.

Our study found a strong association between periodontitis and COPD, and PI seemed to be a major periodontal factor for predicting COPD among Chinese adults.

Inappropriate neutrophil infiltration and subsequent neutrophil extracellular trap (NET) formation have been confirmed to be involved in chronic inflammatory conditions. Fatty liver disease is an increasingly severe health problem worldwide and currently considered the most common cause of chronic liver disease. Sphingosine 1-phosphate (S1P), a product of membrane sphingolipid metabolism, regulates vital physiological and pathological actions by inducing infiltration and activation of various cell types through S1P receptors (S1PRs). Here, we seek to determine the S1PR-mediated effects on neutrophil activation during chronic liver inflammation. In this study, NETs are detected in the early stage of methionine-choline-deficient and a high-fat (MCDHF) diet-induced liver injury. NET depletion by deoxyribonuclease I intraperitoneal injection significantly protects liver from MCDHF-induced liver injury in vivo. Meanwhile, we show that levels of myeloperoxidase-DNA complex (NET marker) in the serum present positive correlation with sphingosine kinase1 (S1P rate-limiting enzyme) messenger RNA expression or S1P levels in the injured liver of MCDHF-fed mice. In vitro, S1PR2 participates in the redirection of neutrophil apoptosis to NETosis via Gαi/o, extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, and reactive oxygen species signaling pathways. Moreover, S1PR2 knockdown in MCDHF-fed mice by S1PR2-siRNA intravenous injection significantly inhibits NET formation in damaged liver tissue and then alleviates hepatic inflammation and fibrosis. Conclusion: In the early stage of fatty liver disease, S1PR2-mediated neutrophil activation plays an important role in the evolvement of liver injury.

NLR family pyrin domain containing 3 (NLRP3) inflammasome accompanies chronic liver injury and is a critical mediator of inflammation-driven liver fibrosis. Sphingosine 1-phosphate (S1P)/S1P Receptor (S1PR) signaling participates in liver fibrogenesis by affecting bone marrow (BM)-derived monocytes/macrophage (BMM) activation. However, the relationship between S1P/S1PR signaling and NLRP3 inflammasome in BMMs remains unclear. Here, we found significantly elevated gene expression of NLRP3 inflammasome components (NLRP3, pro-interleukin-1β, and pro-interleukin-18) and the activation of NLRP3 inflammasome significantly elevated during murine chronic liver injury induced by a bile duct ligation operation, a methionine-choline-deficient and high-fat diet, or carbon tetrachloride intraperitoneal injection. Moreover, the increased expression of sphingosine kinase 1 (SphK1), the rate-limiting synthetic enzyme of S1P, was positively correlated with NLRP3 inflammasome components in both patients and mouse model livers. Flow cytometry analysis and immunofluorescence staining showed BMMs contributed to the significant proportion of NLRP3 + cells in murine inflammatory livers, but not Kupffer cells, dendritic cells, endothelial cells, T cells, and hepatocytes. Focusing on macrophages, S1P promoted NLRP3 inflammasome priming and activation in a dose-dependent manner. Blockade of S1PR 2 by JTE-013 (antagonist of S1PR 2) or S1PR 2-siRNA inhibited S1P-induced NLRP3 inflammasome priming and inflammatory cytokine (interleukin-1β and interleukin-18) secretion, whereas blockade of S1PR 1 or S1PR 3 had no such effect. in vivo, a β1,3-d-glucan-encapsulated siRNA particle (GeRP) delivery system is capable of silencing genes in macrophages specifically. Treatment with S1PR 2 siRNA-GeRPs markedly reduced NLRP3 inflammasome priming and activation and attenuated liver inflammation and fibrosis. Together, the conclusions indicated that targeting macrophage S1PR 2 retarded liver inflammation and fibrogenesis via downregulating NLRP3 inflammasome, which may represent an effective therapeutic strategy for chronic liver injury.

Objectives: This trial aimed to evaluate the efficacy and safety of vitamin D supplementation on the residual moderate and deep pockets following nonsurgical periodontal therapy.Background: Vitamin D supplementation has potential effects on periodontitis, but current evidence remains inconclusive. Methods: After 3 months of nonsurgical periodontal treatment, 360 patients with moderate or severe periodontitis were randomly assigned to 2000 international unit (IU)/d vitamin D3, 1000 IU/d vitamin D3, or placebo. Clinical periodontal examinations, including probing depth (PD), bleeding index (BI), plaque index (PLI), attachment loss (AL), and alveolar crest height (ACH), were performed at baseline and after 3 months of intervention. Results: There was a slight but significant decrease in AL and PD in both vitamin D groups compared with placebo group for moderate and deep pockets. About 2000 IU/d vitamin D3 group, 1000 IU/d vitamin D3 group, and placebo group all decreased the AL for both moderate pockets (−0.4 mm vs −0.4 mm vs −0.3 mm) and deep pockets (−1.1 mm vs −1.1 mm vs −1.0 mm) (all P < .05). Similarly, PD was also decreased in these three groups for both moderate pockets and deep pockets (all P < .05). In addition, vitamin D supplementation was well tolerated, and no adverse events were reported. Conclusions: Although statistically significant differences were observed in favor to vitamin D supplementation, the magnitude of effect size tended to be modest with limited clinical relevance and the long-term efficacy and safety warrant further investigation. K E Y W O R D S periodontal disease, periodontitis, randomized controlled trial, vitamin D supplementation | 355 GAO et Al.