These results suggest that glycemic level in diabetes is affected by the persistence of P. gingivalis, especially clones with type II fimbriae, in periodontal pockets.

Objectives Lots of bioactive materials have been additionally applied for the treatment of periodontal intrabony defect. However, there is dearth of studies to systematically evaluate the supplementary role of them in periodontal regeneration. The goal of this meta-analysis is to evaluate the adjunctive effects of bioactive materials such as platelet-rich plasma (PRP), platelet-rich fibrin (PRF), enamel matrix derivative (EMD), and amnion membrane (AM) on the outcomes of bone grafting treatment for periodontal intrabony defects. Methods Articles published before December 2017 were searched electronically in three databases (PubMed, Embase, and Cochrane Central), with no date or language limits. Randomized controlled trials (RCTs) on the assessment of effectiveness of the four biomaterials in conjunction with demineralized freeze-dried bone allografts (DFDBA) in the treatment of periodontal intrabony defects were enrolled in this meta-analysis. Data were analyzed with STATA 12. Results Nine studies were included. PRF and PRP significantly improved pocket depth (PD) reduction and clinical attachment loss (CAL) gain. Only PRF exhibited a positive result in recession reduction (RecRed). Only PRP showed a statistically significant increase in bone fill. AM merely gained more CAL. EMD did not improve any clinical outcome. Conclusion Our data suggest that PRF/PRP could be taken as a preferred adjunct to facilitate periodontal regeneration of intrabony defects.

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Mitophagy is a metabolic process to remove excessive or damaged mitochondria in eukaryotic cells. It is well-known that mitochondria are one of the major sources of reactive oxygen species (ROS). Mitochondrial ROS and damage-associated molecular patterns (DAMPs) can activate inflammasomes to induce inflammatory responses. Once the activation is regulated improperly, excessive inflammation will bring about various tissue injuries, resulting in a series of diseases. However, the selective mitochondrial autophagy can specifically eliminate dysfunctional mitochondria to maintain mitochondrial homeostasis and protect against the hyperinflammation induced by ROS and DAMPs. Recent studies demonstrated that a variety of internal and external factors regulate several inflammatory diseases via altering the level of mitophagy. In this review, we summarize the latest research progress of mitophagy and focus on the inflammatory responses regulated by mitophagy, aiming to illuminate the role of mitophagy in inflammation and provide clues to the diagnosis and therapy of inflammatory diseases.

Chronic marginal periodontitis is a destructive inflammatory disease caused by an imbalance between bacterial virulence and host defense ability, resulting in eventual tooth exfoliation. Porphyromonas gingivalis, a major periodontal pathogen, triggers a series of cellular inflammatory responses including the production of prostaglandin E 2 (PGE 2 ), which causes periodontal destruction; thus, anti-inflammatory reagents are considered beneficial for periodontal therapy. In the present study, we examined whether hop-and apple-derived polyphenols (HBP and ACT, respectively) inhibit PGE 2 production by human gingival epithelial (HGE) cells stimulated with P. gingivalis components. HGE cells were stimulated with P. gingivalis membrane vesicles, and the effects of HBP, ACT and epigallocatechin gallate (EGCg) on PGE 2 production by HGE cells were evaluated using an enzyme-linked immunosorbent assay. HBP and EGCg significantly inhibited PGE 2 production, whereas ACT did not. , were found to be elements which significantly inhibited cellular PGE 2 production. These results suggest that HBP is a potent inhibitor of cellular PGE 2 production induced by P. gingivalis, and HBP may be useful for the prevention and attenuation of periodontitis.