The results of this study indicate the presence of a significant relationship between periodontitis, hyperlipidemia, and serum antibodies against P. gingivalis LPS that warrants further examination in a larger patient population. Furthermore, these studies indicate that elevated triglycerides are able to modulate IL-1beta production by PMNs stimulated with P. gingivalis LPS.

Background: Previous systematic reviews of periodontal regeneration with bone replacement grafts and guided tissue regeneration (GTR) were defined as state of the art for clinical periodontal regeneration as of 2002.Methods: The purpose of this systematic review is to update those consensus reports by reviewing periodontal regeneration approaches developed for the correction of intrabony defects with the focus on patient-, tooth-, and site-centered factors, surgical approaches, surgical determinants, and biologics. This review adheres to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines for systematic reviews.A computerized search of the PubMed and Cochrane databases was performed to evaluate the clinically available regenerative approaches for intrabony defects. The search included screening of original reports, review articles, and reference lists of retrieved articles and hand searches of selected journals.All searches were focused on clinically available regenerative approaches with histologic evidence of periodontal regeneration in humans published in English. For topics in which the literature is lacking, non-randomized observational and experimental animal model studies were used.Therapeutic endpoints examined included changes in clinical attachment level, changes in bone level/fill, and probing depth. For purposes of analysis, change in bone fill was used as the primary outcome measure, except in cases in which this information was not available. The SORT (Strength of Recommendation Taxonomy) grading scale was used in evaluating the body of knowledge.Results: 1) Fifty-eight studies provided data on patient, tooth, and surgical-site considerations in the treatment of intrabony defects. 2) Forty-five controlled studies provided outcome analysis on the use of biologics for the treatment of intrabony defects.Conclusions: 1) Biologics (enamel matrix derivative and recombinant human platelet-derived growth factor-BB plus b-tricalcium phosphate) are generally comparable with demineralized freezedried bone allograft and GTR and superior to open flap debridement procedures in improving clinical parameters in the treatment of intrabony defects. 2) Histologic evidence of regeneration has been demonstrated with laser therapy; however, data are limited on clinical predictability and effectiveness. 3) Clinical outcomes appear most appreciably influenced by patient behaviors and surgical approach rather than by tooth and defect characteristics. 4) Long-term studies indicate that improvements in clinical parameters are maintainable up to 10 years, even in severely compromised teeth, consistent with a favorable/good long-term prognosis. J Periodontol 2015;86(Suppl.):S77-S104.

IntroductionThe complex life cycle of HIV-1 involves critical functional interactions with CD4 ϩ host-cell factors. In addition to CD4 ϩ T cells, CD4 ϩ CCR5 ϩ macrophages represent a primary target and host of HIV-1. Infected macrophages replicate copious amounts of virus at their surface and at intracellular membranes where the virions accumulate in vesicles. 1 Macrophages are not typically subject to viral-induced death and may persist as reservoirs of virus in tissues for long periods of time. 2,3 In addition, infected macrophages may be resistant to antiviral agents, 3-6 and the unique attributes and factors that are enabling for this persistent viral host remain elusive. Critically, all monocytic cells are neither equally permissive to HIV-1 nor supportive of the viral life cycle. In vitro or in vivo, dendritic cells (DCs) may or may not become infected, depending on maturational status 7 ; peripheral-blood monocytes are nearly impervious (Ͻ 1% HIV-1 DNA ϩ ) 8,9 ; and of longstanding interest is the enhanced susceptibility of macrophages to HIV-1 compared with immature monocytes, the basis of which remains a mystery. The fact that macrophages, in culture and in tissues, are more susceptible to infection than monocytes cannot be attributed to levels of membrane CD4 or HIV-1 coreceptor expression 10 or multiple other criteria that have been considered. 11 This fundamental question has obvious significance in that if the monocyte-resistance factor(s) can be identified, opportunities may emerge for manipulating susceptible myeloid populations to impose a restrictive barrier to HIV-1. Limited evidence supports an early postentry block that occurs in association with or shortly after reverse transcription (RT). 8 Beyond the well-established CD4 and CCR5/CXCR4 entry requirements, recent evidence implicates additional membrane and intracellular factors that influence early host-cell responsiveness to productive infection. [11][12][13][14][15][16][17] Among the potential innate intracellular viral antagonists, initially characterized in T cells 18 and more recently in monocytes, 19,20 are cytidine deaminases that edit viral RNA and mutate DNA. These cytoplasmic apolipoprotein B mRNA-editing enzyme catalytic polypeptidelike (APOBEC) subunits, particularly APOBEC3G (hA3G), become incorporated into virions, leading to mutation of nascent HIV-1 DNA formed during reverse transcription and its subsequent degradation. 18,21,22 HIV-1, in turn, inhibits hA3G via HIV-1-encoded viral infectivity factor (Vif)-dependent and -independent pathways to thwart this antiviral defense within the target cell. Vif not only facilitates 26S proteasome-mediated degradation of hA3G but also diminishes its synthesis to collectively exclude hA3G incorporation into the budding virions. [23][24][25] Nonetheless, whether differential HIV-1 susceptibility in myeloid populations could be attributed to constitutively expressed hA3G or any other components of this defensive superfamily had not been addressed.In this study, by oligonucleotide microarr...

In periodontitis, a common chronic inflammatory condition, gram negative-rich bacterial biofilms trigger, in susceptible individuals, perpetuating inflammation that results in extensive tissue damage of tooth supporting structures. To delineate immune cell-dependent mechanisms whereby bacterial challenge drives persistent destructive inflammation in periodontitis and other inflammatory diseases, we studied involved tissues ex vivo and investigated host cell responses to the periodontal pathogen P. gingivalis, in vitro. Diseased lesions were populated by abundant Th17 cells, linked to infection, chronic inflammation/autoimmunity and tissue pathology. In vitro, P. gingivalis, particularly the more virulent strain W83, stimulated myeloid antigen presenting cells (APC) to drive Th17 polarization. Supernatants from myeloid APC exposed to P. gingivalis were capable of enhancing Th17 but not Th1 polarization. P. gingivalis favored the generation of Th17 responses by stimulating the production of Th17 related cytokines IL-1β, IL-6 and IL-23, but not Th1 related IL-12. By inducing NFκB activation, P. gingivalis promoted IL-1β, IL-6 and IL-12p40 production, but not IRF-3 phosphorylation, connected to generation of the IL-12p35 chain, ultimately restricting formation of the intact IL-12 molecule. Promotion of Th17 lineage responses was also aided by P. gingivalis proteases, which appeared to differentially degrade pivotal cytokines. In this regard, IL-12 was largely degraded by P. gingivalis, whereas IL-1β was more resistant to proteolysis. Our data unveil multiple pathways by which P. gingivalis may orchestrate chronic inflammation, providing insights into interventional strategies.