In recent years, several new periodontal taxa have been associated with the etiology of periodontitis. A recent systematic review provides further support for the pathogenic role of 17 species/phylotypes. Thus, the aim of this study was to assess the prevalence and levels of these species in subjects with generalized chronic periodontitis (GChP; n = 30), generalized aggressive periodontitis (GAgP; n = 30), and periodontal health (PH; n = 30). All subjects underwent clinical and microbiological assessment. Nine subgingival plaque samples were collected from each subject and analyzed for their content of 20 bacterial species/phylotypes through the RNA-oligonucleotide quantification technique. Subjects from the GChP and GAgP groups presented the highest mean values for all clinical parameters in comparison with the PH group (P < 0.05). Subjects with GChP and GAgP showed significantly higher mean levels of Bacteroidetes sp. human oral taxon (HOT) 274, Fretibacterium sp. HOT 360, and TM7 sp. HOT 356 phylotypes, as well as higher mean levels of Filifactor alocis, Fretibacterium fastidiosum, Porphyromonas gingivalis, Tannerella forsythia, and Selenomonas sputigena species than PH subjects (P < 0.05). GAgP subjects presented higher mean levels of TM7 sp. HOT 356 and F. alocis than GChP subjects (P < 0.05). A significantly higher mean prevalence of Bacteroidales sp. HOT 274, Desulfobulbus sp. HOT 041, Fretibacterium sp. HOT 360, and Fretibacterium sp. HOT 362 was found in subjects with GChP and GAgP than in PH subjects. Mean levels of P. gingivalis (r = 0.68), T. forsythia (r = 0.62), F. alocis (r = 0.51, P = 0.001), and Fretibacterium sp. HOT 360 (r = 0.41) were correlated with pocket depth (P < 0.001). In conclusion, Bacteroidales sp. HOT 274, Desulfobulbus sp. HOT 041, Fretibacterium sp. HOT 360, Fretibacterium sp. HOT 362, and TM7 sp. HOT 356 phylotypes, in addition to F. alocis, F. fastidiosum, and S. sputigena, seem to be associated with periodontitis, and their role in periodontal pathogenesis should be further investigated.

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Phagocytosis and the ability of the two macrophage subtypes to eliminate microbes were not affected by MTA.

This study assessed the influence of mineral trioxide aggregate (MTA) on adaptive immune responses. BALB/c mice were immunized with heat-killed Fusobacterium nucleatum (Fn) in MTA or other control adjuvants, and serum IgG responses to Fn were measured. Either Fn-or Peptostreptococcus anaerobius (Pa)-reactive memory T cells (Tm) were pre-incubated in vitro with/ without MTA and restimulated with Fn or Pa. Tm proliferation and cytokine production were assessed. Compared to control groups, IgG-antibody responses were upregulated in mice immunized with Fn in MTA in a similar manner to animals immunized with Fn in Freund's adjuvant or aluminum hydroxide adjuvant. While MTA did not affect the upregulated expression of IL-10, TNF-α or RANKL by Tm, it suppressed the proliferation of Pa-or Fn-Tm and inhibited their production of Th1-or Th2-signature cytokines. MTA upregulated the adaptive humoral immune responses, but had little or no effect on pro-or anti-inflammatory cytokine production by Tm.

Comparison of MTA and FLPX effects upon macrophages indicates that FLPX may impair macrophage activity and viability, while MTA seems to increase phagocytic activity.

Fillapex impaired effector immune responses during inflammation (M1 macrophages), as well as during healing (M2 macrophages) responses.

Macrophages/foam cells have a pivotal role in atherogenesis although little is known about the way lipid imbalance, a hallmark of atherosclerosis, leads to lipid accumulation in these cells. Modified low‐density lipoproteins are associated with macrophage lipid dysfunction in atherosclerosis, but a possible role for altered lipogenesis leading to lipid accumulation remains to be elucidated. Since endothelium‐derived nitric oxide (NO) and prostaglandins (PGs) are physiological autacoids whose production may be impaired in atherosclerosis, the effects of these mediators on de novo lipid synthesis in 24‐h cultured rat peritoneal macrophages is investigated. In resident (unstimulated) cells, 1 μM PGE2 and the stable analog of PGI2 carbaprostacyclin (cPGI2, 1 μM) deviated the overall [1‐14C]acetate from incorporation into cholesterol, free fatty acids and triacylglycerols favoring the formation of phospholipids. In inflammatory (thioglycollate‐elicited) macrophages, these eicosanoids likewise reduced tac‐incorporations into all the lipid fractions tested. Also, cPGI2 and PGE2 reduced [4‐14C]cholesterol uptake from inflammatory cells but did not interfere in 14C‐cholesterol export. The PGE2‐derivative PGA2 (10‐20 μM) reduced 14C‐incorporations into all the lipids in resident cells while it enhanced phospholipid synthesis by up to 129% at the expense of reduced incorporations into the other test lipids. The NO donor S‐nitroso‐N‐acetylpenicillamine (SNAP, 1‐10 μM), when added to macrophages in the presence of superoxide dismutase (SOD, to avoid the reaction of superoxide with NO), significantly reduced lipogenesis especially in inflammatory cells. These findings suggest that endothelium‐derived NO and PGs may be associated with macrophage lipid accumulation by modulating lipogenesis and cholesterol uptake within these ceils.