lipid-a and Periodontal-Pocket

Porphyromonas gingivalis lipid A heterogeneity modulates cytokine expression in human cells. This study investigates the effects of two lipid A isoforms of P. gingivalis, lipopolysaccharide (LPS)1435/1449 and LPS1690, on the secretion of proinflammatory and regulatory cytokines in total blood cultures from patients with and without chronic periodontitis (CP).. A cross-sectional study was conducted in 38 systemically healthy individuals divided in two groups: 1) the CP group (n = 19), in which patients were diagnosed with CP; and 2) the no periodontitis (NP) group (n = 19), which included control patients without CP. Blood samples were collected from all patients, and whole-blood cell cultures (WBCCs) were stimulated for 48 hours with P. gingivalis LPS1435/1449 and LPS1690 and Escherichia coli LPS. Unstimulated WBCCs served as negative controls. The secretion of interferon-γ (IFN-γ), interleukin-10 (IL-10), and transforming growth factor-β (TGF-β) was detected in WBCC supernatants by enzyme-linked immunosorbent assays.. E. coli LPS significantly increased the expression of all cytokines in WBCCs from both the NP and CP groups when compared to non-stimulated cells (control treatment). P. gingivalis LPS preparations increased IFN-γ levels in the CP group but not in the NP group when compared with controls (P <0.05). P. gingivalis LPS preparations also increased IL-10 and TGF-β levels in both CP and NP groups, but P. gingivalis LPS1690 showed a three-fold increase on IL-10 production in the NP group (P <0.05) when compared to P. gingivalis LPS1435/144.. These data demonstrate that WBCC cell populations obtained from healthy individuals and patients with CP may differ in the cytokine response to P. gingivalis but not E. coli LPS. This is consistent with the notion that CP alters the systemic WBCC response and that this can be detected by the different P. gingivalis LPS structures.

Topics: Adult; Aged; Blood Cells; Chronic Periodontitis; Cross-Sectional Studies; Cytokines; Dental Plaque Index; Escherichia coli; Female; Humans; Inflammation Mediators; Interferon-gamma; Interleukin-10; Lipid A; Male; Middle Aged; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Porphyromonas gingivalis; Transforming Growth Factor beta

We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 non-smokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C(i17.0) (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids associated with the consensus (high potency) enteric LPS structure (3-OH-C(12.0) and 3-OH-C(14.0); 33.3% and 15.8% reduction, respectively) were noted in smokers compared with non-smokers with chronic periodontitis. Thus, smoking is associated with specific structural alterations to the lipid-A-derived 3-OH fatty acid profile in saliva that are consistent with an oral microflora of reduced inflammatory potential. These findings provide much-needed mechanistic insight into the established clinical conundrum of increased infection with periodontal pathogens but reduced clinical inflammation in smokers.

Topics: Adult; Bacteria, Anaerobic; Chronic Periodontitis; Cotinine; Dental Plaque Index; Fatty Acids; Female; Gingival Hemorrhage; Gram-Negative Bacteria; Humans; Lipid A; Lipopolysaccharides; Male; Middle Aged; Mouth; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Saliva; Smoking

In our previous study, we found that the ability of supragingival plaque to induce Toll-like receptor (TLR)4-mediated stimulation was positively associated with plaque score and bleeding on probing (BOP) at the sampled sites and that the ability to induce TLR2-mediated stimulation was negatively associated with probing depth (PD) and clinical attachment level (CAL). Because signaling from TLR leads to the induction of pro- and anti-inflammatory cytokines, we further analyzed the influence of the ability of supragingival plaque to induce TLR2-/TLR4-mediated stimulation of cytokine production by peripheral blood mononuclear cells (PBMCs).. The abilities of 125 plaque samples to induce TLR2- or TLR4-mediated stimulation were determined using genetically engineered Chinese hamster ovary reporter cells that express a reporter molecule upon activation of nuclear factor-kappa B through TLR2 or TLR4. PBMCs were stimulated with each plaque sample, and the production of proinflammatory cytokines (tumor necrosis factor-alpha and interleukin [IL]-6 and -8) and an anti-inflammatory cytokine (IL-10) was analyzed by enzyme-linked immunosorbent assay.. The levels of the cytokines produced by PBMCs all correlated with the ability of supragingival plaque to induce TLR4-mediated stimulation but not with its ability to induce TLR2-mediated stimulation. Cytokine production was inhibited by an anti-TLR4 monoclonal antibody and a TLR4 antagonist, compound 406. The levels of cytokines were associated with plaque index, BOP, PD, and CAL at the sampled sites.. The production of pro-/anti-inflammatory cytokines by PBMCs was associated with the ability of supragingival plaque to induce TLR4-mediated stimulation. The cytokines induced by supragingival plaque via TLR4 might modulate periodontal status.

Topics: Adult; Aged; Aged, 80 and over; Animals; Antibodies, Monoclonal; CHO Cells; Cricetinae; Cricetulus; Cytokines; Dental Plaque; Dental Plaque Index; Female; Gingival Hemorrhage; Glycolipids; Humans; Interleukin-10; Interleukin-6; Interleukin-8; Leukocytes, Mononuclear; Lipid A; Male; Middle Aged; NF-kappa B; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Toll-Like Receptor 2; Toll-Like Receptor 4; Tumor Necrosis Factor-alpha; Young Adult