Periodontitis is an inflammatory disease affecting the connective tissue surrounding the teeth leading to tooth loss. Pathogens associated with periodontitis interact with Toll-like receptors (TLRs) to induce cytokines causing and aggravating disease. We screened 197 individuals suffering from generalized periodontitis for the presence of Asp299Gly and Thr399Ile of TLR-4 as well as Arg753Gln of TLR-2 in comparison to matched controls. Single-nucleotide polymorphisms (SNPs) of TLR-4 were elevated among patients (odd's ratio 3.650, 95% CI 1.573-8.467, P < or = 0.0001), while no difference was observed for TLR-2. TLR-4 SNPs were correlated with chronic periodontitis (odd's ratio 5.562, 95% CI 2.199-14.04, P < or = 0.0001), but not with aggressive periodontitis. This observation was confirmed employing a group of periodontally healthy probands over 60 years of age. These data demonstrate that genetic variants of TLR-4 may act as risk factors for the development of generalized chronic periodontitis in humans.

Within the limits of a retrospective analysis, these findings indicate that administration of amoxicillin/metronidazole immediately after initial SRP provides more PD reduction and RAL "gain" in initially deep sites than late administration at SPT with reinstrumentation after 3 months.

The results indicate that a therapeutical intervention may have a systemic effect on the blood count in GAP patients. This effect seems to differ between smokers and non-smokers.

Periodontal therapy reduces plasma sE-selectin levels. Whether this leads to a reduction in risk of future cardiovascular events in patients with aggressive periodontal disease warrants further studies.