Bone specific alkaline phosphatise activity and tartrate resistant acid phosphatase 5b was statistically lower in CRZHDF-A and CRZHDF-B groups as compared to the untreated periodontitis group (p < 0.0001).
This study indicates that extraction of a lipopolysaccharide-like macromolecule is feasible from the assay spirochetes, and this macromolecule may be used as an antigen for the diagnosis of ADA types II-IV periodontitis.
In stepwise logistic regression models, high relative expression levels of ECE1 and ADAM17 mRNAs were significantly associated with moderate/advanced periodontitis.
Both soluble TNF-α and sRANKL are found in the periodontitis lesion, leading to the hypothesis that TACE expressed on lymphocytes is engaged in RANKL shedding and that the resulting sRANKL induces osteoclastogenesis.
Two SNPs at the known CAD risk loci ADAMTS7 (rs11634042) and VAMP8 (rs1561198) passed the pre-assigned selection criteria (P<sub>AgP-Ger</sub> < 0.05; P<sub>CAD</sub> < 5 × 10<sup>-8</sup>; concordant effect direction) and were replicated in an independent GWAS meta-analysis dataset of PD (4,415 cases vs 5,935 controls).
Significantly elevated serum levels of leptin and decreased serum levels of adiponectin in patients with periodontitis were observed in the subgroup analysis of body mass index (BMI) <30.
Same results were achieved by APR treatment of periodontitis induced in adiponectin (APN) knockout mice, indicating the ability of APR to activate the endogenous APN receptors to exert osteoanabolic effects.
Previous work in our groups has shown that a region of the streptococcal antigen denoted BAR (SspB Adherence Region) inhibits P. gingivalis/S. gordonii interaction and biofilm formation both in vitro and in a mouse model of periodontitis (Daep et al. in Infect Immun 74:5756-5762, 2006; Daep et al. in Infect immun 76:3273-3280, 2008; Daep et al. in Infect Immun 79:67-74, 2011).
Naringin-carrying CHC-β-GP-glycerol hydrogel sites showed significantly reduced periodontal bone loss (P <0.05) and inflammatory infiltration (P <0.01) as well as significantly downregulated TLR2 (P <0.05), RAGE (P <0.01), and TNF-α (P <0.05) relative to the sites with experimental periodontitis alone.
In this study, we investigate the underlying mechanisms behind PH exacerbation of periodontitis by using a bacteria-induced periodontitis model in normotensive and hypertensive (Nos3<sup>-/-</sup> ) mice treated with or without an Angiotensin II (Ang II) specific receptor 1 (AT1) antagonist, losartan.
Subjects with the haplotype AGT had a significantly higher risk of periodontitis than those with the most common haplotype GGT (OR=1.91, 95% CI=1.32-2.76, p(c)<0.001).
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, block inflammatory mediators, upregulate antioxidant enzymes and bone formation markers.
However, the destructive potential of IL-22-expressing AhR<sup>+</sup> Th22 lymphocytes over periodontal tissues during periodontitis has not been demonstrated in vivo yet.