Background—: Genetic studies demonstrated the presence of risk alleles in the genes ANRIL and CAMTA1/VAMP3 that are shared between coronary artery disease (CAD) and periodontitis. We aimed to identify further shared genetic risk factors to better understand conjoint disease mechanisms. Methods and Results—: In-depth genotyping of 46 published CAD risk loci of genome-wide significance in the worldwide largest case–control sample of the severe early-onset phenotype aggressive periodontitis (AgP) with the Illumina Immunochip (600 German AgP cases, 1448 controls) and the Affymetrix 500K array set (283 German AgP cases and 972 controls) highlighted ANRIL as the major risk gene and revealed further associations with AgP for the gene PLASMINOGEN ( PLG ; rs4252120: P =5.9×10 ⁻⁵ ; odds ratio, 1.27; 95% confidence interval, 1.3–1.4 [adjusted for smoking and sex]; 818 cases; 5309 controls). Subsequent combined analyses of several genome-wide data sets of CAD and AgP suggested TGFBRAP1 to be associated with AgP (rs2679895: P =0.0016; odds ratio, 1.27 [95% confidence interval, 1.1–1.5]; 703 cases; 2.143 controls) and CAD ( P =0.0003; odds ratio, 0.84 [95% confidence interval, 0.8–0.9]; n=4117 cases; 5824 controls). The study further provides evidence that in addition to PLG , the currently known shared susceptibility loci of CAD and periodontitis, ANRIL and CAMTA1/VAMP3 , are subjected to transforming growth factor-β regulation. Conclusions—: PLG is the third replicated shared genetic risk factor of atherosclerosis and periodontitis. All known shared risk genes of CAD and periodontitis are members of transforming growth factor-β signaling.

Background: The aim of this study is to evaluate proinflammatory and anti‐inflammatory cytokine levels in gingival crevicular fluid (GCF) and serum of rheumatoid arthritis (RA) and chronic periodontitis (CP) patients to assess whether cytokine profiles distinguish patients with RA and patients with CP while using healthy patients as background controls.Methods: A total of 49 patients, 17 patients with RA (three males and 14 females; mean age: 47.82 ± 10.74 years), 16 patients with CP (10 males and six females; mean age: 44.00 ± 7.00 years), and 16 controls (eight males and eight females; mean age: 28.06 ± 6.18 years) were enrolled. Patients with RA were under the supervision of rheumatologists; 15 of the patients with RA were being treated with methotrexate–sulfasalazine combined therapy, and two of the patients were being treated with leflunomid therapy. Periodontal parameters (plaque index, gingival index, probing depth, and clinical attachment level) were recorded. Interleukin (IL)‐1β, IL‐4, IL‐10, and tumor necrosis factor‐α (TNF‐α) were determined in GCF and IL‐1β and IL‐10 in serum by enzyme‐linked immunosorbent assay.Results: There were significant differences found among RA, CP, and control groups for all periodontal parameters (P 0.05). Although the total amount and concentration of serum IL‐10 was not significantly different among the groups (P >0.05), serum IL‐1β was significantly lower in the RA group compared to CP patients and controls and was higher in GCF of the RA group compared to the CP group.Conclusions: Although clinical periodontal disease parameters indicated more severe periodontal disease in CP compared to RA patients, immunologic evaluation did not reveal consistent results regarding proinflammatory and anti‐inflammatory cytokine levels. This might be a result of the use of non‐steroidal anti‐inflammatory drugs and rheumatoid agents by patients with RA.

Background: Preterm low birth weight (PLBW) is a problem encountered worldwide. The many causes of low birth weight (LBW) and premature or preterm birth (PTB) vary among developing/industrialized countries. Few studies have been published, in part because of the paucity of subjects and the ethnic heterogeneity of the populations. Our goals were to correlate maternal periodontal disease with birth outcomes in a Turkish population and evaluate maternal periodontal health.Methods: This study consisted of 3,576 Turkish women who gave birth within 24 hours of the onset of labor. The adjusted odds ratio was generated from various logistic regression models.Results: Codes from the Community Periodontal Index of Treatment Needs (CPITN) were evaluated according to treatment need (TN). The TN‐I rate was 24.2% (N = 866), the TN‐II rate was 73.5% (N = 2,628), and the TN‐III rate was 2.3% (N = 82). There were 566 (15.8%) adverse birth outcomes; the PTB with LBW rate was 4.2%; the PTB with normal birth weight (NBW) rate was 8.3%; the in term birth with LBW rate was 3.3%, and the in term birth with NBW rate was 84.2%. The overall PTB rate was 12.5% (N = 447), and the LBW rate was 7.5% (N = 269). The mean birth weight and weeks of gestation decreased as the CPITN level increased (P <0.001 for both). The LBW rate was 4.6% in the TN‐I group, 8.3% in the TN‐II group, and 14.6% in the TN‐III group. TPTB rates were 10.5%, 12.7%, and 26.8%, respectively, whereas adverse birth outcome rates were 12.0%, 16.6%, and 30.5%, respectively (P <0.01 for all). TN‐II and TN‐III were independent risk factors for LBW, PTB, and abnormal births in regression analyses.Conclusion: Maternal periodontal disease may be a risk factor for an adverse pregnancy outcome.