Scaling and root planing treatment for periodontitis to reduce preterm birth and low birth weight: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: The aim of this study is to perform an updated systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating the efficacy of scaling and root planing (SRP) in reducing the preterm-birth and low-birth-weight risks to analyze important subgroups and to further explore heterogeneity and bias risks in the pooled studies. METHODS: The entire Cochrane Library was searched (from 1990 to September 2011), MEDLINE (from 1950 to September 2011), CINAHL (from 1980 to September 2011), University of Michigan School of Dentistry "Dentistry and Oral Sciences" database (from 1990 to September 2011), conference proceedings, and the ClinicalTrials.gov database. Authors were contacted when clarification was needed. Selection criteria included the following: 1) RCTs that reported preterm-birth risk (<37 weeks) outcomes, 2) compared SRP treatment to either placebo or no treatment in pregnant patients with periodontitis, and 3) had a probing depth >4 mm or clinical attachment loss >2 mm for ≥ 1 site. Reviewers independently extracted data from each included study using a standardized, piloted form and assessed quality using a risk-of-bias tool modeled after Cochrane, and discrepancies were resolved. A random-effects model was used to calculate relative risks and 95% confidence intervals (CIs) for pooled data. For subgroup analysis with heterogeneity <50%, a fixed-effects model was used. RESULTS: After abstract review, 12 studies were identified by the search, and 11 were included in the main meta-analysis (preterm birth <37 weeks). Overall quality and design of included studies was fair or good. For the main meta-analysis, results ranged from risk ratio with periodontal treatment 0.14 (95% CI = 0.01, 2.55) to 1.24 (95% CI = 0.93, 1.67) for an overall risk ratio of 0.81 (95% CI = 0.64, 1.02). When analyzed separately by subgroup for excess prematurity risk, the high-risk group (overall prematurity of 22.2% to 62.8%) showed combined risk ratios of 0.66 (95% CI = 0.54, 0.80). Remaining studies (overall prematurity of 4.0% to 10.4%) showed combined risk ratio of 0.97 (95% CI = 0.75, 1.24). CONCLUSIONS: This systematic review and meta-analysis indicates statistically significant effect in reducing risk of preterm birth for SRP in pregnant women with periodontitis for groups with high risks of preterm birth only. Future research should attempt to confirm these findings and further define groups in which risk reduction may be effective.

Plasma carboxypeptidase B downregulates inflammatory responses in autoimmune arthritis.

The immune and coagulation systems are both implicated in the pathogenesis of rheumatoid arthritis (RA). Plasma carboxypeptidase B (CPB), which is activated by the thrombin/thrombomodulin complex, plays a procoagulant role during fibrin clot formation. However, an antiinflammatory role for CPB is suggested by the recent observation that CPB can cleave proinflammatory mediators, such as C5a, bradykinin, and osteopontin. Here, we show that CPB plays a central role in downregulating C5a-mediated inflammatory responses in autoimmune arthritis. CPB deficiency exacerbated inflammatory arthritis in a mouse model of RA, and cleavage of C5a by CPB suppressed the ability of C5a to recruit immune cells in vivo. In human patients with RA, genotyping of nonsynonymous SNPs in the CPB-encoding gene revealed that the allele encoding a CPB variant with longer half-life was associated with a lower risk of developing radiographically severe RA. Functionally, this CPB variant was more effective at abrogating the proinflammatory properties of C5a. Additionally, expression of both CPB and C5a in synovial fluid was higher in patients with RA than in those with osteoarthritis. These findings suggest that CPB plays a critical role in dampening local, C5a-mediated inflammation and represents a molecular link between inflammation and coagulation in autoimmune arthritis.