Bonnie Clothier

Treatment of localized periodontal disease in pregnancy does not reduce the occurrence of preterm birth: results from the Periodontal Infections and Prematurity Study (PIPS)

OBJECTIVE The purpose of this study was to test whether treating periodontal disease (PD) in pregnancy will reduce the incidence of spontaneous preterm delivery (SPTD) at < or = 35 weeks of gestation. STUDY DESIGN A multicenter, randomized clinical trial was performed. Subjects with PD were randomized to scaling and root planing (active) or tooth polishing (control). The primary outcome was the occurrence of SPTD at <35 weeks of gestation. RESULTS We screened 3563 subjects for PD; the prevalence of PD was 50%. Seven hundred fifty-seven subjects were assigned randomly; 378 subjects were assigned to the active group, and 379 subjects were assigned to the placebo group. Active treatment did not reduce the risk of SPTD at <35 weeks of gestation (relative risk, 1.19; 95% confidence interval [CI], 0.62-2.28) or composite neonatal morbidity (relative risk, 1.30; 95% CI, 0.83-2.04). There was a suggestion of an increase in the risk of indicated SPTD at <35 weeks of gestation in those subjects who received active treatment (relative risk, 3.01; 95% CI, 0.95-4.24). CONCLUSION Treating periodontal disease does not reduce the incidence of SPTD.

Periodontal infection and preterm birth: successful periodontal therapy reduces the risk of preterm birth

Please cite this paper as: Jeffcoat M, Parry S, Sammel M, Clothier B, Catlin A, Macones G. Periodontal infection and preterm birth: successful periodontal therapy reduces the risk of preterm birth. BJOG 2011;118:250–256.

Duration of antibiotic therapy after preterm premature rupture of fetal membranes

OBJECTIVE This study was undertaken to compare the efficacy of 3 days versus 7 days of ampicillin in prolonging gestation for at least 7 days in women with preterm premature rupture of membranes (PPROM). STUDY DESIGN We performed a randomized clinical trial comparing 3 days of ampicillin with 7 days ampicillin in patients with PPROM. Our primary outcome was the prolongation of pregnancy for at least 7 days. Secondary outcomes included rates of chorioamnionitis, postpartum endometritis, and neonatal morbidity and mortality. RESULTS Forty-eight patients were randomly selected. There was no statistically significant difference in the ability to achieve a 7-day latency (relative risk 0.83, 95% CI 0.51-1.38). In addition, there was no statistically significant difference in the rates of chorioamnionitis, endometritis, and our composite neonatal morbidity. CONCLUSION In patients with PPROM, length of antibiotic therapy does not change the rate of a 7-day latency or affect the rate of chorioamnionitis, postpartum endometritis, or neonatal morbidity.

Periodontal infection and preterm birth: successful periodontal therapy reduces the risk of preterm birth: Correspondence

Sir, Despite the great interest in reading the paper from Jeffcoat et al. on the treatment of periodontal infection and preterm birth, a few methodological issues in the study design and interpretation raise doubts on the validity of its conclusion. The aim of the paper was to assess the effect of periodontal therapy in reducing the risk of preterm birth and it concluded that the treatment successfully decreased the incidence of preterm birth. The study was originally designed as a randomised controlled trial. Nevertheless the effectiveness of periodontal therapy is only demonstrated in a nonrandomised comparison between subgroups within the study population: women treated successfully compared with women treated without success. Therefore, there is no certainty that the two populations were comparable with respect to known and unknown confounding factors. Although the authors claimed that they would have conducted a stratified analysis based on severity of periodontal disease (mild versus moderate or severe) and previous preterm birth, such an analysis has neither been published nor commented on. Previous preterm delivery is a well-recognised risk factor for preterm birth and not considering it in such an analysis creates a major methodological issue, particularly as the comparison was carried out between two nonrandomised groups. Furthermore, the study indicated a preterm rate of 49% (52.4% among treated women and 45.6% among untreated women), well above the 4.9% rate of the Periodontal Infections and Prematurity Study (PIPS), of which the present study is part. As 55% of the PIPS population is represented by the study population in Jeffcoat et al., such a huge discrepancy is not understandable and the authors have not commented on it to justify such a difference. Finally, the conclusions of the present study are not consistent with evidence from previous studies: the authors explained the difference by the diverse inclusion criteria (women were selected only if they showed at least three sites with 4 mm or more of attachment loss) and the fact that only successful treatment of periodontal disease should be considered to assess treatment efficacy in reducing preterm birth. In our opinion there is an alternative explanation: the applied study design does not permit the control of confounders and bias and therefore the lack of randomisation and of control for previous preterm birth hinders the validity of this study. j