Background  Recent studies suggest that periodontal disease, as a source of subclinical and persistent infection, may induce systemic inflammatory responses that increase the risk of adverse pregnancy outcomes. Objectives  To examine the existing evidence on the relationship between periodontal disease and adverse pregnancy outcomes. Search strategy  Published studies identified via searches of the MEDLINE, EMBASE, CINAHL, and Current Contents full‐text databases. Selection criteria  We identified and selected observational studies (i.e. case–control, cross‐sectional, and cohort) and nonrandomised controlled studies or randomised controlled trials that examined periodontal disease as a risk factor for adverse pregnancy outcomes. Data collection and analysis  Odds ratios (OR) or risk ratios (RR) were extracted or calculated from the studies’ data. We calculated pooled effect size for two clinical controlled trials but not for the observational studies due to the heterogeneity in definitions for periodontal disease and adverse pregnancy outcomes across studies. Main results  Twenty‐five studies (13 case–control, 9 cohort, and 3 controlled trials) were identified. The studies focused on preterm low birthweight, low birthweight, preterm birth, birthweight by gestational age, miscarriage or pregnancy loss, and pre‐eclampsia. Of the chosen studies, 18 suggested an association between periodontal disease and increased risk of adverse pregnancy outcome (ORs ranging from 1.10 to 20.0) and 7 found no evidence of an association (ORs ranging from 0.78 to 2.54). Three clinical trial studies suggest that oral prophylaxis and periodontal treatment can lead to a 57% reduction in preterm low birthweight (pooled RR 0.43; 95% CI 0.24–0.78) and a 50% reduction in preterm births (RR 0.5; 95% CI 0.20–1.30). Author's conclusions  Periodontal disease may be associated with an increased risk of adverse pregnancy outcome. However, more methodologically rigorous studies are needed for confirmation.

1. Recent studies have suggested that interleukin-6 is a major mediator of the acute-phase protein response in man. The aim of the present study was to investigate the relationships between the response of serum interleukin-6 to surgery, the type of surgical procedure performed and the response of serum C-reactive protein. 2. Timed venous blood samples were taken from 26 patients in five broad surgical categories (minor surgery, cholecystectomy, hip replacement, colorectal surgery and major vascular surgery). C-reactive protein and interleukin-6 were measured in each sample. 3. Serum interleukin-6 rose within 2-4 h of incision in all patients and the magnitude of the response differed among the various surgical groups. The response of interleukin-6 correlated (r = 0.80, P less than 0.001) with the duration of surgery. In contrast, serum C-reactive protein was not detectable after minor surgery (less than 10 mg/l) and the response of C-reactive protein did not differ among the more major surgical groups. The response of interleukin-6 showed a weak, but significant, correlation with the response of C-reactive protein (r = 0.67, P less than 0.001). 4. We conclude that serum interleukin-6 is a sensitive, early marker of tissue damage. In general, the greater the surgical trauma, the greater the response of serum interleukin-6 and the greater the peak serum concentration of interleukin-6. Our results are consistent with a role for interleukin-6 in the induction of C-reactive protein synthesis.

Cardiovascular disease is the leading cause of morbidity and mortality in patients with Type II (non-insulin-dependent) diabetes mellitus accounting for up to 75 % of deaths [1]. Although insulin and insulin resistance have been considered major factors in the pathogenesis of cardiovascular disease [2,3], given the close links between the insulin-like growth factor-system and insulin action we examined the potential role of the insulin-like growth factor-system in the pathogenesis of macrovascular disease. Diabetologia (2001) Abstract Aims/hypothesis. Insulin resistance/hyperinsulinaemia is implicated in the development of cardiovascular disease and diabetes but its role and causal pathways are not clear. We tested the hypothesis that the insulin-like growth factor system is independently associated with cardiovascular risk within susceptible populations based on previous reports of the links between low circulating insulin-like growth factor binding protein-1 concentrations and increased macrovascular disease in Type II (non-insulin-dependent) diabetes mellitus. Methods. In a population-based study 272 subjects (142 subjects of European and 130 Pakistani of origin) underwent a 75 g oral glucose tolerance test and standardised anthropometry. Fasting concentrations of insulin-like growth factor binding protein-1 (IG-FBP-1), insulin-like growth factor-I (IGF-I), insulinlike growth factor-II (IGF-II), intact insulin and lipids were measured and were related to 2-h glucose tolerance test status. Insulin sensitivity was calculated using the homeostasis model assessment (HOMA). Results. Insulin-like growth factor binding protein-1 was significantly lower in subjects with impaired glucose tolerance when compared with normal glucose tolerance in both ethnic groups (Europeans F = 6.7, p = 0.002 and Pakistanis F = 4.4, p = 0.01). Multiple linear regression modelling showed that insulin-like growth factor binding protein-1 was independently associated with 2-h glucose (b = 0.16, p = 0.009) and logistic regression indicated a 40 % reduction in risk of impaired glucose tolerance for every 2.7 ng/ml increase in the insulin-like growth factor binding protein-1 concentration [odds ratio 0.6 (CI = 0.49±0.71), p = 0.001)]. In addition, insulin-like growth factor binding protein-1 was significantly correlated negatively with several established cardiovascular factors, and positively with insulin sensitivity. Conclusion/interpretation. Insulin-like growth factor binding protein-1 is closely related to risk factors for diabetes and cardiovascular disease in people of European and Pakistani origin. It has potential use as a marker of (hepatic) insulin resistance in clinical intervention studies and further implicates the insulin-like growth factor system in the development of macrovascular disease. [Diabetologia (2001) 44: 333±339]

Objective Whether vitamin D deficiency in pregnancy is a cause of pre-eclampsia remains controversial. Most previous studies to date have assessed exposure at only one time-point in pregnancy.We assessed longitudinal vitamin D status during pregnancy and the risk of pre-eclampsia.Design Prospective cohort study.Setting Seventeen urban obstetric hospitals, Canada.Population Pregnant women who were participants in a trial of vitamin C and E supplementation for the prevention of preeclampsia. Canadian participants who consented to participate in a biobank with plasma specimens available at the baseline visit were included (n = 697).Methods Maternal plasma 25-hydroxyvitamin D (25(OH)D) concentrations were measured at 12-18 and 24-26 weeks of gestation using chemiluminescence immunoassay.Main outcome measures Pre-eclampsia.Results Of the women, 39% were vitamin D deficient (25(OH)D <50 nmol/l). A strong positive correlation was observed in maternal 25(OH)D concentrations between the two gestational age windows (r = 0.69, P < 0.0001). Mean maternal 25(OH)D concentrations at 24-26 weeks of gestation were significantly lower in women who subsequently developed pre-eclampsia compared with those who did not (mean ± SD: 48.9 ± 16.8 versus 57.0 ± 19.1 nmol/l, P = 0.03). Women with 25(OH)D < 50 nmol/l at 24-26 weeks gestation experienced an increased risk of pre-eclampsia (adjusted odds ratio 3.24, 95% confidence interval 1.37-7.69), whereas the association was not statistically significant for maternal 25(OH)D level at 12-18 weeks of gestation.Conclusions Lower maternal 25(OH)D levels at late mid-trimester were associated with an increased risk of pre-eclampsia.

Largest study of its kind finds certain species of vaginal Lactobacillus + Bifidobacterium may relate to lower risk of preterm birth.