When viewed in light of the findings from the companion Pine Ridge study and other recent MI studies, the results of this study suggest that when the complex disease of early childhood caries is addressed in high-risk populations, MI is not effective, and alternative approaches are warranted.

In the yeast Saccharomyces cerevisiae unstable mRNAs decay 10-20 fold more rapidly than stable mRNAs. In order to examine the basis for the differences in decay rate of the unstable STE3 mRNA and the stable PGK1 and ACT1 mRNAs we have constructed and measured the decay rates of numerous chimeric mRNAs. These experiments indicate that multiple regions within yeast mRNAs are involved in modulating mRNA decay rates. Our results suggest that at least two regions within the STE3 mRNA are involved in stimulating rapid decay. One region is located within the coding region and requires sequences between codons 13 and 179. In addition, the STE3 3' UT can also function to stimulate decay. Surprisingly, the STE3 3' UT is not sufficient to accelerate the turnover of the stable PGK1 transcript unless portions of the PGK1 coding region are first deleted. These results not only identify sequences that function within yeast to stimulate mRNA turnover but also have important implications for an understanding of the basis of differences in eukaryotic mRNA decay rates.

Background There is a paucity of data on the validity of self-report of periodontal disease in African Americans. The Black Women’s Health Study (BWHS), a United States national cohort study of 59,000 black women followed via mailed questionnaires since 1995, offered the opportunity to clinically validate self-reported periodontitis among a sample of participants. Methods Oral health questionnaires were sent to study participants residing in Massachusetts. Respondents living in the Boston metro area were invited for clinical examination. Self-reports were compared with clinical data obtained from the 77 women (mean age: 59 years) who were examined. The authors examined the predictive ability of individual and combined questionnaire items with respect to clinical periodontal disease severity. Validation parameters were calculated for each question, and receiver operating characteristic statistics were generated to compare questionnaire items. Results Periodontitis prevalence in the validation sample was 24% for severe periodontitis and 61% for moderate disease. Performance of individual questionnaire items with respect to predicting periodontitis was better for severe compared with moderate disease. Combinations of questionnaire items improved the predictive ability with respect to severe disease beyond that of individual questionnaire items. Conclusions Prevalence of severe periodontitis was similar to other age-comparable populations, without regard for race or sex, whereas prevalence of total periodontitis (moderate and severe) among women of similar age and/or race was much higher. Predictive ability of questionnaire items assessed in the BWHS was similar to that in other studies.

Aims Patients with chronic kidney disease (CKD) are also susceptible to periodontitis. The causal link between periodontitis and CKD may be mediated via systemic inflammation/oxidative stress. Using structural equation modelling (SEM), this cross‐sectional study aimed to explore the causal relationship between periodontal inflammation (PI) and renal function. Materials and methods Baseline data on 770 patients with stage 3–5 (pre‐dialysis) CKD from an ongoing cohort study were used. Detailed, bioclinical data on PI and renal function, as well as potential confounders and mediators of the relationship between the two, were collected. SEMs of increasing complexity were created to test the causal assumption that PI affects renal function and vice versa. Results Structural equation modelling confirmed the assumption that PI and renal function are causally linked, mediated by systemic oxidative stress. The magnitude of this effect was such that a 10% increase in PI resulted in a 3.0% decrease in renal function and a 10% decrease in renal function resulted in a 25% increase in PI. Conclusions Periodontal inflammation represents an occult source of oxidative stress in patients with CKD. Further clinical studies are needed to confirm whether periodontal therapy, as a non‐pharmacological approach to reducing systemic inflammatory/oxidative stress burden, can improve outcomes in CKD.

Causal theory and causal models have proven to be helpful in understanding the multi‐factorial causation of many diseases, including periodontitis. The design and application of causal models is essential to the appropriate design, conduct and analysis of studies on periodontal disease causation. This review discusses the principles of causation and causal theory, both in general and as they pertain to studies of the etiology of periodontitis. Specifically, we present an overview of models of causation, including the potential outcomes model, the sufficient component cause model, and directed acyclic graphical models. More thorough explanations and accompanying illustrations are provided for the sufficient component cause model and the directed acyclic graphical model. Topics related to the study of periodontitis, as illustrated by such models, include the principles of confounding and effect measure modification (interaction). Existing models of periodontitis etiology are critically reviewed in this context.