The survival probability for critical spread-out oriented percolation above 4+1 dimensions. II. Expansion

Article / Letter to editorMathematisch Instituu

Projections of U.S. Edentulism Prevalence Following 5 Decades of Decline

After decades of decline in prevalence of complete tooth loss (edentulism), the trend continues to be misinterpreted, producing flawed projections and misdirected health goals. We investigated population trends in edentulism among U.S. adults aged ≥15 yr by creating time-series data from 5 national cross-sectional health surveys: 1957-1958 (n ≈ 100,000 adults), 1971-1975 (n = 14,655 adults), 1988-1998 (n = 18,011 adults), 1999-2002 (n = 12,336 adults), and 2009-2012 (n = 10,522 adults). Birth cohort analysis was used to isolate age and cohort effects. Geographic and sociodemographic variation in prevalence was investigated with a sixth U.S. survey of 432,519 adults conducted in 2010. Prevalence through 2050 was projected with age-cohort regression models using Monte-Carlo simulation of prediction intervals. Across the 5-decade observation period, edentulism prevalence declined from 18.9% in 1957-1958 (95% confidence limits: 18.4%, 19.4%) to 4.9% in 2009-2012 (95% confidence limits: 4.0%, 5.8%). The most influential determinant of the decline was the passing of generations born before the 1940s, whose rate of edentulism incidence (5%-6% per decade of age) far exceeded later cohorts (1%-3% per decade of age). High-income households experienced a greater relative decline, although a smaller absolute decline, than low-income households. By 2010, edentulism was a rare condition in high-income households, and it had contracted geographically to states with disproportionately high poverty. With the passing of generations born in the mid-20th century, the rate of decline in edentulism is projected to slow, reaching 2.6% (95% prediction limits: 2.1%, 3.1%) by 2050. The continuing decline will be offset only partially by population growth and population aging such that the predicted number of edentulous people in 2050 (8.6 million; 95% prediction limits: 6.8 million, 10.3 million) will be 30% lower than the 12.2 million edentulous people in 2010

Response to letter to the Editor, "directed acyclic graphs for oral disease research"

We thank Dr. Schwan and colleagues (2016) for their comments on our paper (Akinkugbe et al. 2016)

Cognitive Decline and Oral Health in Middle-aged Adults in the ARIC Study

Even before dementia becomes apparent, cognitive decline may contribute to deterioration in oral health. This cohort study of middle-aged adults evaluated associations of six-year change in cognitive function with oral health behaviors and conditions in the Atherosclerosis Risk in Communities (ARIC) study. Cognitive function was measured at study visits in 1990-1992 and 1996-1998 with three tests: (a) Delayed Word Recall (DWR), (b) Digit Symbol Substitution (DSS), and (c) Word Fluency (WF). Cognitive decline scores were computed as ‘studentized’ residuals of 1996-1998 scores regressed against 1990-1992 scores. In 1996-1998, 10,050 participants answered dental screening questions, and 5,878 of 8,782 dentate participants received a comprehensive oral examination. Multiple regression models used cognitive change to predict oral health behaviors and conditions with adjustment for covariates. In the fully adjusted models, greater decline in all three measures of cognitive function was associated with increased odds of complete tooth loss. Greater decline in DSS and WF scores was associated with infrequent toothbrushing. Decline in WF scores was also associated with higher plaque levels. In these middle-aged adults, six-year cognitive decline was modestly associated with less frequent toothbrushing, plaque deposit, and greater odds of edentulism, but not with other oral behaviors or diseases

COMT Genotype and Efficacy of Propranolol for TMD Pain: A Randomized Trial

Propranolol is a nonselective β-adrenergic receptor antagonist that is efficacious in reducing facial pain. There is evidence that its analgesic efficacy might be modified by variants of the catechol-O-methyltransferase (COMT) gene. We tested the hypothesis in a subset of 143 non-Hispanic Whites from a randomized controlled trial of patients with painful temporomandibular disorder (TMD). Patients were genotyped for rs4680, a single nucleotide polymorphism of COMT, and randomly allocated to either propranolol 60 mg twice daily or placebo. During the 9-wk follow-up period, patients recorded daily ratings of facial pain intensity and duration; the product was computed as an index of facial pain. Postbaseline change in the index at week 9 (the primary endpoint) was analyzed as a continuous variable and dichotomized at thresholds of ≥30% and ≥50% reduction. Mixed models for repeated measures tested for the genotype × treatment group interaction and estimated means, odds ratios (ORs), and 95% confidence limits (95% CLs) of efficacy within COMT genotypes assuming an additive genetic model. In secondary analysis, the cumulative response curves were plotted for dichotomized reductions ranging from ≥20% to ≥70%, and genotype differences in area under the curve percentages (%AUC) were calculated to signify efficacy. Mean index reduction did not differ significantly (P = 0.277) according to genotype, whereas the dichotomized ≥30% reduction revealed greater efficacy among G:G homozygotes (OR = 10.9, 95%CL = 2.4, 50.7) than among A:A homozygotes (OR = 0.8, 95%CL = 0.2, 3.2) with statistically significant interaction (P = 0.035). Cumulative response curves confirmed greater (P = 0.003) efficacy for G:G homozygotes (%AUC difference = 43.7, 95%CL = 15.4, 72.1) than for A:A homozygotes (%AUC difference = 6.5, 95%CL = -30.2, 43.2). The observed antagonistic effect of the A allele on propranolol’s efficacy was opposite the synergistic effect hypothesized a priori. This unexpected result highlights the need for better knowledge of COMT’s role in pain pathogenesis if the gene is to be used for precision-medicine treatment of TMD (ClinicalTrials.gov NCT02437383)

COMT Diplotype Amplifies Effect of Stress on Risk of Temporomandibular Pain

When measured once, psychological stress predicts development of painful temporomandibular disorder (TMD). However, a single measurement fails to characterize the dynamic nature of stress over time. Moreover, effects of stress on pain likely vary according to biological susceptibility. We hypothesized that temporal escalation in stress exacerbates risk for TMD, and the effect is amplified by allelic variants in a gene, catechol-O-methyltransferase (COMT), regulating catechol neurotransmitter catabolism. We used data from the Orofacial Pain: Prospective Evaluation and Risk Assessment prospective cohort study of 2,707 community-dwelling adults with no lifetime history of TMD on enrollment. At baseline and quarterly periods thereafter, the Perceived Stress Scale (PSS) measured psychological stress. Genotyped DNA from blood samples determined COMT diplotypes. During follow-up of 0.25 to 5.2 y, 248 adults developed examiner-verified incident TMD. PSS scores at baseline were 20% greater (P < 0.001) in adults who developed incident TMD compared with TMD-free controls. Baseline PSS scores increased by 9% (P = 0.003) during follow-up in cases but remained stable in controls. This stress escalation was limited to incident cases with COMT diplotypes coding for low-activity COMT, signifying impaired catabolism of catecholamines. Cox regression models confirmed significant effects on TMD hazard of both baseline PSS (P < 0.001), modeled as a time-constant covariate, and change in PSS (P < 0.001), modeled as a time-varying covariate. Furthermore, a significant (P = 0.04) interaction of COMT diplotype and time-varying stress showed that a postbaseline increase of 1.0 standard deviation in PSS more than doubled risk of TMD incidence in subjects with low-activity COMT diplotypes (hazard ratio = 2.35; 95% confidence limits: 1.66, 3.32), an effect not found in subjects with high-activity COMT diplotypes (hazard ratio = 1.42; 95% confidence limits: 0.96, 2.09). Findings provide novel insights into dynamic effects of psychological stress on TMD pain, highlighting that effects are most pronounced in individuals whose genetic susceptibility increases responsiveness to catecholamine neurotransmitters

Characteristics Associated With High-Impact Pain in People With Temporomandibular Disorder: A Cross-Sectional Study

High-impact (disabling) pain diminishes the quality of life and increases health care costs. The purpose of this study was to identify the variables that distinguish between high- and low-impact pain among individuals with painful temporomandibular disorder (TMD). Community-dwelling adults (N = 846) with chronic TMD completed standardized questionnaires that assessed the following: 1) sociodemographic characteristics, 2) psychological distress, 3) clinical pain, and 4) experimental pain. We used high-impact pain, classified using the Graded Chronic Pain Scale, as the dependent variable in logistic regression modeling to evaluate the contribution of variables from each domain. Cross-validated area under the receiver operating characteristic curve (AUC) quantified model discrimination. One-third of the participants had high-impact pain. Sociodemographic variables discriminated weakly between low- and high-impact pain (AUC =.61, 95% confidence interval [CI] = 0.57, 0.65), with the exception of race. An 18-variable model encompassing all 4 domains had good discrimination (AUC = 0.79, 95% CI = 0.75, 0.82), as did a simplified model (sociodemographic variables plus catastrophizing, jaw limitation, and number of painful body sites) (AUC = 0.79, 95% CI = 0.76, 0.82). Duration of pain, sex, and experimental pain testing results were not associated. The characteristics that discriminated most effectively between people with low- and high-impact TMD pain included clinical pain features and the ability to cope with pain. Perspective: This article presents the results of a multivariable model designed to discriminate between people with high- and low-impact pain in a community-based sample of people with painful chronic TMD. The findings emphasize the importance of catastrophizing, jaw limitation, and painful body sites associated with pain-related impact

Sleep Apnea Symptoms and Risk of Temporomandibular Disorder: OPPERA Cohort

The authors tested the hypothesis that obstructive sleep apnea (OSA) signs/symptoms are associated with the occurrence of temporomandibular disorder (TMD), using the OPPERA prospective cohort study of adults aged 18 to 44 years at enrollment (n = 2,604) and the OPPERA case-control study of chronic TMD (n = 1,716). In both the OPPERA cohort and case-control studies, TMD was examiner determined according to established research diagnostic criteria. People were considered to have high likelihood of OSA if they reported a history of sleep apnea or ≥ 2 hallmarks of OSA: loud snoring, daytime sleepiness, witnessed apnea, and hypertension. Cox proportional hazards regression estimated hazard ratios (HRs) and 95% confidence limits (CL) for first-onset TMD. Logistic regression estimated odds ratios (OR) and 95% CL for chronic TMD. In the cohort, 248 individuals developed first-onset TMD during the median 2.8-year follow-up. High likelihood of OSA was associated with greater incidence of first-onset TMD (adjusted HR = 1.73; 95% CL, 1.14, 2.62). In the case-control study, high likelihood of OSA was associated with higher odds of chronic TMD (adjusted OR = 3.63; 95% CL, 2.03, 6.52). Both studies supported a significant association of OSA symptoms and TMD, with prospective cohort evidence finding that OSA symptoms preceded first-onset TMD

Periodontitis and Non-alcoholic Fatty Liver Disease, a population-based cohort investigation in the Study of Health in Pomerania

Background: Non‐alcoholic fatty liver disease (NAFLD) affects 20%–30% of adults with risk factors like obesity and insulin resistance putatively acting through chronic low‐grade inflammation. Because periodontitis elicits low‐grade inflammation, we hypothesized that it could contribute to NAFLD occurrence. Objective: To investigate epidemiologic associations between periodontitis and the incidence of NAFLD among 2,623 participants of the Study of Health in Pomerania. Methods: Periodontitis at baseline was defined as the percentage of sites (0%, <30%, ≥30%) with (i) clinical attachment level (CAL) ≥3 mm; (ii) probing pocket depth (PD) ≥4 mm. Incident NAFLD was defined as a significant increase in liver echogenicity on ultrasound relative to the kidneys, with the diaphragm indistinct or the echogenic walls of the portal veins invisible.Results: After a median 7.7 years of follow‐up, 605 incident NAFLD cases occurred at a rate of 32.5 cases per 1,000 person‐years. Relative to participants without CAL ≥3 mm, NAFLD incidence was elevated slightly in participants with <30% of sites affected and moderately in participants with ≥30% of sites affected (multivariable‐adjusted incidence rate ratio = 1.28, 95% CI, 0.84, 1.95 and 1.60, 95% CI, 1.05–2.43), respectively. A similar dose–response relationship was not observed for PD. Conclusion: History of periodontitis may be a risk factor for NAFLD

Cohort profile: Zoe 2.0—a community-based genetic epidemiologic study of early childhood oral health

Early childhood caries (ECC) is an aggressive form of dental caries occurring in the first five years of life. Despite its prevalence and consequences, little progress has been made in its prevention and even less is known about individuals’ susceptibility or genomic risk factors. The genome-wide association study (GWAS) of ECC (“ZOE 2.0”) is a community-based, multi-ethnic, cross-sectional, genetic epidemiologic study seeking to address this knowledge gap. This paper describes the study’s design, the cohort’s demographic profile, data domains, and key oral health outcomes. Between 2016 and 2019, the study enrolled 8059 3–5-year-old children attending public preschools in North Carolina, United States. Participants resided in 86 of the state’s 100 counties and racial/ethnic minorities predominated—for example, 48% (n = 3872) were African American, 22% white, and 20% (n = 1611) were Hispanic/Latino. Seventy-nine percent (n = 6404) of participants underwent clinical dental examinations yielding ECC outcome measures—ECC (defined at the established caries lesion threshold) prevalence was 54% and the mean number of decayed, missing, filled surfaces due to caries was eight. Nearly all (98%) examined children provided sufficient DNA from saliva for genotyping. The cohort’s community-based nature and rich data offer excellent opportunities for addressing important clinical, epidemiologic, and biological questions in early childhood