Anne E. Sanders

Impact of oral disease on quality of life in the US and Australian populations

UNLABELLED The US National Health and Nutrition Examination Survey (NHANES 2003-2004) evaluated oral health quality of life for the first time using a previously untested subset of seven Oral Health Impact Profile (OHIP) questions, i.e. the NHANES-OHIP. OBJECTIVES (i) To describe the impact of dental conditions on quality of life in the US adult population; (ii) to evaluate construct validity and adequacy of the NHANES-OHIP in NHANES 2003-2004 and a comparable Australian survey. METHODS In the cross-sectional NHANES 2003-2004 survey of a nationally representative sample of US adults (n=4907), prevalence was quantified as the proportion of adults who reported experiencing one or more impacts fairly often or very often within the past year. Construct validity was tested by comparing prevalence estimates across categories of sociodemographic, dental health and utilization characteristics known to vary in oral health. In 2002, Australian cross-sectional survey of a nationally representative sample of adults (n=2644), adequacy of the NHANES-OHIP questions were tested with reference to a slightly modified version of the OHIP-14 questions. RESULTS NHANES-OHIP prevalence estimates were markedly similar in the United States (15.3%) and Australia (15.7%). In the US construct, validity was evidenced by higher NHANES-OHIP scores among groups with greater levels of tooth loss, perceived treatment need and problem-oriented visiting and with lack of private dental insurance and low income. In Australia, prevalence for the NHANES-OHIP closely resembled prevalence estimates of the modified OHIP-14. Both varied to a similar degree across levels of tooth loss, perceived treatment need, problem-oriented visiting, and private dental insurance and income, demonstrating adequacy of the NHANES-OHIP as a brief independent instrument. CONCLUSIONS There was acceptable construct validity and adequacy of the NHANES-OHIP questionnaire. In the United States, the impact of oral disease disproportionately affected disadvantaged groups, a finding that supports application of the US Healthy People 2010 major goals of improved quality of life and reduced health disparities.

Smoking-attributable periodontal disease in the Australian adult population.

BACKGROUND The extent to which periodontitis is attributable to smoking in Australia has not been examined. OBJECTIVES To investigate the smoking-periodontitis relationship and to estimate the public health impact of smoking on periodontitis in Australia. MATERIAL AND METHODS The National Survey of Adult Oral Health 2004-2006 collected nationally representative oral epidemiologic data for the Australian adult population. Examiners measured probing pocket depth (PPD) and gingival recession at three sites per tooth to compute clinical attachment level (CAL). Moderate-severe cases were defined as having: >/=2 interproximal sites (not on same tooth) with >/=4 mm CAL or with >/=5 mm PPD. Smoking status was defined as never-, former- or current-smoker. Current-smokers were further classified into light-, moderate- or heavy-smoker using calculated pack-years. Age, sex and socioeconomic position were examined as potential confounders. RESULTS Twenty-three per cent were former-smokers and 15% were current-smokers. Prevalence of periodontitis was 23%. In unadjusted analyses, former- and current-smokers had significantly higher periodontitis prevalence than never-smokers. Relative to non-smokers, adjusted prevalence ratios (95% confidence interval) for periodontitis were as follows: former-smokers: 1.22 (1.03-1.46), moderate-smokers: 1.63 (1.16-2.30); and heavy-smokers: 1.64 (1.27-2.12). The population attributable fraction of smoking for moderate-severe periodontitis was 32% (equivalent to 700,000 adults). CONCLUSION Smoking has a significant impact on periodontal health of the Australian adults.

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.

Social inequality in perceived oral health among adults in Australia.

Objective: To establish population estimates of self‐assessed tooth loss and subjective oral health and describe the social distribution of these measures among dentate adults in Australia.

Effects of Fluoridated Drinking Water on Dental Caries in Australian Adults

Systematic reviews produce conflicting conclusions regarding dental caries-preventive effects of water fluoridation in adults. The authors investigated the relationship using data from the nationally representative 2004−2006 Australian National Survey of Adult Oral Health. Effects were compared between the pre-fluoridation cohort born before 1960 (n = 2,270) and the cohort born between 1960 and 1990 (n = 1,509), when widespread implementation of fluoridation increased population coverage from < 1% to 67%. Residential history questionnaires determined the percentage of each person’s lifetime exposed to fluoridated water. Examiners recorded decayed, missing, and filled teeth (DMF-Teeth) and decayed and filled tooth surfaces (DF-Surfaces). Socio-demographic and preventive dental behaviors were included in multivariable least-squares regression models adjusted for potential confounding. In fully adjusted models, > 75% of lifetime exposure to fluoridation relative to < 25% of lifetime exposure was associated with 11% and 10% fewer DMF-Teeth in the pre-1960 (p < .0001) and 1960–1990 cohorts (p = .018), respectively. Corresponding reductions in DF-Surfaces were 30% (p < .001) and 21% (p < .001). Findings for intermediate fluoridation exposure suggested a dose-response relationship. Results were consistent in sensitivity analyses accounting for missing data. In this nationally representative sample of Australian adults, caries-preventive effects of water fluoridation were at least as great in adults born before widespread implementation of fluoridation as after widespread implementation of fluoridation.

A cross-national comparison of income gradients in oral health quality-of-life in four welfare states: application of the Korpi and Palme typology

Background: The extent to which welfare states may influence health outcomes has not been explored. It was hypothesised that policies which target the poor are associated with greater income inequality in oral health quality of life than those that provide earnings-related benefits to all citizens. Methods: Data were from nationally representative surveys in the UK (n = 4064), Finland (n = 5078), Germany (n = 1454) and Australia (n = 2292) conducted from 1998 to 2002. The typology of Korpi and Palme classifies these countries into four different welfare states. In each survey, subjects completed the Oral Health Impact Profile (OHIP-14) questionnaire, which evaluates the adverse consequence of dental conditions on quality of life. For each country, survey estimation commands were used to create linear regression models that estimated the slope of the gradient between four quartiles of income and OHIP-14 severity scores. Parameter estimates for income gradients were contrasted across countries using Wald χ2 tests specifying a critical p value of 0.008, equivalent to a Bonferroni correction of p<0.05 for the six pairwise tests. Results: Statistically significant income gradients in OHIP-14 severity scores were found in all countries except Germany. A global test confirmed significant cross-national differences in the magnitude of income gradients. In Australia, where a flat rate of benefits targeted the poor, the mean OHIP-14 severity score reduced by 1.7 units (95% CI −2.15 to −1.34) with each increasing quartile of household income, a significantly steeper gradient than in other countries. Conclusion: The coverage and generosity of welfare state benefits appear to influence levels of inequality in population oral health quality of life.

Trends in prevalence of complete tooth loss among Australians, 1979–2002

Edentulism is a key indicator of the oral health status of populations and is associated with reduced quality of life.

Summary of Findings From the OPPERA Prospective Cohort Study of Incidence of First-Onset Temporomandibular Disorder: Implications and Future Directions

UNLABELLED Papers in this issue investigate when and how putative risk factors influence development of first-onset, painful temporomandibular disorder (TMD). The results represent first findings from the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) prospective cohort study that monitored 2,737 men and women aged 18 to 44 years recruited at 4 U.S. study sites. During a median 2.8-year follow-up period, 260 participants developed TMD. The average incidence rate of 4% per annum was influenced by a broad range of phenotypic risk factors including sociodemographic characteristics, health status, clinical orofacial factors, psychological functioning, pain sensitivity, and cardiac autonomic responses. A novel method of multivariable analysis used random forest models to simultaneously evaluate contributions of all 202 phenotypic variables. Variables from the health status domain made the greatest contribution to TMD incidence, followed closely by psychological and clinical orofacial domains. However, only a few measures of pain sensitivity and autonomic function contributed to TMD incidence, and their effects were modest. Meanwhile, age and study site were independent predictors of TMD incidence, even after controlling for other phenotypes. Separate analysis of 358 genes that regulate pain found several novel genetic associations with intermediate phenotypes that, themselves, are risk factors for TMD, suggesting new avenues to investigate biological pathways contributing to TMD. PERSPECTIVE Collectively, the papers in this issue demonstrate that TMD is a complex disorder with multiple causes consistent with a biopsychosocial model of illness. It is a misnomer and no longer appropriate to regard TMD solely as a localized orofacial pain condition.

Resilience to Urban Poverty: Theoretical and Empirical Considerations for Population Health

OBJECTIVES To better understand the trajectory that propels people from poverty to poor health, we investigated health resilience longitudinally among African American families with incomes below 250% of the federal poverty level. METHODS Health resilience is the capacity to maintain good health in the face of significant adversity. With higher levels of tooth retention as a marker of health resilience, we used a social-epidemiological framework to define capacity for health resilience through a chain of determinants starting in the built environment (housing quality) and community context (social support) to familial influences (religiosity) and individual mental health and health behavior. RESULTS Odds of retaining 20 or more teeth were 3 times as likely among adults with resilience versus more-vulnerable adults (odds ratio=3.1; 95% confidence interval [CI]=1.3, 7.4). Children of caregivers with resilience had a lower incident rate of noncavitated tooth decay at 18- to 24-month follow-up (incidence risk ratio=0.8; 95% CI=0.7, 0.9) compared with other children. CONCLUSIONS Health resilience to poverty was supported by protective factors in the built and social environments. When poverty itself cannot be eliminated, improving the quality of the built and social environments will foster resilience to its harmful health effects.

Painful Temporomandibular Disorder Decade of Discovery from OPPERA Studies

In 2006, the OPPERA project (Orofacial Pain: Prospective Evaluation and Risk Assessment) set out to identify risk factors for development of painful temporomandibular disorder (TMD). A decade later, this review summarizes its key findings. At 4 US study sites, OPPERA recruited and examined 3,258 community-based TMD-free adults assessing genetic and phenotypic measures of biological, psychosocial, clinical, and health status characteristics. During follow-up, 4% of participants per annum developed clinically verified TMD, although that was a “symptom iceberg” when compared with the 19% annual rate of facial pain symptoms. The most influential predictors of clinical TMD were simple checklists of comorbid health conditions and nonpainful orofacial symptoms. Self-reports of jaw parafunction were markedly stronger predictors than corresponding examiner assessments. The strongest psychosocial predictor was frequency of somatic symptoms, although not somatic reactivity. Pressure pain thresholds measured at cranial sites only weakly predicted incident TMD yet were strongly associated with chronic TMD, cross-sectionally, in OPPERA’s separate case-control study. The puzzle was resolved in OPPERA’s nested case-control study where repeated measures of pressure pain thresholds revealed fluctuation that coincided with TMD’s onset, persistence, and recovery but did not predict its incidence. The nested case-control study likewise furnished novel evidence that deteriorating sleep quality predicted TMD incidence. Three hundred genes were investigated, implicating 6 single-nucleotide polymorphisms (SNPs) as risk factors for chronic TMD, while another 6 SNPs were associated with intermediate phenotypes for TMD. One study identified a serotonergic pathway in which multiple SNPs influenced risk of chronic TMD. Two other studies investigating gene-environment interactions found that effects of stress on pain were modified by variation in the gene encoding catechol O-methyltransferase. Lessons learned from OPPERA have verified some implicated risk factors for TMD and refuted others, redirecting our thinking. Now it is time to apply those lessons to studies investigating treatment and prevention of TMD.