Assessing risk factors for dental caries a statistical modeling approach

We confirmed the proportionality assumption for all models Hosmer and Lemeshow In our analyses, we used tertiles of the lead biomarkers and estimated separate models for lead concentrations in tibia, patella, and blood.

We also considered the effects of including questionnaire-recorded tooth brushing frequency and dietary calcium intake. However, because these variables did not alter the relationship between the lead biomarkers and tooth loss and were not significant predictors of tooth loss, we excluded them from our final analyses.

To further examine the effects of socioeconomic factors on our analyses, we estimated the association of lead biomarkers and tooth loss in separate categories of education—those with high school or lower education versus participants who had technical, college, or higher training.

Our sample was racially homo genous, with all but six of our participants identifying themselves as white Americans. To confirm that race was not a confounding factor in our analyses, we excluded the six non white participants from the analyses and observed no appreciable change in the results. We therefore included all participants in our final analyses.

We also compared key characteristics of Normative Aging Study participants included in our study with those excluded because of missing data on dental or lead biomarker variables. For all data analyses, we used SAS version 9. Our participants had a median age of 67 years range, 50—94 years.

Compared with those excluded from our analyses because of missing data on tooth loss or lead biomarkers, our study participants were younger by an average of 1.

However, there were no significant differences between these groups in terms of pack-years of smoking, educational attainment, or physician diagnoses of diabetes. They were also more likely to be current smokers and have experienced more than 10 pack-years of smoking. As has been described earlier in this cohort Schaumberg et al. Men who had not completed high school had the highest bone and blood lead concentrations.

Multivariable-adjusted ORs for the association between lead biomarkers and tooth loss. To put the results for lead exposure in the context of more established risk factors for tooth loss, we estimated the relationship of cigarette smoking with tooth loss. Similar associations were observed for models that included patella or blood. Participants with less than high school education and those with diabetes controlled or uncontrolled also had increased odds of tooth loss; however, these associations were not statistically significant.

When we stratified our analyses by level of educational attainment, we observed that the association of bone lead biomarkers with tooth loss was similar among the different categories of education. Similarly, for men with education levels of high school or lower, the ORs of tooth loss were 3.

In our study, men with elevated bone lead levels had approximately three times the odds of having experienced an elevated degree of tooth loss compared with those participants who were in the lowest tertile of bone lead concentrations. This association showed a clear trend across tertiles of bone lead biomarkers and remained significant when we adjusted for a number of confounding factors, including age, smoking, and diabetes.

Moreover, blood lead levels were not associated with tooth loss, suggesting that bone lead concentrations are a better indicator of the risk of tooth loss posed by cumulative long-term environmental lead exposure.

Tooth loss is a multifactorial disease and is influenced by numerous sociodemographic and lifestyle factors Beltran-Aguilar et al. Notably, environmental lead exposure has been linked to dental caries and periodontal disease Moss et al.

It is, therefore, possible that the rate of tooth loss over the to year period, from baseline to the early s, was greater in those participants with higher lead levels.

Although the biological mechanisms linking lead exposure and dental disease are not completely clear, it has been suggested that lead may disrupt salivary gland function, thereby increasing the risk of dental caries Watson et al. Studies on rats have shown that exposure to lead during the prenatal and peri natal periods resulted in significantly higher levels of dental caries and markedly reduced salivary flow rate Watson et al.

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Similarly, adult rats exposed to lead through drinking water showed decreased salivary calcium and protein concentrations Abdollahi et al. Although adult animals showed no change in salivary flow rate, increased lipid peroxidation and a decrease in total antioxidant capacity and thiol group levels in salivary gland tissue indicated the presence of lead-induced oxidative stress Abdollahi et al. The disruption of bone remodeling due to lead exposure has been suggested as a possible mechanism linking this toxicant with periodontal disease Saraiva et al.

That lead disrupts bone remodeling is supported by studies in laboratory animals where long-term lead exposure induced osteopenia Gruber et al.

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Studies in children, however, suggest that this interaction is complex, and those exposed to lead may undergo accelerated bone maturation resulting in lower peak bone mass and, therefore, a greater risk of osteoporosis in older age Campbell et al.

Historical exposure to lead as reflected in bone lead concentrations may also be important in establishing susceptibility. The mechanisms behind the pathologic effects of lead on bone include the ability to promote inflammation, which is pertinent to perio dontal disease, where disruption of the host inflammatory response is considered an important factor in disease progression and subsequent alveolar bone loss.

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In our multivariable-adjusted analyses, the association between bone lead biomarkers and tooth loss was similar in magnitude to the increase in odds observed among current smokers, indicating that long-term cumulative lead exposure may be a potentially important predictor of tooth loss. Like the participants in our study, the older members of the U.

A number of studies have reported that bone lead levels increase with age Hu et al. Our study is limited by its cross-sectional design. However, bone lead concentrations reflect exposure over decades Hu et al. Furthermore, reverse causality, such that tooth loss could lead to increased bone lead levels, is unlikely. We have adjusted for a number obesite grenoble webmail important potential confounders, including smoking.

However, both lead exposure and tooth loss are influenced by a multitude of socioeconomic and environmental factors and, as in any observational study, the possibility of residual confounding due to unmeasured or mismeasured shared risk factors cannot be excluded.

All of our study participants were male, with a majority identifying themselves as white Americans, limiting the generalizability of our results to the wider U. Furthermore, in the present study, we analyzed data on a subgroup of participants recruited from the wider Normative Aging Study cohort.

However, the self-selection of participants for dental examinations occurred independently from their bone lead measurements and is unlikely to bias the results of our study. Differential selection into the study on the basis of greater degrees of tooth loss and exposure to lead the most likely pattern of selection would only have underestimated the associations of lead biomarkers with tooth loss.

All of our participants received dental care from private dental practitioners, and the clinical diagnoses and interventions leading to the removal of teeth would have been consistent with general population in the region.

Our participants were younger and more likely to be never-smokers, making it unlikely that they were at greater risk of tooth loss than those who were not included in the study. Although the proportion of men with physician diagnosis of diabetes was similar in our participants and those not enrolled in our study, mean fasting plasma glucose levels were higher among those who were included in our analyses.

Our study is strengthened by a large number of participants with detailed measures on a number of important covariates. Notably, we have used a validated KXRF method to measure in vivo lead concentrations in both the cortical and trabecular bone compartments.

To the best of our knowledge, this is the first epidemiologic investigation to show that bone lead levels are associated with tooth loss.

Assessing risk factors for dental caries a statistical modeling approach

Despite the decline in blood lead levels, lead exposure remains an important public health issue. The oral health implications of accumulated lead, however, are yet to be fully realized, and further work is needed to uncover the biological mechanisms underlying the association between bone lead and tooth loss. National Center for Biotechnology InformationU. Journal List Environ Health Perspect v. Environ Health Perspect. Published online Jun Garcia5, 7 and Howard Hu 4, 8.

Marc G. Raul I. Conspicuous social patterning of caries was observed in both the index- and co-sibling populations even after adjustment for all study covariates. Significant sibling-specific familial aggregation of caries was observed, which varied in a stepwise graded fashion across the social hierarchy. Overall, Co-siblings of affected probands had 3. This sibling similarity was further amplified in those with relative socioeconomic disadvantage e. Graded clustering patterns of caries and socioeconomic disadvantage are encapsulated within families in Denmark, contributing to the engendering of health inequalities in society.

With sibling caries being such a pertinent marker of increased caries risk, caries in a sibling should elicit preventive family-based approaches targeting co-siblings, particularly in socially disadvantaged households.

Since caries shares common risk factors with other non-communicable diseases and conditions such as diabetes and obesitysuch policy constructs could reduce not only caries experience but also wider health inequalities in society. Ainsi, vous pouvez exiger que soient rectifiées, complétées, clarifiées, mises à jour ou effacées les informations vous concernant qui sont inexactes, incomplètes, équivoques, périmées ou dont la collecte ou l'utilisation ou la conservation est interdite.

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Assessing risk factors for dental caries a statistical modeling approach

Nous adhérons aux principes de la charte HONcode. Valider Annuler. Médecine générale Médecine interne Médecine légale Médecines complémentaires Neurologie, neuropsychologie Ophtalmologie Oto-rhino-laryngologie Pédiatrie Pharmacologie, Thérapeutique. Biologie, Bactériologie, maladies infectieuses Cancérologie Cardiologie, Médecine vasculaire Chirurgie générale et digestive Chirurgie orthopédique, Traumatologie Chirurgie plastique Chirurgie, autres Dermatologie, Vénérologie Dictionnaires et lexiques.

Oxidative stress and dysregulated immune responses are implicated in both organophosphate neurodevelopmental effects and ASD etiopathogenesis. In the present study, we aimed at investigating whether the behavioral effects of gestational CPF administration are associated with brain increased oxidative stress and altered lipid mediator profile. Measures were performed in mice of both sexes, at different postnatal stages PNDs 1, 21, and CPF treatment also induced a reduction of somatic growth, which reached statistical significance at PND The results further support the hypothesis that oxidative stress might be the link between environmental neurotoxicants such as CPF and ASD.

The increased levels of oxidative stress during early postnatal life could result in delayed and long-lasting alterations in specific pathways relevant to ASD, of which PGE2 signaling represents an important one. Autism spectrum disorder prevalence and associations with air concentrations of lead, mercury, and arsenic. Lead, mercury, and arsenic are neurotoxicants with known effects on neurodevelopment. Autism spectrum disorder ASD is a neurodevelopmental disorder apparent by early childhood.

In unadjusted analyses, ambient metal concentrations were negatively associated with ASD prevalence. Our results suggest a possible association between ambient lead concentrations and ASD prevalence and demonstrate that exposure to multiple metals may have synergistic effects on ASD prevalence.

Autism spectrum disorders ASDs are one of the life long existing disorders. Abnormal methylation status of gene promoters of oxytonergic system has been implicated as among the etiologic factors of ASDs. We, therefore, investigated the methylation frequency of oxytocin receptor gene OXTR promoter from peripheral blood samples of children with autistic features.

Although our findings indicate high frequency of OXTR promoter hypomethylation in ASDs, there is need for independent replication of the results in a bigger sample set.

We expect that future studies with the inclusion of larger, more homogeneous samples will attempt to disentangle the causes of ASDs. However, when we consider semantic competence, this group could compensate with a higher capacity to imagine the meaning of words referring to emotions. This is indeed what we found when we asked people with different levels of autistic and empathic traits to rate the degree of imageability of various kinds of words.

But this was not the whole story. Individuals with marked autistic traits demonstrated outstanding ability to imagine theoretical concepts, i. We speculate that this quasi-perceptual ability to imagine theoretical concepts represents a specific cognitive pattern that, while hindering social interaction, may favor problem solving in abstract, non-socially related tasks.

This would allow people with marked autistic traits to make use of perceptual, possibly visuo-spatial, information for "higher" cognitive processing. Animal models provide preclinical tools to investigate the causal can i drink 24 hours after botox of genetic mutations and environmental factors in the etiology of autism spectrum disorder ASD.

Knockout and humanized knock-in mice, and more recently knockout rats, have been generated for many of the de novo single gene mutations and copy number variants CNVs detected in ASD and comorbid neurodevelopmental disorders.

Mouse models incorporating genetic and environmental manipulations have been employed for preclinical testing of hypothesis-driven pharmacological targets, to begin to develop treatments for the diagnostic and associated symptoms of autism.