Documents

Family History and Oral Health

Description
ww
Categories
Published
of 12
All materials on our website are shared by users. If you have any questions about copyright issues, please report us to resolve them. We are always happy to assist you.
Related Documents
Share
Transcript
  The life-course approach to chronic disease epide-miology considers the long-term biological, behavioural, psychological, social and environmen-tal influences that link adult health and adultdisease risk to exposures acting during theindividual’s lifespan (1). It is also concerned withhow these influences can contribute to healthacross generations (1). Research suggests that thehealth status of one generation can have a pro-found effect on that of the next; studies have foundintergenerational and familial associations for car-diovascular disease (2–7), non-insulin-dependentdiabetes mellitus (8–12), metabolic syndrome (13,14), cancer (15–18), asthma (19), obesity (20, 21) andhealth-related behaviours, including smoking,drug and alcohol use (22–25), and diet and exercise(26, 27). However, little research has been carriedout on intergenerational associations for oralhealth.Is family history a risk factor for oral disease?Intriguingly, twin studies suggest a strong geneticcontribution to dental caries experience (28–30). Anearly attempt was made in 1974 to investigatecaries experience across three generations; unfor-tunately, the study suffered from high rates of attrition and insufficient power (31). Since then, Community Dent Oral Epidemiol 2012; 40: 105–115 All rights reserved   2011 John Wiley & Sons A/S Family history and oral health:findings from the DunedinStudy Shearer DM, Thomson WM, Caspi A, Moffitt TE, Broadbent JM, Poulton R.Family history and oral health: findings from the Dunedin Family HistoryStudy. Community Dent Oral Epidemiol 2012; 40: 105–115.    2011 John Wiley &Sons A   ⁄   SAbstract –  Context:  The effects of the oral health status of one generation onthat of the next within families are unclear.  Objective:  To determine whetherparental oral health history is a risk factor for oral disease.  Methods:  Oralexamination and interview data were collected during the age-32 assessmentsin the Dunedin Study. Parental data were also collected on this occasion. Thesample was divided into two familial-risk groups for caries   ⁄   tooth loss (high riskand low risk) based on parents’ self-reported history of tooth loss at the age-32assessment interview.  Main outcome measures:  Probands’ dental caries and toothloss status at age 32, together with lifelong dental caries trajectory (age 5–32). Results:  Caries   ⁄   tooth loss risk analysis was conducted for 640 proband-parentgroups. Reference groups were the low-familial-risk groups. After controllingfor confounding factors (sex, episodic use of dental services, socio-economicstatus and plaque trajectory), the prevalence ratio (PR) for having lost 1+ teeth by age 32 for the high-familial-risk group was 1.41 [95% confidence interval (CI)1.05, 1.88] and the rate ratio for DMFS at age 32 was 1.41 (95% CI 1.24, 1.60). Inthe high-familial-risk group, the PR of following a high caries trajectory was2.05 (95% CI 1.37, 3.06). Associations were strongest when information wasavailable about both parents’ oral health. Nonetheless, when information wasavailable for one parent only, associations were significant for some outcomes. Conclusions:  People with poor oral health tend to have parents with poor oralhealth. Family   ⁄   parental history of oral health is a valid representation of theintricacies of the shared genetic and environmental factors that contribute to anindividual’s oral health status. Associations are strongest when data from bothparents can be obtained. Dara M. Shearer  1  , W. Murray Thomson 1  ,Avshalom Caspi 2,3  , Terrie E. Moffitt 2,3  , Jonathan M. Broadbent 1 and RichiePoulton 4 1 Department of Oral Sciences, School of Dentistry, Dunedin, New Zealand,  2 Social,Genetic and Developmental PsychiatryCentre, Institute of Psychiatry, King’sCollege, London, England,  3 Departments of Psychology and Neuroscience andPsychiatry and Behavioural Science, Institutefor Genome Sciences and Policy, DukeUniversity, Durham, North Carolina, 4 Department of Preventive and SocialMedicine, Dunedin School of Medicine,Dunedin, New ZealandKey words: family history; intergenerational;oral health; riskDara M. Shearer, Department of OralSciences, School of Dentistry, PO Box 647,Dunedin 9054, New Zealande-mail: shearer@es.co.nzSubmitted 20 December 2010;accepted 9 September 2011 doi: 10.1111/j.1600-0528.2011.00641.x  105  little research has investigated the mechanisms thatlink oral health (and oral disease risk) to exposuresacross generations. What has been done has almostexclusively concentrated on oral health in childrenor young adolescents (32–41). Most researchershave focused on narrow aspects of intergenera-tional continuity, such as oral cancer (42), or Streptococcus mutans  acquisition (36). Some studieswere cross-sectional in design (and so do not offerstrong evidence), and many have tended to exam-ine the effects of exposures at only one point intime. Others have suffered from methodologicalproblems (such as selection bias, attrition or insuf-ficient statistical power). Many studies have notcontrolled for confounding factors. In summary, itis unclear whether the oral health status of onegeneration has an effect on that of the next.Oral health, in common with virtually all traits,is likely to be the result of gene–environmentinteraction (43–45). Family history reflects theresults of shared genetic variations and sharednongenetic factors (environmental factors, expo-sures and common behaviours) (46). Whileresearch has increased awareness of the numerousand diverse risk factors contributing to oral dis-ease, an understanding of these shared genetic andenvironmental influences acting through genera-tions on the oral health of adults is a clear gap inthe knowledge base. Using intergenerational datafrom an adult sample with sufficient statisticalpower, and controlling for putative confounders,the aim of this study was to determine whether anindividual’s oral health and disease risk are influ-enced by those of his or her parents. Methods Study design and participants This study is an analysis of data from the DunedinMultidisciplinary Health and Development Study(DMHDS) using dental data collected from Studymembers (hereafter referred to as ‘probands’) andtheir parents during the age-32 assessments. TheDMHDS is a longitudinal epidemiological study of a birth cohort of 1037 children born at the QueenMary Hospital, Dunedin, New Zealand, between 1April 1972 and 31 March 1973. These 1037 childrenrepresent 91% of the 1139 eligible children born between these dates, and 972 (95.8% of the surviv-ing cohort) were assessed at age 32. Of these 972,932 (95.9%) were dentally examined (Fig. 1). Of those who were dentally examined, the majority(882, 94.6%) had one or both parents participate inthe family health history study; two-thirds (648,69.5%) had both parents participate. Data from 16 23 deceased 16 with incomplete  parental information 1014 surviving at age 32 972 assessed at age 32932 dentally examined at age 32 1037 participants 882 had at least one parent assessed at age 32 assessment 1139 Eligible High familial risk if one or both parents had lost six or more teeth due to caries at the age-32 assessment  N   = 313 (36.1%) High familial risk if one or both parents had lost six or more teeth due to caries at the age-32 assessment  N   = 254 (39.7%) 640 had both parents interviewed (complete information)866 had one or both parents interviewed (complete information) Low familial risk  N   = 553 (63.9%) Low familial risk  N   = 386(60.3%)849 with caries trajectories626 with caries trajectories 625 with plaque trajectories 848 with plaque trajectories High familial risk  N   = 305 (36.0%) High familial risk  N   = 247 (39.5%) High familial risk  N   = 306 (36.0%) High familial risk  N   = 248 (39.6%)Low familial risk  N   = 543 (64.0%) Low familial risk  N   = 378 (60.5%) Low familial risk  N   = 378 (60.4%) Low familial risk  N   = 543 (64.0%)High familial risk  N   = 305 (36.0%) 848 with caries and  plaque trajectories 625 with caries and  plaque trajectories High familial risk  N   = 247 (39.5%) Low familial risk  N   = 543 (64.0%) Low familial risk  N   = 378 (60.5%)  Fig. 1.  Participation rates, sample sizes and familial-risk groups. 106 Shearer et al.  probands were excluded from the analysis becauseof incomplete parental information. Analyses werecarried out for two samples. The first sample( N   = 866) comprised probands who had one or both parents interviewed at the age-32 assessment(generalizable to households where data fromeither one parent only or both parents wereavailable); the second ( N   = 640) consisted of pro- bands who had both parents interviewed at theage-32 assessment (a more complete parentalhistory is obtained, but is only generalizable totwo-parent families). As the ‘one or both parentsinterviewed’ sample encompasses the ‘both parentsinterviewed’ sample, the samples are not mutuallyexclusive.M  aori (7.5%) were under-represented (in com-parison with 15% in the total New Zealand pop-ulation) in the cohort at age 32. There werestatistically significant differences between thoseincluded and those excluded in the analyses; thoseexcluded had a greater prevalence of one or moremissing teeth ( P  < 0.05), higher mean DMFS( P  < 0.05) and higher mean MS ( P  < 0.05) at age32 than those included (unpublished data, avail-able on request). Those excluded did not signifi-cantly differ from those included with respect tosex, SES, self-rated oral health, use of dentalservices, smoking status, caries prevalence, severecaries prevalence, mean DS and mean FS at age 32.Ethics approval for the study was granted by theOtago Research Ethics Committee, and participantsgave informed consent.  Measurements The study used data collected from probands’ oralexaminations and interviews and from interviewswith their parents, at the age-32 assessments. Proband caries and tooth loss measurement.  In the age-32 assessments (conducted in 2004–2005),calibrated examiners carried out dental examina-tions for caries and missing teeth on 932 (95.6%) of the 972 probands who were assessed at age 32.Accumulated tooth loss caused by caries wasdetermined by recording the presence or absenceof each tooth, and noting the reason for its absence.Third molars were not included in the estimation of caries-associated tooth loss. Teeth were examinedfor caries and restorations; four surfaces werecoded for the anterior teeth (buccal, lingual, mesialand distal), and five (including the occlusal surface)for the posterior teeth.As reported previously, longitudinal caries expe-rience data were used to identify three distincttrajectories of dental caries experience betweenages 5 and 32 (47). Briefly, a modified DMFS wascomputed for participants who had three or moredental examinations (and dental caries data) between ages 5 and 32. Group-based trajectoryanalysis, based on the zero-inflated Poisson distri- bution, was performed with the PROC TRAJ macroin SAS 9.1 to identify low, moderate and highcaries trajectory groups. Regarding the familyhistory samples, 849 individuals had a cariestrajectory in the ‘one or both parents in’ sample(low,  N   = 349, 41.1%; moderate,  N   = 374, 44.1%;and high,  N   = 126, 14.8%), and 626 individuals hada caries trajectory in the ‘both parents in’ sample(low,  N   = 256, 40.9%; moderate,  N   = 283, 45.2%;and high,  N   = 87, 13.9%). Plaque measurement.  The simplified oral hygieneindex was used to quantify plaque accumulationon six index teeth (48), and the overall plaque scorewas the sum of the scores divided by the number of teeth scored. Long-term plaque exposure wasdescribed through trajectory analysis. The longitu-dinal data on plaque scores measured at three ormore assessments between the ages 5 and 32(including at age 32) were used to split the cohortinto three distinct ‘plaque groups’ using a group- based trajectory analysis model, based on thecensored normal distribution, in SAS 9.2 (49). Inthe family history samples, 848 individuals had aplaque trajectory in the ‘one or both parents in’sample (group 1, low levels of plaque,  N   = 333,39.3%; group 2, moderate levels of plaque, N   = 419, 49.4%; and group 3, high levels of plaque,  N   = 96, 11.3 %), and 625 individuals hada plaque trajectory in the ‘both parents in’ sample(group 1, low levels of plaque,  N   = 257, 41.1%;group 2, moderate levels of plaque,  N   = 306, 49.0%;and group 3, high levels of plaque,  N   = 62, 9.9%). Proband interviews.  A measure of socio-economicstatus (SES) at phase 32 was obtained from eachstudy member using standard New Zealand indi-ces that apply a six-interval classification accordingto occupation, for example, a doctor scores ‘1’ and alabourer scores ‘6’ (50, 51). Study members with ascore of ‘1’ or ‘2’ were allocated to the ‘high SESgroup’; those with a score of ‘3’ or ‘4’ were assignedto the ‘medium SES group’; and those with a scoreof ‘5’ or ‘6’ were assigned to the ‘low SES group’.Participants were asked to indicate whether theywere routine or episodic users of dental careservices. Routine users were those who usuallyvisited for a check-up and had made a dental visitin the previous 12 months (52). 107 Family history and oral health  Parental interviews.  Around the same time as theage-32 assessment (2003–2006), the parents of probands took part in an interview on their oralhealth status and history (53). They were askedwhether they had lost any teeth (for any reason)and if so, how many. In addition, they were askedabout the main reason for their tooth loss (toothdecay, periodontal disease, trauma or anotherreason).The parental interview information on theirdental caries and tooth loss experience was usedto allocate each proband (their child) to either a‘high-familial-risk’ group or a ‘low-familial-risk’group for dental caries (Fig. 1). Probands wereallocated to the high-familial-risk category if one or both of their parents reported having lost six ormore teeth, because of caries, at the age-32 assess-ment. All other probands (those whose parents didnot report having lost six or more teeth, because of caries, at the age-32 assessment) were grouped inthe low-familial-risk category. These groups werefurther refined for some analyses according towhether the probands had been assigned to a cariestrajectory, a plaque trajectory or both (Fig. 1). Statistical analysis Descriptive and bivariate analyses were performedusing SPSS version 16.0 (SPSS Inc. Chicago, IL,USA). Multivariable analyses used Stata version10.0 (StataCorp, College Station, TX, USA). Chi-square tests were used to examine the statisticalsignificance of associations observed betweenfamilial-risk groups and proband caries and toothloss prevalence at age 32. Independent sample t -tests were used for continuous dependent vari-ables mean DMFS, mean DS, mean MS, mean FSand mean plaque score at age 32. Statistical testswere two tailed, and the threshold for statisticalsignificance was set at  P  < 0.05. In the multivari-able analysis, the generalized linear model (GLM)command with modified Poisson regression anal-ysis was used to estimate prevalence ratio (withconfidence intervals) for proband prevalence of oneor more missing teeth owing to caries, and of having a high caries trajectory, and a rate ratio formean DMFS, at age 32, using a robust errorvariance procedure. Confounding factors (sex, epi-sodic use of dental services, SES and plaquetrajectory) were selected based on the biologicalplausibility and were guided by the literature (49,54–56). In the causal directed acyclic graph (DAG),an arrow connecting two variables indicates cau-sation (Fig. 2). This graphical representation of causal effects between variables facilitates theidentification of confounders that should be ad- justed for to minimize bias (57, 58). Results Dental caries and tooth loss by familial-riskcategory In bivariate analyses for both samples, there weremarked caries   ⁄   tooth loss risk category differences between the familial-risk groups in: the prevalenceof severe caries experience (DMFS > 20); one ormore teeth missing owing to caries; having a DMFSscore greater than the median (median DMFS = 12)at age 32; and having a high caries trajectory between ages 5 and 32 (Tables 1 and 2, and Fig. 3).This was also the case for mean DMFS, mean DS,mean FS, mean MS and mean plaque score(Tables 1 and 2, and Fig. 4).  Multivariable analyses Multivariable modelling was used to determine theprevalence ratio (PR) for one or more missing teethat age 32, the rate ratio (RR) for DMFS at age 32,and the PR of having a high caries trajectory between ages 5 and 32 in the high-familial-riskgroup (using the low-familial-risk group as areferent) while controlling for the confoundingfactors of sex, episodic use of dental services, SESand plaque trajectory. For the ‘one or both parentsinterviewed’ sample, the age-32 mean DMFS in the  Fig. 2.  DAG for exposure (familial-risk), outcome (pro- band caries   ⁄   tooth loss status at age 32) and confoundingfactors. 108 Shearer et al.

Layout Byblos

Sep 19, 2017

Sea Monsters.

Sep 19, 2017
Search
Tags
Related Search
We Need Your Support
Thank you for visiting our website and your interest in our free products and services. We are nonprofit website to share and download documents. To the running of this website, we need your help to support us.

Thanks to everyone for your continued support.

No, Thanks
SAVE OUR EARTH

We need your sign to support Project to invent "SMART AND CONTROLLABLE REFLECTIVE BALLOONS" to cover the Sun and Save Our Earth.

More details...

Sign Now!

We are very appreciated for your Prompt Action!

x