Original Paper Caries Research Caries Res 2001,38:236-238 Desens anor melon: Mere 8, 2001 Is Asthma a Risk Factor for Dental Caries? Findings from a Cohort Study A.M. Meldrum? W.M. Thomsons B.K. Drummond* MLR. Sears® “Department of Oral Health, School of Dentistry, University of Otago, Dunedin, New Zealand 'MeMaster University, Hamilton, Ont, Canada Key Words Asthma Asthma pharmacotherapy « Caries risk - Cohort study « Dental caries Abstract Ithas been suggested that asthmatic children may have a higher caries risk, both as a result of their medical con: dition and the physical and physiological effects of their pharmacotherapy. By examining the association over time between asthma and caries increment, this study tested the hypothesis thet childhood asthma is associat: ed with an increased caries increment. In a long-stand: ing New Zealand cohort study, participants’ long-term asthma histories and the 3-year net caries increment be- tween the ages of 15 and 18 years were examined. Of the 781 who were examined at 15 and 18 years, 39 par- ticipants were consistently taking anti-asthma medica- tion at the ages of 9, 11, 13 and 15 years (and were labelled in this study as ‘medication-determined asth- matics’), 56 were identified as consistent wheezers at the ages of 9, 11, 13 and 15 years ("wheeze-determined asthmatics’) and 36 were members of both groups. A smaller group in = 9) was identified as being very-long- term asthmatics (asthma at 5 years of age and at the ages of 9, 11, 13 and 15 years). Some 206 study mem- bers were identified as having no history of asthma, asthma medication or significant wheeze at any time up to and including 18 years. The overall mean net caries increment between the ages of 18 and 18 years was 2.06 KARGER (au ese tse aS 17500 surfaces (SD, 3.76). There were no significant differ- ences in caries increment between the 206 asthma-free participants and any of the asthma groups. This study provides little evidence for an asthma-caries causative relationship. A link between dental caries and asthma (either the con dition per se or the commonly used anti-asthma inhalant medications) has biological credibility, but there is only limited clinical and epidemiological support for such an as sociation, The international literature, however, presents few studies investigating the relationship between asthma and oral disease, Previous attempts to investigate the asso- ciation have produced conflicting results and mostly equiv ‘ocal conclusions [Hyyppa et al., 1979; Hyyppa and Paunio, 1979; Bjerkeborn et al., 1987; Kankaala et al., 1998: MeDerra et al., 1998]. Two factors are largely responsible for this current lack of consensus. First, both asthma and caries are chronic conditions with variable presentations, complex aetiologies and challenges in diagnosis which complicate attempts to study them, Second, most reported studies have been of cross-sectional design and have in- volved small, non-representative samples. ‘Asthmatics may have altered salivary composition and flow rates due to the presence of specific auto-antibodies to Br-adrenergic receptors, These receptors are affected by the administration of f-agonist anti-asthmatic drugs [Ryberg et al., 1987, 1990, 1991), This has led to the suggestion that,through either their disease or their pharmacotherapy. asth matics may be more susceptible to dental caries. Decreased salivary and plaque pH has been observed in asthmatic chil- dren who were using inhalers [Kargul et al. 1998]. The de- livery mode of common asthma medications may further enhance this risk: inhaled drugs are delivered in a carrier powder which may contain a sugar to assist the user in recognising the delivery of their medication by taste. Be- codisk (beclomethasone dipropionate, Glaxo Wellcome) and Flixotide Rotadisk (fluticasone propionate, Glaxo Well- come) contain as much as 25 mg of large-particle lactose per dose. Almost all inhalant powders have a pH of less than 5.5 [0 Sullivan and Curzon, 1998}, and while lactose is less, cariogenic than other common sugars, it has caries-promot- f potential when associated with reduced salivary flow [Pearce and Sissons, 1987] Asthmatics may use erosive drinks [MeDerra et al., 1998} to alleviate the effects of mouth breathing or eliminate the residual taste of medication, some 60% of which may re ‘main in the oropharynx (Pedersen, 1996]. Accordingly, there ray be a heightened caries risk among asthmatics from (1) their disease, (2) their anti-asthma medication or (3) their at- tempts to alleviate the condition’s physiological sequelae. ‘There are no reports from prospective cohort studies of asthma and dental caries. The cohort study design offers distinct methodological advantages over the cross-sectional approach used in previous studies. Repeated observations of participants over time enable: (1) the time-ordering of exposure and outcome to be made explicit: (2) more accu- rate identification of long-term asthmatics, and (3) the ex amination of caries experience over time, rather than at a single point in time. The objective of this study was to test the hypothesis that, among participants in a longitudinal New Zealand cohort study, long-term exposure to asthma is, associated with increased caries experience in adolescence. Materials and Methods The Sample Te participants were children enrolled in the Dunedin Multis ciplnary Health and Development Study (DMHDS). an ongoing lon sitadinal study of th health, development and well-being of a large sample of young New Zealanders [Silva and Stanton, 1996]. The chil- drea were born at Queen Mary Hospital in Dunedin between April 1972, and March 31, 1973, Children still resident inthe province of Otago at 3 years of age were invited to cake pat inthe study, and 91% {n= 1.037) of those eligible were enrolled. In comparison with New Zealand as-a whole, the sample s slightly under representative ofthe ‘more socio-economically disadvantaged but includes abroad range of socio-economic levels, The participants were assessed every 2 ‘uml he age of 1 and theo at 18 years, 26 Collection of Exposure and Ouscome Dare [Long-term asthmatics were identitied from information collected teach of the ages of 9 11,13 and 15 years (table 1), Two approach cs were used identify the long-term asthmatics: (1) “wheeze-deter mined asthmatics’ (WDA) were identified by a reported history of ‘wheeze at cach ofthe ages of 9, 11,13 and 15 years, and (2) ‘medica tion-determined asthmaties'(MDA) were identified by a reported his- tory of anti-astha medication at each ofthe ages of 9,11, 13 and 15 years, Very long-term asthmaties were identified by a tepdrted histo Fy of asthma at the age ofS years as well as meeting the criteria forthe MDA and WDA groups. Parental socio-economic status was cate orised at the age of 15 years using the Elley-Irving scale, which al locates individuals to a 6-category occupational scale [Eley and Irv- ing, 1985} “The dependent variable for the current study Was the net coronal caries inerement between the ages of 1 and 18 years. This was com. puted by comparing the status of each tooth surface atthe age of 18 ‘with that at che age of 15 using World Health Organisation evteria [World Health Organisation, 1977], The diagnosis was based on clin- ical examinations, and no radiographs were taken, All questionable lesions were recorded as sound. The 3-yeur net increments of decayed surfaces (DS), filled surfaces (FS) and decayed and filled surfaces (DFS) were computed for each individual by subtracting the number of reversals from the gross caries increment. AS well as the overall caries increment, separate surface-specitie analyses were conducted fie smooth-sueface and pt-andsfissure caries. Three dental examiners were involved inthe collection of data at 1S years and 4 dental exam- iners a 18 years, All wre calibrated before the collection of data, but no formal reproducibility procedures were undertaken due to logst cal constraints. A consistent and systematic approach to each deat ‘examination was adopted. At both ages, the same examination proce lures were followed. Examination was made using fibre-optic light, plane dental mirror and sickle explorer. Concerns that iatrogenic da ‘age may be caused by probing the teeth Ted to the abandonment of the sharp probe to confirm the presence (or otherwise) of caries during the examination at 18 years, and visual assessment only was used at that ime, Data were entered onto individual data forms by a recorder atthe time of the examination Analysis Data were entered into an electronic data set and analysed using $8, Afer the computation of univariate staistis, bivariate analy- ses explored the association of asthma stats and disease experience. 1 sola tess were used to test associations with categorical depen- ‘dent variables, while analysis of variance or Mann-Whitney U tests ‘were used (where appropriate) for continuous dependent variables ‘The critical level of significance was 0.05 Results At the age of 15 years, 976 members were assessed, of whom 848 were dentally examined, and at the age of 18 years, 993 members were assessed, of whom 867 were dem: tally examined. Dental data from the ages of 15 and 18 years were avail- able for 781 (75.8% of the original cohort) of the members Meldrum/Thomson/Drummond/SearsTable 1. Identification of asthmatic study members Y (1) Paediatric interview VIL (1) Health questionnaire Phase Method of identification Specific item used Has... ever had any problems with asthma or wheezing? Hus... ever had asthma? (2) Family history of asthma, TX (1) Asthma questionnaire (2) Asthma medication (a) Overall history indicative of asthma? (b) History of wheezing, chest whistling or noisy breathing? (2) Oral or inhaled bronchodilator? (b) Oral or inhaled steroids? (Gy Lung funetion tests XL (1) Asthma questionnaire (2) Asthma medication G) Lung function {a) Diagnosis from reported history (by Ever had whoezy breathing? ‘What drug? Intermittent/regular? (4) Measurements of allergy xi (2) Asthma medication Whi (1) Asthma questionnaire (a) Self-reported asthma inthe last 2 years (b) Self-reported wheezy bresthing in the last 2 years rug? Intermittent/regular? G) Lung funetion ests (4) Skin tess XV (1) Respiratory questionnaire 2) Asthma medication {a) Diagnosis from reported history () History of current wheeze {¢} Age commenced regular smoking ‘What drug? Intermittent/regular? (G3) Lung function tests xvii (1) Respiratory questionnaire (2) Asthma medication Do you still have asthma? Current asthma medication? {G) Lang fonction tests ‘There were no sex or socio-economic status differences be- tween the 781 members who were dentally examined at both ages and the 87 who were not, or between the former and the 195 who were not dentally examined at either age. Of the 781 participants, 39 (5.0%) were identified as MDA, 56 (7.2%) were WDA and 36 (4.6%) were identified as members of both groups. A smaller group of 9 (1.2%) ‘were asthmatic at the age of 5 years and at the ages of 9, 11, 13 and 15 years (and categorised as “very-long-term asth- matics"), and met the criteria for both the MDA and WDA groups. The 9 very-long-term asthmatics were included in both the asthma groups. The groups overlapped, with only 3 members of the MDA group not also represented in the WDA group. A group of 206 (26.3%) were identified as having no history of asthma, that is no asthma medication or significant wheeze at any time up 10 (and including) 18 years, These individuals were used as the comparison group for subsequent analyses in order to maximise the chance of detecting a difference between asthmatics and non-asthmat- ics. The remaining 516 participants reported wheezing symptoms at one (or more) but not all of the study phases and were not included in either the ‘asthma’ groups or the control group. The overall 3-year mean net DFS increment from the ages of 15 10 18 years was 2,06 (SD, 3.76), which com- prised a mean DS of 0.17 (SD, 0.87) and a mean FS of 1.89 (SD, 3.76). The mean net DFS increment for pits and fis- sures was 1,29 (SD, 2.18). and for smooth surfaces 0.78 (SD, 2.21) Three-year net caries increment data are presented in table 2. Among the WDA, the mean net DFS increment for all surfaces was 2.39 (SD, 4.12), while the pit-and-fissure [6 Asthma a Risk Factor for Dental Caries? ose SRE =