Sugar, dental caries and the incidence of

acute rheumatic fever: a cohort study of

Māori and Pacific children
Original article
Simon Thornley,1 Roger J Marshall,2 Katie Bach,3 Pauline Koopu,4 Gary Reynolds,5 Gerhard
Sundborn,6 Win Le Shwe Sin Ei.7

1. Epidemiologist, Auckland Regional Public Health Service, Cornwall Complex, Greenlane,

Auckland, 1051, New Zealand.
2. Associate-Professor of Biostatistics, Section of Epidemiology and Biostatistics, The
University of Auckland, Tamaki Campus, Auckland, 1142, New Zealand.
3. Paediatric Dentist, Paediatric Services, Oral Health Department, Level 1, Building 4,
Greenlane Clinical Centre, Auckland District Health Board, Auckland, 1051, New
Zealand.
4. Dentist, Paediatric Services, Oral Health Department, Level 1, Building 4, Greenlane
Clinical Centre, Auckland District Health Board, Auckland, 1051, New Zealand.
5. Medical Officer, Auckland Regional Public Health Service, Cornwall Complex,
Greenlane, Auckland, 1051, New Zealand.
6. Research Fellow, Section of Epidemiology and Biostatistics, The University of Auckland,
Tamaki Campus, Auckland, 1142, New Zealand.
7. Postgraduate student, Section of Epidemiology and Biostatistics, The University of
Auckland, Tamaki Campus, Auckland, 1142, New Zealand.

Correspondence to: Simon Thornley

Epidemiologist, Auckland Regional Public Health Service, Cornwall Complex, Greenlane,

Auckland, 1051, New Zealand.

email: sithor@gmail.com

Phone (mobile): +64212991752

Key words
Epidemiology; rheumatic fever; dental caries; cohort study; dietary sucrose.

Word count
3,232

1
Licence for Publication

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behalf of all authors, an exclusive licence (or non exclusive for government employees) on a

worldwide basis to the BMJ Publishing Group Ltd to permit this article (if accepted) to be

published in JECH and any other BMJPGL products and sublicences such use and exploit all

subsidiary rights, as set out in our licence (http://group.bmj.com/products/journals/instructions-

for-authors/licence-forms).

Competing interests

None declared.

2
Abstract

Objective

To determine whether dental caries, as an indicator of cumulative exposure to sugar, is

associated with the incidence of acute rheumatic fever and chronic rheumatic heart disease, in

Māori and Pacific children aged five and six years at their first dental visit.

Materials and Methods

A cohort study was undertaken which linked school dental service records of caries with national

hospital discharge and mortality records. Cox models were used to investigate the strength of

the association between dental caries and rheumatic fever incidence.

Results

A total of 20,333 children who were free of rheumatic heart disease at enrolment were available

for analysis. During a mean follow-up time of five years, 96 children developed acute rheumatic

fever or chronic rheumatic heart disease. After adjustment for potential confounders, children

with five primary teeth affected by caries were 57% (95% confidence interval: 20% to 106%)

more likely to develop disease during follow-up, compared to children whose primary teeth were

caries free. The population attributable risk for caries in this cohort was 22%.

Conclusions

Dental caries is positively associated with the incidence of acute rheumatic fever and chronic

rheumatic heart disease in Māori and Pacific children. Sugar intake, an important risk factor for

dental caries, is also likely to influence the aetiology of rheumatic fever.

3
What is already known about this topic?

Acute rheumatic fever is strongly associated with Streptococcus pyogenes infection. A closely

related bacterium, S. mutans, is associated with dental caries.

Indices of a poor diet, such as low body weight and low serum albumin have been historically

associated with rheumatic fever incidence.

Māori and Pacific children have both a high prevalence of dental caries and acute rheumatic

fever.

What does this study add?

Dental caries in childhood is positively associated with the incidence of acute rheumatic fever,

after adjusting for known risk factors.

This finding suggests that dietary sugar intake, a known risk factor for dental caries, is also likely

to influence the onset of acute rheumatic fever.

4
INTRODUCTION

Acute rheumatic fever (ARF) is almost absent from most developed countries, yet New Zealand

continues to carry a high burden among Pacific and Māori populations.1 The disease leads to

degeneration of heart valvular function, usually in adulthood, and is an important cause of

ethnic inequality in health status. The incidence and prevalence has declined substantially in

New Zealand, but remains similar to countries such as China, Russia, and Qatar.2

A new hypothesis is that ARF is related to sugar (sucrose) intake.3 It is plausible because

Streptococcus pyogenes, a bacterium associated with acute rheumatic fever, is able to ferment

sugar.4 This bacterium uses glucose as its primary carbon source during growth, but is also able

to ferment fructose, a monosaccharide that is present when sucrose is digested.5

At the same time, a closely related bacterium, S. mutans, is associated with dental caries, so that

a relationship between ARF and dental caries would signal an ARF - sugar relationship. The

hypothesis is supported by evidence that Māori and Pacific children are most susceptible to ARF

and also have a high prevalence of dental caries, compared to other ethnic groups. 6

In a recent review of the relationship between sugar and caries, Sheiham and James7 conclude

that the main cause of caries is sugar intake. Other, less important influences that were

discussed are oral hygiene and water fluoridation. Their argument is supported by many

ecological studies which show a reduction of caries when sugar is restricted due to rationing, for

5
example.8-10 If sugar causes dental caries and caries is predominately the result of sugar intake

(figure 1; solid grey arrow), then caries is effectively a surrogate for sugar and may be used to

estimate the presence of an association between sugar intake and acute rheumatic fever (figure

1; dashed black arrow). Just as the bacteria that cause dental caries to thrive in the presence of

sugar, it is plausible that sugar will also fuel the growth of bacteria that cause streptococcal

throat infection – a frequent precursor to rheumatic fever.

[figure 1 here]

Auckland city has a single provider of dental care for children. All children in Auckland are

invited to participate in the service from birth to thirteen years, and are, ideally, seen annually

for review. Since these records and databases of hospital diagnoses exist for state run hospitals,

we conducted a cohort study linking these two databases to investigate the nature of the

association between dental caries and rheumatic fever incidence. Since ARF, in New Zealand, is

almost exclusively a disease of Māori and Pacific Island children (there were just four cases of

ARF in other groups) the study is confined to them.

MATERIALS AND METHODS

Study Population

Data was extracted from the Auckland Regional Dental Service (ARDS). This service provides

preventive, restorative and surgical dental services, mostly undertaken by dental therapists.

Estimates of enrolment in the service vary by age, but are between 90 to 96% of children age 3 to

4 years. Despite high enrolments, many do not attend clinics. The proportion that do not attend

is estimated to be about 20% at the age of 5 years.11

The data extract included individuals at their first dental examination, between 14/5/2007 and

24/3/2015. Items available in the dental service data included date of birth, date of visit, ethnic

group (as claimed by parents: “Māori”, “Pacific” and “Other” ethnicity), gender, a unique

6
National Health Index code (NHI) and measures of dental caries. If a child’s parents claimed

both Māori and Pacific heritage, the child was classified as “Māori”. The caries measures

included decayed, missing (due to caries) and filled teeth with primary (dmft), and permanent

teeth (DMFT) coded separately. The NHI code enabled these records to be combined with

records of hospital treatment, coded as ICD-10 diagnoses.

Exclusion criteria

Children with potentially life-limiting conditions were excluded by searching for any conditions

in the first five diagnosis categories in hospital records before they first appeared in the dental

database. This was carried out to reduce possible confounding by chronic disease status.

Diagnoses that were excluded were obtained from a study which specifically focused on children

with life-limiting illnesses.12 These were specifically: C00-D48 neoplasms, D60-D64 aplastic and

other anaemias, D80-89 immune disorders, E70-84, E88 metabolic syndromes, G00-G99

nervous system diseases, I42 cardiomyopathies, J40-J47 chronic lower respiratory diseases,

J80-84 interstitial respiratory diseases, J96.1 respiratory failure, N18 renal failure, Q00-Q99

congenital malformations, P27 perinatal chronic respiratory disease, and P91 cerebral

conditions of the newborn.

All children who otherwise met the entry criteria had records checked for codes consistent with

rheumatic fever or heart disease (any, rather than principal diagnosis) before their first visit to

the dental service. Children with such codes were excluded. Individuals without an NHI code

were also excluded.

Inclusion criteria

The study population was restricted to Māori and Pacific children aged between five and six

years of age on the date of their first dental visit. The exclusion of children of other ethnicities

was applied as the incidence of ARF is very low in this group, with the likely effect of an unstable

statistical model, due to the presence of a strong association between ethnicity and disease

7
incidence. The age restriction was applied to limit the effects of exfoliation of carious primary

teeth.

Caries measures

The sum of decayed, missing (due to caries) and filled primary teeth (dmft), was recorded in the

dental register. Scores range from 0 to 20. If a carious lesion was found, or both a lesion and

restoration, then the tooth is labelled ‘d’, if a filling was present, the tooth is an ‘f’, and if

extracted due to caries it was ‘m’. DMFT similarly applies to permanent teeth. As a child ages,

between 5 and 12 years, the primary teeth are shed. If a child exfoliates a tooth affected by caries

(decayed), or a filled tooth, then dmft will decrease; however, an extracted tooth (‘m’) remains.

Both permanent (DMFT) and primary teeth (dmft) caries were considered as predictors of ARF.

Outcomes

The first appearance, after first dental examination, of an ICD-10 diagnosis of acute rheumatic

fever (I00-I02), or chronic rheumatic heart disease (I05-I09) in either death or hospital

discharge records (primary diagnosis only), during follow-up, was considered the outcome of

interest.13 Only primary diagnoses were used to reduce false-positive cases. The final date that

follow-up data was available was 22/04/2015.

Loss to follow-up

We assumed that all children remained in New Zealand during follow-up, and none were lost, as

we had no way of checking emigration status.

Ethical considerations
Ethical approval was granted by the New Zealand Health and Disability Ethics Committee

(14/STH/133).

8
Analysis

Checks were made for duplicate records and implausible data (wrongly recorded age, for

example). Differences in outcomes by caries status were assessed with Kaplan-Meier plots, by

initially splitting the distribution at the median value of dmft. Cox proportional hazard models

were used to assess the strength of association between dental caries and time until first hospital

diagnosis of ARF. If individuals had no such outcome, they were considered censored at the end

of the study period (22/04/2015), or in the event of death from another cause. Age at the time of

an ARF event, in those in whom it occurred, or at 22/04/2015 was considered the time scale for

analysis, since it is now recommended in the analysis of cohort studies in which conditions are

age-related.14

Results are presented as crude associations and adjusted for potential confounders (gender,

ethnic group and socioeconomic status) using Cox regression modelling. Restricted cubic splines

were used to check on the modelling assumption of linearity for continuous covariates.

Confounders included gender, ethnic group (Māori, and Pacific) and socioeconomic status

(NZdep06). NZDep06 is an area-based measure of socioeconomic deprivation based on a range

of characteristics derived from the New Zealand census (car and telephone access, receipt of

benefits, unemployment, income, education, home ownership and living space). All these

variables were considered to be common causes of caries and ARF, and so were adjusted for in

the analysis.

The assumption of proportional hazards throughout the duration of follow-up was checked by

creating interaction terms with time for each covariate and calculating the Pearson product-

moment correlation between scaled Schöenfeld residuals for this term with a log transformation

of time. A significant correlation between residuals and transformed time suggests deviation

from proportionality during follow-up. Evidence for interactions was checked between ethnic

group and severity of dental caries and survival, using a likelihood ratio test. A two-sided type-1

9
error rate was set at 5%. Very few missing values were present, mainly in people without NHI,

who were excluded.

Population attributable risk (PAR) for significant dental exposures was calculated using the

formula for multiple exposure levels15 with estimated risk ratios taken from the fitted Cox

model. PAR here is effectively the percentage reduction in ARF incidence that would result if

caries were completely eliminated.

R software was used for all analyses (version 3.2.1).16 The rms, survival, magrittr and epicalc

packages were used for data analysis.

RESULTS
The flow of individuals into the study is outlined in figure 2.

[Figure 2 here]

After age and ethnicity restrictions were applied, a total of 20,333 individuals were available for

analysis, totalling 103,588 person-years of follow-up. Mean follow-up time for the cohort was

five years, over which time 94 cases developed. Table 1 shows the characteristics of the study

population, divided by the level of caries in the primary teeth (dmft = 3 represents the median

value). The table shows that Pacific children had higher levels of caries than Māori, and those

subjects with lower socioeconomic status and boys had higher levels of caries. Lesions in the

primary teeth mainly consisted of decay, which are presumably treated at subsequent visits, as

did those in the permanent teeth. The proportion of children who developed ARF or chronic

rheumatic heart disease during follow-up was about doubled in the high caries group (dmft ≥

3), compared to the low.

10
Table 1. Baseline characteristics, by caries status (dmft) at enrolment.

dmft
<3 ≥3 Total P-
mean (sd)* mean (sd)* mean (sd)* value†
Total 11,593 8,740 20,333
Gender (Male); n (col. %) 5,669 (48.9) 4,440 (50.8) 10,109 (49.7) 0.008
Age at first visit (years) 5.84 (0.57) 5.92 (0.57) 5.88 (0.57) <0.001
Ethnic group; n (col. %) < 0.001
Māori 5,891 (50.8) 3,408 (39.0) 9,299 (45.7)
Pacific Island 5,702 (49.2) 5,332 (61.0) 11,034 (54.3)
Deprivation quintile; n (col. %) < 0.001
1 and 2; least deprived 896 (7.7) 286 (3.3) 1,182 (5.8)
3 and 4 1,131 (9.8) 481 (5.5) 1,612 (7.9)
5 and 6 1,356 (11.7) 777 (8.9) 2,133 (10.5)
7 and 8 2,459 (21.2) 1,776 (20.3) 4,235 (20.8)
9 and 10; most deprived 5,514 (47.6) 5,189 (59.4) 10,703 (52.6)
Rural (not categorised) 237 (2.0) 231 (2.6) 468 (2.3)
Primary teeth caries
decayed 0.408 (0.709) 4.697 (3.008) 2.252 (2.947) < 0.001
missing 0.005 (0.078) 0.212 (0.893) 0.094 (0.597) <0.001
filled 0.067 (0.306) 1.010 (1.830) 0.472 (1.308) < 0.001
dmft 0.480 (0.755) 5.919 (2.660) 2.818 (3.258) < 0.001
Adult teeth caries
Decayed 0.022 (0.219) 0.100 (0.438) 0.055 (0.334) < 0.001
Missing 0.003 (0.214) 0.004 (0.151) 0.003 (0.189) < 0.001
Filled 0.002 (0.060) 0.014 (0.155) 0.007 (0.112) 0.004
DMFT 0.026 (0.313) 0.117 (0.492) 0.065 (0.403) < 0.001
Outcomes
Acute rheumatic fever; 31 (0.267) 50 (0.572) 81 (0.398) <0.001
n (col. %)
Chronic rheumatic heart 9 (0.078) 10 (0.114) 19 (0.093) 0.537
disease; n (col. %)
ARF or CRHD‡ ; n (col. %) 36 (0.311) 58 (0.664) 94 (0.462) < 0.001
Follow-up time (days) 1,865 (726) 1,852 (706) 1,861 (719) 0.224
*Mean (standard deviation) unless categorical variable, then n (column %). †Chi-square
test for categorical variables and Wilcoxon rank-sum test for continuous. ‡ARF: acute
rheumatic fever. CRHD: chronic rheumatic heart disease. dmft: sum of decayed, missing
(due to caries) and filled primary teeth. DMFT: sum of decayed, missing and filled
permanent teeth. sd: standard deviation.

[Insert figure 3 here]

11
Table 2 highlights the differences in the distribution of socio-demographic factors and oral

health status between children that went on to become cases and those who did not. Cases were

more likely to live in deprived neighbourhoods (P = 0.002), and were more likely to have higher

levels of decay in the primary (mean dmft 50% higher in cases than non-cases) and permanent

teeth (mean DMFT 260% higher in cases than non-cases).

Table 2. Baseline characteristics, by disease status at the end of follow-up.

Disease free Rheumatic fever Total P-value†

mean (sd)* mean (sd)* mean (sd)*
Total 20,239 94 20,333
Gender (Male); n (col. %) 10,055 (49.7) 54 (57.5) 10,109 (49.7) 0.162
Age at first visit (years) 5.88 (0.57) 5.95 (0.54) 5.88 (0.57) 0.232
Ethnic group; n (col. %) 0.078
Māori 9,265 (45.8) 34 (36.2) 9,299 (45.7)
Pacific 10,974 (54.2) 60 (63.8) 11,034 (54.3)
Deprivation quintile; n (col. %) 0.002
1 and 2; least deprived 1,182 (5.8) 0 (0.0) 1,182 (5.8)
3 and 4 1,608 (8.0) 4 (4.3) 1,612 (7.9)
5 and 6 2,129 (10.5) 4 (4.3) 2,133 (10.5)
7 and 8 4,220 (20.9) 15 (16.0) 4,235 (20.8)
9 and 10; most deprived 10,636 (52.6) 67 (71.3) 10,703 (52.6)
Rural (not categorised) 464 (2.3) 4 (4.3) 468 (2.3)
Primary teeth caries
decayed 2.246 (2.944) 3.468 (3.413) 2.252 (2.947) < 0.001
missing 0.094 (0.598) 0.096 (0.465) 0.094 (0.597) 0.908
filled 0.471 (1.307) 0.681 (1.594) 0.472 (1.308) 0.074
dmft 2.811 (3.255) 4.245 (3.656) 2.818 (3.258) < 0.001
Adult teeth caries
Decayed 0.054 (0.330) 0.234 (0.739) 0.055 (0.334) < 0.001
Missing 0.003 (0.190) 0.000 (0.000) 0.003 (0.189) 0.792
Filled 0.007 (0.112) 0.000 (0.000) 0.007 (0.112) 0.478
DMFT 0.065 (0.400) 0.234 (0.739) 0.065 (0.403) < 0.001
* Mean (standard deviation) unless categorical variable, then n (column %). † Chi-square
test for categorical variables and Wilcoxon-Mann-Whitney rank-sum test for continuous.
dmft: sum of decayed, missing (due to caries) and filled primary teeth. DMFT: sum of
decayed, missing and filled permanent teeth. sd: standard deviation.

12
The Kaplan-Meier cumulative hazard, which compared children with <3 to ≥ 3 dmft, shows a

gradual departure of the risk of ARF with age, with clear separation between the two groups

after 12 years (figure 3). By the age of 13 years, the cumulative hazard of disease in the high

decay group (10.0 per 1000 per year; 95% confidence interval (CI): 7.0 to 13.1) was just over

twice the incidence in the low decay group (5.0 per 1000 per year; 95% CI: 3.0 to 7.0).

The c-statistic for the adjusted model was 0.67 (standard error: 0.031), which indicates

moderate discriminative ability.

Table 3. Cox proportional hazard model showing the crude and adjusted
association between dental caries and the incidence of ARF or chronic rheumatic
heart disease (n = 20,333; number of events during follow-up = 94).

Risk factors Crude hazard ratio Adjusted* hazard ratio

(95% CI) (95% CI)
Gender (male vs. female) 1.37 (0.91 to 2.06) 1.35 (0.89 to 2.03)
Ethnicity (Pacific vs. Māori) 1.48 (0.97 to 2.25) 1.17 (0.76 to 1.79)
Deprivation 2.55 (1.51 to 4.31) 2.27 (1.32 to 3.88)
(deciles 8 to 10 vs. higher
socioeconomic status or missing)
Caries (per 5 affected teeth)
Primary
dmft 1.72 (1.33 to 2.23) 1.57 (1.20 to 2.06)
Permanent
DMFT 2.52 (1.38 to 4.64) 2.70 (1.32 to 5.53)
Deprivation: based on NZdep06 deciles (most deprived: 8 to 10), from subject’s
address. CI: confidence interval. vs: versus. *Adjusted for all variables shown in
table. DMFT: total decayed, missing and filled permanent teeth. dmft: total
decayed, missing and filled primary teeth.

Table 3 outlines the crude and adjusted hazard ratios, derived from a Cox model. The

comparisons for continuous variables are illustrated for the difference between zero and five

primary teeth affected by caries. In the model, male gender and Pacific ethnicity (compared to

Māori) were associated with increased risk of disease, but neither association was statistically

significant.

13
Of the indices of caries, decay in the primary and permanent teeth were both significantly

associated with disease incidence in both the crude and adjusted models. After adjustment for

other covariates, a five unit increment in dmft was associated with a 57% increase in risk of

disease (95% confidence interval: 20 to 106%). The presence of caries on permanent teeth was

also significantly associated with disease incidence, with a five unit increase in caries associated

with a 170% increase in risk (95% confidence interval: 32 to 453% increase). A five unit change

in dmft was chosen as this roughly approximates the change in a binary variable, with five units

being approximately the 16th and 84th centiles of the distribution of dmft values.17

Although the model did show some departure from hazard proportionality (the P-value for the

cox.zph test for the ethnicity term was 0.03), the adjusted effect estimate and confidence

interval for total caries did not change, if separate baseline hazards were estimated for different

ethnic groups. This departure from the proportional hazards assumption showed that the

increasing hazard of identifying as Pacific, compared to Māori, increased disproportionately

with time during follow-up. The use of restricted cubic splines as a check on the modelling

assumption of linearity did not show any convincing departure.

A population attributable risk calculation showed that factors that lead to decay of the primary

teeth were responsible for 22% of the disease burden. This compared to 2.0% for caries of the

permanent teeth, since these teeth were relatively caries free in the study population.

DISCUSSION
This study reports a positive association between dental caries and ARF. If this association is

assumed causal, and caries were entirely eliminated, the population risk calculation suggests

that there would be a 22% drop in ARF incidence. This figure assumes the fitted Cox model,

with its exponential increase in risk with number of decayed teeth, is a reasonable

representation.

14
The study has some limitations. We relied on hospital records, rather than physician review of

charts to determine ARF status at follow-up. We believe, however, that coding of ARF is likely to

be reasonably accurate. One review of the accuracy of hospital records, compared to a physician-

curated register, to identify cases of ARF in New Zealand showed a sensitivity of 88% (481/548),

but the number of false positives was high, returning a positive-predictive value of 64%

(483/749).18 We used the principal diagnosis to identify new cases of disease during follow-up to

improve the specificity of the outcome, compared to searching any diagnosis.

Mis-measurement of dental caries is likely to be present, due to variation in diagnostic skills. In

many cases, radiographs were not undertaken, so that under-diagnosis was likely. Another

source of mis-measurement is that of a child’s socioeconomic status, which was taken as the

deprivation code of a child’s residential address.

Residual confounding may also explain our results, since these findings are observational. It

may be that dental caries and sugar intake are a proxy for another condition. Sugar intake and

poverty are likely to closely co-exist. It may be that sugar intake represents an effect of residual

confounding by socioeconomic status. In our study, however, we adjusted for socioeconomic

status by using the New Zealand standard (NZdep06), and after adjusting for this, the caries–

ARF link remained. This lack of attenuation of the strength of association between caries and

rheumatic fever, after adjustment for confounders, strengthens the evidence for a causal

interpretation. In an alternative analysis of the data,19 taken over all dental check-ups of

children as they age, the results were very similar to those reported here, which are based on

the initial dental check.

15
The main strength of the study is that it is a large, population-based sample with consistently

reported exposure and outcome measures that allowed us to achieve adequate statistical power

to detect an association.

The interpretation of the study findings is important. One is that dental caries is a proxy

indicator of exposure to sugar and that sugar is a direct cause of ARF by allowing pathogens

associated with ARF to grow. An alternative is that untreated caries itself may predispose to

rheumatic fever incidence. We believe the former explanation to be more likely. The correlation

coefficient between sugar intake and caries is high, 0.7 in one study.8 A narrative review of a

wide range of observational and ecological evidence supports the idea that sugar intake and

caries are strongly causally linked.7 Caries is therefore a reasonable surrogate measure of sugar

intake. The latter explanation we believe to be less likely as most lesions in the community oral

service data were recorded as ‘decayed’, and were likely to be rapidly treated subsequently

according to clinical protocols. The strong association between caries status and disease

incidence would be attenuated by such a causal mechanism.

In the introduction, we speculated that group A streptococcal infection is likely to mediate the

sugar-ARF link. Since we did not collect information about these infections, it was not possible

to assess whether statistical evidence supports such a mechanism.

Since this study is confined to Māori and Pacific populations, the findings do not generalise to

NZ European children. It remains to be seen whether this link between caries and rheumatic

fever can be replicated in other high prevalence populations.

Two other studies have reported a higher incidence of caries in cases of rheumatic fever,

compared to controls. A case-control study (n = 200) carried out in 1949 in Philadelphia,

showed that 132 extractions due to caries had been carried out in the 100 cases, compared to 44

in the same number of controls.20 Gingivitis, a bacterial infection of the gums which is linked

16
with dental caries, was present in 33% of cases, compared to 4% of controls. The distribution of

age and socio-economic status was similar in the two groups. A second study, carried out in

Utah (n = 264), showed similar caries levels between cases and controls, although caries levels

were generally higher in cases, compared to controls (5 to 9 year olds; mean dmft: 7.2 in cases,

compared to 6.1 in controls).21 Other studies have reported the association between ARF, ethnic

group and socioeconomic deprivation.22 Indeed, the similarity between the risk factors for caries

and rheumatic fever was a stimulus for this study.

Our study is consistent with other epidemiological analyses that show population-based

incidence of ARF is higher among Pacific people than Māori, although age-standardised reports

showed almost twice the incidence in Pacific compared to Māori. In this study, crude incidence

was 50% higher in Pacific people, with adjusted rates about 17% lower than that.1 The annual

incidence of new ARF or chronic rheumatic heart disease in our study was 92/100,000 per year;

higher than that reported by Jaine and colleagues in 2008,1 by ethnic group for all of New

Zealand (34.1/100,000/year for Māori and 67.1/100,000/year for Pacific children).

Other studies have explored dietary links to rheumatic fever, but sugar has not been implicated.

Observational studies have reported an association between low body weight, low egg intake,

low serum albumin and prevalent rheumatic heart disease in the United States23, Yugoslavia24,

Zaire22 and Bangladesh.25 26 These results suggest that nutritional status is a risk factor for

disease onset.

In New Zealand, the recent focus of preventive effort for rheumatic fever has been early use of

antibiotics in high risk populations to treat Streptococcus pyogenes throat infection. A cluster

randomised trial, however, showed no convincing difference in disease incidence between the

schools who received the early antibiotic-based intervention and those that did not.27 Our study

suggests alternative dietary interventions may be useful. While we have seen a strong

relationship between caries and rheumatic fever incidence, these findings would be

17
strengthened by an independently conducted study using different methods, for example, a

case-control design could be carried out in a geographically separated area.

Given the importance of sugar intake in the aetiology of dental caries,7 as well as its role in

childhood obesity and other morbidities, we advocate for sugar reduction in Māori and Pacific

populations. Dietary interventions which limit sugar intake could play an important part in

reducing socioeconomic and ethnic health disparities in New Zealand.

Acknowledgements

We thank Dr Satha Kanagaratnam and Gene Becconsall from Auckland Regional Dental Service

for their co-operation and work in obtaining and extracting the data. The authors also thank

Dean Papaconstantinou for his work in linking the dental data with hospital records. We also

thank Dr Julia Peters from Auckland Regional Public Health Service who supported this work.

Funding

This work did not receive any specific funding.

Data sharing statement

These data are, at present, unable to be shared due to ethical considerations.

REFERENCES

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2005. J Paediatr Child Health 2008;44(10):564-71. doi: 10.1111/j.1440-1754.2008.01384.x

2. Seckeler MD, Hoke TR. The worldwide epidemiology of acute rheumatic fever and rheumatic

heart disease. Clinical epidemiology 2011;3:67.

3. Thornley S, Sundborn G, Schmidt-Uili SM. Rheumatic fever in New Zealand: what are the teeth

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Figure legends

Figure 1. A plausible causal diagram which explains the nature of the association
between dental caries and acute rheumatic fever. Solid arrows indicate the
proposed direction of causation (but unobserved in this study; grey colour), while
the dashed arrow shows the observed (black) association, expected from the
unobserved causal relationships.

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Figure 2. Study population flow.

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Figure 3. Cumulative hazard of developing acute rheumatic fever or chronic
rheumatic heart disease during follow-up, comparing those with ≥ 3 primary teeth
affected by caries compared with those who had < 3, by age (years). 95%
confidence intervals surround the point estimate.

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