The aim of this study was to describe the caries experience and severity of periodontal disease in a convenience sample of Indigenous Australians living in the Northern Territory.
The aim of this study was to describe the caries experience and severity of periodontal disease in a convenience sample of Indigenous Australians living in the Northern Territory.
Data were gathered via self-reported questionnaire and dental examination by calibrated examiners. Socio-demographic characteristics were compared with data from the 2011 Australian census while prevalence of periodontal disease and dental caries was compared against weighted estimates from the National Survey of Adult Oral Health 2004–2006. In each comparison, non-overlapping 95% confidence intervals inferred a significant difference. Within-study comparisons were assessed via chi-square, t-tests and analysis of variance for differences among study participants.
A total of 312 Indigenous Australian participants provided completed data (average age 39.5 ± 10.5 years, 174 males). Of these, 87.5% were confirmed periodontitis cases; 3.5 times that of national-level estimates. The experience of untreated caries was five times that of national estimates (mean decayed 3.0 versus 0.6). Periodontitis case status was positively associated with older age, male gender and presence of diabetes.
Periodontal disease and untreated caries were significantly more prevalent in this sample of Indigenous Australians compared to the general Australian population. The prevalence of periodontal disease was markedly higher than that previously described for Indigenous Australians.
clinical attachment loss
decayed, missing and filled teeth
National Survey of Adult Oral Health
Indigenous Australians represent 2.5% of Australia's 22 million population and it is estimated that the Northern Territory (NT) has the largest proportion of Indigenous Australians per capita in the country. The life expectancy of Indigenous Australians is estimated to be some 10–12 years lower than non-Indigenous Australians owing to high rates of infection and chronic diseases.[3-5] Indigenous Australians exhibit social and economic disadvantage resultant from lower educational attainment, higher unemployment rates and overcrowded housing.
Periodontitis is an inflammation of the periodontal tissues resulting in loss of connective tissue attachment, destruction of alveolar bone and formation of pathological pockets around diseased teeth. In severe cases it may lead to tooth loss. Dental caries arises from a complex interplay between the tooth surface, gram positive bacteria, and a regular source of carbohydrate. Treatment for caries can range from remineralizing the tooth structure to restorations. In the event where a tooth has decayed beyond repair, extraction is required.
The National Survey of Adult Oral Health 2004–2006 (NSAOH) estimated the mean decayed, missing and filled teeth (DMFT) among Indigenous Australian adults was 14.8 compared to 12.8 for non-Indigenous Australians, while the respective estimates for the prevalence of periodontal disease was 29% compared to 23%. These national estimates may under-estimate the true prevalence of caries and periodontal disease among Indigenous Australians due to methodological constraints.
Few studies have examined the oral health status of Indigenous Australian adults. One survey of two towns in western New South Wales identified extensive treatment need for restorations, a high prevalence of periodontal disease and little evidence of oral hygiene practices. More recent research from Western Australian communities have reported consistent findings of problem-associated visiting patterns, infrequent brushing, combined with high proportions of untreated caries and periodontal pocketing.[10, 11] Diabetes has impacted the oral health status of an Indigenous community located in north-western South Australia. Among those with diabetes, almost 80% were reported to have periodontitis compared to 30% without diabetes and the number of missing teeth was 3.5 times higher among persons with diabetes versus those without. A series of dental surveillance studies have also shown differences in caries experience exist between Indigenous Australians living in metropolitan locations compared to remote areas of Australia.
We aimed to determine associations between key risk indicators and oral health status of a convenience sample of Indigenous Australian adults residing in the NT. We also aimed to compare these findings against national level estimates.
A convenience sample of Indigenous Australian adults residing in Darwin, Katherine and correctional facilities in Darwin and Alice Springs in the NT, Australia were recruited. All study participants were otherwise healthy and had no contraindications to undergoing a dental examination. This study reports findings from all participants who underwent an oral health assessment and completed a self-reported questionnaire.
Dental assessments replicated the methods used in the NSAOH. The oral assessment obtained information on tooth presence, caries experience, periodontal destruction, gingival bleeding, dental plaque, and calculus scores. Examiners distinguished missing teeth due to dental caries or periodontal disease as opposed to teeth missing for other reasons which included orthodontic, dental trauma or congenitally missing. Root fragments due to caries were coded separately from fragments arising from dental trauma and were incorporated into the ‘decayed’ component of the index. Caries experience was recorded for each tooth as: decayed, recurrent caries (new decay around existing filling), filled unsatisfactorily (defective restorations without decay), filled, and sound. Oral plaque score was recorded for six index teeth (if present) based on published criteria. Light plaque was defined as present only after scraping tooth surface; moderate as an accumulation visible to naked eye; and heavy, defined when plaque was abundant around the tooth surface. The selected teeth were the most anterior molar in each quadrant, in addition to the maxillary right central and mandibular left central incisors. The same six teeth were assessed for dental calculus.
Periodontal probing and gingival recession was measured at four sites at every tooth excluding third molars. The sites assessed included the mesio-buccal, mid-buccal, disto-buccal and disto-lingual. Periodontitis was based on the US Centers for Disease Control and Prevention and American Academy of Periodontology classification. This case definition was selected to correspond with that used in the NSAOH. Periodontitis was ascertained by algorithm via a combination of probing depth (PD), the distance from the base of the periodontal pocket to the gingival margin, and clinical attachment loss (CAL) determined as the sum of gingival recession and PD. Moderate periodontitis was diagnosed if participants exhibited at least two interproximal sites with CAL ≥4 mm, or at least two interproximal sites with PD ≥5 mm; and severe periodontitis as ≥2 interproximal sites with CAL ≥6 mm and at least one site with PD ≥5 mm. A gingival bleeding score was collected for each tooth periodontally assessed. The extent of periodontal disease was calculated as the average number of sites per person with periodontal destruction relative to the number of teeth using published methods. The extent of PD ≥4 mm in the Australian population has previously been reported in the NSAOH (Table 5.21, p. 131). However, comparisons between NSAOH and the present study participants were made by comparing the number of sites that exhibited both CAL ≥3 mm and PD ≥4 mm. This measure reduces the risk of bias caused by pseudopocketing due to inflammation, and facilitates comparisons between populations that differ in oral hygiene practices.
Dental armamentarium included disposable mirrors (MirrorliteTM Defend, Hauppauge, USA) and a periodontal probe with 2 mm markings (Hu-Friedy, Chicago, USA, product number PCP2).
A questionnaire to obtain information regarding socio-demographic characteristics, including education, employment, and household income, in addition to lifestyle factors and medical history, including diabetes status, was administered to all participants. Lifetime exposure to smoking was quantified as the number of ‘pack years’ using a published formula:
NSAOH contains weighted representative estimates of the Australian population. To facilitate comparisons of periodontal disease between NSAOH and the present study, the disto-lingual measurements were dropped prior to analysis and reinstated for within-sample analyses. Similarly, only data from NSAOH participants aged between 22 to 73 years were analysed to match with the age range of the current study sample. Statistical significance for comparisons of frequencies and means between our study and NSAOH participants and between the present study and the 2011 Australian Census was determined on the basis of non-overlapping 95% confidence intervals. Age and socio-economic data pertaining to the 2011 Australian Census findings for Indigenous Australians residing in Darwin was obtained from the Australian Bureau of Statistics using data from the Darwin local government area (http://www.censusdata.abs.gov.au; accessed 23 May 2013).
Statistical significance was inferred at P < 0.05 for comparisons of frequencies (chi-square test), independent samples t-test for comparisons between moderate and severe periodontitis cases and ANOVA using Student-Neuman-Keuls post hoc tests for means among all participants. Continuous, normally distributed variables are reported as mean ± standard deviation and 95% confidence interval. Data were analysed using SAS Version 9.3 (Cary, North Carolina, USA).
Approval for the present study was obtained from the Human Research Ethics Committee of the NT Department of Health and Menzies School of Health Research, the Central Australian Human Research Ethics Committee, the NT Department of Correctional Services Research Committee, the University of Adelaide Human Research Ethics Committee and the Aboriginal Health Council of South Australia. Study participants gave informed consent before participating. Research was conducted in accordance with the World Medical Association Declaration of Helsinki (Version VII, 2008).
Recruitment commenced in June 2010 and concluded in January 2012. Some 312 participants completed both an oral assessment and self-reported questionnaire.
Compared with Australian Census data of Darwin residents, participants in our study were similarly aged and a comparable number had completed secondary schooling. There were significant differences in mean weekly household income. For example, over half of the participants in the present study reported an income of ≥$1000 per week compared to 21% of Darwin residents in the Census (Table 1). Compared with the NSAOH, participants were younger, had a higher prevalence of self-reported diabetes, and were almost three times more likely to be current smokers (Table 2). Although five times as many participants in the present study had teeth with untreated caries, NSAOH participants had a 50% higher DMFT owing to more teeth missing or filled as a result of oral disease.
|Variable||NT sample % (95% CI)||NT Indigenous Australian 2011 Census % (95% CI)||Ratio (NT sample/Darwin Census)|
|Age (n = 181)||20–34 years||29.8 (23.1–36.6)||34.5 (32.9–36.2)||0.9|
|35–54 years||54.1 (46.8–61.5)||46.2 (44.5–47.9)||1.2|
|55+ years||16.0 (10.6–21.4)||19.3 (18.0–20.7)||0.8|
|Education (n = 172)||Completed Yr 12||29.7 (22.8–36.5)||22.9 (21.0–25.0)||1.3|
|Housing (n = 172)||Own||4.7 (1.5–7.8)||8.2 (7.1–9.4)||0.6|
|Buying||30.2 (23.3–37.2)||25.5 (23.8–27.3)||1.2|
|Renting||53.5 (46.0–61.0)||56.7 (54.7–58.7)||0.9|
|Rent free||11.6 (6.8–16.5)||6.6 (5.9–7.4)||1.8|
|Weekly h-hold income (n = 130)||$0–299||7.7 (3.1–12.3)a||31.7 (30.3–33.2)||0.2|
|$300–599||13.1 (7.2–19.0)a||20.4 (19.2–21.7)||0.6|
|$600–999||23.1 (15.7–30.4)||17.1 (16.0–18.3)||1.4|
|≥$1000||56.2 (47.5–64.8)a||21.0 (19.8–22.2)||2.7|
|NT sample (n = 312)||NSAOH (n = 4967)||Ratio (NT sample/ NSAOH)|
|Mean age yrs (95% CI)||39.5 (38.4–40.7)a||45.5 (44.9–46.0)||0.9|
|% (95% CI)||55.8 (50.2–61.3)||49.5 (47.7–51.4)||1.1|
|Self-reported diabetes – Yes||41||258|
|% (95% CI)||13.2 (9.4–17.0)b||4.7 (3.9–5.4)||2.8|
|Current smoker – Yes||162||726|
|% (95% CI)||51.9 (46.4–57.4)b||17.5 (15.9–19.1)||3.0|
|Former smoker – Yes||41||1380|
|% (95% CI)||13.1 (9.8–17.3)b||30.2 (28.6–31.9)||0.4|
|% (95% CI)||34.9 (29.9–40.4)b||52.3 (50.3–54.2)||0.7|
|% (95% CI)||100c||1.2 (0.8–1.6)|
|CDC periodontitis case||273||1477|
|% (95% CI)||87.5 (83.8–91.2)b||25.2 (23.5–26.9)||3.5|
|Mean no. teeth (95% CI)||26.5 (25.9–27.1)||25.7 (25.5–25.9)||1.0|
|Mean no. decayed (95% CI)||3.0 (2.6–3.4)b||0.6 (0.5–0.6)||5|
|Mean no. filled (95% CI)||2.9 (2.5–3.3)a||8.9 (8.7–9.2)||0.3|
|Mean no. missing (95% CI)||3.8 (3.2–4.4)a||4.9 (4.7–5.1)||0.8|
|Mean no. DMFT (95% CI)||9.7 (8.9–10.6)a||14.4 (14.1–14.8)||0.7|
|Mean no. root fragments||0.6||-|
|Mean no. sites CAL ≥3 mm and ≥PPD 4 mm (95% CI)||11.3 (9.8–12.7)b||0.8 (0.7–0.9)||14.1|
|Extent CAL ≥3 mm and PPD ≥4 mm (% sites) (95% CI)||12.1 (10.6–13.6)b||1.3 (1.1–1.4)||9.3|
|Mean index teeth with calculus (95% CI)||4.1 (3.9–4.2)b||1.1 (1.1–1.2)||3.7|
|Gingival bleeding ≥2||226||929|
|% (95% CI)||72.4 (67.5–77.4)b||20.3 (18.5–22.1)||3.6|
|Plaque score ≥2||147||1412|
|% (95% CI)||47.3 (41.7–52.8)b||28.7 (26.9–30.5)||1.6|
Both indicators of periodontal disease experience (prevalence and extent), were significantly higher in our study sample than in the NSAOH. Of the 312 persons assessed, 273 had moderate or severe periodontitis representing a prevalence of 87.5%; 3.5 times that of national-level estimates of the same age (Table 2). The extent of periodontal sites with attachment loss and periodontal pocketing was nine times higher in the current study compared to the national-level estimates. There were also significant differences in oral hygiene measured in the form of dental calculus, plaque and gingival bleeding.
Tables 3 and 4 are limited to participants of the present study. Periodontal case status did not differ by lifetime exposure to smoking nor location of recruitment. Participants with severe periodontal disease were older, more likely to be male and previously diagnosed with diabetes (Table 3).
|Non-case (n = 39)||Moderate (n = 188)||Severe (n = 83)||P value|
|Mean age (years)*||35.5 ± 9.8||39.1 ± 10.1*||42.6 ± 10.1*||0.01|
|No. male (%)||16 (41.0)||99 (52.4)||57 (68.7)‡||0.01|
|Darwin||29 (74.4)||104 (55.6)||44 (53.0)||0.38|
|Katherine||2 (5.1)||17 (9.1)||9 (10.8)|
|Darwin correctional centre||4 (10.3)||39 (20.9)||15 (18.1)|
|Alice Springs correctional centre||4 (10.3)||27 (14.4)||15 (18.1)|
|bSmoker (pack years) (%)|
|None||15 (42.9)||68 (40.0)||18 (26.1)||0.10|
|>0–5||11 (31.4)||36 (21.2)||17 (24.6)|
|>5||9 (25.7)||66 (38.8)||34 (49.3)|
|cNo. self-reported diabetes – Yes||0||21 (11.2)||20 (24.4)||<0.01|
|Mean sites CAL ≥3 mm and PPD ≥4 mm||0.5 ± 0.6||8.7 ± 8.2*||22.1 ± 18.1*||<0.01|
|Mean extent CAL ≥3 mm and PPD ≥4 mm||0.5 ± 0.6||8.8 ± 8.0*||24.9 ± 17.1*||<0.01|
|Darwin (n = 180)||Katherine (n = 28)||Alice Springs correctional facility (n = 46)||Darwin correctional facility (n = 58)|
|Age||42.1 ± 11.1||39.5 ± 8.9c||34.5 ± 5.7ac||35.7 ± 8.5a|
|Mean no. teeth||25.2 ± 6.6||28.9 ± 2.5a||27.6 ± 4.1a||28.4 ± 4.1a|
|Mean no. decayed teeth||3.1 ± 3.6||2.5 ± 2.6||2.0 ± 2.3ab||3.8 ± 3.7b|
|Mean no. filled teeth||3.8 ± 4.2||1.7 ± 2.4a||1.9 ± 2.4a||1.4 ± 2.3a|
|Mean no. missing teeth||4.8 ± 6.3||1.2 ± 1.5a||3.2 ± 4.1||2.7 ± 4.1|
|Mean no. DMFT||11.6 ± 8.0||5.4 ± 4.2a||7.1 ± 5.8a||8.0 ± 6.4a|
|Mean no. sites with calculus||3.4 ± 1.8||4.3 ± 1.2a||4.9 ± 1.0a||5.2 ± 1.0a|
|Freq mod/heavy plaque (%)||54 (30.2)||10 (35.7)||35 (76.1)d||48 (82.8)d|
|Freq mod/heavy gingival bleeding (%)||112 (62.2)||20 (71.4)||43 (93.5)d||51 (87.9)d|
Marked differences in oral assessment findings were apparent by location of recruitment, with study participants from Darwin exhibiting significantly higher filled teeth and overall DMFT but significantly fewer sites with dental calculus compared to the three other study locations (Table 4). The average number of teeth with untreated caries was almost twice as high in the Darwin correctional facility compared to the Alice Springs correctional centre. Both correctional facility samples were more likely to present with moderate or heavy plaque levels and more sites with bleeding on probing compared to the non-institutionalized samples.
This study describes the dental caries experience and severity of periodontal disease from a convenience sample of Indigenous Australians living in the NT. Information regarding adult Indigenous Australian oral health is scarce.[9, 10, 12, 13, 19] Despite this, the high prevalence of periodontal disease in the current study (87.5%) was unexpected; previous estimates using the same periodontitis case definition had a prevalence at approximately 30%. Although prevalence of periodontal disease in our study differed by gender, age, and employment status, it remained above 80% in all sub-groups assessed.
Most studies that measured periodontitis in Indigenous Australian adults have used indices to describe the various disease states; with reports of between 30% to 61% of participants showed evidence of periodontal pockets.[9-12] The major drawback of these measures is that there are no provisions to account for CAL. By measuring only gingival inflammation and PD, both the CPI and Russell's PI risk underestimating the true prevalence of periodontal disease in older age groups, while potentially overestimating periodontitis in younger people. This bias may be exacerbated if plaque-associated inflammation leads to misclassification of periodontitis due to pseudo-pocketing when oral hygiene is poor. The use of the CDC/AAP periodontitis case definition is thus recommended.
Indigenous participants in NSAOH had 2.3 times the prevalence of untreated dental caries compared with their non-Indigenous counterparts. Our findings are consistent with this, with the mean number of untreated carious teeth being five times that of the national estimate. Conversely, our study participants were less likely to have had teeth filled or extracted due to disease compared to NSAOH estimates. This may suggest our participants were less likely to utilize dental services than those in the NSAOH as both restorations and extractions require clinical intervention. Conversely, the cost of dental treatment has been identified as a barrier[10, 20] and access to timely and culturally-appropriate dental services is known to be problematic for some Indigenous Australians. Our findings clearly reflect an important priority for service providers and policy makers interested in improving the oral health status of vulnerable populations such as Indigenous Australians.
Both caries and periodontal disease arise as a result of a complex interplay between individual factors (including diet and lifestyle habits) and are complicated further by external environmental influences such as water fluoridation, location of primary residence and availability and accessibility of dental services. Rural and remote areas of Australia where one-quarter of the Indigenous Australian population reside have the lowest proportional ratio of practising dentists per capita. These factors may be one part of the explanation why rates of untreated caries, periodontal disease and tooth loss remain high among certain sub-groups of the Australian population.
Differences in overall DMFT between locations of recruitment in the present study could partially be explained by the older age distribution of participants from Darwin as caries experience is cumulative. However, the observational nature of this investigation makes it difficult to identify definitive causes. The variation in untreated caries between correctional facilities may be the result of differences in access to dental services within prisons. It was not possible to ascertain the length of sentence for those incarcerated. Caries may also be influenced by geography. Darwin has low naturally occurring fluoride in the water supply and is fluoridated by water authorities. In contrast, Alice Springs and many of the surrounding communities have naturally occurring levels of fluoride of at least 1 parts per million or higher. Lifetime exposure to fluoride sources was not collected as part of this study. Dental fluorosis has been frequently reported in children living in remote areas of Australia including central Australia. Although recording fluorosis was beyond the aims of the current study, it was often observed by examining clinicians in Alice Springs.
A recent report indicated that almost half (46%) of Indigenous adults were current smokers compared to 21% of Australians overall. This estimate is lower than that recorded in the current study. We have reported smoking in the form of ‘pack years’ as this measure provides information on the lifetime exposure to tobacco products. The effects of smoking as a risk factor for periodontal disease and its dose-dependent association with both the progression and severity of periodontitis is well understood. In light of this, the high proportion of periodontitis cases diagnosed in the present study may be the result of long-term exposure to smoking products. Once again, however, the cross-sectional nature of this investigation prevents any examination of causal pathways.
Type 2 diabetes prevalence among Indigenous Australians is considerably higher than among non-Indigenous Australians. In the current study, 13% of participants reported being previously diagnosed with diabetes, which is lower than estimates for Indigenous Australians published elsewhere. The relationship between periodontal disease and diabetes mellitus is well established. Long-term control of blood glucose levels is paramount in preventing diabetic complications, one of which is periodontal disease. Among participants with severe periodontitis, the extent of periodontal pocketing with 4 mm or more was 25%. This degree of periodontal disease could be a significant source of systemic inflammation which may have metabolic consequences.
Limitations of this study should be noted. One-third of our sample was recruited from correctional facilities in Darwin and Alice Springs. Prison inmates are likely to differ from the general population in terms of oral disease status and risk factors influencing these. Shortcomings aside, our findings provide further evidence that Indigenous Australians appear to have markedly worse clinical oral health status in comparison to their non-Indigenous counterparts. Given the link between periodontal disease and other chronic conditions, and the impact of quality of life resulting from untreated caries, our findings reinforce the importance of making and keeping oral health a priority area in national Aboriginal and Torres Strait Islander health plans.
In conclusion, untreated decay and periodontal disease were significantly more prevalent among a convenience sample of Indigenous Australians in the NT compared to national-level estimates. The prevalence of periodontal disease was markedly higher than previous reports among Indigenous Australians.
The authors gratefully acknowledge the support of the PerioCardio participants, study staff, Danila Dilba Health Services, Northern Territory Oral Health Service, Northern Territory Correctional Services in Darwin and Alice Springs, the Wurli Wurlinjang Aboriginal Health Service in Katherine and the South Australian Dental Service. The PerioCardio study is funded by the National Health and Medical Research Council: Project grant #627100. K Kapellas is supported by a University of Adelaide Divisional Scholarship. The NSAOH was funded by NHMRC: Project grants #299060 and #349514; NHMRC: Capacity building grant #349537; Australian Government Department of Health; Australian Institute of Health and Welfare; Colgate Oral Care; Australian Dental Association and the US Centers for Disease Control and Prevention, Research Participation Program.