Dental caries generates significant health, financial and social costs to individuals and communities, but risk factors are not spread randomly and evenly throughout populations. People from lower socio‐economic status (SES) and disadvantaged groups suffer a disproportionately greater disease burden. Clinicians and public health experts view this problem through a different lens. Dentists at the clinical coalface consider individual risk factors and behaviours, for example sugar consumption, cariogenic bacteria and poor oral hygiene, as major causes of dental caries. However, considerable evidence suggests that low SES, via traditional individual risk factors as mediators and through additional independent pathways, is another significant cause. Progressive clinical practice uses education, prevention and treatment to reduce the impact of individual risk factors. Policy‐makers and health administrators use population‐based approaches to improve the health of societies. The authors use literature review to argue for both a greater awareness of the upstream socio‐economic causes of dental caries, and action from key community sectors to redress the societal inequalities contributing to dental health inequalities.
Policy on fluoride intake involves balancing caries against dental fluorosis in populations. The origin of this balance lies with Dean's research on fluoride concentration in water supplies, caries, and fluorosis. Dean identified cut points in the Index of Dental Fluorosis of 0.4 and 0.6 as critical. These equate to 1.3 and 1.6 mg fluoride (F)/L. However, 1.0 mg F/L, initially called a permissible level, was adopted for fluoridation programs. McClure, in 1943, derived an "optimum" fluoride intake based on this permissible concentration. It was not until 1944 that Dean referred to this concentration as the "optimal" concentration. These were critical steps that have informed health authorities through to today. Several countries have derived toxicological estimates of an adequate and an upper level of intake of fluoride as an important nutrient. The US Institute of Medicine (IOM) in 1997 estimated an Adequate Intake (AI) of 0.05 mg F/kg bodyweight (bw)/d and a Tolerable Upper Intake Level (UL) of 0.10 mg F/kg bw/d. These have been widely promulgated. However, a conundrum has existed with estimates of actual fluoride intake that exceed the UL without the expected adverse fluorosis effects being observed. Both the AI and UL need review. Fluoride intake at an individual level should be interpreted to inform more nuanced guidelines for individual behavior. An "optimum" intake should be based on community perceptions of caries and fluorosis, while the ultimate test for fluoride intake is monitoring caries and fluorosis in populations.
Objectives: In December 2008, artificial water fluoridation was introduced for the first time to the Logan-Beaudesert district in the state of Queensland, Australia. The aim of this study was to evaluate the effects of water fluoridation in the primary dentition in this community after a period of 36 months. Methods: Children aged 4-9 years with clinical examinations and bitewing radiographs (BWs) taken before water fluoridation (pre-F) were randomly selected as comparison controls for age matched children who had been exposed to a mean period of 36 months of water fluoridation (post-F). A total of 201 sets of pre-F BWs from children (mean age 6.95 ± 1.05 years) and 256 sets of post-F BWs from children (mean age 7.19 ± 1.23 years) attending schools in the district were randomly selected. Caries experience in the primary dentition was determined as decayed, missing or filled teeth/surfaces (dmft/dmfs). Results: The caries prevalence for the pre-F group was 87% compared to 75% in the post-F group (Odds ratio (OR): 0.44, 95% CI: 0.27-0.72). Overall, there was a 19 percent reduction of mean dmft from 4.54 in the pre-F group to 3.66 in the post-F group (p = 0.005). After fluoridation, the dmfs was reduced from 6.68 to 5.17 (p = 0.0056). The distal surfaces of maxillary first primary molars experienced the greatest reduction (26%) in caries experience after water fluoridation (p < 0.001). Conclusions: After only 36 months of water fluoridation there was a significant drop in caries prevalence from 87 to 75% and a 19% reduction in caries experience in a community with one of the highest caries rates in Australia.
This case report, involving an indigenous Australian, presents the diagnosis and non-surgical endodontic management of a 22 with developmental abnormalities. They include a dens evaginatus and a dens invaginatus that extends to an apical burst in a second truncated root. Cone-beam computed tomography and endodontic microscopy were not available to the clinician. This case report focuses on ambiguities appearing in the literature relating to classification and terminology associated with the abovementioned developmental anomalies. It also demonstrates the need to methodically collect and cautiously interpret available information before initiating endodontic intervention. Axial inclination, distance perception, internal demarcation and spatial awareness, together with an understanding of dental anatomy, embryology and histology and associated physiology and pathology, allowed the clinician to accurately predict the point, the angle and the depth of coronal access. Sensibility of the dentino-pulpal complex was maintained. Critical thinking, experience, innovation, problem-solving and established principles can compensate for inaccessible technologies.
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