The purpose of this study was to describe the prevalence and incidence of caries in the permanent teeth in a cohort of children over a 7-year period, particularly the disease trajectory of caries in the permanent teeth defined by the presence or absence of caries in the primary teeth (aged 7-9 y); and to explore the role of potential risk factors (demography, dietary and oral health promoting behaviours) in future caries development. In addition, the study aimed to determine whether caries experience in late childhood was predictive of adolescent obesity (ages 12-16 y) to inform the use of a common risk factor approach (CRFA) for prevention. The study also explored the attitudes and beliefs of adolescents towards dental caries and their use or non-use of caries prevention regimens. With ethical approval granted, pupils in Year 3 (aged 7-9 y) at state-funded primary schools in an area of North West England in February 2006 were invited to take part. Positive informed consent was obtained. Clinical examinations (CE1-4) to assess oral health were performed at four time points (mean ages 8, 10, 13 and 15 y) by trained and calibrated dentist examiners using a standardised, national diagnostic protocol. The diagnostic threshold for caries was visual assessment of caries into dentine. At the last two time points, questionnaires were used to assess self-reported oral health related behaviours; and Body Mass Index (BMI) category was calculated from height and weight measurements using age and gender specific cut-offs. In June 2014, semi-structured interviews (n-19) were conducted in 4 secondary schools with a sample of participants (age 16 y). At baseline (CE1), 5470 children (ages 7â9 y) consented. Most identified as White (75.9%) or Asian (22.8%) with over 60% from more deprived backgrounds. The socio-demographic characteristics of consenting pupils were similar to non-consenting pupils. Intra-oral examination was completed at all time points by 2117 children and at least one time point by 6651 children. Mean caries prevalence (%D3MFT > 0) was 16.7% at CE1, increasing to 31.0%, 42.2%, and 45.7% at subsequent examinations. A population-averaged model (generalised estimating equations) was used to model the longitudinal data. The main finding was that estimated mean values indicated a rising D3MFT count as pupils aged (consistent with new teeth emerging) that was significantly higher (4.49 times; 95% confidence interval, 3.90â5.16) in those pupils with caries in their primary dentition than in those without. The odds of developing caries between CE3 and CE4 for those in the most deprived category were 3.37 times those in the least deprived category (OR 3.37, 95% CI 1.71 to 6.65). BMI category in adolescence (available for 2958 (54.1%) participants) was not shown to be significantly associated with: the presence or absence of caries in late childhood (P=0.61); in adolescence (P=0.06); gender (P=0.91); or deprivation (P=0.35). The dominant influence over oral health behaviours was habitual practice of toothbrushing encouraged by parents from a young age but this behaviour was unstable and mitigated by environmental factors later e.g. access to free sugars. This thesis illustrates the life-long consequences of developing caries in early childhood. Children with caries in their primary dentition followed a steep disease development trajectory in their permanent dentition. Children who are caries free and caries active in their primary dentition should be considered as two different populations with targeted and whole population prevention strategies to address their different risk profiles. This also emphasises the need to focus on early prevention to stop children entering the ârapidâ disease trajectory. The finding that deprivation remains an important predictor of future caries, and that adolescent behaviours are mitigated by environmental factors supports strategies that include actions to address social determinants throughout childhood. Two significant future research questions are raised: how do we keep children caries free, and once a child develops the disease how do we slow down the process?