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Dental caries has common risk factors with impairments in growth, cognitive development and child general health. Identifying socioeconomic contexts and parental behaviors in early life that may be associated with negative outcomes in the child's future and their causal mechanisms can contribute to planning early interventions. Therefore, the aim of this paper is to propose and discuss possible ways to explain how early childhood stimulation may be associated with future oral health status, based on the life-course theory of chain-of-risk model and accumulation of risk model. Two hypotheses were suggested: (1) each social exposure or parental behavior in the child's first years of life increase the risk of chronic diseases, such as dental caries in primary dentition, in a simply additive effect; (2) parental factors could negatively influence the establishment of the pattern of child stimulation (child care) or lead to a modification of the established behavior on the risk of dental caries in the child primary dentition. Prevention of dental caries seems to be the most feasible way of solving this serious public health problem. It therefore justifies the importance of identifying exposures in the child's early life that may lead to the occurrence of chronic diseases in the future. The evidence seem to converge to the idea that child stimulation in early life may be associated with future health problems related to behaviors and care by parents, including caries., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Chronic periodontal disease (CPD) is a highly prevalent, multifactorial, bacterially induced inflammatory disease, characterized by pathologic loss of periodontal attachment and alveolar bone with onset mostly in adulthood. While cross-sectional data have demonstrated significant associations between adverse socioeconomic position (SEP) and poor periodontal conditions, there is a gap in the literature on the understanding of how SEPs in different life stages impact on the occurrence of this disease later on. Life-course epidemiology offers different theoretical models to study the pathway of health and illness during the lifespan, and the hypothesis of the present study is that the relationship between SEP and CPD can be explained based on different life-course epidemiology theories: (a) critical period model; (b) critical period with modifier effect model; (c) accumulation of risk model; (d) chain-of-risk model. Under the first theoretical model, the association between SEP and CPD may be explained by an inflammatory hypothesis, considering that childhood adverse socioeconomic backgrounds alter the immunoinflammatory response that leads to disease in adulthood regardless of conditions later in life. The second model postulates that the early life SEP modifies the host immunoinflammatory response, and the risk of disease will be modified over the life-course by socio-behavioural influences. The third, "accumulation of risk model", may explain such relationship taking into account exposures during different periods of life. However, this model does not consider the moment when the exposure occurred, only taking into consideration the number of episodes during the life cycle. Finally, the potential explanation to the role of socioeconomic position on chronic periodontal disease, using a chain-of-risk model, is that early low SEP may cause social stress related to social hierarchies, what may, in turn, trigger endocrine, neural and immune changes, that reflect on elevated levels of cytokines, consequently turning these individuals more likely to develop periodontal disease. To summarize, this paper suggests potential explanations of the relationship between SEP during the lifespan and the occurrence of chronic periodontal disease in adult life, under a life-course framework. Longitudinal studies focusing on such relationship should be conducted, aiming to provide evidence regarding the hypotheses here called in question., (Copyright © 2015 Elsevier Ltd. All rights reserved.)