Abstract

Systemic inflammation links exposure to early childhood adversity to later disease. The associations among adversity and disease risk might in part operate through poor oral hygiene and subsequent periodontal inflammation, which can be measured in saliva. Few studies, however, have examined the association between adversity and salivary inflammation in young children. Further, there is a dearth of literature investigating adverse experiences and salivary inflammation in children and caregivers together, limiting our understanding of the intergenerational, dual effects of adversity on inflammation for both members of the caregiver-child dyad. This study tested child and caregiver adversity and their associations with an inflammatory composite (i.e., IL-6, IL-1β, IL-8, TNF-α) and CRP in 93 preschool-age children and their caregivers. Caregivers reported on their child’s experiences of adversity, as well as on their own adverse experiences, using a comprehensive questionnaire synthesized from previous checklists for complete coverage of possible adverse events. Results showed that caregivers’ salivary inflammatory markers (i.e., IL-6, IL-1β, IL-8, TNF-α, and CRP) were not significantly correlated with the same five inflammatory markers in children’s saliva. Among children, adversity was associated with significantly higher levels of the inflammatory composite, though not CRP. This association was amplified among children whose caregivers also experienced more adversity during adulthood. Among caregivers, childhood adversity and adulthood adversity were each independently associated with significantly higher levels of the inflammatory composite and CRP. The association between caregivers’ own childhood adversity and inflammation was amplified among caregivers whose children also experienced more adversity during their childhoods. These findings provide preliminary evidence for the possible dual role of young children’s and caregivers’ adverse experiences in contributing to salivary inflammation for both members of the dyad, suggesting possible implications for systemic inflammation and future disease.

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