The association between loading of restorations and secondary caries lesions is moderated by the restoration material...

Secondary caries limits the longevity of restorations and is thought to be associated with faulty restorations, e.g. dentin-restoration interfacial gaps. Recent evidence indicates that loading of restorations might aggravate the effects of gaps on interfacial mineral loss. It is unclear if this effect of loading is dose-dependent or not, and if restoration material properties like elasticity moderate the association between load and mineral loss. We hypothesized that mineral loss of secondary lesions increases with increasing load, and that this association is moderated by the elastic modulus of the placed restoration material.

Dentin-restoration specimens with simulated interfacial gaps were submitted to cariogenic Lactobacillus-rhamnosus-biofilms for 10days, and concurrently loaded with different loads (0/42/84/126g per specimen, n=12/group). Two different composites (LEC: low elastic-modulus composite, HEC: high elastic-modulus composite) were employed. Transversal microradiography was used to evaluate the superficial and interfacial (wall) lesion mineral loss. Generalized linear modeling (GLM) was used to evaluate the association between loading, material and their interaction on mineral loss.

Surface mineral loss was not significantly associated with loading, material, or their interaction (p-values ranged between p=0.062 and 0.526). For deep interfacial (wall) lesions, the applied load (p=0.023) but not the material (p=0.382) showed a significant effect. The interaction between both significantly affected mineral loss (p=0.01). Loads of ≥84g per specimens were associated with higher wall lesion mineral loss.

Loads above a certain threshold significantly increased interfacial (wall) lesion mineral loss. This association was moderated by the elasticity of the placed restoration materials.

The clinical relevance of our findings remains unclear, as future studies are needed to understand how exactly both load and material elasticity affect secondary lesion induction.