Secondary caries formation in aged restorations: a clinical review

Abstract

Secondary caries, or recurrent caries, occur at the margins of existing restorations and are influenced by multiple factors, including the characteristics of the restoration material. The pathogenesis of secondary caries mirrors that of primary caries, involving enamel demineralization and the dissolution of organic components, but is modified by the presence of restoration margins. Defective restorations create gaps that allow acidic fluids and biofilms to intrude, while intact restorations can also be susceptible due to the lower buffering capacities of restorative materials compared to natural tooth structure. The incidence of secondary caries differs between restorative materials, with composites exhibiting a higher susceptibility (ranging from 0% to 44%) compared to amalgams. Contributing factors include polymerization shrinkage, microleakage, increased plaque retention, and the lack of antibacterial properties in composites. Diagnosis typically involves visual inspection and radiographic analysis, with indicators such as marginal ditching, staining, and gaps serving as potential predictors. However, reliance on these indicators can lead to misdiagnosis and unnecessary restorative replacements; studies show that 50% to 60% of restorations are replaced due to secondary caries, often overestimated as actual replacement rates range from 2% to 3%. Notably, resin composites display greater sensitivity to application techniques and plaque accumulation, leading to secondary caries. Clinical proficiency in both amalgam and composite restorations can enhance restoration longevity. Key factors influencing the failure rates of restorations include patient age, history of extensive caries, cavity depth, and preparation technique. This review emphasizes understanding secondary caries' impact on restoration longevity and advocates for tailored clinical management in caries treatment and restoration placement. The interaction between caries-related bacteria and the restorative interface further complicates the pathophysiology of secondary caries, underscoring the need for careful assessment and management strategies.