Impact of Amalgam Fillings and Stainless-Steel Crowns on Gingival Crevicular Fluid IL-1β and TNF-α Levels in Children: A Repeated Measures Observational Study

Author:

Doostmohammad Fateme1,Bagherianlemraski Mobina2,Asgarian-Omran Hossein1,Hosseinnataj Abolfazl1,Mirkalaei Fatemeh Mousavi1,Soleimani Banafsheh1,Nahvi Azam1

Affiliation:

1. Mazandaran University of Medical Sciences

2. McMaster University

Abstract

Abstract

Background In chronic inflammation caused by dental amalgam fillings and stainless-steel crowns (SSC), host cells produce cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1). In line with these findings, the present study evaluated the effects of dental amalgam fillings and SSC on the levels of IL-1β and TNF-α cytokines in the gingival crevicular fluid (GCF) of children. Methods This repeated measures observational study targeted 34 children aged 6 to 9 who were candidates for two-surface amalgam filling or SSC for primary mandibular molars. Participants were divided into two groups: amalgam filling and SSC. Healthy contralateral teeth with no caries served as controls. GCF samples were collected at baseline (before treatment), 7 days post-treatment, and 21 days post-treatment using paper points. The levels of IL-1β and TNF-α in the GCF samples were measured using commercially available ELISA kits. Results TNF-α levels significantly decreased after one week in the SSC group compared to the dental amalgam group (p = 0.017). The level of IL-1β increased in both the amalgam filling (p = 0.029) and SSC (p = 0.046) groups during the same period. The levels of IL-1β (p = 0.006) and TNF-α (p = 0.029) were significantly different between the two groups over time. Conclusions IL-1β and TNF-α cytokines can serve as biomarkers for inflammation induced by dental amalgam fillings and SSCs in children. Significant differences were observed between the two groups, particularly in the short-term, but the effects converged over three weeks.

Publisher

Springer Science and Business Media LLC

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