Abstract
Deep carious dentin lesions induce an immune reaction within the pulp-dentin complex, leading to the release of cytokines, which might be suitable biomarkers in pulp diagnostics. This in vivo feasibility study determines the concentration of different cytokines after selective removal of carious infected dentin (SCR). In our methodology, paired samples are obtained from 21 patients—each of them with two deep carious lesions at posterior teeth without clinical symptoms. After SCR, lesions are randomly assigned to treatment strategy: Group 1 (11 patients): Carious dentin is covered either with BiodentineTM (n = 11) or gutta-percha (n = 11) before using the adhesive OptibondTM FL. Group 2 (10 patients): The adhesives ClearfilTM SE Protect Bond (n = 10) or ClearfilTM SE Bond 2 (n = 10) are directly applied. Prepared cavities are rinsed with phosphate buffered saline containing 0.05% Tween 20 (10X) for five minutes immediately after SCR (visit 1) and eight weeks later (visit 2). Rinsing liquid is regained. Concentrations of IL-1β, IL-6, IL-10, C-reactive protein (CRP), TNF-α, IFN-γ, TIMP-1, -2, and MMP-7, -8, -9 are assessed by customized multiplex assays, evaluated with fluorescence analyzer. Non-parametric statistical analysis (Wilcoxon, Mann–Whitney U Test, p < 0.05) is performed (SPSS 25). Our results show that concentrations of CRP, IL-1β, IL-6, TIMP-1, -2, and MMPs were detectable. Median concentrations of CRP, IL-1β und IL-6 were significantly higher in visit 1 (304.9, 107.4, 3.8 pg/mL), compared to visit 2 (67.8, 2.3, 0.0 pg/mL; pi < 0.001). The study revealed that the non-invasive determination of cytokines from prepared dental cavities is possible.
Highlights
Dental caries is a multifactorial disease that is associated with an imbalance of the oral microflora and local environmental factors promoting pathogenic acid-producing bacteria resulting in demineralization processes at an early stage and degradation of organic matrices at an advanced stage of disease [1,2]
An increase of cytokines was found in pulp cells (e.g., transforming growth factor β (TGFβ), interleukin-1β (IL-1β), interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin 10 (IL-10), interferon-γ (IFN-γ), and tumor necrotic factor-α (TNF-α) [3,7,8]
The inflammatory cytokines and chemokines may be detectable in dentin carious lesions close to the pulp and in sample material gained from the pulp [10]
Summary
Dental caries is a multifactorial disease that is associated with an imbalance of the oral microflora and local environmental factors promoting pathogenic acid-producing bacteria resulting in demineralization processes at an early stage and degradation of organic matrices at an advanced stage of disease [1,2]. When the carious lesion reaches the dentin, bacteria, as well as their metabolic products, interact with pulpal cells via dentin tubules, and the pulp-dentin complex reacts with immunological defense mechanisms, releasing pro-inflammatory, as well as anti-inflammatory cytokines [3,4]. Several defenses and regeneration mechanisms exist mediated by odontoblasts, which release antimicrobial peptides and cytokines, initiating the migration of immunocompetent cells. A current systematic review summarized different studies considering several of these cytokines as markers in the detection of pulp inflammation, comparing healthy pulps with irreversibly inflamed pulps [9]. The inflammatory cytokines and chemokines may be detectable in dentin carious lesions close to the pulp and in sample material gained from the pulp [10]
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