ArticleCureus2026
Multi-species Microbial Modulation of the RANK/RANKL (Receptor Activator of Nuclear Factor κB/Receptor Activator of Nuclear Factor κB Ligand) Pathway Induces Osteoclastogenic Priming in Apical Periodontitis.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
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Abstract
backgroundApical periodontitis (AP) is a prevalent inflammatory condition affecting the periapical tissues surrounding the tooth root, often initiated by microbial invasion. Objective: The objective of this study is to evaluate the osteoclastogenic priming effects of microbial species associated with primary and secondary AP on human macrophages and to determine their capacity to modulate the RANK/RANKL-OPG (receptor activator of nuclear factor kappa-B, receptor activator of nuclear factor kappa-B ligand, osteoprotegerin) pathway. MATERIALS AND
methodsTHP-1 monocytes/macrophages were stimulated with live bacteria, with or without RANKL, and analyzed for RANK/RANKL/OPG expression by flow cytometry. Cytokine levels (interleukin-1β (IL-1β), tumoral necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), interleukin-12p70 (IL-12p70)) were measured using cytometric bead arrays. Results: Macrophages challenged with
conclusionOur data suggest that AP-associated bacteria can induce osteoclastogenic priming and promote the release of pro-inflammatory cytokines via RANK/RANKL activation, indicating a potential role in the early processes leading to periapical bone resorption.
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