ArticleScientific reports2018
Secreted products of oral bacteria and biofilms impede mineralization of apical papilla stem cells in TLR-, species-, and culture-dependent fashion.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Inflammation-Regeneration Axis of Dental Pulp Stem Cells: Wnt/NF-κB Crosstalk.International endodontic journal · 2026Review
- Root-like apical hard-tissue structure associated with apical periodontitis in an immature permanent tooth: a case report and literature review.BMC oral health · 2026Review
- Effect of Oral Pathogens Associated With Pulpitis and Apical Periodontitis on Odontogenic Mesenchymal Stem Cells.Stem cells international · 2025Review
- Microbiological assessment of success and failure in pulp revitalization: a randomized clinical trial using calcium hydroxide and chlorhexidine gluconate in traumatized immature necrotic teeth.Journal of oral microbiology · 2024Article
- Article
- Stem Cells from the Apical Papilla (SCAPs): Past, Present, Prospects, and Challenges.Biomedicines · 2023Review
- Different interventions and outcomes in four teeth with regenerative endodontic procedures in the same patient: A case report with 7‑year follow‑up.Experimental and therapeutic medicine · 2023Article
- Exploring the impact of oral bacteria remnants on stem cells from the Apical papilla: mineralization potential and inflammatory response.Frontiers in cellular and infection microbiology · 2023Article
- Microbial identification from traumatized immature permanent teeth with periapical lesions using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry.BMC oral health · 2022Article
- Transcriptome Analysis Reveals Modulation of Human Stem Cells from the Apical Papilla by Species Associated with Dental Root Canal Infection.International journal of molecular sciences · 2022Article
- Endodontic pulp revitalization in traumatized necrotic immature permanent incisors: Early failures and long-term outcomes-A longitudinal cohort study.International endodontic journal · 2022Article
- New Insights into the Microbial Profiles of Infected Root Canals in Traumatized Teeth.Journal of clinical medicine · 2020Article
- Atomic Force Microscopy (AFM) As a Surface Mapping Tool in Microorganisms Resistant Toward Antimicrobials: A Mini-Review.Frontiers in pharmacology · 2020Review
- Cytokine Secretion, Viability, and Real-Time Proliferation of Apical-Papilla Stem Cells Upon Exposure to Oral Bacteria.Frontiers in cellular and infection microbiology · 2020Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regenerative endodontics exploits the mineralization potential of stem cells from the apical papilla (SCAPs) in order to promote root maturation of permanent immature teeth. SCAPs may encounter post-disinfection residual bacteria either in planktonic or in biofilm growth mode. Bacterial components bind to Toll-like receptors (TLRs) and trigger pro-inflammatory responses. We hypothesized that biofilm-triggered TLR activation affects the mineralization potential of human SCAPs. SCAPs were challenged with conditioned media derived from standardized dual-species biofilms and planktonic bacterial cultures and their inflammatory status and mineralization capacity were studied. Bacterial products from both growth modes (planktonic vs. biofilm) compromised cell viability, proliferation and mineralization capacity of SCAPs, but in a species- and growth mode-dependent fashion. While TLR4 expression remained unaffected, TLR2 expression was upregulated coinciding with a pro-inflammatory activation of SCAPs. Moreover, TLR and its downstream TGF-β-associated kinase (TAK1) appeared to be blocking mineralization, as inhibition of these factors restored it. In conclusion, bacterial products promoted the pro-inflammatory status and inhibited mineralization of human SCAPs in a TLR-, species-, and culture-dependent fashion. TLR2 emerged as the pivotal mediator of these responses and further research is warranted towards the judicious manipulation of SCAPs in order to modify the untoward events of TLR-priming and signaling.
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