Publications by authors named "Claudia Waha"

Article Synopsis
  • - The study investigates how dental pulp cells respond to immunogenic components like LPS and LTA from bacteria, particularly focusing on the production of inflammatory cytokines TNFα and IL-6 when these cells are treated with the resin monomer HEMA under different oxidative conditions.
  • - Human pulp fibroblasts and odontoblast-like cells were exposed to LTA, LPS, or HEMA for 1 to 24 hours, with results showing that LPS and LTA significantly increased IL-6 production after longer exposure, while HEMA inhibited this inflammatory response, influenced by redox conditions.
  • - The findings suggest that HEMA compromises the normal immune function of dental pulp cells by affecting their oxidative stress balance, potentially impairing their
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Objective: The release of inflammatory cytokines from antigen-stimulated cells of the immune system is inhibited by resin monomers such as 2-hydroxyethyl methacrylate (HEMA). Although the formation of oxidative stress in cells exposed to HEMA is firmly established, the mechanism behind the inhibited cytokine secretion is only partly known. The present investigation presents evidence regarding the role of HEMA-induced oxidative stress in the secretion of the pro-inflammatory cytokine TNFα from cells exposed to the antigens LTA (lipoteichoic acid) or LPS (lipopolysaccharide) of cariogenic microorganisms using BSO (L-buthionine sulfoximine) or NAC (N-acetyl cysteine) to inhibit or stabilize the amounts of the antioxidant glutathione.

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Objectives: The photoinitiator diphenyl-(2,4,6-trimethylbenzoyl)phosphine oxide (TPO) is more reactive than a camphorquinone/amine (CQ) system, and TPO-based adhesives obtained a higher degree of conversion (DC) with fewer leached monomers. The hypothesis tested here is that a TPO-based adhesive is less toxic than a CQ-based adhesive.

Methods: A CQ-based adhesive (SBU-CQ) (Scotchbond Universal, 3M ESPE) and its experimental counterpart with TPO (SBU-TPO) were tested for cytotoxicity in human pulp-derived cells (tHPC).

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The development of strategies for the protection of oral tissues against the adverse effects of resin monomers is primarily based on the elucidation of underlying molecular mechanisms. The generation of reactive oxygen species beyond the capacity of a balanced redox regulation in cells is probably a cause of cell damage. This study was designed to investigate oxidative DNA damage, the activation of ATM, a reporter of DNA damage, and redox-sensitive signal transduction through mitogen-activated protein kinases (MAPKs) by the monomer triethylene glycol dimethacrylate (TEGDMA).

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