Apototic and Necrotic Influence of Dental Resin Polymerization Initiators in Human Gingival Fibroblast Cultures

Masuki, Kouhei; Nomura, Yuji; Bhawal, Ujjal K.; Sawajiri, Masahiko; Hirata, Isao; Nahara, Yukinori; Okazaki, Masanori

doi:10.4012/dmj.26.861

Cited by 24 publications

(21 citation statements)

References 36 publications

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“…p21 WAF1 is a potent cyclin-dependent kinase inhibitor that inhibits cell cycle progression at the G1 phase (19). In line with this finding, previous cell cycle analysis with CQ revealed significant cell cycle arrest at the G1 phase (20), suggesting that p21 WAF1 is the primary mediator that causes arrest of the cell cycle and cell division of dental pulp cells by CQ.…”

Section: Discussionsupporting

confidence: 73%

Camphorquinone Inhibits Odontogenic Differentiation of Dental Pulp Cells and Triggers Release of Inflammatory Cytokines

Kim¹,

Williams²,

Bae³

et al. 2013

Journal of Endodontics

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Introduction Camphorquinone (CQ) is a photoinitiator that triggers polymerization of light-curing materials such as dental adhesives and composites. CQ does not become a part of the polymer network, suggesting that CQ can be leached out into surrounding environment including dental pulp and exert adversary effects on tissues. In order to understand the mechanisms of CQ-induced side effects, we investigated the effect of CQ on cell viability, cytokine secretion, and odontogenic differentiation of dental pulp stem cells in vitro. Methods Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay after CQ exposure. Western blotting was performed for p16INK4A, p21WAF1, and p53. Secretory cytokines were evaluated using the membrane–enzyme-linked immunosorbent assay as well as conventional and quantitative reverse-transcription polymerase chain reaction. The effects of CQ on odontogenic differentiation were evaluated using alkaline phosphatase and alizarin red S staining methods. Results CQ treatment suppressed the proliferation of DPSCs and induced the expression of p16INK4A, p21WAF1, and p53. Levels of proinflammatory cytokines (eg, interleukin 6, interleukin 8, and matrix metalloproteinase-3 [MMP3]) were increased by CQ treatment. CQ also inhibited odontogenic differentiation and mineralization capacities of DPSC and MC3T3-E1 cells. Conclusions Our study showed that CQ may trigger pulpal inflammation by inducing proinflammatory cytokine production from the pulpal cells and may impair odontogenic differentiation of dental pulp cells, resulting in pulpal irritation and inflammation.

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Section: Discussionsupporting

confidence: 73%

Camphorquinone Inhibits Odontogenic Differentiation of Dental Pulp Cells and Triggers Release of Inflammatory Cytokines

Kim¹,

Williams²,

Bae³

et al. 2013

Journal of Endodontics

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“…In the presence of calcium ions, annexin V binds specifically to PS, and the externalization of PS is an important cell-surface signal for the macrophage clearance of apoptotic cells. 31,32 Apoptosis is a physiological process involved in cell deletion during organogenesis, and it controls cell proliferation and differentiation in adult tissues. 33 The deregulation of apoptosis has been implicated in a variety of diseases.…”

Section: Discussionmentioning

confidence: 99%

Influence of chlorine dioxide on cell death and cell cycle of human gingival fibroblasts

Nishikiori¹,

Nomura²,

Sawajiri³

et al. 2008

Journal of Dentistry

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“…This ability of DMPT to form free radicals with subsequent DNA damage may explain the DMPT carcinogenic mechanism (Li et al 2008; Masuki et al 2007; Pereira, Telo, and Nunes 2008; Winter, Pagoria, and Geurtsen 2005). DMPT has been reported to have estrogen antagonist activity in vitro (yeast reporter gene assay; Nomura et al 2003), but whether this activity contributes to DMPT carcinogenic activity is not known.…”

Section: Discussionmentioning

confidence: 99%

N,N-Dimethyl-p-toluidine, a Component in Dental Materials, Causes Hematologic Toxic and Carcinogenic Responses in Rodent Model Systems

et al. 2013

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Because of the potential for exposure to N,N-dimethyl-p-toluidine (DMPT) in medical devices and the lack of toxicity and carcinogenicity information available in the literature, the National Toxicology Program conducted toxicity and carcinogenicity studies of DMPT in male and female F344/N rats and B6C3F1/N mice. In these studies, a treatment-related macrocytic regenerative anemia characterized by increased levels of methemoglobin and Heinz body formation developed within a few weeks of DMPT exposure in rats and mice. DMPT induced nasal cavity, splenic, and liver toxicity in rats and mice at 3 months and 2 years. DMPT carcinogenic effects were seen in the liver of male and female rats and mice, the nasal cavity of male and female rats, and the lung and forestomach of female mice. In rodents, DMPT is distributed to many of the sites where toxic and carcinogenic effects occurred. DMPT-induced oxidative damage at these target sites may be one mechanism for the treatment-related lesions. Methemoglobinemia, as seen in these DMPT studies, is caused by oxidation of the heme moiety, and this end point served as an early alert for other target organ toxicities and carcinogenic responses that followed with longer term exposure.

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Apototic and Necrotic Influence of Dental Resin Polymerization Initiators in Human Gingival Fibroblast Cultures

Cited by 24 publications

References 36 publications

Camphorquinone Inhibits Odontogenic Differentiation of Dental Pulp Cells and Triggers Release of Inflammatory Cytokines

Camphorquinone Inhibits Odontogenic Differentiation of Dental Pulp Cells and Triggers Release of Inflammatory Cytokines

Influence of chlorine dioxide on cell death and cell cycle of human gingival fibroblasts

N,N-Dimethyl-p-toluidine, a Component in Dental Materials, Causes Hematologic Toxic and Carcinogenic Responses in Rodent Model Systems

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