Quantitative radiographic evaluation of periapical bone resorption in dog's teeth contaminated with bacterial endotoxin (LPS) associated or not with calcium hydroxide

Silva, Léa Assed Bezerra da; Branco, Luis Guilherme Siqueira; Navarro, Valéria Pontelli; Filho, Paulo Nelson

doi:10.1590/s0103-64402008000400002

Cited by 22 publications

(21 citation statements)

References 20 publications

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“…2011). In an in vivo study, da Silva et al. (2008) concluded that calcium hydroxide was effective in inactivating LPS as demonstrated by the absence of periodontitis in roots simultaneously filled with the two agents.…”

Section: Discussionmentioning

confidence: 99%

Chlorhexidine, ethanol, lipopolysaccharide and nicotine do not enhance the cytotoxicity of a calcium hydroxide pulp capping material

et al. 2012

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Wheater MA, Falvo J, Ruiz F, Byars M. Chlorhexidine, ethanol, lipopolysaccharide and nicotine do not enhance the cytotoxicity of a calcium hydroxide pulp capping material. International Endodontic Journal, 45, 989–995, 2012. Abstract Aim To determine whether cells pre‐stressed by known cytotoxic or inflammatory agents are more susceptible to the deleterious effects of a calcium hydroxide formulation used in pulp capping. Methodology Adult human dermal fibroblasts were treated for 48 h with 0.001% chlorhexidine, 0.2% ethanol, 5 μg mL−1Escherichia coli lipopolysaccharide (LPS) or 0.05 mmol L−1 nicotine. Cells were subsequently treated with the soluble materials extracted from Dycal pellets for an additional 24 h. Controls included cells cultured in medium only and cells exposed to Dycal only. Cytotoxicity was measured using colorimetric MTT, WST and secreted lactate dehydrogenase assays. In addition, mitotic activity was evaluated using a colorimetric histone H3 phosphorylation assay. Data were statistically analysed using anova with Tukey’s multiple comparison post‐test and significance at P ≤ 0.05. Results For all assays, measured values for cells treated with chlorhexidine, ethanol, LPS or nicotine plus the soluble materials extracted from Dycal pellets were significantly lower compared to control (P < 0.05) for all comparisons between experimental conditions. However, between treatments and for comparisons of treatments with Dycal, there were no differences observed for any assay. Conclusions Calcium hydroxide in a formulation used in dental clinical procedures is highly cytotoxic to cultured cells, as evidenced by several cellular assays. However, other known toxic agents, including chlorhexidine, ethanol, bacterial LPS and nicotine, do not appear to function synergistically to increase the deleterious cellular effects of the calcium hydroxide in an in vitro model of cytotoxicity.

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Section: Discussionmentioning

confidence: 99%

Chlorhexidine, ethanol, lipopolysaccharide and nicotine do not enhance the cytotoxicity of a calcium hydroxide pulp capping material

et al. 2012

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“…Among the beneficial properties of calcium hydroxide are its biocompatibility (10,11), antibacterial activity (12), induction of mineralized tissue formation (13)(14)(15), activation of alkaline phosphatase and collagen synthesis (16) and ability to produce hydrolysis of bacterial endotoxin (17).…”

Section: Introductionmentioning

confidence: 99%

Histopathological evaluation of root canal filling materials for primary teeth

et al. 2010

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This study aimed to assess the response of apical and periapical tissues of dogs' teeth after root canal filling with different materials. Forty roots from dogs' premolars were prepared biomechanically and assigned to 4 groups filled with: Group I: commercial calcium hydroxide and polyethylene glycol-based paste (Calen®) thickened with zinc oxide; Group II: paste composed of iodoform, Rifocort® and camphorated paramonochlorophenol; Group III: zinc oxide-eugenol cement; Group IV: sterile saline. After 30 days, the samples were subjected to histological processing. The histopathological findings revealed that in Groups I and IV the apical and periapical regions exhibited normal appearance, with large number of fibers and cells and no resorption of mineralized tissues. In Group II, mild inflammatory infiltrate and mild edema were observed, with discrete fibrogenesis and bone resorption. Group III showed altered periapical region and thickened periodontal ligament with presence of inflammatory cells and edema. It may be concluded that the Calen paste thickened with zinc oxide yielded the best tissue response, being the most indicated material for root canal filling of primary teeth with pulp vitality.

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“…This stimulates the synthesis and release of cytokines that activate osteoclasts, such as IL-1 and TNF, as previously described, and also stimulates the release of prostaglandin E2, which also has an influence on these cells 8,31 .…”

Section: Etiology Of Periapical Lesions and The Role Of Endotoxin In mentioning

confidence: 53%

Role of endotoxin in the etiology of periapical lesions: molecular mechanisms involved in endotoxin's recognition and cell activation

Lucisano

Filho

Silva

et al. 2014

RGO, Rev. Gaúch. Odontol.

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Periapical lesions are diseases resulting from contamination and necrosis of dental pulp and the progression of this infection toward the periapical tissues. Technological advances in microbiological culture and identification have shown that anaerobic microorganisms, especially Gram-negative, are RESUMOAs lesões periapicais são patologias resultantes da contaminação e necrose da polpa dental e progressão da infecção em direção aos tecidos periapicais. Os avanços tecnológicos na cultura e identificação microbiana demonstraram que, em canais radiculares de dentes portadores de necrose pulpar e lesão periapical crônica, predominam os microrganismos anaeróbios, particularmente os Gram-negativos. As bactérias Gram-negativas, além de possuírem diferentes fatores de virulência e gerarem produtos e subprodutos tóxicos aos tecidos apicais e periapicais, contêm a endotoxina em sua parede celular. Esse conhecimento é importante, uma vez que a endotoxina é liberada durante a multiplicação ou morte bacteriana, exercendo uma série de efeitos biológicos relevantes, que conduzem a uma reação inflamatória e à reabsorção dos tecidos mineralizados. Sendo assim, o objetivo deste trabalho foi efetuar uma revisão da literatura relativa ao papel da endotoxina bacteriana na etiologia das lesões periapicais, seu mecanismo de ação, bem como elucidar mecanismos moleculares envolvidos no seu reconhecimento pelo sistema imunológico e na ativação celular. Role of endotoxin in the etiology of periapical lesions: molecular mechanisms involved in endotoxin's recognition and cell activationPapel da endotoxina na etiologia da lesão periapical: mecanismos moleculares envolvidos no seu reconhecimento e na ativação celular

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Quantitative radiographic evaluation of periapical bone resorption in dog's teeth contaminated with bacterial endotoxin (LPS) associated or not with calcium hydroxide

Cited by 22 publications

References 20 publications

Chlorhexidine, ethanol, lipopolysaccharide and nicotine do not enhance the cytotoxicity of a calcium hydroxide pulp capping material

Chlorhexidine, ethanol, lipopolysaccharide and nicotine do not enhance the cytotoxicity of a calcium hydroxide pulp capping material

Histopathological evaluation of root canal filling materials for primary teeth

Role of endotoxin in the etiology of periapical lesions: molecular mechanisms involved in endotoxin's recognition and cell activation

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