Periapical lesion progression and cytokine expression in an LPS hyporesponsive model

Fouad, Ashraf F.; Acosta, A.W.

doi:10.1046/j.1365-2591.2001.00423.x

Cited by 23 publications

(19 citation statements)

References 37 publications

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“…30 Larger lesions may also be slower to heal completely, and therefore appear to have incomplete healing in some studies. 26 Numerous studies have used lesion size to examine the pathogenesis and healing of PR lesions in animal models and have documented their findings in terms of lesion size either histomorphometrically [31][32][33][34] or radiographically. [35][36][37] More studies are needed to determine if the radiographic size of PR lesions in patients is related to the virulence of root canal microorganisms and if the rate of reduction in size correlates with the effectiveness of treatment.…”

Section: Epidemiology and Pathogenesis Of Periradicular Lesionsmentioning

confidence: 99%

Diabetes Mellitus as a Modulating Factor of Endodontic Infections

Fouad

2003

Journal of Dental Education

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Diabetes mellitus is a chronic disease with serious health consequences. The association between diabetes and periodontal disease is well documented. However, the progression and healing of endodontic infections in diabetic patients has not been adequately studied. In this review, diabetes mellitus is explored as a potential modulating factor of endodontic pathosis. Recent data on the relationship between the clinical presentation of pulpal and periradicular disease, as well as the outcome of endodontic treatment in diabetic and nondiabetic patients, are presented. Diabetics who present for endodontic treatment, particularly those with periradicular pathosis, may have increased perioperative symptoms. Cases with preoperative periradicular lesions are less likely to be determined successful two years or longer postoperatively if the patient reports a history of diabetes. Studies examining the pathogenesis of periradicular lesions in mouse models with uncontrolled type 1 diabetes suggest that the lesion size may be increased and the animals have increased serious sequelae. Preliminary findings suggest that some bacterial species may be more prevalent in necrotic pulp of diabetic than nondiabetic patients. More studies are needed to further explore the microbiology of endodontic infections and to determine effective treatment strategies in both diabetic and nondiabetic patients.Dr. Fouad is Associate Professor,

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Section: Epidemiology and Pathogenesis Of Periradicular Lesionsmentioning

confidence: 99%

Diabetes Mellitus as a Modulating Factor of Endodontic Infections

Fouad

2003

Journal of Dental Education

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“…, Kawashima & Stashenko , Kent et al . , Fouad & Acosta ). In addition, LPS can induce the expression of cytokines and chemokines and elicit the innate immune response in DPSCs (Chang et al .…”

Section: Introductionmentioning

confidence: 99%

“…Lipopolysaccharide (LPS) is a major component of the gram-negative bacterial membrane that persists in dentine and resists its elimination and is responsible for pulp infection (Vianna et al 2007). Lipopolysaccharide can induce the expression of pro-inflammatory cytokines and chemokines, such as TNF-a, IL-6 and IL-8, and elicit a variety of immune responses in the odontoblasts, fibroblasts and monocytes of dental pulp tissue (Nagaoka et al 1996, Kawashima & Stashenko 1999, Kent et al 1999, Fouad & Acosta 2001. In addition, LPS can induce the expression of cytokines and chemokines and elicit the innate immune response in DPSCs (Chang et al 2005).…”

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confidence: 99%

LPS induces IL‐8 expression through TLR4, MyD88, NF‐kappaB and MAPK pathways in human dental pulp stem cells

Wang

et al. 2012

Int Endodontic J

149

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“…). In addition, IL‐6 levels were measured at 2, 4, 6 and 8 weeks, and increased expression was observed at 8 weeks (Fouad & Acosta ). Another study suggested that macrophages and osteoblasts are involved in the development of periapical lesions and that they promote bone resorption by producing mediators such as IL‐6 (Lin et al .…”

Section: Resultsmentioning

confidence: 99%

The role of IL‐6 on apical periodontitis: a systematic review

et al. 2013

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The aim of this review was to examine current knowledge of the role of interleukin-6 (IL-6) in apical periodontitis (AP) pathogenesis as an inflammatory or pro-inflammatory cytokine. It also looked at whether IL-6 could serve as a measure for differential diagnosis or as a biomarker that can further predict the progression of bone resorption. A systematic review relating to AP and IL-6 was made via PubMed, BIOSIS, Cochrane, EMBASE and Web of Science databases using keywords and controlled vocabulary. Two independent reviewers first screened titles and abstracts and then the full texts. The reference lists of the identified publications were examined for additional titles. Eighteen papers were studied in total. In vitro studies (n = 6) revealed that IL-6 is present in AP, and its levels are proportional to the size of the periapical lesions. Neutrophils and macrophages resident in these lesions can produce IL-6 in vitro after a bacterial stimulus. Animal studies (n = 5) showed that IL-6 is present in AP and that osteoblasts can produce IL-6 in vivo. On the other hand, two studies using IL-6 knockout mice revealed larger periapical lesions when compared with control groups, demonstrating IL-6's role as an anti-inflammatory cytokine. In human studies (n = 7), IL-6 was identified in AP, and its levels were higher in symptomatic, epithelialized and large lesions than in asymptomatic and small lesions. These data lead to the conclusion that IL-6 may play a pro-inflammatory role, increasing its levels and reabsorbing bone in the presence of infections. When IL-6 is not present, other cytokines such as IL-1 and TNF-α induce bone resorption. Further studies about the relationship between AP development and the cytokine network must be performed to establish the exact role of each cytokine in the inflammatory process.

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Periapical lesion progression and cytokine expression in an LPS hyporesponsive model

Abstract: Responsiveness to LPS may not be significant in the pathogenesis of periapical lesions and in cytokine expression within the lesions, when the lesions are induced by non-specific oral flora.

Cited by 23 publications

References 37 publications

Diabetes Mellitus as a Modulating Factor of Endodontic Infections

Diabetes Mellitus as a Modulating Factor of Endodontic Infections

LPS induces IL‐8 expression through TLR4, MyD88, NF‐kappaB and MAPK pathways in human dental pulp stem cells

The role of IL‐6 on apical periodontitis: a systematic review

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