Higher Expression of Galectin-3 and Galectin-9 in Periapical Granulomas than in Radicular Cysts and an Increased Toll-like Receptor-2 and Toll-like Receptor-4 Expression Are Associated with Reactivation of Periapical Inflammation

Oliveira, Rita De Cássia Medeiros De; Beghini, Marcela; Borges, Cláudia Renata Bibiano; Alves, Polyanna Miranda; Araújo, Marcelo Sivieri de; Pereira, Sanívia Aparecida de Lima; Rodrigues, Virmondés; Rodrigues, Denise Bertulucci Rocha

doi:10.1016/j.joen.2013.10.031

Cited by 19 publications

(20 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Periodontitis is distinguished by immune-mediated damage of periodontal supporting tissues and loss of teeth. Apical lesions can progress to form an RC, and the RC's level of growth is mainly due to the increased levels of MMP-9 [4].…”

Section: Discussionmentioning

confidence: 99%

“…The outcome is an elevated intracystic pressure that can result in osteoclastic bone resorption and cyst enlargement [1][2][3]. A radicular cyst (RC) is a result of chronic inflammation in response to inflammatory mediators created from the necrosis of dental pulp [4]. According to Khot et al, RCs "derive their epithelial lining from the proliferation of small odontogenic epithelial residues within the periodontal ligament," which contributes to the progression of the lesion [2].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association of Oxidative Stress and Production of Inflammatory Mediators Matrix Metalloproteinase-9 and Interleukin 6: Systemic Events in Radicular Cysts

Malik¹,

Chawla²,

Tauseef³

et al. 2020

Cureus

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Association of Oxidative Stress and Production of Inflammatory Mediators Matrix Metalloproteinase-9 and Interleukin 6: Systemic Events in Radicular Cysts

Malik¹,

Chawla²,

Tauseef³

et al. 2020

Cureus

View full text Add to dashboard Cite

show abstract

“…PL were diagnosed based on clinical and histopathological findings, as previously described. 9 Inclusion criteria were sufficient material for immunohistochemistry and presence of epithelial cell rests of Malassez (ERM) in PG. Exclusion criteria were evidence of previous endodontic treatment, refractory endodontic disease and specimens with sinus tract.…”

Section: Methodsmentioning

confidence: 99%

“…Previous investigations have addressed TLR expression in periodontal 8 and periapical disease. 5 , 9-11 In the latter, TLR2 and TLR4 involvement has been demonstrated at the onset of the experimentally induced furcation lesions of endodontic origin. 11 Furthermore, TLR2 and TLR4 up-regulation has been described in PG and PC from patients, 5 , 9 demonstrating that their expression is associated with reactive periapical inflammation.…”

Section: Introductionmentioning

confidence: 99%

“… 5 , 9-11 In the latter, TLR2 and TLR4 involvement has been demonstrated at the onset of the experimentally induced furcation lesions of endodontic origin. 11 Furthermore, TLR2 and TLR4 up-regulation has been described in PG and PC from patients, 5 , 9 demonstrating that their expression is associated with reactive periapical inflammation. Yet, where periapical disease is concerned, such investigations have largely focused on TLR expression in immunocompetent cells, whereas their association with microbial pathogens and their expression in the epithelium of inflammatory periapical lesions (PL) have been neglected.TLR are also expressed in epithelial cells of other tissues including tumor cells.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Toll-like receptor 4 expression in the epithelium of inflammatory periapical lesions. An immunohistochemical study

et al. 2015

View full text Add to dashboard Cite

Toll-like receptors (TLR) are essential for the innate immune response against invading pathogens and have been described in immunocompetent cells of areas affected by periapical disease. Besides initiating the inflammatory response, they also directly regulate epithelial cell proliferation and survival in a variety of settings. This study evaluates the in situ expression of TLR4 in periapical granulomas (PG) and radicular cysts, focusing on the epithelial compartment.Twenty-one periapical cysts (PC) and 10 PG were analyzed; 7 dentigerous non-inflamed follicular cyst (DC) served as control. TLR4 expression was assessed by immunohistochemistry. TLR4 immunoreaction products were detected in the epithelium of all specimens, with a higher percentage of immunostained cells in PG. Although TLR4 overexpression was detected in both PG and PC, there were differences that seemed to be related to the nature of the lesion, since in PG all epithelial cells of strands, islands and trabeculae were strongly immunoreactive for TLR4, whereas in PC only some areas of the basal and suprabasal epithelial layers were immunostained. This staining pattern is consistent with the action of TLR4: in PG it could promote formation of epithelial cell rests of Malassez and in epithelial strands and islands the enhancement of cell survival, proliferation and migration, whereas in PC TLR4 could protect the lining epithelium from extensive apoptosis. These findings go some way towards answering the intriguing question of why many epithelial strands or islands in PG and the lining epithelium of apical cysts regress after non-surgical endodontic therapy, and suggest that TLR4 plays a key role in the pathobiology of the inflammatory process related to periapical disease.

show abstract

Necroptosis in apical periodontitis: A programmed cell death with multiple roles

Liu

Fan

2023

Journal Cellular Physiology

View full text Add to dashboard Cite

Programmed cell death (PCD) has been a research focus for decades and different mechanisms of cell death, such as necroptosis, pyroptosis, ferroptosis, and cuproptosis have been discovered. Necroptosis, a form of inflammatory PCD, has gained increasing attention in recent years due to its critical role in disease progression and development. Unlike apoptosis, which is mediated by caspases and characterized by cell shrinkage and membrane blebbing, necroptosis is mediated by mixed lineage kinase domain‐like protein (MLKL) and characterized by cell enlargement and plasma membrane rupture. Necroptosis can be triggered by bacterial infection, which on the one hand represents a host defense mechanism against the infection, but on the other hand can facilitate bacterial escape and worsen inflammation. Despite its importance in various diseases, a comprehensive review on the involvement and roles of necroptosis in apical periodontitis is still lacking. In this review, we tried to provide an overview of recent progresses in necroptosis research, summarized the pathways involved in apical periodontitis (AP) activation, and discussed how bacterial pathogens induce and regulated necroptosis and how necroptosis would inhibit bacteria. Furthermore, the interplay between various types of cell death in AP and the potential treatment strategy for AP by targeting necroptosis were also discussed.

show abstract

Higher Expression of Galectin-3 and Galectin-9 in Periapical Granulomas than in Radicular Cysts and an Increased Toll-like Receptor-2 and Toll-like Receptor-4 Expression Are Associated with Reactivation of Periapical Inflammation

Cited by 19 publications

References 35 publications

Association of Oxidative Stress and Production of Inflammatory Mediators Matrix Metalloproteinase-9 and Interleukin 6: Systemic Events in Radicular Cysts

Association of Oxidative Stress and Production of Inflammatory Mediators Matrix Metalloproteinase-9 and Interleukin 6: Systemic Events in Radicular Cysts

Toll-like receptor 4 expression in the epithelium of inflammatory periapical lesions. An immunohistochemical study

Necroptosis in apical periodontitis: A programmed cell death with multiple roles

Contact Info

Product

Resources

About