Detection Of Rankl Positive Cells in Gingival Tissue in Healthy &amp; Chronic Periodontal Disease Patients -A Comparative Study

Bhuvaneswarri, J.; Gita, Bagavad; Chandrasekaran, SC

doi:10.7860/jcdr/2014/9876.5125

Cited by 5 publications

(5 citation statements)

References 16 publications

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“…In this study, bisleuconothine A treatment significantly reversed the altered expressions of OPG and RANKL in gingival tissue of periodontitis rats. These results are in agreement with those of previous studies [19,20]. The results of histopathological examination which showed that bisleuconothine A treatment significantly reversed histological changes in periodontal tissues of periodontitis rats provided supportive evidence for results from biochemical assays.…”

Section: Discussionsupporting

confidence: 93%

“…In periodontitis, gingival tissues are destroyed due to increased secretion of IL-6 and TNF-α, a process mediated by RANKL/OPG [19]. It has been reported that in periodontitis, the expression of RANKL is increased, while that of OPG is reduced in gingival tissue, with subsequent tooth loss [20]. In this study, bisleuconothine A treatment significantly reversed the altered expressions of OPG and RANKL in gingival tissue of periodontitis rats.…”

Section: Discussionmentioning

confidence: 54%

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Bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells

Wang¹,

Sun²,

Sun³

2020

Trop. J. Pharm Res

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Purpose: To investigate the protective effect of bisleuconothine A on periodontal tissue in rats and the mechanism involved. Methods: Adult male Sprague Dawley rats (n = 32) weighing 180 - 200 g (mean weight, 190 ± 10 g) were randomly assigned to four groups of eight rats each: control group, periodontitis group, bisleuconothine A (50 mg/kg) group and bisleuconothine A (100 mg/kg) group. Rats in the treatment groups received bisleuconothine intraperitoneally for two weeks. Periodontitis was induced in the rats using standard procedures. Serum and tissue samples were used for biochemical analysis. Alveolar bone loss was measured in rat maxillae, while the activity of bone alkaline phosphatase (BALP) was determined in serum. Tumor necrosis factor α (TNF-α) interleukin-1β and interleukin-6 (IL-1β and IL-6) were determined in gingival tissue using enzyme-linked immunosorbent assay (ELISA) kit. Gene and protein expressions of receptor activator of nuclear factor kappa-Β ligand (RANKL), osteoprotegerin (OPG), and matrix metallopeptidase-9 (MMP-9) were measured in gingival tissue using real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting, respectively. Results: Bisleuconothine A treatment significantly and dose-dependently reduced alveolar bone loss, as well as serum levels of TNF-α, IL-1β and IL-6, but increased BALP activity in periodontitis rats (p < 0.05). It also significantly and dose-dependently reduced mRNA expressions of RANKL and MMP-9, but significantly increased OPG mRNA expression (p < 0.05). Similarly, treatment with bisleuconothine A significantly and dose-dependently down-regulated RANKL, p-NF-kB, p-IkBα and iNOS proteins in gingival tissue of periodontitis rats (p < 0.05). The results of histopathological examination indicated that bisleuconothine A treatment significantly reversed histological changes in periodontal tissues of periodontitis rats. It also significantly reduced the degree of polymorphonuclear (PMN) cell infiltration in periodontal tissue. Conclusion: The results obtained show that bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells. Keywords: Bisleuconothine A, Expression, Inflammation, Periodontitis, RANKL

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 54%

Bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells

Wang¹,

Sun²,

Sun³

2020

Trop. J. Pharm Res

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“…Moreover, an increase of TNF- α , IL-1 β , IL-6, IL-11, and IL-17 can induce osteoclastogenesis by increasing the expression of Receptor Activator of NF- κ B Ligand (RANKL) and by reducing the osteoprotegerin (OPG) production in osteoblasts and stromal cells [ 13 ]. In fact, it was demonstrated that IL-17 and RANKL were overregulated and IL-10, an anti-inflammatory cytokine, and TGF- β 1 were downregulated in active periodontal lesions compared with inactive lesions [ 14 , 15 ] ( Figure 1(a) ).…”

Section: Introductionmentioning

confidence: 99%

Relationship between Periodontitis and Rheumatoid Arthritis: Review of the Literature

Araújo

Melo

Lima

2015

Mediators of Inflammation

123

115

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Periodontitis (PD) and rheumatoid arthritis (RA) are immunoinflammatory diseases where leukocyte infiltration and inflammatory mediators induce alveolar bone loss, synovitis, and joint destruction, respectively. Thus, we reviewed the relationship between both diseases considering epidemiological aspects, mechanical periodontal treatment, inflammatory mediators, oral microbiota, and antibodies, using the keywords “periodontitis” and “rheumatoid arthritis” in PubMed database between January 2012 and March 2015, resulting in 162 articles. After critical reading based on titles and abstracts and following the inclusion and exclusion criteria, 26 articles were included. In the articles, women over 40 years old, smokers and nonsmokers, mainly constituted the analyzed groups. Eight studies broached the epidemiological relationship with PD and RA. Four trials demonstrated that the periodontal treatment influenced the severity of RA and periodontal clinical parameters. Nine studies were related with bacteria influence in the pathogenesis of RA and the presence of citrullinated proteins, autoantibodies, or rheumatoid factor in patients with PD and RA. Five studies investigated the presence of mediators of inflammation in PD and RA. In summary, the majority of the articles have confirmed that there is a correlation between PD and RA, since both disorders have characteristics in common and result from an imbalance in the immunoinflammatory response.

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“…Indeed, gingival samples from periodontal lesions have been shown to have significantly higher RANKL and lower OPG mRNA levels than those of healthy subjects (Bostanci et al, 2007 ). Similarly, abundant RANKL-positive cells were found in the inflammatory epithelium and connective tissues of gingiva of patients with chronic periodontitis (Bhuvaneswarri et al, 2014 ). Our results showed that RANK overexpression in cells of the monocyte/macrophage lineage and in gingival epithelium cells in mice led to the loss of alveolar bone height and an increase in the number of TRAP-positive cells in alveolar bone, reflecting the over-activation of osteoclasts and accelerated resorption whose origin may be the inflammation of the gingival epithelium that precede any sign of bone lost (Figures 4 , 6 ).…”

Section: Discussionmentioning

confidence: 94%

RANK/RANKL/OPG Signalization Implication in Periodontitis: New Evidence from a RANK Transgenic Mouse Model

et al. 2017

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Periodontitis is based on a complex inflammatory over-response combined with possible genetic predisposition factors. The RANKL/RANK/OPG signaling pathway is implicated in bone resorption through its key function in osteoclast differentiation and activation, as well as in the inflammatory response. This central element of osteo-immunology has been suggested to be perturbed in several diseases, including periodontitis, as it is a predisposing factor for this disease. The aim of the present study was to validate this hypothesis using a transgenic mouse line, which over-expresses RANK (RTg) and develops a periodontitis-like phenotype at 5 months of age. RTg mice exhibited severe alveolar bone loss, an increased number of TRAP positive cells, and disorganization of periodontal ligaments. This phenotype was more pronounced in females. We also observed dental root resorption lacunas. Hyperplasia of the gingival epithelium, including Malassez epithelial rests, was visible as early as 25 days, preceding any other symptoms. These results demonstrate that perturbations of the RANKL/RANK/OPG system constitute a core element of periodontitis, and more globally, osteo-immune diseases.

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Detection Of Rankl Positive Cells in Gingival Tissue in Healthy & Chronic Periodontal Disease Patients -A Comparative Study

Abstract: These findings imply that in this comparative study of gingival tissue for, RANKL positive cells, these cells were present in both healthy & chronic periodontitis samples, but number of positive cells present is significantly increased in chronic periodontitis.

Cited by 5 publications

References 16 publications

Bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells

Bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells

Relationship between Periodontitis and Rheumatoid Arthritis: Review of the Literature

RANK/RANKL/OPG Signalization Implication in Periodontitis: New Evidence from a RANK Transgenic Mouse Model

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