scholarly journals Retraction: Yu, X., Hu, Y., Freire, M., Yu, P., Kawai, T., Han X. (2017) Role of toll‐like receptor 2 in inflammation and alveolar bone loss in experimental peri‐implantitis versus periodontitis. Journal of Periodontal Research 53(1), 98‐106. https://doi.org/10.1111/jre.12492

2020 ◽  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Periodontal Research

scholarly journals Mixed lineage kinase domain-like pseudokinase mediated necroptosis aggravates periodontitis progression

2021 ◽  
Author(s):  
Yanan Yang ◽  
Lingxia Wang ◽  
Haibing Zhang ◽  
Lijun Luo
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Porphyromonas Gingivalis ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Mrna Levels ◽  
Genetic Ablation ◽  
Osteoclast Activation

Abstract Necroptosis is a form of cell death that is reportedly involved in the pathogenesis of periodontitis. However, the role of Mlkl-involved necroptosis remains unclear. Herein, we aim to explore the role of MLKL-mediated necroptosis in periodontitis in vitro and in vivo. Expression of RIPK3, MLKL, and phosphorylated MLKL is observed in gingival tissues obtained from healthy subjects or patients with periodontitis. Viability of Porphyromonas gingivalis lipopolysaccharide (LPS-Pg)-treated cells was detected. In wild type or Mlkl deficiency mice with ligature-induced periodontitis, alveolar bone loss and osteoclast activation were assessed. mRNA levels of inflammatory cytokines in bone marrow-derived macrophages were tested by qRT-PCR. Increased expression of RIPK3, MLKL, and phosphorylated MLKL is observed in gingival tissues obtained from patients with periodontitis. Porphyromonas gingivalis lipopolysaccharide (LPS-Pg)-treated cells developed necroptosis after caspase inhibition and negatively regulated the NF-κB signaling pathway. In mice with ligature-induced periodontitis, Mlkl deficiency reduced alveolar bone loss and weakened osteoclast activation. Furthermore, genetic ablation of Mlkl in LPS-Pg-treated bone marrow-derived macrophages increased the mRNA levels of tumor necrosis factor-α, interleukin (Il)-1β, Il-6, cyclooxygenase 2, matrix metalloproteinase 9, and receptor activator of nuclear factor kappa-B ligand. Our data indicated that MLKL-mediated necroptosis aggravates the development of periodontitis in a Mlkl-deficient mouse. And this will provide a new sight for the understanding of etiology and therapies of periodontitis.

The role of 5-lipoxygenase inAggregatibacter actinomycetemcomitans-induced alveolar bone loss

2017 ◽  
Vol 44 (8) ◽  
pp. 793-802 ◽  
Author(s):  
Mila F. M. Madeira ◽  
Celso M. Queiroz-Junior ◽  
Jôice D. Corrêa ◽  
Sílvia M. C. Werneck ◽  
Fabiana S. Machado ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss

scholarly journals The roles of osteocytes in alveolar bone destruction in periodontitis

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Xiaofei Huang ◽  
Mengru Xie ◽  
Yanling Xie ◽  
Feng Mei ◽  
Xiaofeng Lu ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Remodeling ◽  
Alveolar Bone ◽  
Bone Cells ◽  
Bone Destruction ◽  
Alveolar Bone Loss ◽  
Receptor Activator ◽  
Local Destruction ◽  
Underlying Mechanisms

AbstractPeriodontitis, a bacterium-induced inflammatory disease that is characterized by alveolar bone loss, is highly prevalent worldwide. Elucidating the underlying mechanisms of alveolar bone loss in periodontitis is crucial for understanding its pathogenesis. Classically, bone cells, such as osteoclasts, osteoblasts and bone marrow stromal cells, are thought to dominate the development of bone destruction in periodontitis. Recently, osteocytes, the cells embedded in the mineral matrix, have gained attention. This review demonstrates the key contributing role of osteocytes in periodontitis, especially in alveolar bone loss. Osteocytes not only initiate physiological bone remodeling but also assist in inflammation-related changes in bone remodeling. The latest evidence suggests that osteocytes are involved in regulating bone anabolism and catabolism in the progression of periodontitis. The altered secretion of receptor activator of NF-κB ligand (RANKL), sclerostin and Dickkopf-related protein 1 (DKK1) by osteocytes affects the balance of bone resorption and formation and promotes bone loss. In addition, the accumulation of prematurely senescent and apoptotic osteocytes observed in alveolar bone may exacerbate local destruction. Based on their communication with the bloodstream, it is noteworthy that osteocytes may participate in the interaction between local periodontitis lesions and systemic diseases. Overall, further investigations of osteocytes may provide vital insights that improve our understanding of the pathophysiology of periodontitis.

scholarly journals Mangiferin alleviates experimental peri-implantitis via suppressing interleukin-6 production and Toll-like receptor 2 signaling pathway

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Hao Li ◽  
Zhiyong Chen ◽  
Xinghua Zhong ◽  
Jiaquan Li ◽  
Wei Li
Keyword(s):  
Bone Loss ◽  
Western Blot ◽  
Inflammatory Infiltrate ◽  
Alveolar Bone ◽  
Pcr Analysis ◽  
Micro Ct ◽  
Toll Like Receptor ◽  
Qrt Pcr ◽  
Toll Like Receptor 2 ◽  
Tlr2 Signaling

Abstract Background TLR2 (Toll-like receptor 2) signaling and its downstream proinflammatory cytokines are considered to be important in the progression of peri-implantitis. A natural medicine, mangiferin has exhibited modulatory effect on TLR2 signaling and anti-inflammatory effects on different diseases. The objective of the present study is to investigate the effect of mangiferin on peri-implantitis and the potential mechanisms by administering this drug to an experimental peri-implantitis mouse model. Methods Maxillary left first, second, and third molars of mice were extracted, and dental implants were placed in the region of the maxillary left second molars. Then, peri-implantitis was induced by tying ligatures around implants, and mangiferin was given orally to the mice. After 6-week mangiferin treatment, bone loss around the implants was detected using micro-computerized tomography (micro-CT). Alveolar bone and inflammatory infiltrate in peri-implant tissues were examined using hematoxylin and eosin (H&E) staining. Production of interleukin-6 (IL6), a TLR2 downstream proinflammatory cytokine, in the tissue surrounding implants was measured using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) analysis. IL6 protein expression and TLR2 signaling pathway activation in peri-implant tissues were detected using western blot analysis. Results Micro-CT demonstrated reduced bone loss in peri-implantitis upon mangiferin administration. Additionally, H&E staining showed more alveolar bone and less inflammatory infiltrate in peri-implant tissues after mangiferin application. Moreover, qRT-PCR analysis demonstrated lower levels of IL6 gene expression, and western blot analysis showed decreased protein expression of IL6 and TLR2, and suppressed phosphorylation of TLR2 downstream nuclear factor-κB, p38 mitogen-activated protein kinase, and c-Jun N-terminal kinase after mangiferin treatment. Conclusions These results suggest the suppressive effect of mangiferin on bone damage and inflammatory infiltrate in peri-implantitis. These therapeutic effects may be associated with inhibited IL6 production and reduced TLR2 signaling activation in peri-implant tissues.

scholarly journals The Potential Role of Suppressors of Cytokine Signaling in the Attenuation of Inflammatory Reaction and Alveolar Bone Loss Associated with Apical Periodontitis

2008 ◽  
Vol 34 (12) ◽  
pp. 1480-1484 ◽  
Author(s):  
Renato Menezes ◽  
Thiago Pompermaier Garlet ◽  
Ana Paula Fávaro Trombone ◽  
Carlos Eduardo Repeke ◽  
Ariadne Letra ◽  
...  
Keyword(s):  
Bone Loss ◽  
Inflammatory Reaction ◽  
Potential Role ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Apical Periodontitis ◽  
Cytokine Signaling ◽  
Suppressors Of Cytokine Signaling

scholarly journals The effect of dexamethasone in the pathogenesis of ligature-induced periodontal disease in Wistar rats

2005 ◽  
Vol 19 (4) ◽  
pp. 290-294 ◽  
Author(s):  
Juliano Cavagni ◽  
Ana Cristina Soletti ◽  
Eduardo José Gaio ◽  
Cassiano Kuchenbecker Rösing
Keyword(s):  
Bone Loss ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Pearson Correlation ◽  
Test Group ◽  
Alveolar Bone Loss ◽  
Control Group ◽  
Female Wistar Rats ◽  
The Mean

The aim of this study was to evaluate, in rats, the role of the systemic use of dexamethasone in the pathogenesis of induced alveolar bone loss. In 26 female Wistar rats, ligatures were placed around the second upper molars, and the contralateral ones served as intra-group controls. Two groups were formed. The test group received 0.5 mg/kg of dexamethasone subcutaneously every third day during thirty days. The control group received the same amount of saline solution. After thirty days, the animals were sacrificed and their maxillae were removed. Sodium hypochlorite was used to prepare the specimens, and the cementum-enamel junction was stained with 1% methylene blue. Morphometric analysis of the alveolar bone loss was performed with standardized digital photographs, and the distance between the cementum-enamel junction and the alveolar bone crest was measured with the software ImageTool 3.0. Intra-examiner calibration revealed a Pearson correlation coefficient of 0.99. Statistical analysis was performed by paired or independent samplet tests, as appropriate (alpha = 0.05). Dexamethasone increased the mean alveolar bone loss in ligature-induced periodontitis in relation to the control group (0.77 and 0.61 buccally, and 0.65 and 0.56 palatally, respectively). No significant differences were observed intergroups in the teeth without ligatures. In the animal model used here, the use of dexamethasone increased the progression of ligature-induced alveolar bone loss.

EFFECTS OF ALENDRONATE THERAPY ON CYCLOSPORINE INDUCED ALVEOLAR BONE LOSS : A MORPHO-METRIC AND BIO-CHEMICAL STUDY IN RATS

2016 ◽  
Vol 4 (4) ◽  
pp. 947-955
Author(s):  
Sneha R Bhat ◽  
◽  
Aravind R Kudva ◽  
Dhoom S Mehta ◽  
◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Chemical Study ◽  
Alveolar Bone Loss
Sign in / Sign up

Export Citation Format

Share Document