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 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.

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 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

3,4,5-Trihydroxybenzoic acid attenuates ligature-induced periodontal disease in Wistar rats.

2020 ◽  
Vol 19 ◽  
Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek
Keyword(s):  
Bone Loss ◽  
Gallic Acid ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Collagenase Activity ◽  
Osteoblastic Activity ◽  
Cell Counts ◽  
Experimental Periodontitis ◽  
Anti Inflammatory

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.

scholarly journals Gram-positive bacteria cell wall-derived lipoteichoic acid induces inflammatory alveolar bone loss through prostaglandin E production in osteoblasts

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tsukasa Tominari ◽  
Ayumi Sanada ◽  
Ryota Ichimaru ◽  
Chiho Matsumoto ◽  
Michiko Hirata ◽  
...  
Keyword(s):  
Cell Wall ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Osteoclast Differentiation ◽  
Lipoteichoic Acid ◽  
Alveolar Bone Loss ◽  
Gram Negative Bacteria ◽  
Gram Positive ◽  
Gram Negative ◽  
Gram Positive Bacteria

AbstractPeriodontitis is an inflammatory disease associated with severe alveolar bone loss and is dominantly induced by lipopolysaccharide from Gram-negative bacteria; however, the role of Gram-positive bacteria in periodontal bone resorption remains unclear. In this study, we examined the effects of lipoteichoic acid (LTA), a major cell-wall factor of Gram-positive bacteria, on the progression of inflammatory alveolar bone loss in a model of periodontitis. In coculture of mouse primary osteoblasts and bone marrow cells, LTA induced osteoclast differentiation in a dose-dependent manner. LTA enhanced the production of PGE2 accompanying the upregulation of the mRNA expression of mPGES-1, COX-2 and RANKL in osteoblasts. The addition of indomethacin effectively blocked the LTA-induced osteoclast differentiation by suppressing the production of PGE2. Using ex vivo organ cultures of mouse alveolar bone, we found that LTA induced alveolar bone resorption and that this was suppressed by indomethacin. In an experimental model of periodontitis, LTA was locally injected into the mouse lower gingiva, and we clearly detected alveolar bone destruction using 3D-μCT. We herein demonstrate a new concept indicating that Gram-positive bacteria in addition to Gram-negative bacteria are associated with the progression of periodontal bone loss.

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