Evaluation of the protective effects of non-thermal atmospheric plasma on alveolar bone loss in experimental periodontitis

Author(s):  
Basak Kusakcı-Seker ◽  
Hakan Ozdemir ◽  
Suna Karadeniz-Saygili
Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek

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.


2016 ◽  
Vol 95 (9) ◽  
pp. 1018-1025 ◽  
Author(s):  
E. Papathanasiou ◽  
A. Kantarci ◽  
A. Konstantinidis ◽  
H. Gao ◽  
T.E. Van Dyke

2019 ◽  
Vol 36 (4) ◽  
pp. 257-265
Author(s):  
Metin Çalışır ◽  
Aysun Akpınar ◽  
Ömer Poyraz ◽  
Fahrettin Göze ◽  
Ziynet Çınar

The purpose of this study was to evaluate the biochemical, morphometric, and histopathological changes associated with experimental periodontitis in rats in response to local administration of humic acid. Thirty-eight Wistar rats were divided into 5 experimental groups: nonligated (NL) group, ligature-only (LO) group, and ligature + local administration of humic acid (20, 80, and 150 mg/kg body weight per day for 15 days, respectively; L-20, L-80, and L-150 groups). Changes in alveolar bone levels were clinically measured as the distance from the cementoenamel junction to the alveolar bone crest with a stereomicroscope. Tissues were histopathologically examined to assess the osteoclast numbers, osteoblastic activity, and inflammatory cell infiltration among the study groups. Enzyme-linked immunosorbent assay interleukin1β (IL-1β) and IL-10 levels in serum and gingival homogenates were evaluated. At the end of 15 days, the alveolar bone loss was significantly higher in the LO group compared to the NL, L-20, and L-150 groups ( P < .05). The osteoclast number in the LO group was significantly higher than the NL, L-20, and L-150 groups ( P < .05). Inflammatory cell infiltration was significantly higher in the LO and L-80 groups than the other groups ( P < .05). The highest serum and gingival homogenate IL-10 levels were determined in the NL group ( P < .05). The serum and gingival homogenate IL-1β levels in LO group were significantly higher than the NL, L-20, and L-150 groups ( P < .05). Within the limits of this study, it can be suggested that humic acid, when administered locally at 20 and 80 mg/kg doses, may prevent alveolar bone loss in the rat model.


Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 934 ◽  
Author(s):  
Hae Jin Lee ◽  
Dong-Ryung Lee ◽  
Bong-Keun Choi ◽  
Seung Hwan Yang

Over the past decades, periodontitis has become a rising health problem and caused various diseases. In the many studies shows that some extracts and compound to the prevention and treatment of periodontitis. This study focuses on the effects of inhibition of gingival damage and alveolar bone loss. The aim of this study was to evaluate the protective effects of Magnolia biondii extract (MBE) against ligature-induced periodontitis in rats. A ligature was placed around the molar teeth for 8 weeks, and MBE was administered for 8 weeks. Gingival tissue damage and alveolar bone loss were measured by microcomputed tomography (CT) analysis and histopathological examination. Serum Interluekin-1 β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenases-2 (COX-2), and receptor activator of nuclear factor–κB ligand (RANKL) levels were investigated using commercial kits to confirm the antiperiodontitis effects of MBE. We confirmed that ligature-induced periodontitis resulted in gingival tissue damage and alveolar bone loss. However, treatment for 8 weeks with MBE protected from periodontal tissue damage and downregulated serum inflammatory cytokine factors and RANKL levels. These results suggest that MBE exerts antiperiodontitis effects by inhibiting gingival tissue destruction and alveolar bone loss through regulation of anti-inflammatory cytokines in periodontitis-induced rats.


2010 ◽  
Vol 89 (2) ◽  
pp. 192-197 ◽  
Author(s):  
T. Ohnishi ◽  
A. Okamoto ◽  
K. Kakimoto ◽  
K. Bandow ◽  
N. Chiba ◽  
...  

Periodontitis causes resorption of alveolar bone, in which RANKL induces osteoclastogenesis. The binding of lipopolysaccharide to Toll-like receptors causes phosphorylation of Cot/Tp12 to activate the MAPK cascade. Previous in vitro studies showed that Cot/Tp12 was essential for the induction of RANKL expression by lipopolysaccharide. In this study, we examined whether Cot/Tp12 deficiency reduced the progression of alveolar bone loss and osteoclastogenesis during experimental periodontitis. We found that the extent of alveolar bone loss and osteoclastogenesis induced by ligature-induced periodontitis was decreased in Cot/Tp12-deficient mice. In addition, reduction of RANKL expression was observed in periodontal tissues of Cot/Tp12-deficient mice with experimental periodontitis. Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-α mRNA expression in gingiva of mice with experimental periodontitis. Our observations suggested that Cot/Tp12 is essential for the progression of alveolar bone loss and osteoclastogenesis in periodontal tissue during experimental periodontitis mediated through increased RANKL expression.


2012 ◽  
Vol 57 (1) ◽  
pp. 60-65 ◽  
Author(s):  
Serhat Demirer ◽  
M. Isa Kara ◽  
Kamile Erciyas ◽  
Hakan Ozdemir ◽  
Hatice Ozer ◽  
...  

2017 ◽  
Vol 8 ◽  
Author(s):  
Alrieta H. Teixeira ◽  
Jordânia M. de Oliveira Freire ◽  
Luzia H. T. de Sousa ◽  
Antônia T. Parente ◽  
Nayara A. de Sousa ◽  
...  

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