Effects of colchicine on gingival inflammation, apoptosis, and alveolar bone loss in experimental periodontitis

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.

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Investigating the Effects of Systemically Administered Strontium Ranelate on Alveolar Bone Loss Histomorphometrically and Histopathologically on Experimental Periodontitis in Rats

Journal of Periodontology ◽

10.1902/jop.2016.160227 ◽

2017 ◽

Vol 88 (2) ◽

pp. e24-e31 ◽

Cited By ~ 8

Author(s):

Nebi Cansın Karakan ◽

Aysun Akpınar ◽

Fahrettin Göze ◽

Ömer Poyraz

Keyword(s):

Bone Loss ◽

Strontium Ranelate ◽

Alveolar Bone ◽

Alveolar Bone Loss ◽

Experimental Periodontitis

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SOCS-3 Regulates Alveolar Bone Loss in Experimental Periodontitis

Journal of Dental Research ◽

10.1177/0022034516645332 ◽

2016 ◽

Vol 95 (9) ◽

pp. 1018-1025 ◽

Cited By ~ 20

Author(s):

E. Papathanasiou ◽

A. Kantarci ◽

A. Konstantinidis ◽

H. Gao ◽

T.E. Van Dyke

Keyword(s):

Bone Loss ◽

Alveolar Bone ◽

Alveolar Bone Loss ◽

Experimental Periodontitis

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Humic Acid, a Polyphenolic Substance, Decreases Alveolar Bone Loss in Experimental Periodontitis in Rats

Journal of Veterinary Dentistry ◽

10.1177/0898756420910531 ◽

2019 ◽

Vol 36 (4) ◽

pp. 257-265

Author(s):

Metin Çalışır ◽

Aysun Akpınar ◽

Ömer Poyraz ◽

Fahrettin Göze ◽

Ziynet Çınar

Keyword(s):

Humic Acid ◽

Bone Loss ◽

Inflammatory Cell ◽

Alveolar Bone ◽

Alveolar Bone Loss ◽

Inflammatory Cell Infiltration ◽

Cell Infiltration ◽

Enzyme Linked Immunosorbent Assay ◽

Local Administration ◽

Experimental Periodontitis

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.

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N-acetylcysteine decreases alveolar bone loss on experimental periodontitis in streptozotocin-induced diabetic rats

Journal of Periodontal Research ◽

10.1111/j.1600-0765.2012.01497.x ◽

2012 ◽

Vol 47 (6) ◽

pp. 793-799 ◽

Cited By ~ 17

Author(s):

H. Toker ◽

H. Ozdemir ◽

H. Balcı ◽

H. Ozer

Keyword(s):

Bone Loss ◽

Alveolar Bone ◽

Diabetic Rats ◽

Alveolar Bone Loss ◽

Experimental Periodontitis

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Involvement of Cot/Tp12 in Bone Loss during Periodontitis

Journal of Dental Research ◽

10.1177/0022034509353405 ◽

2010 ◽

Vol 89 (2) ◽

pp. 192-197 ◽

Cited By ~ 10

Author(s):

T. Ohnishi ◽

A. Okamoto ◽

K. Kakimoto ◽

K. Bandow ◽

N. Chiba ◽

...

Keyword(s):

Bone Loss ◽

Alveolar Bone ◽

Alveolar Bone Loss ◽

Periodontal Tissue ◽

Rankl Expression ◽

Periodontal Tissues ◽

Tnf Α ◽

Experimental Periodontitis ◽

Deficient Mice

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.

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