Occlusal trauma accelerates attachment loss at the onset of experimental periodontitis in rats

2013 ◽  
Vol 49 (3) ◽  
pp. 314-322 ◽  
Author(s):  
S. Nakatsu ◽  
Y. Yoshinaga ◽  
A. Kuramoto ◽  
F. Nagano ◽  
I. Ichimura ◽  
...  
Keyword(s):  
Attachment Loss ◽  
Experimental Periodontitis

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 POS0581 PERIODONTAL DISEASE IN RHEUMATOID ARTHRITIS: RESULTS FROM A COHORT AT TREATMENT WITH BIOLOGICAL, CLASSICAL AND TARGETED SYNTHETIC DMARDs

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 524.1-524
Author(s):  
R. Dos-Santos ◽  
F. Otero ◽  
E. Perez-Pampín ◽  
A. Mera Varela
Keyword(s):  
Rheumatoid Arthritis ◽  
Oral Health ◽  
Periodontal Disease ◽  
Disease Activity ◽  
Health Problem ◽  
Multivariable Analysis ◽  
Testing Time ◽  
Univariable Analysis ◽  
Clinical Attachment Loss ◽  
Attachment Loss

Background:Periodontal disease (PD) has been widely studied in the pathogenesis of rheumatoid arthritis (RA). As well, its relationship with severity and disease activity, has also been investigated with ambiguous results. It has been suggested that the improvement of oral health could enhance disease activity scores.1 PD prevalence worldwide stands around 60% in older adults (>65 years) and its frequency increases with aging.2Objectives:To asses oral health in RA patients and to identify predictors of PD in this population.Methods:Patients diagnosed of RA at treatment with biological, classical or targeted synthetic disease modifying anti-rheumatic drugs (b/cs/tsDMARDs) in the aforementioned hospital during 2020 performed a dental review with a specialized periodontal odontologist. Oral health patterns were given for all patients, following criteria of American Academy of Periodontology, and reevaluation of disease activity was made 2 months later.Clinical, demographic and treatment data were collected from participants.Univariable logistic regression was performed to identify predictors of PD. Variables with p<0.20 were selected for multivariable analysis.Stata 15.1 was used to perform statistical analysis.Results:81 patients were recruited. 82.72% were female. Mean age was 56.17 years (SD 14.15) and mean time since diagnosis was 15.58 years (SD 8.17). 25% were current or past smokers. 21 patients had comorbidities (arterial hypertension the most frequent). 66.67% were rheumatoid factor (RF) positive and 72.73% anti-citrullinated peptide autoantibody (ACPA) positive. Median erythrocyte sedimentation rate (ESR) was 12 mm (IQR 6;23) and mean C-reactive protein (CRP) was 0.48 mg/dl (SD 1.18). Mean disease activity score (DAS28-VSG) at the testing time was 2.62 (SD 1.21) and after 2 months was 2.39 (SD 0.97). 96.30% of patients were at treatment with csDMARDs, 64.20% with glucocorticoids, 96.30% with bDMARDs and 6 patients with tsDMARDs.Univariable analysis identified higher age, at least one autoantibody positive and ESR/CRP as potential predictors of medium/severe PD (p<0.20). Multivariable testing including these variables pointed out higher age, lower ESR and at least one autoantibody positive (OR 1.09 [CI95% 1.04-1.14] p=0.001, OR 0.18 [CI95% 0.04-0.95] p=0.044 and OR 0.94 [CI95% 0.88-1.00] p=0.042, respectively) as predictors of medium or severe PD (≥3 mm interdental clinical attachment loss).Univariable analysis identified higher age, the presence of any comorbidity and anti tumour-necrosis factor alpha treatment (anti-TNF) as potential predictors of severe PD (p<0.20). Multivariable testing including these variables pointed out higher age (OR 1.15 [CI95%1.02-1.30] p=0.026) as predictor of severe PD (≥5 mm interdental clinical attachment loss).Conclusion:Periodontal disease is still an extended health problem among the entire population. Its prevalence in RA is increased, therefore higher age and RF or ACPA positive are risk factors for developing severe PD. This analysis might suggest that an aggressive management of PD could implement better responses in DAS28. Also anti-TNF treatment could delimit a “penumbra” group of patients at risk of developing severe PD, where intensive manage could modify the final outcome.References:[1]C O Bingham, M Moni. Periodontal disease and rheumatoid arthritis: the evidence accumulates for complex pathobiologic interactions. Curr Opin Rheumatol. 2013;25(3):345-353.[2]P Carvajal. Periodontal disease as a public health problem: the challenge for primary health care. Rev Clin Periodoncia inplantol. 2016;9(2):177-183.Disclosure of Interests:None declared

scholarly journals Granulocyte colony-stimulating factor (G-CSF) mediates bone resorption in periodontitis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hui Yu ◽  
Tianyi Zhang ◽  
Haibin Lu ◽  
Qi Ma ◽  
Dong Zhao ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Bone Volume ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Periodontal Tissues ◽  
Gingival Epithelial Cells ◽  
Trap Staining ◽  
Experimental Periodontitis ◽  
Stimulating Factor

Abstract Background Granulocyte colony-stimulating factor (G-CSF) is an important immune factor that mediates bone metabolism by regulating the functions of osteoclasts and osteoblasts. Bone loss is a serious and progressive result of periodontitis. However, the mechanisms underlying the effects of G-CSF on periodontal inflammation have yet not been completely elucidated. Here, we examined whether an anti-G-CSF antibody could inhibit bone resorption in a model of experimental periodontitis and investigated the local expression of G-CSF in periodontal tissues. Methods Experimental periodontitis was induced in mice using ligatures. The levels of G-CSF in serum and bone marrow were measured; immunofluorescence was then performed to analyze the localization and expression of G-CSF in periodontal tissues. Mice with periodontitis were administered anti-G-CSF antibody by tail vein injection to assess the inhibition of bone resorption. Three-dimensional reconstruction was performed to measure bone destruction‐related parameters via micro-computed tomography analysis. Immunofluorescence staining was used to investigate the presence of osteocalcin-positive osteoblasts; tartrate-resistant acid phosphatase (TRAP) staining was used to observe osteoclast activity in alveolar bone. Results The level of G-CSF in serum was significantly elevated in mice with periodontitis. Immunofluorescence analyses showed that G-CSF was mostly expressed in the cell membrane of gingival epithelial cells; this expression was enhanced in the periodontitis group. Additionally, systemic administration of anti-G-CSF antibody significantly inhibited alveolar bone resorption, as evidenced by improvements in bone volume/total volume, bone surface area/bone volume, trabecular thickness, trabecular spacing, and trabecular pattern factor values. Immunofluorescence analysis revealed an enhanced number of osteocalcin-positive osteoblasts, while TRAP staining revealed reduction of osteoclast activity. Conclusions G-CSF expression levels were significantly up-regulated in the serum and gingival epithelial cells. Together, anti-G-CSF antibody administration could alleviates alveolar bone resorption, suggesting that G-CSF may be one of the essential immune factors that mediate the bone loss in periodontitis.

Sign in / Sign up

Export Citation Format

Share Document