scholarly journals Effect of Psoralen on the Intestinal Barrier and Alveolar Bone Loss in Rats With Chronic Periodontitis

Inflammation ◽  
2021 ◽  
Author(s):  
Hua Liu ◽  
Yingjie Xu ◽  
Qi Cui ◽  
Ning Liu ◽  
Fuhang Chu ◽  
...  
2014 ◽  
Vol 5 (4) ◽  
pp. 199-203
Author(s):  
Harshal Liladhar Chaudhari ◽  
Nipun Ashok ◽  
Veena Kalburgi ◽  
Haziel Dina Jenifer

ABSTRACT Introduction Tobacco in the form of Gutkha is commonly used in India. The present study was done to analyze the extent and pattern of alveolar bone loss (ABL) among gutkha chewers who were having chronic periodontitis. Materials and methods A total of 55 habitual gutkha chewers within the age range of 18 to 35 years with chronic periodontitis, who were otherwise healthy were recruited for the study. Fourteen full mouth intraoral periapical (IOPA) radiographs were taken for each individual (a total of 770 radiographs) with the help of radiovisiography. Kodak dental software was used to analyze and measure the alveolar bone loss at each proximal site and data were computed as percentage alveolar bone loss. Results Almost all the subjects had poor oral hygiene status. Clinical parameters of periodontal examination represented by clinical attachment level, probing depth, gingival bleeding index had positive correlation with frequency and duration of gutkha chewing. The study population had a mean alveolar bone loss of 17%. Mean bone loss was more severe in mandible 18.3% ± 2.6, when compared with maxillary arch 15.7% ± 3.7. Conclusion Maximum bone loss was observed with molars and incisors. Alveolar bone loss was more frequently found in mandibular arch as compared to maxillary arch. How to cite this article Warad S, Chaudhari HL, Ashok N, Kalburgi V, Kalburgi NB, Jenifer HD. Clinical Evaluation of Gutkha chewing and Pattern of Bone Loss in Periodontitis. World J Dent 2014;5(4):199-203.


2018 ◽  
Vol 98 (1) ◽  
pp. 107-116 ◽  
Author(s):  
X. Jia ◽  
L. Jia ◽  
L. Mo ◽  
S. Yuan ◽  
X. Zheng ◽  
...  

Postmenopausal osteoporosis (PMO) is a risk factor for periodontitis, and current therapeutics against PMO prevent the aggravated alveolar bone loss of periodontitis in estrogen-deficient women. Gut microbiota is recognized as a promising therapeutic target for PMO. Berberine extracted from Chinese medicinal plants has shown its effectiveness in the treatment of metabolic diseases such as obesity and diabetes via regulating gut microbiota. Here, we hypothesize that berberine ameliorates periodontal bone loss by improving the intestinal barriers by regulating gut microbiota under an estrogen-deficient condition. Experimental periodontitis was established in ovariectomized (OVX) rats, and the OVX-periodontitis rats were treated with berberine for 7 wk before sacrifice for analyses. Micro–computed tomography and histologic analyses showed that berberine treatment significantly reduced alveolar bone loss and improved bone metabolism of OVX-periodontitis rats as compared with the vehicle-treated OVX-periodontitis rats. In parallel, berberine-treated OVX-periodontitis rats harbored a higher abundance of butyrate-producing gut microbiota with elevated butyrate generation, as demonstrated by 16S rRNA sequencing and high-performance liquid chromatography analysis. Berberine-treated OVX-periodontitis rats consistently showed improved intestinal barrier integrity and decreased intestinal paracellular permeability with a lower level of serum endotoxin. In parallel, IL-17A-related immune responses were attenuated in berberine-treated OVX-periodontitis rats with a lower serum level of proinflammatory cytokines and reduced IL-17A+ cells in alveolar bone as compared with vehicle-treated OVX-periodontitis rats. Our data indicate that gut microbiota is a potential target for the treatment of estrogen deficiency–aggravated periodontal bone loss, and berberine represents a promising adjuvant therapeutic by modulating gut microbiota.


2021 ◽  
Author(s):  
Hua Liu ◽  
Yingjie Xu ◽  
Qi Cui ◽  
Ning Liu ◽  
Fuhang Chu ◽  
...  

Abstract ObjectivesTo study the effects of psoralen on the intestinal barrier and alveolar bone loss (ABL) in rats with chronic periodontitis.MethodsFifty-two 8-week-old specific pathogen-free (SPF) male Sprague-Dawley (SD) rats were randomly divided into the following four groups: Control group (Control), Psoralen group of healthy rats (Pso), Periodontitis model group (Model), and Psoralen group of periodontitis rats (Peri+Pso). The alveolar bone resorption of maxillary molars was observed via hematoxylin-eosin staining and micro-computed tomography. The expression level of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) in periodontal tissues were evaluated by immunofluorescence staining. The changes in serum tumour necrosis factor (TNF)-α, interleukin (IL)-10, IL-6, intestinal mucosal occludin and claudin-5 were detected using enzyme-linked immunosorbent assay (ELISA). The level of intestinal mucosal NOD2 was detected using immunohistochemical methods. DNA was extracted from the intestinal contents and the 16s rRNA gene was sequenced using an Illumina Miseq platform.ResultsThe expression of NOD2 protein in the intestinal tract of periodontitis rats decreased after intragastric psoralen administration. Psoralen increased the intestinal microbiota diversity of rats. The level of serum pro-inflammatory factor TNF-α decreased and the level of anti-inflammatory factor IL-10 increased. ABL was observed to be significantly decreased in rats treated with psoralen. Psoralen decreased the RANKL/OPG ratio of periodontitis rats.ConclusionsPsoralen may affect the intestinal immune barrier and ecological barrier, mediate immune response, promote the secretion of anti-inflammatory factor IL-10, and reduce the secretion of the pro-inflammatory factor TNF-α, thus reducing ABL in experimental periodontitis in rats.


2019 ◽  
Vol 22 (1) ◽  
pp. 6-11
Author(s):  
Aini Hariyani Nasution ◽  
Martina Amalia ◽  
Cornelia Christy Tarigan

Periodontitis is one of most common oral disease. Chronic periodontitis is characterised by gingival inflamation, periodontal pocket, lost of attachment, and alveolar bone loss. Smoking is a risk factor of periodontal disease that has direct effect to periodontal tissue. Smoking prevalence in Indonesia during 2013 was about 56,7% among men and about 1,9% among women. Smoking modifies the periodontal microbial challenge and host cytokine levels. Some studies showed that smoker has greater alveolar bone loss than non-smoker, and teeth that have the greatest alveolar bone loss are incisor and followed by molar. The aim of this study is to know the upper incisor and upper molar alveolar bone loss differences between smoker and non-smoker patient with chronic periodontitis. The study’s samples are 92 chronic periodontitis statuses and 200 periapical radiographs that selected by purposive sampling techinque. This study will measure the distance between cementoenamel junction to alveolar bone crest, cementoenamel junction to tooth apex, and alveolar bone loss percentage at upper incisor and upper molar. To compare the differences upper incisor and upper molar alveolar bone loss at patient with chronic periodontitis between smoker and non-smoker will be analyzed by independent t test and Mann-Whitney U test. The result showed that smoker has greater alveolar bone loss than non-smoker. There is no significant differences at upper incisor alveolar bone loss and there is significant differences at upper molar alveolar bone loss between smoker and non-smoker patient with chronic periodontitis.


2013 ◽  
Vol 72 (1) ◽  
pp. 42-47 ◽  
Author(s):  
Daniela Miricescu ◽  
Alexandra Totan ◽  
Bogdan Calenic ◽  
Brandusa Mocanu ◽  
Andreea Didilescu ◽  
...  

1990 ◽  
Vol 69 (1) ◽  
pp. 82-86 ◽  
Author(s):  
M. Sashima ◽  
M. Satoh ◽  
A. Suzuki

SAM-R/1/Iw (senescence-accelerated mouse, resistant) and Pl2/Iw (senescence-accelerated mouse, prone) under a conventional environment and eating standard pellets were examined for alveolar bone loss and the presence of periodontitis around maxillary and mandibular molars as a function of age. Neither SAM strain manifested a chronic periodontitis similar to that in humans, and no obvious plaque and calculus were observed. However, in both strains, 15% of M3 was lost after 13 months of age, and alveolar bone loss gradually increased with advancing age. Though there was no significant difference in the incidence of M3 loss between the two strains, P/2/Iw showed a higher alveolar bone loss around all molars than did Rl1/ Iw after one month of age throughout their life span. For Ml, the difference in alveolar bone loss between Pl2/Iw and Rl1/Iw was significant, and it was probably caused by the difference in degree of molar eruption. Other factors, such as occlusal trauma and gingivitis, may play some role in alveolar bone loss.


2016 ◽  
Vol 4 (4) ◽  
pp. 947-955
Author(s):  
Sneha R Bhat ◽  
◽  
Aravind R Kudva ◽  
Dhoom S Mehta ◽  
◽  
...  

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.


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