scholarly journals Effects of Smoking on the Microbiota and Periodontal Tissue: Literature Review

2018 ◽  
Vol 3 (2) ◽  
pp. 855-862
Author(s):  
Felipe Cid ◽  
Bárbara Soto

Periodontitis is a chronic local inflammatory disease of tissue supporting the teeth that leads to progressive loss of periodontal ligament and alveolar bone. Smoking is a known risk factor for many diseases and increasing evidence suggests that smoking negatively affects periodontal health. Cigarette smoking increased periodontal pathogenic bacterial flora, increasing their pathogenicity and alterations in the periodontal tissue, however the effect of smoking is not directly to these bacteria. Nicotine causes a decreased blood flow and decreased capillary hindering the immune response against pathogenic bacteria. In addition, the immune system is suppressed, so the action of leukocytes is poorly effective against periodontal disease. In conclusion, smoking, mainly nicotine, affects the gingival blood flow, cytokine production, the neutrophil function, replacement of connective tissue and because of these factors, increases the number of periodontal pathogenic bacteria which negatively affects the periodontal tissue.

2021 ◽  
Vol 12 ◽  
Author(s):  
Dragana Stanisic ◽  
Nevena Jeremic ◽  
Suravi Majumder ◽  
Sathnur Pushpakumar ◽  
Akash George ◽  
...  

The gut microbiome has a very important role in human health and its influence on the development of numerous diseases is well known. In this study, we investigated the effect of high fat diet (HFD) on the onset of dysbiosis, gingival blood flow decreases, and the periodontal matrix remodeling. We established a dysbiosis model (HFD group) and probiotic model by Lactobacillus rhamnosus GG (LGG) treatment for 12weeks. Fecal samples were collected 24h before mice sacrificing, while short chain fatty acids (SCFA) analysis, DNA extraction, and sequencing for metagenomic analysis were performed afterwards. After sacrificing the animals, we collected periodontal tissues and conducted comprehensive morphological and genetic analyses. While HFD reduced Bacteroidetes, SCFA, and gingival blood flow, this type of diet increased Firmicutes, lipopolysaccharide (LPS) binding protein, TLR4, pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), matrix metalloproteinases (MMP-2 and MMP-9) expression, and also altered markers of bone resorption (OPG and RANKL). However, LGG treatment mitigated these effects. Thus, it was observed that HFD increased molecular remodeling via inflammation, matrix degradation, and functional remodeling and consequently cause reduced gingival blood flow. All of these changes may lead to the alveolar bone loss and the development of periodontal disease.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yi Hu ◽  
Xu Zhang ◽  
Jing Zhang ◽  
Xinyi Xia ◽  
Huxiao Li ◽  
...  

Abstract Background Increasing evidence suggests a causal link between periodontitis and cognitive disorders. Systemic inflammation initiated by periodontitis may mediate the development of cognitive impairment. Our study aims to investigate the effect of ligature-induced periodontitis on cognitive function and the role of signal transducers and activators of transcription 3 (STAT3) in this process. Materials and methods Ligature-induced periodontitis was established, and the rats were treated intraperitoneally with/without the pSTAT3 inhibitor cryptotanshinone (CTS). Alveolar bone resorption and periodontal inflammation were detected by micro-computed tomography analysis and histopathological evaluation. Locomotor activity and cognitive function were evaluated by the open field test and the Morris water maze test, respectively. The activation of microglia and astrocytes in the hippocampus and cortex was assessed by immunohistochemistry (IHC). The expression of interleukins (IL-1β, IL-6, IL-8, IL-21) in both the periphery and cortex was evaluated by RT-PCR and ELISA. The expression of TLR/NF-κB and ROS cascades was evaluated by RT-PCR. The expression of pSTAT3 and the activation of the STAT3 signaling pathway (JAK2, STAT3, and pSTAT3) in the periodontal tissue and cortex were assessed by IHC and Western blot. The expression of amyloid precursor protein (APP) and its key secretases was evaluated by RT-PCR. The level of amyloid β-protein (Aβ) and the ratio of Aβ1-40/1-42 were measured via ELISA in the plasma and cortex while IHC was used to detect the level of Aβ1-42 in the brain. Results In periodontal ligature rats, significant alveolar bone resorption and local inflammatory cell infiltration were present. Apparent increases in inflammatory cytokines (IL-1β, IL-6, IL-8, and IL-21) were detected in peripherial blood and brain. Additionally, spatial learning and memory ability was impaired, while locomotor activity was not affected. Activated microglia and astrocytes were found in the cortex and hippocampus, presenting as enlarged cell bodies and irregular protrusions. Levels of TLR/NF-kB, PPAR and ROS were altered. The STAT3 signaling pathway was activated in both the periodontal tissue and cortex, and the processing of APP by β- and γ-secretases was promoted. The changes mentioned above could be relieved by the pSTAT3 inhibitor CTS. Conclusions Ligature-induced periodontitis in rats resulted in systemic inflammation and further abnormal APP processing, leading to cognitive impairments. In this progress, the activation of the STAT3 signaling pathway may play an important role by increasing inflammatory load and promoting neuroinflammation.


2017 ◽  
Vol 2 (s1) ◽  
pp. 49-52 ◽  
Author(s):  
Monica Monea ◽  
Tudor Hănțoiu ◽  
Alexandra Stoica ◽  
Ramona Vlad ◽  
Alexandru Sitaru

Abstract Background: Desquamative gingivitis (DG) is a non-plaque-induced, blistering and painful condition occurring most frequently on the labial aspect of the attached gingiva of anterior teeth. The incidence of DG is highest around 50 years of age, and usually indicates the presence of oral or systemic diseases. The purpose of our study was to determine the impact of DG on periodontal health by recording the plaque index, gingival index and gingival bleeding index in a group of patients with DG, compared to healthy controls. Materials and methods: Recordings of specific indices were performed in a group of 26 patients with DG and compared with 24 healthy individuals. These were followed by radiographic examinations in order to assess the loss of marginal alveolar bone. Results: The results showed that patients with DG had a statistically significant increase in periodontal indices, with more gingival inflammation and plaque retention compared to the control group (p <0.05). The highest scores for gingival inflammation were recorded in patients with DG, but on radiographic evaluation the difference was related only to gender, men being more affected by alveolar bone loss in both groups (p <0.05). Conclusions: The incidence and severity of gingival inflammation proved to be higher in patients with DG, which calls for better preventive and maintenance treatment protocols in this group of patients. Early diagnosis and initial-phase periodontal treatment are very important in preventing further tissue breakdown.


1990 ◽  
Vol 39 (1) ◽  
pp. 94-104 ◽  
Author(s):  
Hiroshi Izumi ◽  
Shizuko Kuriwada ◽  
Keishiro Karita ◽  
Takashi Sasano ◽  
Daisuke Sanjo

2019 ◽  
Vol 12 (9) ◽  
pp. 1491-1498 ◽  
Author(s):  
Yu Vatnikov ◽  
A. Rudenko ◽  
P. Rudenko ◽  
Ev Kulikov ◽  
A. Karamyan ◽  
...  

Background: Dilated cardiomyopathy is common in dogs. This form of cardiomyopathy is the main cause of death due to heart disease in dogs. Death can occur suddenly in clinically normal animals as a result of the progression of congestive heart failure (CHF). The pathogenesis of heart failure syndrome in dogs with dilated cardiomyopathy involves activation of the neurohumoral system and immune-mediated inflammation, which leads to further progression of the condition. Heart failure syndrome in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, the involvement of other key internal organs, and intestinal dysbiosis. Aim: This study aimed to determine the immunological and inflammatory mechanisms surrounding the development of heart failure syndrome in dogs with dilated cardiomyopathy. Materials and Methods: The subjects of this study were dogs with a dilated form of cardiomyopathy (n=159), complicated by various functional classes of heart failure syndrome. Evaluation of myocardial remodeling, systolic function, and systemic hemodynamics was performed using EMP-860 Vet and PU-2200V ultrasound scanners according to the standard technique. Electrocardiography was performed with all dogs in right lateral recumbency using the EK1T-04 Midas electrocardiograph (50 mm/s speed and 1 mV gain = 1 cm). Results: In some affected animals, especially in cases of compensated dilated cardiomyopathy, leukocytosis was noted. In patients with dilated cardiomyopathy complicated by heart failure syndrome of various functional classes, the number of neutrophils was significantly increased, and the number of lymphocytes was decreased by 1.9-2.1 times when compared with those in clinically normal animals. In dogs with dilated cardiomyopathy, neutrophilic leukocytosis develops with a simple regenerative shift to the left. The results of immunological studies indicate that dogs with dilated cardiomyopathy develop T lymphocytopenia as compared with clinically normal animals. Conclusion: The central component of heart failure syndrome in dogs with dilated cardiomyopathy is the activation of the neurohumoral system and immune-mediated inflammation. The development of CHF in dogs with dilated cardiomyopathy is caused by the progressive loss of cardiomyocytes, apoptosis, remodeling of the left ventricle, systolic and diastolic dysfunction, arrhythmias, reduced cerebral blood flow, involvement of other key internal organs, and intestinal dysbiosis.


2020 ◽  
Vol 17 (35) ◽  
pp. 381-390
Author(s):  
Andrei SEVBITOV ◽  
Alla DAVIDYANTS ◽  
Roman BALYKIN ◽  
Anton TIMOSHIN ◽  
Mariya KUZNETSOVA

Periodontal disease in the adult population is one of the most pressing problems of dentistry around the world. Thanks to the introduction of modern technologies in practice, it was possible to identify the main mechanisms of the development of this disease at the molecular and genetic level. The interaction of periodontal pathogens with immune factors of antimicrobial protection of the body is the basis of periodontal tissue inflammation and further leads to the destruction of the alveolar bone. Epithelial cells of the gum mucosa play a crucial role against periodontal pathogenic bacteria. Factors of innate immunity play a role not only in antimicrobial protection, but they also support the conditions necessary for the healing and regeneration of periodontal tissues. Therefore, various therapeutic approaches that affect the factors of innate immunity are considered as effective and promising. Clinical examination and determination of factors of innate immunity were performed in 115 patients. Healthy individuals made up a group of 30 people. Patients with chronic generalized periodontitis with varying degrees of severity were 85 people. Each patient underwent orthopantomography on the orthopantomograph Orthophosis XG DS/Ceph (SIRONA Dental System GmbH, Germany) in order to assess the state of the bone tissue of the jaws (the degree of destruction of the cortical layer, the degree of resorption of the interalveolar partitions). Targeted intraoral radiographs were used to assess the state of bone tissue and the quality of surgical treatment. Immunological methods of research were carried out in several stages. The findings of this article make the claim that the use of autologous complex immunopeptides in the surgical treatment of periodontitis reduces the time of achieving a therapeutic effect 2 times, resulting in the rapid relief of the symptoms of inflammation and acceleration of reparative processes.


2021 ◽  
Author(s):  
Rongrong Jiang ◽  
Miao Wang ◽  
Xiaobo Shen ◽  
Shuai Huang ◽  
Jianpeng Han ◽  
...  

Abstract Background: Periodontal disease, an oral disease characterized by loss of alveolar bone and progressive teeth loss, is the sixth major complication of diabetes. It is spreading worldwide as it is difficult to be cured. The insulin-like growth factor 1 receptor (IGF-1R) plays an important role in regulating functional impairment associated with diabetes. However, it is unclear whether IGF-1R expression in periodontal tissue is associated with periodontal bone tissue destruction in diabetic patients. SUMO modification has been reported in various diseases and are associated with an increasing number of biological processes, but previous studies have not focused on diabetic periodontitis.Methods: Periodontal membrane stem cells (PDLSCs) were isolated and cultured from healthy human obstructed teeth after extraction or adolescent orthodontic subtractive extraction. PDLSCs were cultured with medical 5% sterile glucose solution formulated as osteogenic differentiation induction solution with different glucose concentrations. The effects of different glucose concentrations on the osteogenic differentiation ability of PDLSCs were investigated at the genetic and cellular levels using staining assay, Western Blot, RT-PCR, Co-IP and cytofluorescence.Results: We found that SLUG, RUNX2 expression was decreased in PDLSCs cultured in high glucose osteogenic induction solution compared with normal glucose osteogenic induction solution. In addition, the IGF-1R expression levels, osteogenic differentiation and sumoylation of IGF-1R in PDLSCs cultured in high glucose osteogenic induction solution were not consistent with those cultured in normal glucose osteogenic induction solution.Conclusion: Our data demonstrated that SUMO1 modification of IGF-1R in high glucose environment inhibited osteogenic differentiation of PDLSCs by binding to SLUG, a key factor leading to periodontal bone tissue loss in diabetic patients. Thus we can maximize the control of multiple downstream damage signaling factors and bring new hope for periodontal tissue regeneration in diabetic patients.


2002 ◽  
Vol 29 (2) ◽  
pp. 103-107 ◽  
Author(s):  
Pascal Ambrosini ◽  
Sabine Cherene ◽  
Neal Miller ◽  
Michel Weissenbach ◽  
Jacques Penaud

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