Species of Yeast Identified in the Plaque of Healthy Patients versus Periodontal Patients

Although many study the human oral cavity for bacteria, different species of yeast that are also present are often overlooked. Therefore, the different strains of yeasts found in the mouth have not yet been identified. This study focuses on developing a PCR-based technique to identify species of yeast in the mouth. The relationship between the species of yeast found in patients with periodontal disease versus healthy patients was also analyzed

Longitudinal evaluation of prostaglandin E2 (PGE2) and periodontal status in HIV\u3csup\u3e+\u3c/sup\u3e patients

The study aim was to determine whether prostaglandin E2 (PGE2) in gingival crevicular fluid (GCF) could serve as a risk factor for periodontitis in human immunodeficiency virus-positive (HIV+) patients. Clinical measurements, including gingival index (GI), plaque index, bleeding index, probing depth (PD), attachment loss (AL) and GCF samples were taken from two healthy sites (including sites with gingival recession, GI = 0; PD ≤ 3 mm; AL ≤ 2 mm), three gingivitis sites (GI \u3e 0; PD ≤ 3 mm; AL = 0) and three periodontitis sites (GI \u3e 0; PD ≥ 5 mm; AL ≥ 3 mm) of each of the 30 patients at baseline and 6-month visits. GCF samples were also taken by means of paper strips. GCF PGE2 levels were determined by a sandwich ELISA. The progressing site was defined as a site which had 2 mm or more attachment loss during the 6-month study period. The mean amounts of PGE2 were significantly higher in gingivitis and periodontitis sites than in healthy sites (p \u3c 0.0001). GCF levels of PGE2 were significantly correlated with probing depth, attachment loss, CD4+ cells, viral load, age and smoking pack-years at baseline and 6-month visits (0.0001 \u3c p \u3c 0.05). Repeated measures analysis of 19 active sites versus 221 inactive sites indicated that PGE2 levels were significantly higher in active sites than in inactive sites (p \u3c 0.0001). It is likely that the compromised immune system contributes to the pathogenesis of periodontitis in HIV+ patients. It is well known that the activated inflammatory cells produce inflammatory mediators which stimulate the production of PGE2. Longitudinal evaluation of GCF PGE2 with respect to the progression of untreated periodontitis sites in HIV+ subjects will contribute to the understanding of the pathogenesis of periodontitis in HIV+ patients. These data indicate that sites with high GCF levels of PGE2 in HIV+ patients are at significantly greater risk for progression of periodontitis. © 2007 Elsevier Ltd. All rights reserved

Literature Review: Comparison of the Effects of Cigarette Smoke on Mesenchymal Stem Cells and Dental Stem Cells

Stem cells are distinguished from other cell types due to two important defining characteristics. First, stem cells must exhibit selfrenewal potential, which is the ability to produce identical copies of themselves through mitotic divisions over time. Second, stem cells must exhibit multilineage differentiation potential – pluripotency, which is the ability to give rise to various specialized cell types and serves as the driving concept behind stem cell regeneration. They also possess migration potential in order to reach sites of injury. These abilities allow stem cells to participate in the body’s natural processes of wound healing and tissue generation and raise the potential of using stem cells in various applications in regenerative medicine. However, certain environmental predisposing conditions such as cigarette smoke can negatively impact these abilities and stem cell viability for transplantation and regeneration. Most of the research conducted on stem cells involves mesenchymal stem cells (MSCs), typically from the bone marrow. The substantial growth in this research has allowed further understanding of the deleterious effects of cigarette smoke on MSCs, as well as improved our knowledge on the therapeutic usage of MSCs for smoking patients. As of now, there is a considerable lack of research focused on dental stem cells. Given that the first exposure to smoke occurs in the oral cavity, and that the content of nicotine is estimated to be nearly 8 times higher in saliva than in blood plasma (8 hours following application of nicotine patch; saliva: 76.8 ng/ml, plasma: 10.0 ng/ml)1, the potentially more susceptible stem cell populations in the oral cavity deserve more attention. Dental stem cells share many properties with MSCs, and a disruption in their function by higher concentrations of a known inhibitor of stem cell function would create significant problems in the repair process

Literature Review: Comparison of the Effects of Cigarette Smoke on Mesenchymal Stem Cells and Dental Stem Cells

Stem cells are distinguished from other cell types due to two important defining characteristics. First, stem cells must exhibit selfrenewal potential, which is the ability to produce identical copies of themselves through mitotic divisions over time. Second, stem cells must exhibit multilineage differentiation potential – pluripotency, which is the ability to give rise to various specialized cell types and serves as the driving concept behind stem cell regeneration. They also possess migration potential in order to reach sites of injury. These abilities allow stem cells to participate in the body’s natural processes of wound healing and tissue generation and raise the potential of using stem cells in various applications in regenerative medicine. However, certain environmental predisposing conditions such as cigarette smoke can negatively impact these abilities and stem cell viability for transplantation and regeneration. Most of the research conducted on stem cells involves mesenchymal stem cells (MSCs), typically from the bone marrow. The substantial growth in this research has allowed further understanding of the deleterious effects of cigarette smoke on MSCs, as well as improved our knowledge on the therapeutic usage of MSCs for smoking patients. As of now, there is a considerable lack of research focused on dental stem cells. Given that the first exposure to smoke occurs in the oral cavity, and that the content of nicotine is estimated to be nearly 8 times higher in saliva than in blood plasma (8 hours following application of nicotine patch; saliva: 76.8 ng/ml, plasma: 10.0 ng/ml)1, the potentially more susceptible stem cell populations in the oral cavity deserve more attention. Dental stem cells share many properties with MSCs, and a disruption in their function by higher concentrations of a known inhibitor of stem cell function would create significant problems in the repair process

Chlamydia pneumoniae is present in the dental plaque of periodontitis patients and stimulates an inflammatory response in gingival epithelial cells

Chlamydia pneumoniae is an airborne, Gram-negative, obligate intracellular bacterium which causes human respiratory infections and has been associated with atherosclerosis. Because individuals with periodontitis are at greater risk for atherosclerosis as well as respiratory infections, we in-vestigated the role of C. pneumoniae in inflammation and periodontal dis-ease. We found that C. pneumoniae was more frequently found in subgingival dental plaque obtained from periodontally diseased sites of the mouth versus healthy sites. The known periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were also found in the plaque. In addition, C. pneumoniae could efficiently invade human gingival epithelial cells (GECs) in vitro, causing translocation of NF-κB to the nucleus along with increased secretion of mature IL-1β cytokine. Supernatants collected from C. pneumoniae-infected GECs showed increased activation of caspase-1 protein, which was significantly reduced when nlrp3 gene expression was silenced using shRNA lentiviral vectors. Our results demonstrate that C. pneumoniae was found in higher levels in periodontitis patients compared to control pa-tients. Additionally, C. pneumoniae could infect GECs, leading to inflammation caused by activation of NF-κB and the NLRP3 inflammasome. We propose that the presence of C. pneumoniae in subgingival dental plaque may contribute to periodontal disease and could be used as a potential risk indicator of perio-dontal disease

Systemic Immunologic Consequences of Chronic Periodontitis

Chronic periodontitis (ChP) is a prevalent inflammatory disease affecting 46% of the US population. ChP produces a profound local inflammatory response to dysbiotic oral microbiota that leads to destruction of alveolar bone and tooth loss. ChP is also associated with systemic illnesses, including cardiovascular diseases, malignancies, and adverse pregnancy outcomes. However, the mechanisms underlying these adverse health outcomes are poorly understood. In this prospective cohort study, we used a highly multiplex mass cytometry immunoassay to perform an in-depth analysis of the systemic consequences of ChP in patients before (n = 28) and after (n = 16) periodontal treatment. A high-dimensional analysis of intracellular signaling networks revealed immune system–wide dysfunctions differentiating patients with ChP from healthy controls. Notably, we observed exaggerated proinflammatory responses to Porphyromonas gingivalis–derived lipopolysaccharide in circulating neutrophils and monocytes from patients with ChP. Simultaneously, natural killer cell responses to inflammatory cytokines were attenuated. Importantly, the immune alterations associated with ChP were no longer detectable 3 wk after periodontal treatment. Our findings demarcate systemic and cell-specific immune dysfunctions in patients with ChP, which can be temporarily reversed by the local treatment of ChP. Future studies in larger cohorts are needed to test the boundaries of generalizability of our results

Systemic Immunological Consequences of Chronic Periodontitis

Chronic Periodontitis (ChP) is a prevalent inflammatory disease affecting 46% of the US population. ChP produces a profound local inflammatory response to dysbiotic oral microbiota that leads to destruction of alveolar bone and tooth loss. ChP is also associated with systemic illnesses including cardiovascular diseases, malignancies, and adverse pregnancy outcomes. However, the mechanisms underlying these adverse health outcomes are poorly understood. We used a highly multiplex mass cytometry immunoassay to perform an in-depth analysis of the systemic consequences of ChP in patients, before and after periodontal treatment in this prospective cohort study. A high-dimensional analysis of intracellular signaling networks revealed immune system-wide dysfunctions differentiating patients with ChP from healthy controls. Notably, we observed exaggerated pro-inflammatory responses to P. gingivalis-derived lipopolysaccharide in circulating neutrophils and monocytes from patients with ChP. Simultaneously, natural killer cell responses to inflammatory cytokines were attenuated. Importantly, the immune alterations associated with ChP were no longer detectable three weeks after periodontal treatment. Our findings demarcate systemic and cell-specific immune dysfunctions in patients with ChP which can be temporarily reversed by the local treatment of ChP

Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats

BACKGROUND: Periodontal disease in diabetic patients presents higher severity and prevalence; and increased severity of ligature-induced periodontal disease has been verified in diabetic rats. However, in absence of aggressive stimuli such as ligatures, the influence of diabetes on rat periodontal tissues is incompletely explored. The aim of this study was to evaluate the establishment and progression of periodontal diseases in rats only with diabetes induction. METHODOLOGY/PRINCIPAL FINDINGS: Diabetes was induced in Wistar rats (n = 25) by intravenous administration of alloxan (42 mg/kg) and were analyzed at 1, 3, 6, 9 and 12 months after diabetes induction. The hemimandibles were removed and submitted to radiographical and histopathological procedures. A significant reduction was observed in height of bone crest in diabetic animals at 3, 6, 9 and 12 months, which was associated with increased numbers of osteoclasts and inflammatory cells. The histopathological analyses of diabetic rats also showed a reduction in density of collagen fibers, fibroblasts and blood vessels. Severe caries were also detected in the diabetic group. CONCLUSIONS/SIGNIFICANCE: The results demonstrate that diabetes induction triggers, or even co-induces the onset of alterations which are typical of periodontal diseases even in the absence of aggressive factors such as ligatures. Therefore, diabetes induction renders a previously resistant host into a susceptible phenotype, and hence diabetes can be considered a very important risk factor to the development of periodontal disease