Periodontitis is one of the most prevalent bacterial diseases affecting man with up to 90% of the global population affected. Its severe form can lead to the tooth loss in 10-15% of the population worldwide. The disease is caused by a dysbiosis of the local microbiota and one organism that contributes to this alteration in the bacterial population is Prophyromonas gingivalis. This organism possesses a range of virulence factors that appear to contribute to its growth and survival at a periodontal site amongst which is its ability to invade oral epithelial cells. Such an invasion strategy provides a means of evasion of host defence mechanisms, persistence at a site and the opportunity for dissemination to other sites in the mouth. However, previous studies have demonstrated that invasion of the mammalian cells in a population by P. gingivalis is heterogenous, with some cells becoming heavily invaded while others harbour no or only a few bacteria. An understanding of this heterogeneity may throw light on the mechanisms involved and we hypothesised that the phase of the host cell cycle may explain this phenomenon. In an attempt to study the factors influencing P. gingivalis invasion and the cell response to that invasion, a standard antibiotic protection assay was employed and an oral keratinocyte cell line, H357. The results showed that P. gingivalis NCTC 11834 invasion was significantly increased with increasing time of exposure to the cells and the cell density. This may reflect an increased host cell surface area available for bacterial attachment. No effect on invasion of P. gingivalis invasion was observed by the bacterial growth phase, H357 cell passage number or whether cells were pre-incubated with P. gingivalis lipopolysaccharide. Epithelial cells did, however, respond to the presence of P. gingivalis in a number of ways. For example, the mRNA expression of endothelin-1 and urokinase receptor were upregulated with increasing P. gingivalis infection time, suggesting that these proteins could act as inflammatory mediators and possibly as useful markers of the severity of periodontal disease or in the diagnosis and treatment of periodontitis. iii Secondly, in an attempt to investigate the reason for the observed heterogeneous P. gingivalis invasion of H357 cell populations, the effect of cell cycle phase on P. gingivalis invasion was investigated. H357 cells were synchronized by serum starvation. On re-introduction of serum, characterisation of cell cycle phase distribution was performed by flow cytometry following staining with propidium idodide (PI) or by immunofluorescence using bromodeoxyuridine (BrdU), which specifically identifies cells in S-phase. The effect of cell cycle phases on P. gingivalis invasion was measured using the antibiotic protection assay, immunofluorescence and flow cytometry and these were correlated with gene and surface expression of the urokinase receptor and the α5-integrin subunit, which is thought to mediate P. gingivalis invasion. Results showed that the percentage invasion was enhanced with increasing serum re-introduction time, and positively correlated with the number of cells in S-phase. In addition, flow cytometry data showed that the highest association of fluorescent P. gingivalis was with PI positive S-phase cells. Moreover, BrdU positive S-phase cells were 3 times more likely to be invaded and contained 10 times more P. gingivalis than cells in other phases. Also, α5-integrin was more highly expressed in cells in S-phase than other phases, which could explain the mechanism underlying this enhanced invasion. Data presented here have suggested that P. gingivalis targeting of cells in S- phase could, in vivo, allow preferential invasion of the junctional epithelial cells which turns over rapidly. The data presented in this thesis suggest that P. gingivalis invasion is greatly dependent on several factors attributed to the host, the bacteria itself, and to the environment which the bacteria reside in. The invasion occurs within a population of host cells in a heterogeneous fashion, and is dependent on the cell cycle phase, specifically S-phase. This novel finding, in addition to the previously reported mechanisms of P. gingivalis invasion, increases our understanding of this virulence trait and suggests that such a strategy is a highly organised process which the bacteria can follow to ensure its survival within the host. Furthermore, knowledge of these mechanisms could provide novel approaches to treatment of periodontal diseases.
Periodontitis is a chronic inflammatory disease resulted from aggravated immune response to a dysbiotic subgingival microbiota of a susceptible host. Consequences of periodontitis are not only limited to the devastating effect on the oral cavity but extends to affect general health of the individual and also exerts economic burdens on the health systems worldwide. Despite these serious outcomes of periodontitis; however, they are avoidable by early diagnosis with proper preventive measures or non-invasive interventions at earlier stages of the disease. Clinically, diagnosis of periodontitis could be overlooked due to certain limitations of the conventional diagnostic methods such as periodontal charting and radiographs. Utilization of re
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In this review of literature, the light will be concentrated on the role of stem cells as an approach in periodontal regeneration.
Periodontal diseases such as gingivitis and periodontitis are considered common diseases. This study is aimed to predicate these diseases using non-harmful specimens such as saliva throughout the detection of some parameters. In the beginning, a random 51 patients' saliva was collected from outpatients who suffered from different degrees of periodontal diseases. Concurrently, another 40 people who appeared to be healthy were collected, and both patients and healthy people were subjected to a questionnaire form and diagnosed by a specialist dentist. The results of this study revealed that there is no significant difference between males and females in infection with periodontal diseases. As well, smoking is not acting as the main f
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Background: Anemia of chronic disease (ACD) occurs in the presence of chronic infection, inflammatory conditions or neoplastic conditions despite of adequate iron and vitamins storage. Gingivitis is the inflammation of the gingiva, periodontitis is the inflammation in the periodontium that extend deeper with loss of connective tissue attachment and supporting bone. The main pathogenesis of periodontal diseases and ACD is immune activation. Aims of study: Determine and compare the clinical periodontal parameters (plaque index (PLI), gingival index (GI), bleeding on probing (BOP), probing pocket depth (PPD) and clinical attachment level (CAL)). Evaluate the hematocrit (Hct) level, red blood cells (RBCs) count and white blood cells (WBCs) c
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Background: Cluster of differentiation 14 (CD14) is a serum/cell surface glycoprotein; and it is a pattern recognition receptor. CD14 expressed on the surface of various cells, or it found soluble in saliva and other body fluids. It has been proposed that soluble CD14 (sCD14) may play a protective role by controlling Gram negative bacterial infections through its capacity to bind lipopolysaccharide. This study was conducted to assess the level of soluble CD14 in saliva of patients with different periodontal diseases and healthy subjects and determine its correlation with clinical periodontal parameters. Materials & Methods: A total of 80 subjects, age ranged (25-50) years old, divided into three main groups, group ? consisted of 45 chronic
... Show MoreThe aims of this paper is investigating the spread of AIDS both within-host, through the contact between healthy cells with free virus inside the body, and between-host, through sexual contact among individuals and external sources of infectious. The outbreak of AIDS is described by a mathematical model consisting of two stages. The first stage describes the within-host spread of AIDS and is represented by the first three equations. While the second stage describes the between-host spread of AIDS and represented by the last four equations. The existence, uniqueness and boundedness of the solution of the model are discussed and all possible equilibrium points are determined. The local asymptotic stability (LAS) of the model is studied, wh
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Background: Chronic periodontitis is an inflammatory disease of tissues supporting the teeth. Salivary compositions have been most intensely studied as a potential marker for periodontal disease. In this study, analysis of saliva provides a simple and non-invasive method of evaluating the role of salivary IgA (s-IgA) levels in periodontal disease by detecting the level of (s-IgA) in patients with chronic periodontitis smokers and non smokers patients and correlate the mean (s-IgA) levels with clinical periodontal parameters Plaque index (PLI) gingival index (GI), probing pocket depth (PPD) and clinical attachment level (CAL). Materials and Methods: The study samples consists of (15) patients with chronic periodontitis who were non smokers (
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Abstract Inflammation of periodontal tissues is the consequence of interaction between periodontal pathogens and immune system. This is associated with increased expression of inflammatory cytokines, which may exert destructive effect to the periodontal tissues when released over long period. The aim of this study was to chronologically track the homeostasis of oral keratinocytes following removal of periodontal pathogens. This was done by investigating expression of selected inflammatory markers and integrity of epithelial monolayers in vitro. Rat oral keratinocytes were stimulated with heat-killed Fusobacterium nucleatum and Porphyromonas gingivalis over 7-days then bacteria were washed away and epithelial cells re-cultured for 3-
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