Immune Responses to Periodontal Bio Film

Question: Discuss about the Immune Responses to Periodontal Bio Film. Answer: Introduction The immune system of the periodontal diseases has been under evolution that has spanned many foundational transformations that are founded on the individual microbiology studies. It is the study that has long been known to provide a basis for the understanding and the appreciation of the primary stimuli for the infection. Periodontal disease is a chronic infection caused by bacteria affecting the gingiva and the bone supporting the teeth. It is a result of the response to the bacteria in the dental biofilm where most of them remain hosts to the gingival tissues where the tissues have minimal changes (Stathopoulou, Benakanakere, Galicia Kinane, 2010). The infection can be severe to the extent of causing destruction to the teeth resulting in a loss of attachment and the alveolar bone. Another evolution has been linked to the ongoing process in the parsing out of the technicality of the inflammatory in humans, innate and adaptive immune response that go along with the findings in the f ield of microbiology. The natural immune response entails the homeostatic system as the first defense line that can recognize the bacteria and triggers the immune systems to fight back. Along the innate immunity is the adaptive immunity cells believed to be critical in the pathogenesis scenes of the periodontal disease, the T-cells, and B-cells. The T-cells are essential for the human resistance. It is a kind of a lymphocyte that is very active in the immune response. The B-cell is also a type of lymphocyte that is responsible for the production of antibodies (Peyyala, Ebersole, 2013). The B-cells functions in the humoral immunity element of the adaptive immune system by secreting antibodies. The T-and B-cells are the cells in a human body specially designed for defensive purposes. The cells are differently tailored to different germs in the sense that when the body is attacked by a virus, the cell responding will have recognized that virus, rapidly disperses around forming an army of identical cells to combat the infection. The principal purpose of this paper is to research onto the immune responses towards the periodontal Biofilm (Guggenheim et al. 2009). Innate Immune Response in Periodontal Disease According to a histological evaluation, polymorphonuclear leukocyte (PMN) is a key player in the maintenance of the periodontal health. These cells can be found in large numbers in the junction epithelium covering the tissues beneath from the reach of the bacterial infection. The existence of the PNM is because of the availability of the chemotactic factor in the gingival sulcus as well as the tissues beneath. When the PMNs fails to transmigrate into the endothelium, there is an increase in the inflammatory response that lowers the immune response against the bacteria causing periodontal infections (Mikihito et al. 2010). The periodontal epithelium offers a physical barrier to the infection and also plays active roles in the host defense of the innate because the epithelial cells are usually in contact with the bacterial products. In the existence of the active disease, the shifts in the epithelial results in the severe periodontal pocket that causes the bacteria to invade, also caus ing inflammation and destruction of the connective tissue associated with loss of bone and also the possible loss of the tooth. The epithelial can always take part in the in the infection by promoting further innate as well as the acquired immune responses. The epithelial cells may as well answer the calls by the bacterial by increasing their proliferation, by changing their cell initiation activities and also by transforming the cell differentiation and the death of cells (Peyyala, Kirakodu, Novak, 2012). After a variety of studies, it can now be concluded that the epithelia in the human bodies produce a wider range of antimicrobial peptides. These peptides have as well been discovered to have links with saliva and are in the case also present in the den to gingival junction area. The oral secular pocket and the epithelia in the junctions of the gingival have been associated with the generation of defensins and in most cases, the beta-defensin hBD-1, hBD-2, and hBD-3 (Turi et al. 2012). The integrity of the defensin epithelial is as well found to be disrupted by the different microbial pathogens that attack cell-cell junctions dissociating the cells from each other. The innate immunity is appreciated for its abilities to recognize bacteria as non-self agents because of the available microorganisms PAMPs in the bacterial wall acknowledged by the pattern recognition receptors on the surfaces of the immune wall. The PAMPs in the bacterial wall have been recognized to be invariant, and th ey represent conserved molecular patterns that are necessary for the microbial to survive. They are present in the bacterial lipopeptides, peptidoglycan, flagellin and DNA (Ali, Tahir and Ansari, 2011). Adaptive Immune Response in the Periodontal Infection The adaptive immune system is usually activated in cases where there has been a breach in the epithelial barrier along with the antimicrobial peptides and the other elements found in the innate system. The cytokines and the interleukins are found to be an integral part of the response, and they usually represent the intercellular messengers (Dickinson et al. 2011). According to Gemmel et al., the immune responses to the infection are usually under the control of the balance between the T helper (Th) 1 and two cytokines. To distinguish between the Th1 and two cell subsets, one would consider certain factors as the antigen and the antigen dose, the route of administration and the nature of the antigen presenting cell as well as the co-stimulatory molecules. Studies dated towards the end of the 19th century identified that the diapedesis was the fundamental mechanism involved in the process of leukocyte emigration. The invasion of the tissues by the leukocyte is usually influenced by di fferent elements including the IL-1, tumor necrosis factor as well as the LPS bacterial when injected (Li et al. 2007). Other chemokines have however raised significant interests regarding their selective recruitment and the activation of the leukocytes. The Chemikines are found to be a large family of small proteins almost similar to the heparin-proteins regarding their structures and are classified into four subfamilies based on the configuration of the cystein residues. Both the B and T cells are found to be present in the periodontal tissues. The infiltrate in the periodontal lesion is inclusive of the lymphocytes and mast cells that usually move to the tissues through the guidance of the various concentrations of the chemiokines and cytokines. The Th1 responses generated by the T cells are known to have the ability to enhance the phagocytic activity of the macrophages and neutrophils, and they also appear to host the infection. The B cells are activated and begin to produce ant ibodies when there is a Th 2 response. Many studies have declared and proved strong reactions of the antibodies against specific bacterial antigens that are associated with less severe diseases in the patients with aggressive and chronic periodontosis (Kenneth, 2008). Host inflammatory reaction related stimuli The environment is believed to be an ideal place rich in nutrients and can promote the growth of bacteria that will in the end form communities. The initial parts of the digestive tract give the bacteria a real surface of the teeth where they apply and multiply. The biofilm bacteria on the surface of the tooth usually activate the innate and the adaptive host responses that affect the biofilm. During the inflammation process, the changes in the surrounding might come along with effect on the biofilm (Siege et al. 2007). The environmental changes in temperature usually affect different functions and virulence of the full species of microbiology. The bacteria usually sense the variations in the temperature by proteins and also through the membrane lipids. In the periodontal pocket, there have been reports of an increase of 2 degrees Celsius in the affected sites as compared to the good sites. The increase in the temperature is believed to be a host defense mechanism that initiates the valance and the heat shock gene expression in the bacteria in response. Thus, the rise the temperature has also been noted to affect the attachment of the bacteria and the production of protease. The gingival in the case have as well been found to have been hit by the temperature. In the elevated temperatures, there is an expression of the rising volumes of the monophosphorylated penta-acylated lipid A. The fat is seen to be a rapid activator to the host Toll-like receptor four making the bacteria more susceptible to the host defensins. The overall effect of the temperature is however found to be favoring the periodontal pathogens in the sublingual films due to the increased portions of the Prevotella intermedia, P. gingivalisand A. actinomycetemcomitans associated with the high temperatures in the sites (Umeda et al. 2012). Host Defense Mechanisms The defense mechanisms of the host interrelating with each other are a reflection of the reaction of the host to the aggression. The response entails the ignition of both innate and the adaptive components of the immune systems. In the field of periodontists, the bacteria includes in an inflammatory response that is accompanied by their destructive effects and are the key players for the destruction of the tissues. Inflammatory and the immune responses have been found to dynamically interact even though the majority of the responses have been declared immunological. The gingival cervicular fluid is known as the serum tyransudate coming from the gingival plexus of the gingival corium blood vessels. Because if flows through the sulcular and the junctional epithelial and the periodontal tissues, the fluid has molecular biological markers. With an increase in the inflammation and the severity of the infection, the fluid augments. The GCF has been evaluated and found to contain serum comp onents available in the blood but is comprised with the particular component in the periodontist because it is enriched with specific elements in the periodontitis. This is because of the infiltration and the inflammatory cells that reflect on the local metabolic nature of the periodontal tissues. Many techniques have been used to sample the GCF, and many have since been developed where more than 100 different components of have been examined for periodontal diagnosis (Paino et al. 2013). The LPS is a known virulence factor in the Gram-negative bacteria membrane that comprises of Lipids A, antigen O, and oligosaccharide that unites them all. In the three portions, lipid A is the component that triggers an inflammatory reaction. LPS is a potent activator of the innate immune system that it usually meets through influencing the toll-like receptor 4. The receptor is a cell surface that appreciates the products of the bacteria. On entering the blood circulation, the LPS triggers many biological responses that may include death. Different researchers have confirmed that the rise of the serum LPS in the periodontitis comes along with the increase in the risks to systematic problems. The LPS oral fungi have instilled the effect on many types of cell found in the periodontal tissues that include the lymphocytes and osteoclasts. An LPS binding protein is referred to as an acute stage reactant that has been synthesized by the hepatocytes that intervenes LPS movement to its rece ptors. The ignition of the CD14 receptor incites monocytes and endothelial cells through a TLR4-pathway that in turn produces the secretion of the prionflammatory molecules. The molecules later trigger the release of the secondary inflammatory mediators (Paino et al. 2011). Complement system The complement system is a collection of close to 30 proteins that take part on the destructions of tissues and in the inflammatory process. It can always be triggured by the option pathway or by the classical pathway. The complement activation is usually considered proactive technique in the immunity of the antibacterial. However, some of the products in the channel may destroy the tissues. Many components of the system are discovered in the GFC of the periodontal patients that are usually retrieved from the serum or are generated through system activation locally (Paino et al. 12013). Many research papers have pointed out the significance of the regime in the case of the periodontal infection and the role it is playing in the protection against the pathogenic bacteria. The activation of the substitute system is one of the pioneer host immune response in the cervical space in the gingival. The activation though varies with the depth of the effect of the inflammation and could assist in differentiating the different forums of periodontitis. The bacteria related to the periodontal infection have been declared to have distinguished techniques to dodge the complement system. Some strains come with polysaccharides on their surfaces masking the molecules activating the complement while promoting the affinity of the traces that inhibits the activity or development of a steric impediment (Vardar-Sengul Mercola, 2009). Antibodies and Immunoglobulins (Igs) These are glycoproteins that are synthesized by the B lymphocytes and plasma cells that have the property designed for binding to the antigen. The pathogens in the periodontitis generate marked humoral immune responses that will be measured locally in the saliva of in the GFC. The existence of the antibodies in the fighting the pathogens in the GFC has been displayed in the patients suffering periodontitis with the predominance of the IgG1where there is the low presence of the IgG2. Various binding antigens have been explored in different distinct groups. The differences can be in the immunoreactivity profile where they are related to the hydrocarbon molecules and proteins. However, there are still no clear immune-dominance models established for any of the pathogens or patient groups (Simone et al. 2011). Conclusion Periodontal disease is a chronic infection caused by bacteria affecting the gingiva and the bone supporting the teeth. It is a result of the response to the bacteria in the dental biofilm where most of them remain hosts to the gingival tissues where the tissues have minimal changes. The natural immune response entails the homeostatic system as the first defense line that can recognize the bacteria and triggers the immune systems to fight back. Along the innate immunity is the adaptive immunity cells believed to be critical in the pathogenesis scenes of the periodontal disease, the T-cells, and B-cells. The periodontal epithelium offers a physical barrier to the infection and also plays active roles in the host defense of the innate because the epithelial cells are usually in contact with the bacterial products. 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