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When the immune system is activated to eliminate oral irritants and prevent the spread of infection, its main objective is to recognize the antigen and communicate with the other cells to destroy it. This occurs when the PMN's and macrophages cannot destroy the invaders. The next step is the immune response, which consists of two parts to the reactions, the humoral immunity response and cellular immunity. Humoral immunity is effective against bacteria that are related to periodontitis. There are nine events that depict the humoral response to plaque accumulation, first the bacteria and by products accumulate in the gingival crevice and penetrate through the protective wall of Junctional epithelium and neutrophils, the inflammatory response is then triggered. Antigen substances are then carried to the lymph nodes and then are presented by B-cells and are recognized by their antigen and transform into plasma and memory cells. The plasma cells make antibodies and the memory cells remain inactivated. Antibodies are secreted into the bloodstream and are a part of the immunoglobulins. Once the antigens are destroyed the macrophages will stimulate repair and the memory cells remain in circulation. In cellular immunity, T-lymphocytes target and kill cells infected, T cells can cause alveolar bone loss through the production of interleukin 1, however this does not play an important role in periodontal disease. Various antigens such as endotoxins, bacterial enzymes and by-products that are present in the mass of plaque in the gingival crevice will pass through the wall of the PMN's. The activation of the inflammatory and immune system helps to eliminate harmful pathogens, prevent the spread of destruction and will begin to heal while still protecting the host, and if this fails disease will occur. In the oral cavity, the process of inflammation can accomplish an acute inflammatory response, and if the stimulus (plaque) is not removed, and healing does not occur, it will when become chronic and added defense cells become involved. In some cases the damage is permanent even after the infection is gone. Acute inflammation is caused by bacteria and will become chronic when it is unresolved. Various elements are involved in the inflammatory process such as neutophils, macrophages, mast cells, serum complement and Gingival Crevicular Fluid. There are three phases of the inflammatory process the first is the Acute Transient Phase which consists of local vasodilatation and an increased capillary permeability. The second phase is the Delayed Subacute Phase when migration of PMN's and phagocytic cells occurs. Lastly, the Chronic Phase which causes tissue destruction. Time lengths for gingivitis development vary; the initial onset is two to four days in which there is no attachment loss. Early stage is four to seven days clinical signs of redness, and bleeding are visible. Established stage onset is two to three weeks, and the gingiva can appear a bluish-red color and have increased probing depths. The most important sign of gingival inflammation is bleeding. Bleeding occurs when there is a disruption of the sulcus and junctional epithelium that allows the passage of blood from the lamia propria and into the sulcus. Neutrophils are the first line of defense. They migrate from the inside blood to the surrounding tissues and then enter the gingival crevice and junctional epithelium in response to chemotactic substances. Impaired PMN's are seen in patients with medical conditions such as aggressive periodonitits and diabetes. These PMN's engulf bacteria which when inside will leak, causing destruction of the tissues which in turn causes periodontal disease. Macrophages also known as monocytes are phagocytic. Macrophages remain after PMN's are gone and they function to clean up the body's damaged tissues as well as to secrete prostaglandins and cytokines. Macrophages function in periodontitis is to stay in the connective tissue for weeks up to months and keep the body's damaged tissues clean. The complement system also plays a role in periodontitis, as it works with the rest of the immune system to destroy the invaders and to signal to other immune system cells that the attack is occurring. For inflammation to be considered chronic it must be present for two to three weeks and can last for months even years due to an unresolved acute inflammation. Host responses are made up of bacterial components such as endotoxin and leukotoxin. The purpose of a natural host defense mechanism to defend and protect individuals after injury, bacterial or viral infections (Weinberg, Westphal, Froum, Palat, & Schoor, 2010).
Various substances such as endotoxins, leukotoxin which are gram negative bacteria are released from bacteria that effect the host. They release waste products such as ammonia which is toxic to host cells. They also secrete enzymes which can help with the breakdown of tissues. Matrix metalloproteinase are a family of enzymes that have components that break down the extracellular matrix. There are over 25 members including collagenases, gelatinases, stromelysins, matrilysins, and membrane type (MMPs). The bacteria and host cells synthesize the enzymes and prepare the tissues for absorption of toxic bacterial products. The defense mechanisms that exist around the periodontium in the oral cavity are saliva which contains various antibacterial factors. Gingival Cervicular Fluid functions as the cleansing system in the sulcus. The higher the flow of fluid the more antimicrobial products are delivered deeper into the tissue. The oral epithelium helps to prevent the bacteria by-products from entering the underlying tissues. The shedding of the epithelial cells also works as a defense mechanism in the oral cavity. If the body is unsuccessful in eliminating the pathogenic bacteria, the inflammatory system and immune response work together to stimulate and prevent the spread of infection. Antigens that are present in plaque mass are in the gingival crevice these antigens pass through the PMN protective wall and junctional epithelial barrier and penetrate further into the tissues. Very few bacteria will enter the connective tissue. It has been shown that Actinobacillus actinomycetemcomitans, Prophyromonas gingivalis and spirochetes are usually the bacteria that will invade the connective tissue. There are three steps in the activation of inflammatory and immune system, the first being the elimination of the invader, the second is limitation of further tissue destruction and the third is when the healing begins (Weinberg et al, 2010).
There are over 700 types of bacteria present in bioflims, yet roughly only 20 species are considered to be disease causing for periodontal diseases. Dental plaque is a thick nonmineralized mass of these bacteria. The only way to remove these bacteria is through tooth brushing and regular dental cleaning visits. Once removed, plaque can start reforming within two hours of removal. Calculus is basically hardened plaque; it also can form in the absence of bacteria. Calculus will first form on the top surfaces of your teeth and the process can take up to 12 days. However, it can start to build up in as little as 24-72hrs. Calculus, just like plaque, can also be removed through regular dental cleaning appointments. It is important to go for routine dental appointments to remove the calculus because if it is not removed it can lead to periodontal diseases. The calculus irritants the gums and the bacteria combined with the irritation are a major factor in periodontal disease. Gingivitis is the inflammation or swelling of the gums. When gingivitis occurs, there is no bone loss, but bleeding occurs. It is important to know that gingivitis can be reversed with regular oral self care such as regular toothbrushing and flossing. However, if not treated properly, gingivitis can lead to periodontitis. In periodontitis, bone loss occurs and it is irreversible. Dental plaque is the major risk factor in causing periodontitis. Bone loss occurs when the plaque goes deeper and deeper into the gums, pulling the gum tissue down with it. Bone loss is a major concern because once the bone is lost; there is no way of getting it back. Pockets of four mm or greater are a concern because they are a perfect environment for the plaque to migrate to. The deeper the pocket, the more difficult it is for you to clean your teeth. Ideally your pockets should range from one to three mm. With proper brushing and flossing the gum tissue can return back to being healthy again. Even though the bone will not grow back, the oral cavity can still remain healthy, and when healthy it will prevent any further bone loss from occurring. Other contributing factors can exaggerate the response to periodontitis such as hormones and different medications. So for an example a women who is pregnant may experience and exaggerated response to gingivitis, but after the baby is born the response would be a lot less then it was when she was pregnant. The best way of maintaining healthy gums and to eliminate any further bone loss is proper removal of the plaque. This is why a routine in oral self care is essential to help improve the health of your gums (Weinberg et al, 2010).
The level of tissue damage is dependent on the contact between plaque bacteria and host defense mechanisms. Various contributing factors such as calculus can promote the accumulation of dental biofilms. Systemic and local modifying factors may modify the host response to the bacterial challenge. Periodontal diseases have various risk factors; however, the primary risk factor is dental biofilm. Local and systemic factors also play a significant role as well. Dental plaque is a thick nonmineralized complex accumulation of bacterial colonies that live in a semi-solid intermicrobial matrix. Currently, the only way to remove dental biofilms is mechanically with tooth brushing, flossing, and scaling or root planning. If subginigival biofilm forms it cannot be removed by brushing or flossing only instrumentation will remove it. Over 700 kinds of bacteria are present in the oral cavity; however, only 20 of the species are considered pathogenic. Various criteria all play an important factor in periodontal diseases. Bacteria can be found in large numbers in advancing lesions or in small numbers at healthy or non-progressing sites. Clinical healing can occur by the elimination of the pathogen which is current prior to clinical changes. They produce a tissue reaction as well as are shown to produce disease in both animal and human experimental studies. Dental biofilm formation begins as the bacteria start to accumulate to the pellicle. Plaque formation begins in one to two days at this time it is gram positive and contain streptococcus mutans and streptococcus sanguis. The second phase of plaque formation begins two to four days and the bacteria involved are now gram positive rods and gram negative rods. The third phase begins four to seven days the plaque is now extending down near the coronal portion of the tooth and vibrios and spirochetes are now colonizing. Phase three continues over a period of seven to eleven days, at this time inflammation is at a subclinical level and the gingival is enlarged. Direct toxic effects of host cells are caused by cytotoxic agents which are found in gram negative bacteria, these bacteria initiate inflammation that causes soft tissue destruction and stimulates bone resorption. Endotoxins are released by bacteria such as actinobacillus actinomycetemcomitans these bacteria may cause damage by killing PMN's. Enzymes can adversely affect the gingival and periodontal tissues by building up in the tissues and destroying the connective tissue by breaking down the collagen and ground substance. Host-Derived enzymes are responsible for cleaving the collagen molecule and degrading proteoglycans. Various enzymes that break down periodontal tissue include: Collagenase, Hyaluronidase, Chondroitin, Proteases and Elastases. Indirect activation of host cells consists of immunopathologic mechanisms which can induce inflammation in the periodontal tissue by stimulating the immune response. It works in two ways, and has the potential to cause tissue destruction as well as being protective. Combined mechanisms are when more then one mechanism is involved in the commencement and progression of gingivitis and periodontitis. Transmission of pathogenic bacteria has been shown to occur between individuals. An example would be Actinobacillus actinomycetemcomitans may be transmitted from a parent to a child. It is most commonly transmitted through saliva (Weinberg et al, 2010).