The role of the immune system in periodontal disease
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The role of the immune system in periodontal disease has been well established. Individuals who smoke are more prone to developing periodontitis because of the excess plaque buildup and the immune system's attack of the bacteria on the gingiva. This study aims to examine the role of immunotherapy in the reversal of periodontal disease in individuals who smoke. Further research will not only assist with the reversal of periodontitis, but may also improve other debilitating co-morbid diseases including autoimmune diseases such as human immunodeficiency virus. To examine this question, a variety of research studies from various sources were examined. There are numerous factors, which contribute to the initiation and progression of periodontal disease. Use of nicotine products enhances the accumulation of plaque formation. Accumulation of large amounts of plaque and calculus assist in the progression of periodontal disease. Disease of the gingiva may lead numerous other debilitating diseases such as respiratory infections, Alzheimer's disease and unfavorable pregnancy outcomes. Two components of the immune system play a major role in gingival inflammation observed in smokers; these include cytokine production and inflammation. The concentration of pro-inflammatory cytokines released from the macrophages of smokers is significantly higher than that observed in non-smokers. Pro-inflammatory cytokines, such as TNF-alpha, are responsible for inflammation of the gingiva. The use of pre-existing immunotherapy treatments may be beneficial and assist in the reversal of periodontal disease. Further researcher on immune therapy, which has been shown to be successful in other disease treatments will not only be beneficial for the oral cavity, but for overall systemic health. Both immune and bacterial components should be taken into consideration when developing therapies for periodontal disease. Pro-inflammatory cytokines such as TNF-alpha are dramatically increased in smokers. Researchers should model therapies after existing therapies that have been successful for other diseases such as immunotherapy studies with lamvidine (Hepatitis B), lambrolixumab (melanoma) and infliximad (oral plaque). The mTOR signaling pathway controls the release of pro-inflammatory and anti-inflammatory cytokines. Deletion of the raptor protein causes more inflammation in the colon due to an increased release of pro-inflammatory cytokines. Therapies which directly act upon this signaling pathway should be further researched upon to reverse the effects of periodontal disease. Chromogranin A release showed a significant increase in smokers because of the body's ability to want to automatically attach the harsh environment created by tobacco. Modulating the immune response induced by Chromagranin A or possibly through the use of anti-TNF-alpha therapies which have shown success in patients with rheumatoid arthritis also is open to future research. The shift from gram-negative to gram-positive bacteria was noted in periodontal disease patients. The less diverse bacteria lead to the loss of the ability of ligaments to attach to one another in the oral cavity. The development and testing of bacteria specific antibiotics such as Fusobacterium, Prevotella, and Selenomonas may prove to be very beneficial. There is much optimism among the dental professionals that immunotherapy may lead to the development of future therapies for periodontitis in both smokers and non-smokers. However we must also encourage patients to stop smoking through awareness and education.