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Review article

Recent advances in periodontology

Andrej Aurer

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page 49-59

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Available information on periodontal diseases are numerous, ambiguous and for the most part highly specialised. Through the years most of the research was focused on the microbiological aspects of the periodontitis. It has been noticed that bacteria alone are not sufficient for the initiation of periodontal diseases, although they play an important part in the process. Host response, smoking, stress and other risk factors influence the appearance of the disease, and the susceptibility to aggressive forms of periodontitis is genetically determined. This knowledge brought significant changes to the concept of etiology, prevention and the treatment of periodontal diseases. There is a huge amount of data on the bacterial role in the initiation of periodontal pockets, changes in the junctional epithelium, destruction of periodontal ligament and resorption of the alveolar bone. The bacteria play an indirect role in the tissue destruction, through activation of the host response which becomes pathological. It seems hard to believe that the same host response factors are responsible both for the defence, as well as the appearance of the disease. Therefore one of the basic questions that can be asked today is why isn’t the periodontal disease self –limiting in its nature, or why doesn’t it stop spontaniously. The studies done in the last years are trying to explain this phenomenon by means of molecular and cellular regulatory mechanisms. The studies using multi-variate analysis indicate that the bacterial components participate in the disease expression with a relatively low percentage. Host response factors are at least as, if not more important in the initiation of periodontitis. The complex interaction of the bacterial challenge and native and acquired immunity determine the final outcome of the disease.
Progress in understanding the molecular basics of the disease in the last decade has led to a better understanding of the process of the disease.


periodontitis; oral microbiome; host response; immunomodulation

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