Part of the book: HLA and Associated Important Diseases
Periodontitis is a chronic inflammatory condition characterized by destruction of non-mineralized and mineralized connective tissues. The pathogenesis of periodontitis involves a complex interplay between periodontopathogens and the host immunity, greatly influenced by genetic and environmental factors. Failure in the inflammation resolving mechanism leads to establishment of a chronic inflammatory process, resulting in the progressive destruction of bone and soft tissue. The aim of this chapter is to summarize the role of innate and specific immune response involved in pathogenesis of periodontitis. Cells and inflammatory mediators, those participating in inflammatory process of the ligamentous supporting structure and in resorption of alveolar bone, will be presented.
Part of the book: Periodontitis
Several genetic polymorphisms in immune response genes have been associated to leprosy. This fact converges on the main hypothesis that genetic factors are involved in the disease susceptibility in two distinct steps: leprosy per se and their clinical forms. These genes play an important role in the recognition process, in the activation of the main metabolic pathway of the immune response and in the evolution of the disease. The scope of this project was to highlight the role of the immune response genes in the context of leprosy, emphasizing the participation of some of them in the signaling and targeting processes in response to bacillus infection and on disease evolution, such as HLA, KIR and MIC genes. Some environmental and genetic factors are important when the exposure to the bacillus occurs, leading to cure or not. Factors that favor a cellular or humoral immune response may influence the clinical manifestations after the infection inducting to one of extreme poles. Furthermore, some genetic factors were associated to the type of reaction that some individuals present during the disease development. Thus, it is very important to highlight the participation of some genetic factors in the immunopathogenesis of leprosy.
Part of the book: Hansen's Disease