Microbiological, pathological, inflammatory, immunological and molecular biological aspects of periradicular disease.

Multimicrobial infection of the dental pulp triggers inflammatory responses and ultimately causes bone destruction in the periradicular tissues. Besides bacteria, noxious substances such as degraded protein components and cholesterol could also act as antigens and elicit a host response, which can be harmful to periradicular tissues. Histologically, a dense infiltration of immunocompetent cells is seen in periradicular lesions and their host reactions may induce bone resorption. Polymorphonuclear leucocytes (PMN) and macrophages migrate to the periapical lesions and phagocytose pathogens as a first line of defence. Dead PMN are quickly phagocytosed by macrophages and this disposal system plays a role in maintaining chronicity of the lesions. The pathological roles of periradicular T cells have been assessed through analysing phenotypic markers of cell types, especially CD antigens, but the results are still controversial. Recently, technical developments in immunology and molecular biology have made it possible to investigate the pathogenesis of many diseases at molecular level. The investigation of functional analysis of the immune cells and their regulatory molecules such as apoptosis-associated molecules and adhesion molecules, will lead to a better understanding of the pathogenesis of periradicular lesions. The role of inflammatory mediators including antibodies, cytokines, matrix metalloproteinases, growth factors and arachidonic metabolism is becoming known for these lesions. Knowledge from these investigations improve the understanding of the pathological mechanisms of periradicular infections.