Tissue destruction in periodontitis: bacteria or cytokines fault?
The pathogenesis of periodontal disease involves the sequential activation of a great variety of components of the host immune response, primarily acting to defend periodontal tissues against bacterial aggression, but also functioning as mediators of tissue destruction. The expression of the disease results from the interaction of host, microbiological agents, and environmental factors. Leukocytes play a critical role in the pathogenesis of the disease, producing different cytokines, chemokines, and other mediators, thus generating a host defense response, as well as inducing tissue inflammation and bone destruction. The aim of this review is to address the role of some inflammatory mediators in response to bacterial aggression in periodontitis.
Bascones
Antonio
A
Department of Stomatology, School of Dentistry, University Complutense of Madrid, Madrid, Spain. avances@arrakis.es
Noronha
Susana
S
Gómez
Maria
M
Mota
P
P
Gónzalez Moles
M A
MA
Villarroel Dorrego
Mariana
M
D016207:Cytokines / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D007375:Interleukin-1; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D015232:Dinoprostone