Inflammatory reaction - communication of cells

Abstract

This article presents scientific background information on the animated 3D film "Inflammatory Reactions - Communication of Cells" (Quintessence Publications, ISBN 978-1-85097-231-0). Gingivitis and periodontitis are understood as the result of a coordinated action of a few clearly identified cellular players who communicate with each other via cytokines. For didactic reasons, the course of a periodontal infection is described here in four phases: (1) bacterial biofilm formation and development of a host response in the marginal periodontium, (2) innate immune response leading to gingivitis, (3) role of the adaptive immune system in attachment loss and pocket formation, and (4) down-regulation of inflammation and periodontal regeneration and repair following biofilm removal. The control of the cells is discussed as a cytokine network, which can be modulated in pro- or anti-inflammatory direction depending on the control of the bacterial infection. Degradation of soft tissue structural proteins like collagen and proteoglycans by matrix metalloproteinases and degradation of hard tissue matrix by osteoclasts are explained as an interference of the immune system with the natural equilibrium of tissue remodeling. Five mechanisms of promotion of bone loss through the influence of the immune system are described. One example is bone resorption as a consequence of the shift of the RANKL/osteoprotegerin balance by soluble RANKL synthesized by CD4(+) Th 1 cells as well as the interference with the coupling of osteoclasts and osteoblasts through dedifferentiation of osteoblasts by TNFα. Finally, the signaling required for down-regulation of inflammatory reactions and the reasons for the incomplete regeneration after periodontal bone loss are discussed.

Keywords: RANKL; T lymphocytes; T-reg cells; TNFα; Th1 cells; adaptive immune system biofilm; bone resorption; cytokines; infection control; inflammatory reaction; innate immune system; osteoclastogenesis; periodontitis.