Modulation of osteoclastogenic factors expression and their inhibitors by CCR5+ cells in experimental periodontal disease

Abstract

Periodontal diseases are trigerred by putative Gram-negative periodontopathogens, such as Actinobacillus actinomycetemcomitans. The host responses to periodontopathogens are thought to be protective against infection, but may trigger periodontal destruction. The disease outcome is determined by the nature of host inflammatory and immune reaction, which involves the participation of several cell types and mediators. Inflammatory cytokines, chemokines and their receptors are thought to be involved in the recruitment of leukocytes to the periodontium. However, the exact mechanisms involved in mediate resistance or susceptibility to periodontitis development are not kwon. Previous studies demonstrate the presence of CCR5+ cells in periodontal lesions of humans, as well in the tissues of mouse, in our experimental model. Furthermore, the presence of CCR5+ cells presents positive correlations with high levels of RANKL. In this project, we will evaluate the role of CCR5+ cells in the outcome of experimental periodontal disease induced by A. actinomycetemcomitans in mice evaluating the modulation of osteoclastogenic factors expression by means of RealTimePCR. To our aims, the mice from the experimental groups will be evaluated regarding the disease severity, through the quantification of alveolar bone loss and of the inflammatory infiltrate and RANKL, OPG e CatepsinK expression. Taken together, these data will contribute to the knowledge of role of immune responses to the outcome of periodontal diseases, and may provide the basis for future therapeutic interventions aimed at limiting the inflammatory process in these pathologies.