Recent advances in periodontitis, a prototypic osteo-immunological disease

Abstract

Periodontitis is a highly prevalent infect-inflammatory disease that can lead to bone destruction, tooth mobility and finally, tooth loss if left untreated. The pathophysiology of bone loss in inflammatory conditions, such as periodontitis, has not been completely elucidated yet, but it appears that inflammation shifts the balance between bone resorption and bone formation in favor of bone loss. Besides the classical T helper cell populations (Th1 and Th2), which contribute to periodontitis, new T cell subsets have been defined and are now implicated in the pathogenesis of periodontitis. Th17 cells are strongly correlated with tissue destruction while regulatory T cells (Tregs) act as immune-modulatory cells. In addition to control immune reactions, several immune cell types directly affect bone cell activity, promoting bone resorption and suppressing bone formation. In this context, the RANKL/OPG (receptor activator of nuclear factor κB ligand/osteoprotegerin) ratio is increased in the inflamed periodontium, which stimulates osteoclastogenesis and bone resorption. More recently, inflammation has been associated with suppressed osteoblast differentiation and bone formation which is at least partially dependent on reduced Wnt signaling. This review aims to highlight the role of host response in inflammatory bone loss during periodontitis, emphasizing the role of Th17 and Treg cells and their relationship with RANKL/OPG and Wnt signaling, in order to better understand the network between skeletal and immune systems from the periodontal point of view.