The Role of Chemokines and Cytokines in the Pathogenesis of Periodontal and Periapical Lesions: Current Concepts

Abstract

The oral cavity is a complex environment that may harbor more than 750 bacterial species. Proper oral hygiene is essential to maintain the equilibrium of microbial community and oral health. The ecological balance can be compromised in inadequate microbial control situations and an oral infection can be evoked. The bacteria can aid in the formation of dental plaque and caries, leading to periodontal disease (PD) and periapical lesion (PL). PD is the most common chronic inflammatory disorder of microbial origin that affects toothsupporting tissues including the periodontal ligament and the alveolar bone. Dental caries is characterized by demineralization of enamel and dentine produced by microorganisms’ acids. This process can cause pulp necrosis and root canal infection and the progression through the root apex can induce PL. PD and PLs constitute inflammatory and immune response against oral pathogens. Both processes encompass pathogenic mechanisms of inflammation-mediated soft tissue destruction and bone resorption. The etiopathogenesis of these diseases have been extensively investigated over the last decades and the role of several cell types, cytokines and pathways has been described (Graves, 2008, Graves et al., 2011a, Nair, 1997). Last decades research have documented the importance and commitment of immune system to protect the host from pathogen and also the paradoxical effect accounting for the bone resorption observed in these diseases. More recently, the pattern of immune cell response involved in the lesions progression (i.e. Th1, Th2, Th17, Th9 or T regulatory) has received particular attention (Cardoso et al., 2009, Colic et al., 2009a, Gaffen & Hajishengallis, 2008, Ohlrich et al., 2009, Queiroz-Junior et al, 2011). Although chemokines and cytokines are pivotal to determine these Th patterns, not much is known regarding the expression of these markers in the regulation of bone resorption in sites of PD and PL. This