Present and Future Non-Surgical Therapeutic Strategies for the Management of Periodontal Diseases

Abstract

Periodontal disease is a chronic bacterial infection of the periodontium affecting the tissues surrounding and supporting the teeth. Periodontal disease progression is associated with subgingival bacterial colonization and biofilm formation principal to chronic inflammation of soft tissues, degradation of collagen fibers supporting the tooth to the gingiva and alveolar bone, as well as resorption of the alveolar bone itself. Since the fundamental role of microorganisms in its etiology was systematically demonstrated some forty years ago, research efforts have long focused on identifying the pathogenic microorganisms and their virulence factors (Socransky and Haffajee, 1994). The search for these putative microorganisms was driven, in part, by knowledge indicating that colonization of the oral cavity and presence of dental biofilm is normally associated with health, similarly to the colonization of the colon. To treat periodontal diseases as an infectious disease, numerous therapeutic strategies aimed at eradication of periodontal pathogens have been studied over the years, including local and systemic delivery of antimicrobial and antibiotic agents. This review will cover an update on chemotherapeutic agents used adjunctively to treat and manage periodontal diseases. In the current paradigm of periodontal disease, specific periodontal pathogens are necessary for disease initiation; however, the extent and severity of tissue destruction are largely dependent on the nature of the host-microbial interactions. These interactions are dynamic, since both the microbial composition of the dental biofilm and the competency of host immune responses can vary, in the same individual, over time. This concept was developed in parallel to the advances on the understanding of the immune response, and research on periodontal disease has been emphasizing mechanisms of host-microbial interactions to understand the disease process, as well as for the development of novel therapeutic strategies. For the past two decades, the host response to the bacterial challenge originating from the dental biofilm has been considered to play a major role on both initiation of the disease and on the tissue destruction associated with its progress (Kirkwood, et al., 2007). The importance of host-microbial interactions is reinforced by epidemiological data indicating different susceptibilities to periodontal disease among individuals, in spite of the