Abstract
Periodontal disease is of inflammatory origin and affects the dental support tissues. The initial phase is characterized by the accumulation of biofilm, which is a predisposing factor for several oral pathologies. The combination of extrinsic factors such as lack of hygiene, smoking and diet, and intrinsic factors such as genetics, and major changes in the immune response associated with immune escape mechanisms of biofilm constituents are crucial to the development and progression of the disease, which when untreated entails local irreversible consequences that can lead to systemic changes. In this brief review, we describe general aspects of periodontal disease, its risk factors and ways of preventing the disease. In particular, we discuss some of the mechanisms of immune response to periodontal pathogens, as well as the escape mechanisms of these microorganisms.
Highlights
Periodontal disease is the most common oral condition of human population
By means of IFN-γ, which has a pro-inflammatory action, it leads to increased expression of toll-like receptors (TLRs), promotion of major histocompatibility complex (MHC) class I and II antigen presentation, induction of chemokine secretion, phagocytosis, activation of CD8+ T cells and free radicals that act against pathogenic microorganisms and tumor cells [50]
Periodontal disease is an immune-inflammatory condition caused by a polymicrobial structure, described as the dental biofilm
Summary
Periodontal disease is the most common oral condition of human population It affects about 20% to 50% of the population worldwide, with prevalence in men, especially those who live below the poverty line and are smokers [1] [2]. It is characterized by a chronical inflammation that can lead to the loss of the supportive tissues of affected teeth, considering the proteolytic activity of the infecting microbes and the cascade reaction of the immune system [3]. Failures that may occur in immune response against disease establishment are due to evasive mechanisms that may be exerted by pathogenic bacteria present in the sub-gingival biofilm
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