![]() CD4 T-cells are specialized to activate other cells and fall into two classes: T-helper cells (TH1), inflammatory cells, activate macrophages and TH2 cells activate B cells to start producing antibodies called immunoglobulins (Ig). CD4 T-cells recognize pathogens and their products derived from the cellular vesicular compartment. Cytosolic pathogens are eliminated by cytotoxic T-cells recognized via co-receptor CD8 (viruses and cytosolic bacteria). Dendritic cells engulf and degrade pathogens and maturate to antigen-presenting cells. Subsequently, adaptive immunity is triggered if the pathogens overcome innate immunity targeting to defend the host from potential pathogen invasion and actions. ![]() Complement components C3a, C4a and C5a are proinflammatory peptide mediators. This allows opsonization and destruction of microbes directly or indirectly by the phagocytes. Activation of the complement system occurs, and recognition of microbes follows three different pathways (classical, manna-binding -lectin, alternative). Natural killer (NK) cells contain and kill intracellular pathogens until cytotoxic T-cells are generated. Inflammation-related molecules have been extensively reviewed by Joseph et al. Macrophages engulf microbes fusing with lysosomes to lyse microbes and release toxic and oxidative products (e.g., hydrogen peroxide, superoxide anion, nitric oxide) and at the same time, proinflammatory prostaglandins, leukotrienes and platelet-activating factor (PAF), proinflammatory cytokines (e.g., TNF-α, IL-1, IL-6, IL-12) and chemokines (e.g., monocyte chemoattractant protein (MCP-1)) to attract neutrophils to extravasate and migrate, in order to degranulate to sites of inflammation. ![]() Pathogen recognition triggers inflammatory responses, i.e., “circulus vitious inflammationis”. Monocytes differentiate to macrophages and their receptors recognize microbial surface components: e.g., mannose, glucan, or lipopolysaccharide. The first few hours of interaction with antigenic microbes trigger the host innate immunity. Innate and Adaptive Immunity and Inflammation Infections may develop from low grade inflammation to acute infections and even proceed to life-threatening sepsis.Ģ. Carious, periodontal, candidal or viral infections may follow if defense mechanisms of the host are insufficient and defective. Local tissue oxidative, nutrient or pH conditions may also often favor the coaggregation tendency of certain bacterial species in biofilm formation. The periodontopathogenic bacteria belonging to the red triad ( Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola) are found and occur due to advanced periodontal disease. mitis), and subsequently the secondary colonizers, which tend also to favor anaerobic growth conditions. VPI (visible plaque index), BOP (bleeding on probing), aMMP-8 (active matrix metalloprotease-8).Īfter birth, the oral normal microbiome starts to build up with primary microbial species colonizers, which are mainly Viridans group streptococci : Streptococcus salivarius ( S. Illustration of some factors affecting healthy and diseased state in the oral environment. Broad-spectrum antibiotics may also disturb and interfere with the normal microbiome long after treatment has ended. In the case of, e.g., host immunodeficiency, a dysbiotic microbiome with opportunistic pathogen overgrowth may occur, resulting in a diseased state. The microbial load could be seen as an indicator of the risk in a patient of developing a diseased state initially, high counts of opportunistic pathogens and predisposing factors, e.g., systemic disease, medications and low or immune incompetent saliva, do not tend to overcome the “reservoir” or tolerance of the individual to stay healthy. The main predisposing factors for a dysbiotic microbiome, and consequently predisposition to a diseased state in the oral cavity, are summarized in Figure 1. The normal microbiome competes constantly with pathogenic or opportunistic bacteria, yeasts and viruses for nutrients and attachment sites on host cells. Microbiome research acknowledges the concept of a symbiotic/dysbiotic microbiome in health and disease.
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