Before a discussion of the control of gingivitis, it is necessary to first grasp how inflammation occurs, and its relevance to disease in the periodontium. The word inflammation brings to mind imagery of ‘angry-looking’ tissue. Underlying and precipitating that surface manifestation lies a complex reactionary microcellular process that serves as a biologic defense operation to attack pathogenic microorganisms and other injurious or irritating stimuli. Within body systems, an external threat triggers the release of inflammatory mediators to attenuate or destroy it, and in the process causes characteristic signs of acute inflammation (e.g., heat, edema, erythema, exudate, pain).
The initial step in the inflammatory process involves threat recognition. Cells in bodily tissues functioning as ‘look-outs’ scan for probable irritants/injurious agents and detect that the invaders have unique patterns that differ from the host. This propels the recruitment phase of inflammation, where host inflammatory mediators like cytokines are mobilized, and bring about an immune response through vascular and cellular permeability effects.13,14
While inflammation has benefit as a protective and restorative healing mechanism in acute local reactions, when unresolved, inflammation can become chronic. Pro-inflammatory cytokines are implicated in the development pathways of serious systemic health conditions including Type 2 diabetes, cardiovascular disease, and adverse pregnancy outcomes.15-17 These and other chronic inflammations – including oral health related – may result in irreversible damage unless there is intervention.
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