Periodontal pathogens in plaque biofilm initiate periodontitis, which is influenced by genetic and environmental
factors. The resultant pro-oxidant status imposed on the periodontium, exacerbated by episodic hyperinflammatory
damage contributes to progression of periodontitis and tooth loss in susceptible subjects. Increasing documentation
of bi-directional connections between periodontal and cardiometabolic disorders makes it an intriguing area of
therapeutic intervention for mutual benefit. Periodontitis and associated comorbidities demonstrate similar risk markers of
inflammation during disease progression. Depending on the extent and severity of the inflammatory response, periodontitis
could impact significantly on systemic inflammatory loading and influence the progression of endothelial dysfunction,
atherosclerotic plaque instability, dyslipidaemia and insulin resistance. Some of the common mechanisms involved are
discussed, relevant to periodontal and cardiometabolic disorders which have been documented as having a bidirectional
relationship with periodontal disease progression; abating in response to treatment. Periodontal disease may be a useful
marker of a susceptible immune system, or directly affect the progression of systemic diseases due to inflammatory loading.
These mechanisms mediated by coordinated actions of cytokines, acute phase proteins, enzymes and their sequelae
are addressed in the context of conventional periodontal therapy and its outcome with a modulatory role on metabolic diseases.
Applications for the role of nutritional and therapeutic antioxidants as adjuncts in diseases with a distinctly prooxidant
profile are discussed. Accurate therapeutic targeting as an adjunct to conventional periodontal treatment in this
context, for mutual benefit to subjects with periodontitis and cardiometabolic diseases is a challenge.
Keywords: Periodontitis, cardiometabolic disorders, oxidative stress, lipid peroxidation, risk markers, nutritional antioxidants, statins, therapeutic targets, Periodontal pathogens, genetic and environmental factors, cardiometabolic disorders, systemic inflammatory, endothelial dysfunction, cytokines
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