Periodontal treatment does not result in detectable platelet activation in vivo

Abstract

Objectives Periodontitis is associated with systemic inflammation, elevated platelet activation and enhanced risk for cardiovascular diseases, while periodontal treatment reduces tissue inflammation and shows desirable effects on the oral biofilm and dental health. However, subgingival debridement during conservative treatment can lead to local trauma and transient bacteraemia, which might affect cardiovascular risk in these patients. Therefore, we investigated the effect of periodontal treatment on systemic platelet activation. Materials and methods In a prospective therapeutic trial, 26 patients underwent periodontal treatment and patient blood was analysed immediately before and immediately after intervention for platelet activation markers (flow cytometric analysis of Pselectin, CD63 and CD40L surface expression, integrin αIIbβ3 activation and fibrinogen binding, intra-platelet reactive oxygen species production, platelet-leukocyte aggregate formation and intra-platelet vasodilator-stimulated phosphoprotein phosphorylation) in response to adenosine diphosphate (ADP). Results The present study shows that basal platelet activation levels remain largely unaltered in response to periodontal treatment. We also did not observe significant changes in platelet reactivity in response to different concentrations of platelet agonist ADP. Conclusion Subgingival debridement does not result in relevantly elevated platelet activation. Thus, augmented platelet activation seems unlikely to be a causative triggering factor that increases the short-term risk for platelet-mediated thrombotic events in response to subgingival debridement. Clinical relevance Subgingival debridement is a safe procedure and does not increase the short-term risk for platelet-mediated thrombotic events.

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“… 3 Moreover, increasing reports support that periodontitis is an important cause to aggravate inflammation, which is closely related to the development of cardiovascular diseases. 4 Basic therapy of periodontitis mainly focuses on inhibiting inflammation via the management of the oral biofilm. 5 However, there are still no clinically effective treatment methods specific to periodontitis.…”