Subgingival debridement reduces the risk of aggravated platelet activation and therefore might potentially diminish subsequent diseases such as cardiovascular disease in periodontal patients.
Platelets are involved in a variety of diseases, making their adequate functional assessment is essential. However, due to their easily activatable nature this has some methodological pitfalls. Therefore, the availability of stable, easily measurable surrogate markers would be beneficial. In this regard, some evidence suggests that certain microRNAs (miRNAs) circulating in plasma might be useful. We aimed to corroborate their suitability by analyzing plasma samples obtained in a randomized controlled trial, which assessed the effects of periodontal treatment on platelet function. We hypothesized that miRNA levels mirror changes of platelet activation and -function. Both platelet function and miRNA abundance were quantified using state-of-the-art flow cytometry and qPCR methods. The following miRNAs were quantified: 223-3p, 150-5p, 197-3p, 23a-3p, 126-3p, 24-3p, 21-5p, 27b-3p, 33a-5p, 320a, 191-5p, 28-3p, 451a, 29b-3p, and 1-3p. However, periodontal treatment did not affect the abundance of any investigated miRNAs to a relevant extent. Platelet activation and reactivity indices did neither correlate with any tested miRNA at baseline, nor after the treatment period. In addition, there was no evidence that investigated miRNAs were released by platelets, as suggested previously. In conclusion, our data suggest that in patients suffering from periodontal disease the investigated miRNAs are unlikely to be suitable biomarkers for platelet function. Our data aim to raise awareness that previously determined platelet activation dependent circulating miRNAs are not suitable as platelet biomarkers in all cohorts.
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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