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Background. To improve the efficacy of regenerative treatment for gingival recessions, the autologous platelet concentrates (APCs) combined with coronally advanced flap (CAF) have been investigated. However, few studies systematically assess the complementary effect of APCs in periodontal regeneration. The present study aims to evaluate the additional effect of different types of APCs to CAF in the treatment of gingival recessions. Methods. Electronic databases (EMBASE, MEDLINE, and Cochrane Central Register of Controlled Trails) and relevant journals were searched until May 15, 2019. Only randomized controlled trials (RCTs) in English were included. Outcome variables include root coverage (RC), recession depth (RD), clinical attachment level (CAL), keratinized tissue width (KTW), and gingival thickness (GT). Data were analyzed with Revman5.3. The estimate of effect sizes was expressed as the mean differences and the 95% confidence interval. Results. 8 RCTs involving 170 patients (328 sites) were included. Our meta-analysis indicated RC, RD, CAL, KTW, and GT were better improved in the CAF plus APCs groups than the CAF alone. The subgroup analyses revealed that platelet-rich fibrin (PRF) brought significant improvement in RC, RD, CAL, and GT. Concentrated growth factors (CGF) lead clinic beneficial in CAL, KTW, and GT. No significant effect of platelet-rich plasma (PRP) could be found in any clinical parameters when combined with CAF. Conclusions. PRF could exert additional effect to CAF; the preferred treatment for gingival recessions was considered. Based on the limited studies, it seemed that PRP failed to show any additional effect and it was not suggested for gingival recessions. Given the limited research and high risk of bias, it is still needed to confirm the additional effect of CGF by more high-quality studies.

BackgroundPorphyromonas gingivalis (P. gingivalis), one of the main pathogenic bacteria involved in periodontitis, induces the expression of intercellular adhesion molecule − 1 (ICAM-1) and monocyte-endothelial cell adhesion. This effect plays a pivotal role in atherosclerosis development. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine and critically affects atherosclerosis pathogenesis. In this study, we tested the involvement of MIF in the P. gingivalis ATCC 33277-enhanced adhesive properties of endothelial cells.ResultsEndothelial MIF expression was enhanced by P. gingivalis ATCC 33277 infection. The MIF inhibitor ISO-1 inhibited ICAM-1 production in endothelial cells, and monocyte-endothelial cell adhesion was induced by P. gingivalis ATCC 33277 infection. However, the addition of exogenous human recombinant MIF to P. gingivalis ATCC 33277-infected endothelial cells facilitated monocyte recruitment by promoting ICAM-1 expression in endothelial cells.ConclusionsThese experiments revealed that MIF in endothelial cells participates in the pro-atherosclerotic lesion formation caused by P. gingivalis ATCC 33277 infection. Our novel findings identify a more detailed pathological role of P. gingivalis ATCC 33277 in atherosclerosis.

Porphyromonas gingivalis ( P. gingivalis ) is an important pathogen that contributes to periodontal disease and causes infections that promote the progression of atherosclerosis. Our previous studies showed that macrophage migration inhibitory factor (MIF) facilitates monocyte adhesion to endothelial cells by regulating the expression of intercellular adhesion molecule-1 (ICAM-1) in P. gingivalis- infected endothelial cells. However, the detailed pathological role of MIF has yet to be elucidated in this context. To explore the functional receptor(s) of MIF that underlie its participation in the pathogenesis of atherosclerosis, we investigated the expression of the chemokine receptors CD74 and CXCR4 in endothelial cells, both of which were shown to be involved in the adhesion of monocytes to endothelial cells pretreated with P. gingivalis . Furthermore, the formation of a MIF, CD74, and CXCR4 ligand-receptor complex was revealed by our immunofluorescence staining and coimmunoprecipitation results. By interacting with the CD74/CXCR4 receptor complex, MIF may act as a crucial regulator of monocyte-endothelial cell adhesion and promote the atherosclerotic plaque formation induced by P. gingivalis .

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