The cholesterol-lowering drugs, statins, possess anti-inflammatory, antimicrobial and pro-osteogenic properties, and thus have been tested as an adjunct to periodontal treatment. The present systematic review aimed to answer the following focused research question: What is the effect of local and/or systemic statin use on periodontal tissues in preclinical in vivo studies of experimentally induced periodontitis (EIP) and/or acute/chronified periodontal defect (ACP) models? A literature search (of Medline/PubMed, Embase/Ovid, CENTRAL/Ovid) using the following main eligibility criteria was performed: (i) English or German language; (ii) controlled preclinical in vivo trials; (iii) local and/or systemic statin use in EIP and/or ACP models; and (iv) quantitative evaluation of periodontal tissues (i.e., alveolar bone level/amount, attachment level, cementum formation, periodontal ligament formation). Sixteen studies in EIP models and 7 studies in ACP models evaluated simvastatin, atorvastatin or rosuvastatin. Thirteen of the EIP (81%) and 2 of the ACP (29%) studies presented significantly better results in terms of alveolar bone level/amount in favor of statins. Meta-analysis based on 14 EIP trials confirmed a significant benefit of local and systemic statin use (P < .001) in terms of alveolar bone level/amount; meta-regression revealed that statin type exhibited a significant effect (P = .014) in favor of atorvastatin. Three studies reported a significantly higher periodontal attachment level in favor of statin use (P < .001). Complete periodontal regeneration was never observed; furthermore, statins did not exert any apparent effect on cementum formation. Neither local nor systemic use of statins resulted in severe adverse effects. Statin use in periodontal indications has a positive effect on periodontal tissue parameters, supporting the positive results already observed in clinical trials. Nevertheless, not all statins available have been tested so far, and further research is needed to identify the maximum effective concentration/dose and optimal carrier.

Sinupret extract can safely be administered in patients with CRS. Although the primary endpoint of the study was not significant, a post-hoc subgroup analysis in patients whose disease was diagnosed by a specialist revealed a pronounced treatment effect. Effects in that subgroup were even stronger with longer disease persistence and stronger severity.

Recent researches suggest an association between periodontitis and cardiovascular disease. Periodontopathic bacteria and/or their component might play a role in the development of atherosclerotic lesions. In the present study, we investigated in vitro the effect of Porphyromonas gingivalis lipopolysaccharide (LPS) on the expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs) as well as its effect on Escherichia coli LPS-induced response. The effect of P. gingivalis LPS was compared with that of toll-like receptor 2 agonist synthetic triacylated lipoprotein Pam3-Cys-Ser-(Lys)4 (Pam3CSK4). Gene and protein expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin were measured using RT-PCR and flow cytometry, respectively. P. gingivalis LPS stimulated the expression levels of all adhesion molecules in a dose-dependent manner. However, the response of HUVECs to P. gingivalis LPS was markedly lower than that to E. coli LPS. Moreover, P. gingivalis LPS attenuated E. coli LPS-induced responses when HUVECs were simultaneously stimulated with both kinds of LPS. Treatment with Pam3CSK4 resulted in a minor increase of adhesion molecule expression and did not diminish E. coli LPS-induced responses. Our data suggest that P. gingivalis LPS induces in vitro the expression of adhesion molecules in endothelial cells, which might promote atherogenesis. Qualitatively different responses of HUVECs to P. gingivalis LPS and Pam3CSK4 suggest that besides TLR2 other signaling pathways might be involved in the effects of P. gingivalis LPS.