Hepatitis C virus (HCV) infections could have an important impact on the oral health status of patients, favoring conditions such as periodontal disease and oral cancer. The review of the existing scientific literature written in English was performed, searching for oral and periodontal manifestations of HCV infection and its impact on the oral fluids. HCV infection can determine direct extrahepatic manifestations at the oral and periodontal level including oral lichen planus, Sjögren-like sialadenitis, and oral cancer. The changes caused by the infection in the subjects' immune system, diet, and lifestyle can facilitate the development of oral conditions such as periodontal disease. Important changes also occur in the composition of the infected patients' saliva and gingival fluid. HCV-infected patients need to be carefully monitored in terms of oral health since the infection with the virus can result in oral complications. The cellular and molecular particularities of the gingival fluid of HCV-infected patients can answer some questions regarding its impact upon periodontium impairment and whether this refers to a possible bidirectional relationship, with hepatic biomarker adjustments being induced by the periodontal patients' inflammatory status.

(1) Background: The aim of this split-mouth design study was to analyze the clinical periodontal indexes and oxidative stress markers in gingival crevicular fluid modifications after three periodontal disease treatment possibilities (scaling and root planning—SRP; SRP and diode laser—L; SRP and photodynamic therapy—PDT). (2) Methods: The study was conducted on 52 patients: systemically healthy subjects with periodontal disease—non-RA (n = 26); and test group (n = 26) subjects with rheumatoid arthritis and periodontal disease—RA. Clinical periodontal measurements (probing depth—PD; Löe and Silness gingival index—GI; papillary bleeding index—PBI; and periodontal community index of treatment needs—CPITN) and oxidative stress markers (8-hydroxy-2’-deoxyguanosine (8-OHdG) and 4 hydroxynonenal (4-HNE)) were analyzed at baseline (T0), after three sessions of periodontal treatment (T1), and 6 months after treatment (T2). (3) Results: Periodontal therapy improved clinical periodontal measurements and oxidative stress markers in both analyzed groups, with supplementary benefits for laser- and PDT-treated periodontal pockets. (4) Conclusions: The analyzed oxidative stress markers decreased significantly following non-surgical periodontal therapy in both rheumatoid arthritis and systemically healthy patients. All the periodontal disease treatment possibilities analyzed in this study offered clinical and paraclinical improvements; however, the association of laser with SRP and photodisinfection with SRP yielded the best clinical and paraclinical outcomes when compared to SRP alone.

Background. Wound healing is a tissue repair process after an injury, and two of its main components are inflammation and angiogenesis, in which course a cascade of mediators is involved. The aim of this research was to evaluate the involvement of Pentraxin 3 and Thrombospondin 1 in wound healing after periodontal surgery (gingivectomy) for gingival overgrowth during orthodontic treatment with or without magnification devices, by assessing their levels in GCF. Methods. From 19 patients with gingival overgrowth as a result of fixed orthodontic treatment, the overgrown gingiva was removed by gingivectomy, from one half of the mandibular arch without magnification and from the other under magnification. Pentraxin 3 and Thrombospondin 1 were determined from gingival crevicular fluid by ELISA tests. Results. Statistically significant differences (p < 0.05) and correlations between levels of the two biomarkers were analyzed. Statistically significant differences were established between levels of the two biomarkers at different time points, with significant positive correlation at the point of 24 hours. Conclusions. Within the limitations of this study, the results seem to sustain the involvement of Pentraxin 3 and Thrombospondin 1 in the processes of inflammation and angiogenesis in wound healing of patients with postorthodontic gingivectomy. The dynamics of Pentraxin 3 and Thrombospondin 1 levels could suggest a reduced inflammation and a faster angiogenesis using microsurgery.

Purpose. Nontraditional cardiovascular risk factors as apolipoprotein A (ApoA), apolipoprotein B (ApoB), and the proprotein convertase subtilisin/kexin type 9 (PCSK9) increase the prevalence of cardiovascular mortality in chronic kidney disease (CKD) or in end-stage renal disease (ESRD) through quantitative alterations. This review is aimed at establishing the biomarker (ApoA, ApoB, and PCSK9) level variations in uremic patients, to identify the studies showing the association between these biomarkers and the development of cardiovascular events and to depict the therapeutic options to reduce cardiovascular risk in CKD and ESRD patients. Methods. We searched the electronic database of PubMed, Scopus, EBSCO, and Cochrane CENTRAL for studies evaluating apolipoproteins and PCSK9 in CKD and ESRD. Randomized controlled trials, observational studies (including case-control, prospective or retrospective cohort), and reviews/meta-analysis were included if reference was made to those keys and cardiovascular outcomes in CKD/ESRD. Results. 18 studies met inclusion criteria. Serum ApoA-I has been significantly associated with the development of new cardiovascular event and with cardiovascular mortality in ESRD patients. ApoA-IV level was independently associated with maximum carotid intima-media thickness (cIMT) and was a predictor for sudden cardiac death. The ApoB/ApoA-I ratio represents a strong predictor for coronary artery calcifications, cardiovascular mortality, and myocardial infarction in CKD/ESRD. Plasma levels of PCSK9 were not associated with cardiovascular events in CKD patients. Conclusions. Although the “dyslipidemic status” in CKD/ESRD is not clearly depicted, due to different research findings, ApoA-I, ApoA-IV, and ApoB/ApoA-I ratio could be predictors of cardiovascular risk. Serum PCSK9 levels were not associated with the cardiovascular events in patients with CKD/ESRD. Probably in the future, the treatment of dyslipidemia in CKD/ESRD will be aimed at discovering new effective therapies on the action of these biomarkers.

Periodontal tissues exhibit important vascular, lymphatic, and nervous connections with the rest of the body. Thus, periodontal inflammation caused by the interaction between the subgingival bacterial biofilm and the host immune response has an impact reaching further than the oral cavity. The concept of "periodontal medicine" reunites the bidirectional relationships that exist between periodontal disease and systemic conditions such as diabetes mellitus or cardiovascular disease. The chronic inflammation of hepatic tissues during hepatitis C virus (HCV) infection causes changes in the general homeostasis that can reverberate at periodontal level and influence periodontal inflammation. Various mechanisms such as insulin resistance or pro-inflammatory cytokines production could be the link between the two conditions. In addition, periodontal inflammation could impact HCV transmission, as HCV RNA molecules and antibodies have been found in infected patients' saliva and gingival fluid. During periodontal inflammation, gingival bleeding is frequent, and the viral molecules could enter oral fluids while being carried by peripheral blood cells. Clinical particularities that suggest the onset of periodontal disease have also been frequently observed in HCV-infected patients. The connections between periodontal disease and hepatitis C need to take into consideration by practitioners of both specialties due to their important implications on clinical manifestations and treatment strategies.