Effect of Periodontitis and Periodontal Therapy on Oral and Gut Microbiota.

Mounting evidence indicates that periodontitis-related oral bacteria may contribute to gut microbial dysbiosis. This clinical study aimed to explore the oral-gut microbial signatures associated with periodontitis and to longitudinally evaluate the effect of periodontal treatment on the oral and gut microbial composition. Stool and saliva samples from generalized stage III/IV periodontitis patients (n = 47) were collected and analyzed by 16S ribosomal RNA gene amplicon sequencing, before and 3 mo after steps I to II of periodontal therapy. Periodontally healthy matched subjects (n = 47) were used as controls. Principal component analysis was carried out to identify oral-gut microbial profiles between periodontitis patients at baseline and healthy subjects; periodontitis samples were longitudinally compared before and after treatment. ß-Diversity of gut microbial profiles of periodontitis patients before treatment significantly differed from healthy controls (P < 0.001). Periodontal therapy was associated with a significant change in gut microbiota (P < 0.001), with post-treatment microbial profiles similar to healthy volunteers. A higher abundance of Bacteroides, Faecalibacterium, Fusobacterium, and Lachnospiraceae was noted in fecal samples of periodontitis patients at baseline compared to healthy controls. In contrast, Lactobacillus was the only genus more abundant in the latter. Additionally, periodontal therapy led to a parallel reduction in the salivary carriage of periodontal pathobionts, as well as gut Bacteroides, Lachnoclostridium, Lachnospiraceae, Oscillospiraceae, and Ruminococcaceae, to levels similar to healthy controls. Collectively, discriminating oral-gut microbial signatures of periodontitis were found. Periodontal treatment both mitigated oral dysbiosis and altered gut microbial composition, signifying potential broader implications for gastrointestinal health and disease.

Increased early inflammatory response and osteoclastic activity in gingival tissues following conventional osseous resective surgery compared with the fibre retention technique: a pilot study.

BACKGROUND AND OBJECTIVE: The retention of suprabony connective fibres attached into the root cementum during fibre retention osseous resective surgery (FibReORS) results in a more conservative intrasurgical removal of bone, and limits further bone loss and patient morbidity during healing, compared with conventional osseous resective surgery (ORS). This may be a result of the protective effect of preserved connective tissue over the interproximal sites and the lower activation of the inflammatory mechanisms. Thus, the aim of this pilot study was to compare the expression of inflammatory and osteoclastic activity markers in gingival tissues following FibReORS and ORS in the early postsurgical phase. MATERIAL AND METHODS: Twenty-six posterior sextants requiring osseous resective surgery were selected in 13 patients with chronic periodontitis: 13 sextants were randomly assigned to ORS and 13 to FibReORS in a split-mouth design. Gingival biospies were collected during the surgical sessions and at suture removal. Tissue samples were analysed to evaluate the expression of proinflammatory and immunity regulatory mediators (interleukin-1α, C-X-C motif chemokine ligand 5, interferon-γ and tumour necrosis factor-α), cluster of differentiation 14 (CD14; a monocyte/macrophage marker) and TRAP (an osteoclast marker) using immunohistochemical, immunofluorescence and cytofluorimetric analyses, respectively. RESULTS: Postsurgery, a higher number of inflammatory cells and stronger expression of proinflammatory cytokines were observed in the epithelium and connective tissue of ORS gingival samples compared with FibReORS gingival samples (p < 0.001). This was accompanied by increased numbers of CD14-positive and TRAP-positive cells. CONCLUSION: Retention of the supracrestal connective fibres appears to reduce the postsurgical intensity of the host-mediated inflammatory response.

[HCV and extrahepatic diseases]. / HCV e patologie extraepatiche.

Besides being a hepatotropic virus and a common cause of chronic hepatitis, hepatitis C virus (HCV) has been linked to a variety of extrahepatic immunological manifestations. The high prevalence of HCV infections in some of these conditions suggests an important pathogenetic role of the virus. The recent observation that HCV infects peripheral blood mononuclear cells, such as CD8+ T lymphocytes, CD19+ B lymphocytes and monocytes/microphages, has given an insight into the possible mechanisms of HCV associated autoimmunity. In the clinical practice it is recommended not only to search for symptoms and signs of autoimmune disorders in patients with chronic hepatitis C, but also to test for hepatitis C virus infection patients with extrahepatic conditions known to be related to HCV. Even if the occurrence of autoimmune disorders or the exacerbations of autoimmune diseases has been reported during interferon therapy, antiviral therapy is effective in treating some of the extrahepatic disorders associated with HCV, namely mixed cryoglobulinemia and membranoproliferative glomerulonephritis. The extrahepatic manifestations associated with hepatitis C virus infection are reviewed according to the available data and the option of interferon therapy is discussed.