Despite a relatively high long-term survival rate, biological and technical complications were frequent. Patients with a history of periodontitis may have lower implant survival rates than patients without a history of periodontitis and were more prone to biological complications such as peri-implant mucositis and peri-implantitis.

No abstract

Porphyromonas gingivalis is a major etiological agent of chronic periodontal diseases, the virulence of which has been attributed to different factors, including lipopolysaccharide (LPS). We investigated the differential responses induced by P. gingivalis LPS stimulation of human umbilical vein endothelial cells and human oral epithelial cells. RT-PCR analysis showed that P. gingivalis LPS used Toll-like receptor 2 (TLR2) to activate epithelial cells and Toll-like receptor 4 (TLR4) to activate endothelial cells. Both cell types were stimulated by P. gingivalis LPS to produce pro-inflammatory cytokines. Cytokine Array assay showed that although patterns of cytokine expression were similar in both cell types, some cytokines were specifically secreted by the endothelial cells, and others were specific to epithelial cells. These results support the idea that the same LPS preparation can act as a TLR2 or TLR4 agonist, depending on TLR expression of the host cell, inducing cytokine profiles that differ according to the cell type.

Within the limitations of this study, the findings of this meta-analysis seem to support the adjunctive use of L. reuteri to SRP in CP treatment at short-term, especially in deep pockets. Heterogeneity and limited available data may reduce the impact of these conclusions. Future long-term RCTs evaluating the clinical efficacy of adjunctive probiotics to SRP are needed.

No abstract

Aryl hydrocarbon receptor (AhR) ligands are environmental contaminants found in cigarette smoke and other sources of air pollution. The prototypical compound is TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin), also known as dioxin. There is an increasing body of knowledge linking cigarette smoking to osteoporosis and periodontal disease, but the direct effects of smokeassociated aryl hydrocarbons on bone are not well understood. Through the use of resveratrol (3,5,4 -trihydroxystilbene), a plant antifungal compound that we have recently demonstrated to be a pure AhR antagonist, we have investigated the effects of TCDD on osteogenesis. It was postulated that TCDD would inhibit osteogenesis in bone-forming cultures and that this inhibition would be antagonized by resveratrol. We employed the chicken periosteal osteogenesis (CPO) model, which has been shown to form bone in vitro in a pattern morphologically and biochemically similar to that seen in vivo, as well as a rat stromal cell bone nodule formation model. In the CPO model, alkaline phosphatase (AP) activity was reduced by up to 50% (P<0·01 vs control) in the presence of 10 9 M TCDD and these effects were reversed by 10 6 M resveratrol (P<0·05 vs TCDD alone). TCDD-mediated inhibition of osteogenesis was restricted primarily to the osteoblastic differentiation phase (days 0-2) as later addition did not appear to have any effects. Message levels for important bone-associated proteins (in the CPO model) such as collagen type I, osteopontin, bone sialoprotein and AP were inhibited by TCDD, an effect that was antagonized by resveratrol. Similar findings were obtained using the rat stromal bone cell line. TCDD (at concentrations as low as 10 10 M) caused an approximately 33% reduction in AP activity, which was abrogated by 3·5 10 7 M resveratrol. TCDD also induced a marked reduction in mineralization (75%) which was completely antagonized by resveratrol. These data suggest that AhR ligands inhibit osteogenesis probably through inhibition of osteodifferentiation and that this effect can be antagonized by resveratrol. Since high levels of AhR ligands are found in cigarette smoke, and further since smoking is an important risk factor in both osteoporosis and periodontal disease, it may be postulated that AhR ligands are the component of cigarette smoke linking smoking to osteoporosis and periodontal disease. If so, resveratrol could prove to be a promising preventive or therapeutic agent for smoking-related bone loss.

Successive active phases observed in periodontal diseases may be explained either by a sudden activation of the pro-forms of tissue-stored degradative enzymes such as metalloproteinases (MMPs) or by an imbalance between metalloproteinases and their tissue inhibitors (TIMPs). To discriminate between these two hypotheses, we quantified the levels, the percentage of active form, and the activities of four metalloproteinases (MMPs -1, -2, -3, and -9), as well as the levels of two tissue inhibitors of metalloproteinases (TIMP-1 and -2) and the activity of cathepsin C in tissue extract supernatants and their corresponding gingival crevicular fluid samples collected from periodontitis-affected and healthy patients. Our results supported evidence that tissue destruction results from an imbalance of metalloproteinases over their tissue inhibitors rather than from a sudden activation of the pro-forms of these enzymes. A significant reduction in the activity of cathepsin C also contributed to the degradative process.

This study showed the reliability of PRAS in evaluating long-term TL and patient susceptibility to periodontal disease. Our data confirmed the positive influence of patient compliance on periodontal treatment outcomes.