Background: In healthy periodontal tissue, innate immune responses effectively confine and suppress a bacterial insult. However, a disruption of the host–bacterial equilibrium may produce an overexpression of cytokines and lead to permanent, host‐mediated tissue damage. Although such periodontal destruction primarily results from activated immune mechanisms, the site‐specific damage suggests that local tissues participate in these pathologic changes. Periodontal ligament fibroblasts (PDLFs) are prominent in the periodontium and are critical in homeostasis and regeneration because they have the ability to produce multiple cytokines in response to a bacterial insult. These cells could play a role in the local pathogenesis of periodontal disease.Methods: We studied alkaline phosphatase (ALP) activity, interleukin (IL)‐6 production, and morphologic characteristics of cultured PDLFs that were isolated from periodontally healthy sites (H‐PDLFs) and diseased sites (D‐PDLFs) in humans. Quantitative analyses of 84 genes that are related to inflammation were performed using real‐time polymerase chain reaction arrays.Results: A mineralizing medium induced a significant increase of ALP in H‐PDLFs, but no significant enzymatic changes were detected in D‐PDLFs after such treatment. The protein and gene expression of IL6 showed a significant upregulation in D‐PDLFs, which also demonstrated a significant upregulation of 54% of genes in the inflammatory gene arrays.Conclusions: To our knowledge, these results represent the first biologic evidence that D‐PDLFs retain uniquely inflammatory phenotypes that could maintain localized destructive signals in periodontitis. The overexpression of proinflammatory cytokines by PDLFs could amplify local inflammation by the continuous triggering of immune responses. In addition, the location of these cells could be critical in the progression of the inflammatory front into the deeper tissues.
21 February 2020 in Journal of Periodontal Research
Background: The open, usually contaminated nature of periodontal defects could negatively affect availability and activity of platelet concentrate–suggested growth factors (GF). The aim of this study is to test this hypothesis and investigate concentrations of: 1) vascular endothelial growth factor (VEGF) and 2) platelet‐derived growth factor (PDGF‐BB) in gingival crevicular fluid (GCF) from localized intrabony defects treated with platelets rich in growth factors (PRGF) or platelet‐rich fibrin (PRF) compared with a control xenograft defect filling.Methods: Thirty non‐smoking patients suffering severe chronic periodontitis were allocated to this randomized, prospective, single‐masked trial. Each patient had one interproximal defect randomly distributed to: 1) group 1: bone‐substitute grafting control (n = 10); 2) group 2: experimental PRGF (n = 10); or 3) group 3: PRF (n = 10). Clinical parameters were measured at baseline and 6 and 9 months following therapy. GCF samples were obtained on days 1, 3, 7, 14, 21, and 30 after therapy for evaluation of VEGF and PDGF‐BB levels.Results: On days 1, 3, and 7 following surgery, mean levels of VEGF and PDGF‐BB at sites treated with PRGF and PRF were not significantly different versus the control. Levels of PDGF‐BB and VEGF were higher in the PRGF‐treated group, but differences were not significant. Growth factor levels decreased significantly in samples collected on days 14, 21, and 30 with non‐significant differences among the three groups. No significant clinical differences were reported among the three groups during the two observation periods (early period: days 1, 3, and 7; and later period: days 14, 21, and 30).Conclusions: Within the limits of the present study, it can be concluded that PRF and PRGF platelet concentrate failed to augment clinical effects achieved with the xenograft alone in treating intrabony defects. Periodontal defects could not retain extraphysiologic levels of GF suggested to be associated with platelet concentrate.
1 August 2002 in Journal of Clinical Periodontology
Background: The present study was designed to determine whether exclusion of the gingival connective tissue (CT) and periosteum with contained stem cells has a positive or negative effect on periodontal regeneration by comparing the use of a novel modified perforated collagen membrane with a traditional cell occlusive barrier membrane.Methods: Twenty non‐smoking patients with severe chronic periodontitis were included in the study. Single deep intrabony defects from each of the patients were randomly divided into two groups, as follows: occlusive bovine collagen membranes (OM control group, 10 sites) and modified perforated bovine collagen membranes (MPM test group, 10 sites). Plaque index, gingival index, probing depth (PD), clinical attachment level (CAL), defect base level (DBL), and crestal bone level (CBL) were measured at baseline and were reassessed at 6 and 9 months after therapy to evaluate the quantitative changes in the defect.Results: At 6‐ and 9‐month observation periods, the MPM‐treated sites showed a statistically significant improvement in PD reduction and CAL gain compared with the OM control group. DBL was significantly reduced with no significant difference between the two groups at 6‐ and 9‐month observation periods. CBL was significantly higher in the MPM group when compared with that of the OM group at both observation periods. The postoperative differences between the two groups were 2 and 1.7 mm at 6 and 9 months, respectively, in favor of the MPM‐treated sites.Conclusions: The present study demonstrated enhanced clinical outcomes when using novel MPMs compared to OMs in guided tissue regeneration procedures. These results may be affected by the penetration of gingival CT contained stem cells and periosteal cells and their differentiation into components of the attachment apparatus.