transforming-growth-factor-beta and Periodontal-Pocket

At present there is limited data concerning the efficacy of non-surgical periodontal therapy supplemented with subantimicrobial dose doxycycline (SDD) in the treatment of severe, generalized periodontitis. The purpose of the present study was to evaluate the effect of adjunctive SDD therapy on clinical periodontal parameters and gingival crevicular fluid (GCF) transforming growth factor-beta1 (TGF-beta1) levels in patients with severe, generalized chronic periodontitis over a 6-month period.. Thirty-five patients with severe, generalized periodontitis and 11 periodontally healthy subjects were included in the present study. Patients received full-mouth supragingival debridment at baseline and randomized to take either SDD b.i.d. or placebo b.i.d. for 3 months. Patients received root planing and oral hygiene instruction once a week for four consecutive weeks. Clinical measurements including probing depth (PD), clinical attachment level, papilla bleeding index and plaque index and GCF sampling were performed at baseline, 3 and 6 months. The GCF TGF-beta1 levels were analysed by enzyme-linked immunosorbent assay.. Thirteen patients in both study groups completed the 6-month trial. Following scaling and root planing (SRP) plus SDD and SRP plus placebo therapy significant improvements in clinical periodontal parameters of both groups were observed (p<0.025). In the SDD group a significantly higher percentage (%73.4) of deep pockets resolved (PD reduction > or =3 mm from baseline) when compared with placebo group (%49.7) at 6 months (p<0.05). At baseline there were no significant differences in GCF TGF-beta1 levels between three groups. Both total amount and concentration of GCF TGF-beta1 in SDD and placebo groups increased when compared with baseline at 3 months. However, only GCF TGF-beta1 levels of SDD group was significantly higher than baseline (p<0.025) and placebo group (p<0.017) at 3 months. At 6 months GCF TGF-beta1 levels of both groups were similar to baseline levels (p<0.025).. These data indicate that combination of SDD with non-surgical therapy improves clinical parameters of periodontal disease and increases GCF TGF-beta1 levels together with a decrease in prevalence of residual pockets in patients with severe, generalized chronic periodontitis. Increased GCF TGF-beta1 levels following SDD therapy might suggest a novell pleiotrophic mechanism for tetracyclines to inhibit connective tissue breakdown.

Topics: Adult; Anti-Bacterial Agents; Chronic Disease; Combined Modality Therapy; Dental Plaque Index; Double-Blind Method; Doxycycline; Female; Follow-Up Studies; Gingival Crevicular Fluid; Humans; Male; Middle Aged; Oral Hygiene; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Periodontitis; Placebos; Root Planing; Subgingival Curettage; Transforming Growth Factor beta; Transforming Growth Factor beta1

This study was an initial evaluation of the use of a bovine-derived bone protein (BP) extract that contains various growth factors combined with decalcified freeze-dried bone allograft (DFDBA) as regenerative treatment for class II mandibular furcations. Twenty-five patients were divided into 5 groups according to the dosage of BP present per mg of DFDBA to be grafted: (1) 0.00 microgram/mg, (2) 3.13 micrograms/mg, (3) 6.25 micrograms/mg, (4) 12.5 micrograms/mg, and (5) 25.0 micrograms/mg. Surgical exploration of the furcation defects was performed followed by grafting with BP/DFDBA. Results at 6 months showed that attachment gain in the treated furcation areas was greatest in Groups 4 and 5, suggesting that BP has the potential to increase the effects of DFDBA in gaining clinical attachment in mandibular class II furcations.

Topics: Adult; Aged; Animals; Bone Morphogenetic Proteins; Bone Regeneration; Bone Transplantation; Cattle; Dental Plaque Index; Double-Blind Method; Female; Follow-Up Studies; Furcation Defects; Gingival Recession; Humans; Male; Mandibular Diseases; Middle Aged; Observer Variation; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Prospective Studies; Reproducibility of Results; Statistics as Topic; Surgical Flaps; Transforming Growth Factor beta; Transplantation, Homologous

Porphyromonas gingivalis lipid A heterogeneity modulates cytokine expression in human cells. This study investigates the effects of two lipid A isoforms of P. gingivalis, lipopolysaccharide (LPS)1435/1449 and LPS1690, on the secretion of proinflammatory and regulatory cytokines in total blood cultures from patients with and without chronic periodontitis (CP).. A cross-sectional study was conducted in 38 systemically healthy individuals divided in two groups: 1) the CP group (n = 19), in which patients were diagnosed with CP; and 2) the no periodontitis (NP) group (n = 19), which included control patients without CP. Blood samples were collected from all patients, and whole-blood cell cultures (WBCCs) were stimulated for 48 hours with P. gingivalis LPS1435/1449 and LPS1690 and Escherichia coli LPS. Unstimulated WBCCs served as negative controls. The secretion of interferon-γ (IFN-γ), interleukin-10 (IL-10), and transforming growth factor-β (TGF-β) was detected in WBCC supernatants by enzyme-linked immunosorbent assays.. E. coli LPS significantly increased the expression of all cytokines in WBCCs from both the NP and CP groups when compared to non-stimulated cells (control treatment). P. gingivalis LPS preparations increased IFN-γ levels in the CP group but not in the NP group when compared with controls (P <0.05). P. gingivalis LPS preparations also increased IL-10 and TGF-β levels in both CP and NP groups, but P. gingivalis LPS1690 showed a three-fold increase on IL-10 production in the NP group (P <0.05) when compared to P. gingivalis LPS1435/144.. These data demonstrate that WBCC cell populations obtained from healthy individuals and patients with CP may differ in the cytokine response to P. gingivalis but not E. coli LPS. This is consistent with the notion that CP alters the systemic WBCC response and that this can be detected by the different P. gingivalis LPS structures.

Topics: Adult; Aged; Blood Cells; Chronic Periodontitis; Cross-Sectional Studies; Cytokines; Dental Plaque Index; Escherichia coli; Female; Humans; Inflammation Mediators; Interferon-gamma; Interleukin-10; Lipid A; Male; Middle Aged; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Porphyromonas gingivalis; Transforming Growth Factor beta

Growth factors play a major part in wound healing in many tissues including the periodontium. Transforming growth factor-β1 (TGF-β1) is one of these factors present in the gingival crevicular fluid. In addition, it is considered as one of the most important anti-inflammatory cytokines. Interleukin-1β is a proinflammatory cytokine that presents itself in gingival inflammation and the GCF. Such factors might be of value as prognostic markers of wound healing activity and the therapeutic progress following flap surgery.. The aim of this study was to evaluate the effect of surgical flap on the concentration of IL-1β and TGF-β in the GCF of patients with moderate to severe chronic periodontitis.. The GCF samples were collected, using the Perio-Paper strip at phase 1 (pre-surgery), phase 2 (4th week post surgery) and phase 3 (12th week post surgery) from 20 sites of 10 patients undergoing flap surgery. After the elution, IL-1β and TGF-β concentrations were measured by enzyme-linked immunosorbent assay (ELISA).. The mean TGF-β and IL-1β concentration decreased from phase 1 to phase 3 (p<0.05). There were no significant statistical correlations between IL-1β and TGF-β1 concentrations in the 3 assessment phases. There was a significant statistical correlation between TGF-β1 concentrations and the Plaque Index (PI) in phase 2 (p<0.05). There was a significant statistical correlation (p<0.05) between IL-1β and TGF-β1 concentration and the probing pocket depth (PPD).. The flap surgery has a significant effect on decreasing IL-1β concentration. In the case of TGF-β1, probably the decrease in the concentration after treatment might be due to the removal of the inflammatory stimulants.

Topics: Adult; Chronic Periodontitis; Enzyme-Linked Immunosorbent Assay; Female; Gingival Crevicular Fluid; Humans; Inflammation; Interleukin-1beta; Male; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Transforming Growth Factor beta

Inhibitory signals mediated via molecules such as programmed death-1 (PD-1) play a critical role in downmodulating immune responses and maintaining peripheral tolerance. We investigated the involvement of cytokines and PD-1 engagement in mediating the T-cell unresponsiveness to bacterial and ubiquitous antigens in periodontal diseases.. Gingival and peripheral blood samples from healthy individuals and patients with chronic periodontitis were collected and used for the subsequent assays. Leukocytes in the lesion site and blood were evaluated using flow cytometry. The production of interferon-gamma, interleukin-10, and transforming growth factor-beta proteins was evaluated by enzyme-linked immunosorbent assay (ELISA), and the presence of PD-1+ cells in the inflamed gingiva was confirmed by immunofluorescence confocal microscopy for CD4 and PD-1 colocalization.. T cells from patients with chronic periodontitis proliferated poorly in response to Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) antigen. T-cell unresponsiveness was not associated with imbalanced cytokine production. However, T cells from patients with chronic periodontitis expressed significantly higher levels of PD-1 either upon isolation or after culture with antigens. Moreover, PD-1 blocking did not result in significant T-cell proliferation in cells cultured with phytohemagglutinin or bacterial antigens. The blockade of PD-1 resulted in the increased production of IFN-gamma. In addition, CD4+ and CD8+ T cells expressing PD-1 accumulated in lesions with chronic periodontitis.. These data show that PD-1 engagement could be involved in the modulation of IFN-gamma production by T cells in patients with chronic periodontitis.

Topics: Adult; Aged; Aged, 80 and over; Aggregatibacter actinomycetemcomitans; Alveolar Bone Loss; Antigens, Bacterial; Antigens, CD; Apoptosis Regulatory Proteins; Case-Control Studies; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Chronic Periodontitis; Down-Regulation; Female; Gingiva; Gingivitis; Humans; Interferon-gamma; Interleukin-10; Leukocytes; Lymphocyte Activation; Male; Middle Aged; Periodontal Attachment Loss; Periodontal Pocket; Programmed Cell Death 1 Receptor; T-Lymphocyte Subsets; T-Lymphocytes; Transforming Growth Factor beta

Advances in diagnostic research are moving towards methods whereby the periodontal risk can be identified and quantified by objective measures using biomarkers. Patients with periodontitis may have elevated circulating levels of specific inflammatory markers that can be correlated to the severity of the disease. The purpose of this study was to evaluate whether differences in the serum levels of inflammatory biomarkers are differentially expressed in healthy and periodontitis patients. Twenty-five patients (8 healthy patients and 17 chronic periodontitis patients) were enrolled in the study. A 15 mL blood sample was used for identification of the inflammatory markers, with a human inflammatory flow cytometry multiplex assay. Among 24 assessed cytokines, only 3 (RANTES, MIG and Eotaxin) were statistically different between groups (p<0.05). In conclusion, some of the selected markers of inflammation are differentially expressed in healthy and periodontitis patients. Cytokine profile analysis may be further explored to distinguish the periodontitis patients from the ones free of disease and also to be used as a measure of risk. The present data, however, are limited and larger sample size studies are required to validate the findings of the specific biomarkers.

Topics: Biomarkers; Chemokine CCL2; Chemokine CCL3; Chemokine CCL4; Chemokine CCL5; Chemokine CXCL9; Chemokines, CC; Chronic Periodontitis; Cytokines; Fas Ligand Protein; Fibroblast Growth Factor 2; Gingival Hemorrhage; Granulocyte Colony-Stimulating Factor; Granulocyte-Macrophage Colony-Stimulating Factor; Humans; Inflammation Mediators; Interferon-gamma; Interleukin-9; Interleukins; Lymphotoxin-alpha; Periodontal Attachment Loss; Periodontal Pocket; Transforming Growth Factor beta

The role of polypeptide growth factors in periodontal regeneration has been documented through animal and human studies. Human platelets contain platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) in their alpha granules. PDGF has been shown to play a role in periodontal regeneration. It has been demonstrated that TGF-beta has a very potent effect on cells associated with bone. The case reports presented demonstrate a new biotechnology in which platelet gel is used in combination with demineralized freeze-dried bone allografts for the treatment of periodontal osseous defects. The treated teeth presented with severe bone loss and a guarded prognosis. Platelet gel biotechnology was used as a novel treatment modality. A significant reduction in probing depths was noted, and radiographically significant amounts of new bone were visible as early as 2 months postoperative. Results up to 2 years postoperative are presented.

Topics: Adult; Alveolar Bone Loss; Alveolar Process; Biotechnology; Blood Platelets; Bone Transplantation; Collagen; Decalcification Technique; Female; Follow-Up Studies; Freeze Drying; Gels; Guided Tissue Regeneration, Periodontal; Humans; Male; Membranes, Artificial; Middle Aged; Periodontal Pocket; Platelet-Derived Growth Factor; Prognosis; Radiography; Tissue Preservation; Transforming Growth Factor beta; Transplantation, Autologous; Transplantation, Homologous; Wound Healing

Transforming growth factor-beta (TGF-beta) represents a family of polypeptide growth factors, involved in embryogenesis, inflammation, regulation of immune responses and wound healing. To determine whether TGF-beta contributes to the evolution of periodontal disease, we assayed TGF-beta levels in gingiva and crevicular fluid of patients with gingivitis and periodontitis. In parallel, TGF-beta was quantified in gingival fluid and serum of beagles with experimentally-induced periodontitis. Disease was monitored by several clinical parameters including Plaque Index, Gingival Index, probing depth, and epithelial attachment loss. Gingival tissues were obtained from 9 patients at the time of periodontal surgery, and gingival fluid samples were collected from an additional population of 10 periodontal patients. In 14 beagles, experimental periodontitis was induced and gingival fluids collected 6 months later. Fluid was collected by paper strips and volume measured by Periotron. Additionally, sera was collected before and 9 months after the ligature-induced periodontitis in 7 beagles. The levels of TGF-beta 1 were measured by ELISA. In the patients, a significantly higher concentration of TGF-beta 1 was observed both in the gingival tissues and fluid samples obtained from the sites with deeper periodontal pockets than in the less involved sites. In beagles, TGF-beta 1 levels measured in gingival fluid were elevated in moderate disease, declining in fluid samples obtained from the pockets during more advanced experimental periodontitis. Furthermore, with the progression of experimental periodontitis, a decrease in TGF-beta 1 occurred in the sera of the beagle dogs. These data suggest that TGF-beta 1 may play a rôle in the pathogenesis and diagnosis of periodontal disease, and that its actions can be further explored in an animal model.

Topics: Adult; Aged; Animals; Dental Plaque Index; Disease Models, Animal; Disease Progression; Dogs; Enzyme-Linked Immunosorbent Assay; Female; Gingiva; Gingival Crevicular Fluid; Gingivitis; Humans; Male; Middle Aged; Periodontal Attachment Loss; Periodontal Index; Periodontal Pocket; Periodontitis; Transforming Growth Factor beta