Platelet-activating factor levels of serum and gingival crevicular fluid in nonsmoking patients with periodontitis and/or coronary heart disease

The purpose of the present study was to investigate systemic and local levels of platelet-activating factor (PAF), a potent proinflammatory mediator implicated in cardiovascular pathophysiology in adult nonsmoking patients with periodontitis with or without coronary heart disease (CHD). Eighty-seven volunteers, 25 periodontitis patients, 19 periodontitis with CHD patients, 19 CHD patients, and 24 healthy controls were included, and periodontal conditions were assessed. Gingival crevicular fluid (GCF) and venous blood were collected, and PAF levels were measured by enzyme-linked immunosorbent assay. PAF levels in serum (303.3 ± 204 pg/ml) and in GCF (26.3 ± 6 pg/μl) of the periodontitis group with CHD, the periodontitis group (serum, 302.4 ± 241 pg/ml and GCF, 26.3 ± 8 pg/μl) and the CHD group (serum, 284.7 ± 192 pg/ml and GCF, 20.8 ± 6 pg/μl) were significantly higher than the healthy control group (serum, 65.4 ± 35 pg/ml and GCF, 7.7 ± 3 pg/μl; p < 0.05). In summary, the present study could demonstrate that in patients with periodontitis, the inflammatory mediator PAF is released into serum at least in the same range as for patients with coronary heart disease. However, no additive effects were seen when both conditions were present

A Role for Non-Antimicrobial Actions of Tetracyclines in Combating Oxidative Stress in Periodontal and Metabolic Diseases: A Literature Review

This review addresses the role of adjunctive tetracycline therapy in the management of periodontal diseases and its efficacy in reducing inflammatory burden, oxidative stress and its sequelae in patients with coexisting features of metabolic syndrome. Removal of the dimethylamine group at C4 of the tetracycline molecule reduces its antibiotic properties, enhancing its non-antimicrobial actions; this strategy has aided the development of several chemically modified tetracyclines such as minocycline and doxycycline, by altering different regions of the molecule for focused action on biological targets. Tetracyclines are effective in reducing inflammation by inhibiting matrix metalloproteinases, preventing excessive angiogenesis, inhibiting apoptosis and stimulating bone formation. There are important applications for tetracyclines in the management of diabetic, dyslipidaemic periodontal patients who smoke. The diverse mechanisms of action of tetracyclines in overcoming oxidative stress and enhancing matrix synthesis are discussed in this review

Metalloproteinases and their inhibitors—diagnostic and therapeutic opportunities in orthopedics

Matrix metalloproteinases (MMPs) and related enzymes (ADAMs, ADAMTS) and their inhibitors control matrix turnover and function. Recent advances in our understanding of musculoskeletal conditions such as tendinopathy, arthritis, Dupuytren's disease, degenerative disc disease, and bone and soft tissue healing suggest that MMPs have prominant roles. Importantly, MMPs are amenable to inhibition by cheap, safe, and widely available drugs such as the tetracycline antibiotics and the bisphosphonates. This indicates that these MMP inhibitors, if proven effective for any novel indication, may be quickly brought into clinical practice

Matrix metalloproteinases (MMP-8 and-9) and neutrophil elastase in gingival crevicular fluid of cyclosporin-treated patients

WOS: 000167948100010PubMed ID: 11327063Background: Gingival overgrowth (GO) is one of the most important side effects of cyclosporin A (CsA) medication, but its pathogenesis is not completely understood. The aim of this study was to identify and compare collagenase-2 (MMP-8), gelatinase-B (MMP-9), and neutrophil (PMN)-elastase levels in gingival crevicular fluid (GCF) from 15 renal transplant patients receiving CsA therapy and exhibiting CsA GO, 14 patients with gingivitis, and 10 periodontally healthy subjects. Methods: Clinical data were obtained on plaque index, papilla bleeding index, and hyperplastic index from each site studied. GCF samples and clinical data were collected from: 2 sites exhibiting CsA GO (CsA GO+) and 2 sites not exhibiting CsA GO (CsA GO-) in each CsA-treated patient; 2 diseased sites in each patient with gingivitis; and 2 healthy sites in each subject with clinically healthy periodontium. CsA GO+ and CsA GO- sites were divided into 2 sub-groups as clinically not inflamed (PBI = 0) and inflamed (PBI greater than or equal to1). GCF MMP-8, MMP-9, and PMN-elastase levels were analyzed by immuno-fluorometric assay. Results: GCF MMP-8 and -9 levels and clinical degrees of gingival inflammation in CsA GO+ sites were similar to those in diseased sites. However, GCF elastase levels were significantly lower in CsA GO+ sites compared to those in diseased sites. GCF MMP-8, -9 and PMN-elastase levels were not different between CsA GO- sites and healthy sites. Additionally, GCF MMP-8 and -9 levels in inflamed CsA GO+ sites were higher but not statistically significantly than those in diseased sites. In contrast, GCF PMN-elastase levels in inflamed CsA GO+ sites were significantly lower than the levels in diseased sites. Conclusions: These results show that CsA therapy does not have a significant effect on GCF MMP-8 and MMP-9 levels, but the gingival inflammation seems to be the main reason for their elevations. However, low GCF PMN-elastase levels can be an important factor in the pathogenesis of CsA-induced gingival overgrowth. CsA therapy does not eliminate the potential use of GCF MMP-8 and -9 as future diagnostic markers of gingival inflammation

Evaluation of gingival crevicular fluid adrenomedullin and human neutrophil peptide 1-3 levels of patients with different periodontal diseases

PubMed ID: 20151808Background: Antimicrobial peptides participating in the innate host response are important contributors for maintaining the balance between health and disease. The aim of the present study is to investigate the levels of gingival crevicular fluid (GCF) adrenomedullin and human neutrophil peptides 1 through 3 (HNP1-3) in patients with different periodontal diseases. Methods: A total of 77 subjects, including 20 patients with chronic periodontitis, 18 patients with generalized aggressive periodontitis, 20 patients with gingivitis, and 19 healthy subjects, were included in the present study. The probing depth, clinical attachment level, plaque index, and papilla bleeding index were assessed in all study subjects. GCF samples were analyzed for evaluating adrenomedullin and HNP1-3 levels by enzyme-linked immunosorbent assay. Results: The present study demonstrated that the periodontitis groups had a significantly higher total amount of GCF adrenomedullin compared to the gingivitis and healthy control groups after adjusting for age and gender (P 0.05). Conclusions: Our results suggest a defensive role for adrenomedullin during the host response in periodontal disease. Additionally, the lack of the HNP1-3 antimicrobial peptide might point to the deficiency of one of the protective mechanisms for periodontal tissues

Gingival crevicular fluid EMAP-II, MIP-1 alpha and MIP-1 beta levels of patients with periodontal disease

WOS: 000230290200007PubMed ID: 15998272Background: Periodontal diseases may differ, which could be attributed to the factors that might modify the host response to microbial pathogens. The aim of this study was to examine gingival crevicular fluid (GCF) levels of EMAP-II, MIP-1 alpha and MIP-1 beta in patients with different periodontal diseases (EMAP-II, endothelial-monocyte activating polypeptide; MIP-1 alpha, macrophage inflammatory protein-1 alpha; MIP-1 beta, macrophage inflammatory protein-1 beta). Methods: Eighty-two subjects were included in this study. GCF samples were collected from 26 patients with generalized aggressive periodontitis (G-AgP), 26 patients with chronic periodontitis (CP), 15 with gingivitis and 15 periodontally healthy subjects. Clinical periodontal parameters were recorded. GCF EMAP-II, MIP-1 alpha and MIP-1 beta levels were quantified by enzyme immunoassay. Results: GCF EMAP-II levels of G-AgP group were higher than those of gingivitis and healthy groups (p 0.008). G-AgP, CP, gingivitis and healthy groups had comparable GCF MIP-1 alpha and MIP-1 beta levels. Conclusions: Our results suggest that elevated GCF EMAP-II could contribute to the pathogenesis of G-AgP. Alternatively, EMAP-II reflects the extent of the inflammatory activity in the periodontal tissues. At this point, MIP-1 alpha and MIP-1 beta levels in GCF do not seem to play a discriminatory role in periodontitis. Our data document for the first time the essential role of EMAP-II in the pathogenesis of different periodontal diseases

Sister chromatid exchange (SCE) analysis in periodontitis

WOS: 000179451300004PubMed ID: 12423293Background: Emerging data indicate that genetic factors may be associated with the etiopathogenesis of aggressive periodontitis. Sister chromatid exchange (SCE) is a sensitive method that might reflect an instability of DNA or a deficiency of DNA repair. The aim of the present study was to investigate SCE frequency of patients with different forms of periodontal disease and to determine whether this cytogenetic marker in patients with aggressive periodontitis can be differential compared to patients with chronic periodontitis and control subjects. Methods: SCE was analysed in peripheral blood lymphocyte chromosomes of 13 patients with generalised aggressive periodontitis (G-AP), 10 patients with chronic periodontitis (CP) and 10 control subjects. The periodontal parameters of probing depth, clinical attachment level, the presence of bleeding on probing and plaque were recorded. Peripheral blood lymphocytes obtained from both patient groups and control subjects were cultured in the presence of 5-Bromo-2-deoxyuridine in complete darkness for 72 h. For scoring SCE frequency, 20 metaphases were studied from each donor. Results: The frequency of SCE was found to be 6.7 +/- 0.9 per cell in patients with G-AP, 6.5 +/- 1.5 per cell in CP patients and 6.9 +/- 1.1 in control subjects. No statistically significant differences were found between groups (p > 0.05). Conclusions: The data indicate that there the cyotogenetic damage in the aggressive type of periodontal disease is not greater than in chronic periodontitis and control subjects. Although no aberrant cytogenetic damage was observed in different forms of periodontitis compared to control, this does not discount the importance of other genetic factors in the pathogenesis of periodontal disease