121 research outputs found

    Trading Rights for Responsibility

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    Clinical, Microbiological and Immunological Responses to Two Non-Surgical Periodontal Treatment Modalities

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    The current study compared the clinical, microbiological and immunological parameters of chronic periodontitis patients that received two different treatment strategies: one-day full-mouth scaling and root planing (FM-SRP) versus quadrant scaling and root planing at two-weekly intervals (Q-SRP). In addition, the effects of smoking on the periodontal status, subgingival microflora and humoral immune response were examined. Clinical measurements, subgingival plaque samples, gingival crevicular fluid (GCF) and sera were collected from 42 patients with moderate to advanced chronic periodontitis before and after treatment over a period of six months. Patients were randomly allocated into two treatment groups and received FM-SRP or Q-SRP. Polymerase chain reaction (PCR) was used to determine the presence of P. gingivalis, A. actinomycetemcomitans, P. intermedia, T denticola and B. forsythus in plaque. Enzyme-linked immunosorbent assay (ELISA) was used to examine systemic and local antibody titres to these bacteria and thiocyanate disassociation was used to determine antibody avidity. Q-SRP and FM-SRP were found to be equally efficacious periodontal treatments. Therefore, the clinician should decide which treatment strategy to choose on a practical basis. No evidence emerged from this study to document a strong immunological reaction elicited by FM-SRP, as was speculated by Quirynen et al. (1995). In fact, during therapy the host responses of patients in both treatment groups followed a similar pattern. In general, both treatments resulted in significant clinical improvement and reduced titres of antibodies, but which were of similar avidity for the majority of the tested organisms. These changes paralleled marked reductions in the site and subject prevalence of putative periodontopathogens. In addition the present data do not support the hypothesis that, during the active phase of quadrant root planing therapy, the treated sites are re-infected with organisms that are possibly transmitted from the remaining untreated pockets and from other intra-oral niches (Quirynen et al. 1995). In contrast, the commencement of quadrant root planing and meticulous oral hygiene measures had a significant positive effect on the periodontal conditions of the remaining untreated quadrants. Nevertheless, this clinical improvement was smaller compared to changes seen after the completion of mechanical debridement. Despite the fact that FM-SRP resulted in significantly higher pain scores and more patients taking analgesics compared to Q-SRP, it still seemed to be well tolerated by patients. Smoking had a significant adverse effect on the inflammatory response to the bacterial challenge and on the treatment outcome. The outcome of each treatment strategy (Q-SRP and FM-SRP) was affected significantly by smoking over the course of treatment, having a significant impact on pocket depth (PD) and relative attachment level (RAL) of selected sites. A smaller PD reduction and less gain in RAL were noted after both treatment strategies at selected sites of smokers compared with those of non-smokers. Smoking appeared to modify both local and systemic host responses by producing lower levels of GCF and serum antibodies, respectively, but appeared to have no significant effect on the subgingival microflora. This study associated systemic antibody levels with the presence of homologous organisms in subgingival plaque. Furthermore, the present study showed that subjects with less severe disease and a better clinical outcome retained higher levels of serum antibodies compared to patients who had more advanced disease and a moderate clinical outcome. These findings confirm the suggestions from other studies that antibodies are protective against the progression of periodontal disease. GCF antibody titres were low compared to serum antibody levels, which agrees with previous findings and a large site-to-site variability was evident, making interpretation of the results difficult. Nevertheless, it was apparent that deep pockets and sites that harboured a bacterial species gave rise to higher levels of GCF antibodies for that species

    Stem cell-like populations and immunoregulatory molecules in periodontal granulation tissue

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    Background and Objectives: Determine the presence of mesenchymal stem cells (MSCs) in healthy periodontal tissue and periodontal granulation tissue (GT) and explore associations between immuno‐regulatory molecules and selected subgingival microorganisms. Material and Methods: Mesenchymal stem cells were isolated, propagated and characterised by flow cytometry from a region of healthy gingival tissue and inflamed GT of 10 systemically healthy non‐smokers with chronic periodontitis. Tissue levels of immunoregulatory molecules were determined by qPCR and Gingival Crevicular Fluid (GCF) levels by ELISA. Subgingival plaque levels of periodontal pathogens were determined by qPCR Results: Cells with MSC‐properties were isolated from both inflamed GT and healthy gingival (G) tissue. A pro‐inflammatory process predominated in GT which was partly reflected in GCF and putative periodontal pathogens were higher at diseased sites. However, there was no significant difference in surface levels of mesenchymal (CD90, CD73, CD146, CD271, STRO‐1), endothelial (CD105, CD106), hematopoietic (CD34, CD45) and embryonic (SSEA‐4) stem cell markers between MSCs isolated from GT and G tissue. Conclusion: Periodontal lesions, albeit inflamed, retain healing potential as inferred by the presence of MSC‐like cells with similar immunophenotypic characteristics to those found in healthy periodontal tissue. Therefore, there might be merits for healing in preserving sufficient GT in‐situ during periodontal surgery

    Principles of Periodontology

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    Periodontal diseases are among the most common diseases affecting humans. Dental biofilm is a contributor to the etiology of most periodontal diseases. It is also widely accepted that immunological and inflammatory responses to biofilm components are manifested by signs and symptoms of periodontal disease. The outcome of such interaction is modulated by risk factors (modifiers), either inherent (genetic) or acquired (environmental), significantly affecting the initiation and progression of different periodontal disease phenotypes. While definitive genetic determinants responsible for either susceptibility or resistance to periodontal disease have yet to be identified, many factors affecting the pathogenesis have been described, including smoking, diabetes, obesity, medications, and nutrition. Currently, periodontal diseases are classified based upon clinical disease traits using radiographs and clinical examination. Advances in genomics, molecular biology, and personalized medicine may result in new guidelines for unambiguous disease definition and diagnosis in the future. Recent studies have implied relationships between periodontal diseases and systemic conditions. Answering critical questions regarding host‐parasite interactions in periodontal diseases may provide new insight in the pathogenesis of other biomedical disorders. Therapeutic efforts have focused on the microbial nature of the infection, as active treatment centers on biofilm disruption by non‐surgical mechanical debridement with antimicrobial and sometimes anti‐inflammatory adjuncts. The surgical treatment aims at gaining access to periodontal lesions and correcting unfavorable gingival/osseous contours to achieve a periodontal architecture that will provide for more effective oral hygiene and periodontal maintenance. In addition, advances in tissue engineering have provided innovative means to regenerate/repair periodontal defects, based upon principles of guided tissue regeneration and utilization of growth factors/biologic mediators. To maintain periodontal stability, these treatments need to be supplemented with long‐term maintenance (supportive periodontal therapy) programs

    Trading Rights for Responsibility

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    The newly published compromise text of the Asylum Procedures Regulation (APR) suggests to render border procedures mandatory in some cases, while also permitting first-entry states to derogate from them once their “adequate capacity” is reached. This adaptable approach to the use of border procedures seeks to resolve a long-standing disagreement between central EU countries and first-entry states. While the former consider the obligatory use of border procedures necessary to prevent onwards or  ‘secondary’ movement of asylum-seekers, southern EU states argue that their mandatory use would place a further strain on their resources and overburden their capacities for processing asylum claims. This blogpost first explains the problems with border procedures, reviews their role in increasing responsibility of first-entry states, and explains why the new compromise Draft is unlikely to resolve the disagreement between first-entry states and other Members States.</p

    Quadrant root planing versus same-day full-mouth root planing - III. Dynamics of the immune response

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    The aim of this study was to determine whether same-day full-mouth scaling and root planing (FM-SRP) and quadrant scaling and root planing (Q-SRP) resulted in variations in the systemic humoral immune response dynamics (antibody titres and avidity) during active treatment and 3 and 6 months post-therapy. Material and Methods: Forty patients with chronic periodontitis were recruited into this study. Subjects were randomised into two groups and received either scaling and root planing quadrant by quadrant at 2-weekly intervals (Q-SRP group) or same-day full-mouth scaling and root planing (FM-SRP group). Clinical measurements and serum samples were obtained at baseline and approximately 6 weeks after the last clinical intervention (R1) and 6 months after the initiation of therapy (R2). Furthermore, serum samples were obtained from each patient undergoing therapy (Q-SRP and FM-SRP) at 3 bi-weekly instances so as to determine the short-term effects of each session of scaling and root planing on the dynamics of the humoral immune response. Serum antibody titre was assayed by enzyme-linked immunosorbent assay (ELISA) and antibody avidity was measured by thiocyanate dissociation against five putative periodontal pathogens: Porphyromonas gingivalis; Actinobacillus actinomycetemcomitans; Prevotella intermedia; Treponema denticola and Bacteroides forsythus. Results: Both therapies resulted in similar antibody titre reductions against the majority of the organisms tested and although there was a distinct trend for antibody avidity to increase following therapy, this was not found to be statistically significant, reflecting marked inter-individual variation. In addition, no evidence emerged from this study to support increased antibody titres following the active phases of both treatment approaches due to an inoculation effect. Nevertheless, significant short-term increases in antibody avidity to most test bacteria were noted for both treatment strategies. Conclusion: Both therapies were associated with a reduction in antibody titres and an increase in the binding ability or avidity of antibodies, but there was a marked inter-subject variability and statistical significance was reached for only some of the test bacteria. No significant differences in the humoral antibody dynamics were found between the two treatment approaches
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