Clopidogrel Enhances Periodontal Repair in Rats Through Decreased Inflammation

Aim We hypothesized that platelet inactivation induced by drugs might interfere with periodontal repair in experimental periodontitis by suppressing the release of biological mediators from platelets at the site of injury. Material and Methods 60 rats were randomly assigned to 6 groups (n=10) and ligatures were placed around lower first molars of three groups. The other three groups were used as negative controls. Ligatures were removed after 10 days of periodontitis induction and all groups were submitted to treatment with aspirin (Asp) (30 mg/kg), clopidogrel (Clop) (75 mg/kg) or NaCl 0.9% intragastrically once daily for 3 days. Periodontal tissue was assessed by the measurement of CXCL12, CXCL4, CCL5 and PDGF by ELISA; histomorphometric analysis of PMN infiltration, attachment loss, bone loss and osteoclast numbers and quantification of blood vessels by imunnohistochemistry. Results During periodontal repair and treatment with NaCl 0.9%, CCL5 was decreased and CXCL12 increased when compared to negative control groups. Asp and Clop did not affect CCL5 expression, decreased CXCL12 but only Clop decreased CXCL4 and PDGF content compared to saline-treated animals. Clop increased blood vessel number, reduced PMN count, and decreased attachment and bone loss, also decreased osteoclast number in animals submitted or not to periodontal repair. Conclusion Systemic administration of Clop during 3 days improved the repair process associated with experimental periodontal disease, suggesting that it may have therapeutic value under situations where tissues undergo a transition from inflammation to repair

Telomere length and its relationship with chronic diseases - New perspectives for periodontal research

Objective: The ageing process is accompanied by a variety of cellular modifications, and telomere shortening is a common finding. Large epidemiological studies have reported an association between shorter telomere length in peripheral leukocytes and several inflammatory diseases of the elderly including diabetes, atherosclerosis and, recently, periodontitis. The primary aim of this study was to critically discuss available evidence regarding the potential mechanisms relating shorter telomeres to periodontitis. Design: A narrative literature review was performed to report evidence relating shorter telomeres to the ageing process and inflammation. Then, we searched MEDLINE (1950 to May 2012) and ISI WEB OF SCIENCE (1950 to May 2012) databases for the combination of the terms 'telomere' and 'periodontitis'. Results: Although these associations suggest a possible role of telomere attrition in the onset or evolution of chronic inflammatory diseases, only two studies addressed the relationship between telomere length and periodontitis. Conclusion: We suggest that the chronic inflammatory burden observed in people with chronic periodontitis could represent the driver of telomere shortening. However, further evidence is needed to confirm whether inflammation is the cause or the consequence of the shorter leukocyte telomere length observed in people with periodontitis. © 2012 Elsevier Ltd. All rights reserved

The Use of Etoricoxib and Celecoxib for Pain Prevention After Periodontal Surgery: A Double-Masked, Parallel-Group, Placebo-Controlled, Randomized Clinical Trial

Background: Postoperative pain is an adverse effect of periodontal surgeries and may therefore be prevented or minimized. This study was conducted to evaluate the clinical efficacy of two selective cyclooxygenase-2 inhibitors, celecoxib and etoricoxib, on pain prevention after periodontal surgery.Methods: For this double-masked, parallel-group, placebo-controlled, and randomized clinical trial, 56 open-flap debridement surgeries were performed. The groups received three different protocols 1 hour before surgery: 1) 200 mg celecoxib (and another 200 mg 12 hours after the first dose); 2) 120 mg etoricoxib; or 3) placebo. Pain intensity and discomfort were assessed up to 2 days after surgery using the visual analog scale and the four-point verbal rating scale, respectively. Patients were instructed to take 750 mg acetaminophen as a rescue medication if necessary.Results: Pain intensity levels in the etoricoxib group were lower than in the placebo group at the 2-, 3-, 4-, 5-, 6-, and 7-hour periods after surgery (Kruskal-Wallis test; P < 0.05). There was no statistically significant difference between celecoxib and etoricoxib. Discomfort in the celecoxib group was significantly lower than in the placebo group only at the 3-hour period (P = 0.03). Rescue medication intake was significantly less frequent in the etoricoxib group than in the placebo and celecoxib groups (analysis of variance; P = 0.009).Conclusion: It was concluded that a single etoricoxib dose is not superior to two split doses of celecoxib when used for pain prevention after open-flap debridement surgery. J Periodontol 2011;82:1238-1244.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES

Preemptive dexamethasone and etoricoxib for pain and discomfort prevention after periodontal surgery: A double-masked, crossover, controlled clinical trial

Background: Several anti-inflammatory drugs have been used to reduce pain and discomfort after periodontal surgeries. This study evaluates the efficacy of using etoricoxib and dexamethasone for pain prevention after open-flap debridement surgery. Methods: For this prospective, double-masked, crossover, placebo-controlled, randomized clinical trial, open-flap debridement surgeries were performed on 15 patients (eight males and seven females, age range 20 to 56 years: mean age ± SD: 40 ± 9.7 years) who presented with chronic periodontitis after nonsurgical periodontal therapy at three quadrants. Each patient underwent three surgical procedures at intervals of 30 days and received one of the following premedication protocols 1-hour before surgery: group 1 = placebo, group 2 = 8 mg dexamethasone, and group 3 = 120 mg etoricoxib. Rescue medication (750 mg acetaminophen) was given to each patient who was instructed to take it when necessary. Pain intensity and discomfort were evaluated by a 101-point numeric rate scale and a four-point verbal rate scale, respectively, hourly for the first 8 hours after surgery and three times a day on the following 3 days. Results: The results demonstrate that groups 2 and 3 present reduced postoperative pain-intensity levels compared to group 1. There were statistically significant differences at the 4, 5, 6, 7, and 8 hour-periods after surgery (Friedman test; P<0.05). Furthermore, rescue-medication intake was significantly lower for groups 2 and 3 than for group 1 (analysis of variance; P<0.02). Conclusion: The adoption of a preemptive medication protocol using etoricoxib or dexamethasone may be considered effective for pain and discomfort prevention after open-flap debridement surgeries

Influencia de la enfermedad periodontal en el control metabólico de pacientes con diabetes mellitus tipo 2: revisión de la literatura

There may be an interaction between periodontal disease and sonic systemic diseases such as diabetes mellitus The objective of this review was to verify by means of a review of clinical trials if is a positive association between periodontal disease and the glycerine control of type 2 diabetes mellitus (DM 2) patients Eleven articles that fit the study criteria were revised It was concluded that periodontal disease may influence the metabolic control of 2 Additional studies with larger sample sizes and longer follow up are necessary for a better clarification of this issue (Rev Med Chile 2010 138 1172 1178

Efficacy of Anesthetic Agents to Delay Pain Onset After Periodontal Surgery

The aim of this study was to evaluate the influence of 2 anesthetic agents on patients' postoperative pain perception after periodontal surgery. For this parallel-group, double-blinded, randomized clinical trial, 36 open flap debridement surgeries were performed on patients who presented with periodontal disease with clinical signs of inflammation after nonsurgical treatment on at least 1 quadrant. Patients were allocated to 1 of the following groups: group 1, 2% lidocaine with 1 ∶ 100,000 epinephrine; group 2, 2% mepivacaine with 1 ∶ 100,000 norepinephrine. Pain intensity was assessed using the visual analog scale during the first 8 hours after surgery. All patients received 750-mg acetaminophen tablets, which they were instructed to take as a rescue medication if necessary. The results demonstrated that postoperative pain intensity was statistically lower in group 2 than in group 1 at the 1-, 2-, and 3-hour periods after surgery, although the pain intensity for all groups could be considered mild. In conclusion, patients in both groups reported similar mild pain after periodontal surgery

Influence of Parstatin on Experimental Periodontal Disease and Repair in Rats

Background: Parstatin is a 41-amino acid peptide, formed by proteolytic cleavage on activation of the protease activated receptor-1, with antiangiogenic properties. The purpose of this study is to evaluate the influence of synthetic parstatin on experimental periodontal disease and repair in rats.Methods: Ligature-induced periodontitis was established in rats and the influence of parstatin administration was assessed after 8 and 15 days for periodontal disease and 24 hours and 8 days after repair after ligature removal.Results: Parstatin administration significantly inhibited gingival myeloperoxidase activity, interleukin (IL)-1 beta, tumor necrosis factor-alpha, and IL-6 levels and led to suppression of macrophages and collagen degradation. At periodontal tissues under repair, parstatin increased the gingival levels of endostatin and decreased vascular endothelial growth factor expression and blood vessel number but did not influence histologic healing. In addition, the tomographic linear bone loss was significantly reduced at 15 days of periodontitis when the rats were treated with parstatin compared to their respective phosphate-buffered saline-treated controls.Conclusions: Parstatin suppresses the periodontal tissue breakdown followed by experimental periodontitis in rats and did not impair periodontal tissue repair, despite its antiangiogenic effect. Parstatin may represent a novel approach to modulate host response in chronic periodontal disease.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP