Orthodontic movement after periodontal regeneration of class II furcation: a pilot study in dogs

Purpose: the effect of orthodontic movement on the periodontal tissues of maxillary second pre-molars, after regenerative treatment for class II furcations, was evaluated in four mongrel dogs.Material and Methods: Class II furcation lesions were created. After 75 days they were treated with bovine bone mineral matrix and guided tissue regeneration with absorbable membrane. After 2 months of daily plaque control, each of the dog's furcation pre-molars was randomly assigned to a test or control group. Orthodontic appliances were placed on both sides of the maxilla using third pre-molars and canines as anchorages. In the test group, bodily orthodontic movement of the second pre-molars was performed in the mesial direction for 3 months while control pre-molars remained unmoved. The dogs were sacrificed for histometric and histologic analyses.Results: There were no statistically significant differences between the two groups in total bone and biomaterial areas or linear extension of periodontal regeneration on the radicular surfaces. In the test group, however, there was a tendency to a greater quantity of bone and a lesser quantity of biomaterial.Conclusion: the orthodontic movement was not pre-judicial to the results obtained with the regenerative periodontal treatment.

Protective effects of Tacrolimus, a calcineurin inhibitor, in experimental periodontitis in rats

Objective: Periodontitis is a well-appreciated example of leukocyte-mediated bone loss and inflammation with pathogenic features similar to those observed in other inflammatory diseases, such as arthritis. Since Tacrolimus, is an immunomodulatory drug used for the treatment of some cases of arthritis, we hypothesized that it may modulate periodontal disease.Design: Using a murine model of ligature-induced periodontal disease, we assessed the effects of daily administrations of Tacrolimus (1 mg/kg body weight) on bone loss, enzymatic (myeloperoxidase) analysis, differential white blood cells counts, airpouch exudate and cytokine expression for 5-30 days.Results: Radiographic, enzymatic (myeloperoxidase) and histological analysis revealed that Tacrolimus reduced the severity of periodontitis. More specifically, Tacrolimus suppressed the expression of serum interleukin (IL-1 beta), tumour necrosis factor (TNF-alpha), IL-6, airpouch exudate PGE(2) and leukocytosis usually observed after the induction of periodontitis. Tacrolimus treatment in periodontitis-induced rats conferred protection against the inflammation-induced tissue and bone loss associated with periodontitis, through a mechanism involving IL-1 beta, TNF-alpha and IL-6.Conclusions: the effects of Tacrolimus on periodontal disease pathogenesis may provide clues to a novel approach to host modulation therapy in destructive periodontal disease. (C) 2007 Elsevier Ltd. All rights reserved.

Accuracy of zoomed digital image in the detection of periodontal bone defect: in vitro study

Objectives: (1) To evaluate the intraobserver agreement related to image interpretation and (2) to compare the accuracy of 100%, 200% and 400% zoomed digital images in the detection of simulated periodontal bone defects.Methods: Periodontal bone defects were created in 60 pig hemi-mandibles with slow-speed burs 0.5 mm, 1.0 mm, 1.5 mm, 2.0 mm and 3.0 mm in diameter. 180 standardized digital radiographs were made using Schick sensor and evaluated at 100%, 200% and 400% zooming. The intraobserver agreement was estimated by Kappa statistic (kappa). For the evaluation of diagnostic accuracy receiver operating characteristic (ROC) analysis was performed followed by chi-square test to compare the areas under ROC curves according to each level of zooming.Results: For 100%, 200% and 400% zooming the intraobserver agreement was moderate (kappa = 0.48, kappa = 0.54 and kappa = 0.43, respectively) and there were similar performances in the discrimination capacity, with ROC areas of 0.8611 (95% CI: 0.7660-0.9562), 0.8600 (95% CI: 0.7659-0.9540), and 0.8368 (95% CI: 0.7346-0.9390), respectively, with no statistical significant differences (chi(2)-test; P = 0.8440).Conclusions: A moderate intraobserver agreement was observed in the classification of periodontal bone defects and the 100%, 200% and 400% zoomed digital images presented similar performances in the detection of periodontal bone defects.

Actinobacillus actinomycetemcomitans lipopolysaccharide induces interleukin-6 expression through multiple mitogen-activated protein kinase pathways in periodontal ligament fibroblasts

Actinobacillus actinomycetemcomitans plays a major role in the pathogenesis of aggressive periodontitis. Lipopolysaccharide (LPS) derived from A. actinomycetemcomitans is a key factor in inflammatory cytokine generation within periodontal tissues. In this study, we identify major mitogen-activated protein kinase (MAPK) signaling pathways induced by A. actinomycetemcomitans LPS, Escherichia coli LPS and interleukin-1 beta (IL-1 beta) in a murine periodontal ligament (mPDL) fibroblast cell line. Immunoblot analysis was used to assess the phosphorylated forms of p38, extracellular-regulated kinase (ERK) and c-jun N-terminal kinase (JNK) MAPK following stimulation with A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta. IL-6 mRNA induction was detected via reverse transcription-polymerase chain reaction, while protein levels were quantified via enzyme-linked immunosorbent assays (ELISA). We utilized biochemical inhibitors of p38, ERK and JNK MAPK to identify the MAPK signaling pathways needed for IL-6 expression. Additional use of stable mPDL cell lines containing dominant negative mutant constructs of MAPK kinase-3 and -6 (MKK-3/6) and p38 null mutant mouse embryonic fibroblast (MEF) cells were used to substantiate the biochemical inhibitor data. Blocking p38 MAPK with SB203580 reduced the induction of IL-6 mRNA by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta by > 70%, > 95% and similar to 60%, respectively. IL-6 ELISA indicated that blocking p38 MAPK reduced the IL-6 protein levels induced by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta by similar to 60%, similar to 50% and similar to 70%, respectively. All MAPK inhibitors significantly reduced the IL-6 protein levels induced by A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta whereas only p38 inhibitors consistently reduced the A. actinomycetemcomitans LPS, E. coli LPS and IL-1 beta induction of IL-6 mRNA steady-state levels. The contribution of p38 MAPK LPS-induced IL-6 expression was confirmed using MKK-3/6 dominant negative stable mPDL cell lines. Wild-type and p38 alpha(-/-) MEF cells provided additional evidence to support the role of p38 alpha MAPK in A. actinomycetemcomitans LPS-stimulated IL-6. Our results indicate that induction of IL-6 by E. coli LPS, IL-1 beta and A. actinomycetemcomitans LPS requires signaling through MKK-3-p38 alpha ERK, JNK and p38 MAPK in mPDL cells.

Combined periodontal, orthodontic, and restorative treatment of pathologic migration of anterior teeth: A case report

Pathologic tooth migration related to periodontal disease is a common chief complaint of periodontal patients. This paper describes the treatment of a case of severe periodontal disease and disfiguring pathologic migration of maxillary central incisors, which required a multidisciplinary approach. After conventional pert. odontal treatment was performed, the anterior diastema was closed using a combination of orthodontic therapy and restorative treatment. A 6-month follow-up examination of this case revealed resolution of the anterior pathologic migration, with gains in clinical attachment levels and a successful esthetic and functional final result.

Curcumin modulates the immune response associated with LPS-induced periodontal disease in rats

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Polymorphisms and Haplotypes in the Interleukin-4 Gene are Associated With Chronic Periodontitis in a Brazilian Population

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Differential regulation of MMP-13 expression in two models of experimentally induced periodontal disease in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)