Influência do FK-506 sobre a expressão de RANKL e OPG na doença periodontal induzida: estudo in vivo e in vitro

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Papel do receptor tipo-2 ativado por protease (PAR-2) na doença periodontal

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Impacto de drogas antiplaquetárias na doença e no reparo periodontal experimental em ratos

Pós-graduação em Odontologia - FOAR

Evidências da associação entre testosteronas e doença periodontal no sexo masculino

Pós-graduação em Odontologia - FOAR

O efeito da carga oclusal no processo de reparo do ligamento periodontal após reimplante imediato em molar de ratos: avaliação histológica e imunoistoquímica

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

Efeitos do laser e da terapia fotodinâmica no tratamento periodontal mecânico em ratas ovariectomizadas e sob influência sistêmica de nicotina: estudo histomorfométrico e imunoistoquímico

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

Modulation of cell proliferation, survival and gene expression by RAGE and TLR signaling in cells of the innate and adaptive immune response: role of p38 MAPK and NF-KB

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Implications of Surface and Bulk Properties of Abutment Implants and Their Degradation in the Health of Periodontal Tissue

The aim of the current review was to investigate the implications of the surface and bulk properties of abutment implants and their degradation in relation to periodontal health. The success of dental implants is no longer a challenge for dentistry. The scientific literature presents several types of implants that are specific for each case. However, in cases of prosthetics components, such as abutments, further research is needed to improve the materials used to avoid bacterial adhesion and enhance contact with epithelial cells. The implanted surfaces of the abutments are composed of chemical elements that may degrade under different temperatures or be damaged by the forces applied onto them. This study showed that the resulting release of such chemical elements could cause inflammation in the periodontal tissue. At the same time, the surface characteristics can be altered, thus favoring biofilm development and further increasing the inflammation. Finally, if not treated, this inflammation can cause the loss of the implant.

Alcoholic and isocaloric diet, but not ovariectomy, influence the apoptosis of bone cells within the alveolar bone crest of rats

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

Synergistic Anti-Inflammatory Activity of the Antimicrobial Peptides Human Beta-Defensin-3 (hBD-3) and Cathelicidin (LL-37) in a Three-Dimensional Co-Culture Model of Gingival Epithelial Cells and Fibroblasts

Given the spread of antibiotic resistance in bacterial pathogens, antimicrobial peptides that can also modulate the immune response may be a novel approach for effectively controlling periodontal infections. In the present study, we used a three-dimensional (3D) co-culture model of gingival epithelial cells and fibroblasts stimulated with Aggregatibacter actinomycetemcomitans lipopolysaccharide (LPS) to investigate the anti-inflammatory properties of human beta-defensin-3 (hBD-3) and cathelicidin (LL-37) and to determine whether these antimicrobial peptides can act in synergy. The 3D co-culture model composed of gingival fibroblasts embedded in a collagen matrix overlaid with gingival epithelial cells had a synergistic effect with respect to the secretion of IL-6 and IL-8 in response to LPS stimulation compared to fibroblasts and epithelial cells alone. The 3D co-culture model was stimulated with non-cytotoxic concentrations of hBD-3 (10 and 20 mu M) and LL-37 (0.1 and 0.2 mu M) individually and in combination in the presence of A. actinomycetemcomitans LPS. A multiplex ELISA assay was used to quantify the secretion of 41 different cytokines. hBD-3 and LL-37 acted in synergy to reduce the secretion of GRO-alpha, G-CSF, IP-10, IL-6, and MCP-1, but only had an additive effect on reducing the secretion of IL-8 in response to A. actinomycetemcomitans LPS stimulation. The present study showed that hBD-3 acted in synergy with LL-37 to reduce the secretion of cytokines by an LPS-stimulated 3D model of gingival mucosa. This combination of antimicrobial peptides thus shows promising potential as an adjunctive therapy for treating inflammatory periodontitis.

Análise hematológica por hemograma, creatinina, triglicérides e colesterol em ratos diabéticos portadores de infecção pulpar e/ou periodontal

Pós-graduação em Ciência Odontólogica - FOA

Periodontal disease-associated compensatory expression of osteoprotegerin is lost in type 1 diabetes mellitus and correlates with alveolar bone destruction by regulating osteoclastogenesis

Alveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.

Host responses induced by different animal models of periodontal disease: a literature review

Periodontitis is an infectious disease characterized by chronic inflammation of the periodontium, and it is mediated and modulated by the host immune system. In the presence of microorganisms or other antigens, immune cells (macrophages/monocytes, dendritic cells, lymphocytes, neutrophils), endothelial cells and fibroblasts secrete cytokines and trigger immune and inflammatory reactions. However, when synthesized at high levels, cytokines modify the pattern of cellular response, participating substantially in the development of chronic inflammatory pathologies, such as periodontal disease. Understanding the origin and progression of bone resorption is one of the primary goals of the field of periodontics, aiming to arrest the disease progression and to optimize future treatments. For this purpose, the development of experimental models is an important and necessary step before entering into clinical trials with new therapies. The purpose of this study is to characterize/evaluate the tissue changes induced by various models of experimental periodontitis through a literature review.

Periodontal pathogens directly promote autoimmune experimental arthritis by inducing a TLR2- and IL-1-Driven Th17 response

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Green tea polyphenol epigallocatechin-3-gallate and cranberry proanthocyanidins act in synergy with cathelicidin (LL-37) to reduce the LPS-induced inflammatory response in a three-dimensional co-culture model of gingival epithelial cells and fibroblasts

Objectives: The human antimicrobial peptide cathelicidin (LL-37) possesses anti-inflammatory properties that may contribute to attenuating the inflammatory process associated with chronic periodontitis. Plant polyphenols, including those from cranberry and green tea, have been reported to reduce inflammatory cytokine secretion by host cells. In the present study, we hypothesized that A-type cranberry proanthocyanidins (AC-PACs) and green tea epigallocatechin-3-gallate (EGCG) act in synergy with LL-37 to reduce the secretion of inflammatory mediators by oral mucosal cells. Methods: A three-dimensional (3D) co-culture model of gingival epithelial cells and fibroblasts treated with non-cytotoxic concentrations of AC-PACs (25 and 50 mg/ml), EGCG (1 and 5 mg/ml), and LL-37 (0.1 and 0.2 mM) individually and in combination (AC-PACs + LL-37 and EGCG + LL-37) were stimulated with Aggregatibacter actinomycetemcomitans lipopolysaccharide (LPS). Multiplex ELISA assays were used to quantify the secretion of 54 host factors, including chemokines, cytokines, growth factors, matrix metalloproteinases (MMPs), and tissue inhibitors of metalloproteinases (TIMPs). Results: LL-37, AC-PACs, and EGCG, individually or in combination, had no effect on the regulation of MMP and TIMP secretion but inhibited the secretion of several cytokines. ACPACs and LL-37 acted in synergy to reduce the secretion of CXC-chemokine ligand 1 (GRO-a), granulocyte colony-stimulating factor (G-CSF), and interleukin-6 (IL-6), and had an additive effect on reducing the secretion of interleukin-8 (IL-8), interferon-g inducible protein 10 (IP-10), and monocyte chemoattractant protein-1 (MCP-1) in response to LPS stimulation. EGCG and LL-37 acted in synergy to reduce the secretion of GRO-a, G-CSF, IL-6, IL-8, and IP-10, and had an additive effect on MCP-1 secretion. Conclusion: The combination of LL-37 and natural polyphenols from cranberry and green tea acted in synergy to reduce the secretion of several cytokines by an LPS-stimulated 3D coculture model of oral mucosal cells. Such combinations show promising results as potential adjunctive therapies for treating inflammatory periodontitis.