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AIM: To evaluate the specific role of ICAM-1 in host responses against endodontic infection. METHODS: Apical periodontitis was experimentally induced in the mandibular first molars of ICAM-1 knockout and wild-type (WT) mice by pulp exposure to the oral environment. At 7, 21 and 42 days following pulp infection, the animals were euthanized and the jaws were prepared for analysis under conventional and fluorescence microscopy (histopathologic and morphometric analysis), immunohistochemistry (polymorphonuclear leucocytes), enzyme histochemistry (osteoclasts and cementoclasts) and RT-PCR (IL-1 α, TNF-α, INF-γ, IL-10, RANK, RANKL and OPG). A generalized linear model with GLIMMIX procedure with Satterthwaite approximation method of degrees of freedom, Tukey-Kramer, pseudo-ranking nonparametric, Bonferroni-Holm multiple testing adjustment, analysis of variance (ANOVA) and the Tukey's multiple comparisons tests were used to evaluate the statistical differences between the groups using SAS 9.4 and the GraphPad Prism 5.0 software (α = 0.05). RESULTS: Compared to WT mice, ICAM-1 knockout mice had significantly greater bone resorption (P < 0.05), reduced recruitment of neutrophils to periapical inflammatory tissues (P < 0.05) and an increased number of fibroblasts (P < 0.05) at all experimental periods. The osteoclast number was significantly higher in ICAM-1 KO than that of WT animals at all times (P < 0.05), while there was no significant difference between the groups regarding cementoclasts. At day 21, the level of IL-1α, RANK, RANKL and IL-10 had increased significantly in tissues from ICAM-1 KO versus WT mice (P < 0.05), while no significant difference was observed in TNF-α and OPG levels (P > 0.05). Tissue levels of INF-γ were significantly lower in ICAM-1 KO than those in WT mice (P < 0.05). CONCLUSION: ICAM-1 deficiency impaired the host response against endodontic infection, resulting in increased tissue destruction.

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Background: Reconstruction of customized cranial implants with a mesh structure using computer-assisted design and additive manufacturing improves the implant design, surgical planning, defect evaluation, implant-tissue interaction and surgeon's accuracy. The objective of this study is to design, develop and fabricate cranial implant with mechanical properties closer to that of bone and drastically decreases the implant failure and to improve the esthetic outcome in cranial surgery with precision fitting for a better quality of life. A customized cranial mesh implant is designed digitally, based on the Digital Imaging and Communication in Medicine files and fabricated using state of the Art-Electron Beam Melting an Additive Manufacturing technology. The EBM produced titanium implant was evaluated based on their mechanical strength and structural characterization. Results: The result shows, the produced mesh implants have a high permeability of bone ingrowth with its reduced weight and modulus of elasticity closer to that the natural bone thus reducing the stress shielding effect. Scanning electron microscope and micro-computed tomography (CT) scanning confirms, that the produced cranial implant has a highly regular pattern of the porous structure with interconnected channels without any internal defect and voids. Conclusions: The study reveals that the use of mesh implants in cranial reconstruction satisfies the need of lighter implants with an adequate mechanical strength, thus restoring better functionality and esthetic outcomes for the patients.

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La periodontitis es una enfermedad inflamatoria crónica multifactorial, la cual se inicia a partir de la biopelícula que se forma alrededor de los dientes y se acumula en margen gingival, colonizando el surco gingival. La complejidad de la biopelícula madura genera estímulos para las células epiteliales e inflamatorias y sobre las demás células del tejido conectivo activando los mecanismos de la respuesta inmune innata y adaptativa. Se reconoce que la acumulación de placa dental genera de forma indefectible gingivitis, pero se desconocen las señales específicas que disparan la periodontitis. Se reconoce también que microorganismos periodontopáticos como Aggregatibacter actynomicetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Prevotella intermedia, Prevotella nigrescens, entre otros, poseen mediadores osteolíticos que actúan directa o indirectamente en las células del hueso y que son responsables del proceso de remodelación ósea, lo cual desequilibra el eje RANKL-RANK/OPG. Los productos microbianos y la respuesta inflamatoria inducen la secreción de citoquinas específicas como IL-1B, TNFalfa y otros mediadores pro-inflamatorios como PGE2, metalloproteinases, MMP-8, MMP-3, RANKL, además los linfocitos T y B activados inducen la pérdida de hueso alveolar al sintetizar y secretar directamente RANKL. Debido a que la pérdida de hueso alveolar es uno de los signos patognomónicos de la enfermedad periodontal, se hace importante revisar los mecanismos moleculares que explican la destrucción ósea, así como algunos avances en el tratamiento óseo.

Periodontitis is a multifactorial chronic inflammatory disease started by biofilm accumulation around the teeth and the gingival margin including the gingival sulcus. Mature biofilm is complex in microbial nature and it triggers signals to the boundary connective tissue and epithelial cells activating mechanisms of innate and acquired immune response. It is known that the dental plaque accumulation indefectibly results in gingivitis. However the specific signals that lead to periodontitis are unknown. The main periodontopathic organisms are Aggregatibacter actynomicetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Prevotella intermedia, Prevotella nigrescens among others. Those microorganisms produce osteolytic mediators that act directly and indirectly on bone cells affecting the bone turnover rate, regulated by the axis RANKL-RANK/OPG. Microbial products and periodontal inflammation induce the release of specific cytokines IL-1B, TNFalpha, PGE2, metalloproteinases, MMP-8, MMP-3, RANKL, T and B lymphocytes elicit bone resorption. Indeed, alveolar bone loss is one of the most pathognomonic features of periodontal disease. Therefore it is essential to review the molecular mechanisms explaining periodontal destruction, as well as the advances in bone therapy.

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