Host response and peri-implantitis

Abstract Considering the absence of predictable and effective therapeutic interventions for the treatment of peri-implantitis, scientific evidence concerning the host response profile around dental implants could be important for providing in the future a wider preventive and/or therapeutic window for this peri-implant lesion, indicating biomarkers that provide quantifiable measure of response to peri-implant therapy. Moreover, a better knowledge of pattern of host osteo-immunoinflammatory modulation in the presence of peri-implantitis could either benefit the early diagnostic of the disease or to cooperate to prognostic information related to the status of the peri-implant breakdown. Finally, new evidences concerning the host profile of modulators of inflammation and of osseous tissue metabolism around dental implants could explain the individual susceptibility for developing peri-implant lesions, identifying individuals or sites with increased risk for peri-implantitis. The focus of this chapter was, based on a systematically searched and critically reviewed literature, summarizing the existing knowledge in the scientific research concerning the host osteo-immunoinflammatory response to the microbiological challenge related to periimplantitis.

Evaluation of the Impact of Alveolar Bone Resorption on the Root Formation of Molars in Transgenic Mice with RANK Over-expression / Evaluación del Imapacto de la Resorción Ósea Alveolar sobre la Formación Radicular de Molares en Ratones Transgénicos con Sobreexpresión de RANK

Alterations in the balance of the osteoblastic-osteoclastic activity (osteopetrosis, osteolysis) have an impact on the dental development. The over activation of the osteoclastogenesis pathway RANK/RANKL/OPG in RANKTg mice produces an acceleration of tooth eruption and root elongation, suggesting this pathway could control the speed of tooth formation. Evaluate the effect of osteoclastic hyperactivity on the root formation of molars in RANKTg mice. Histologic study both descriptive and comparative of the impact of hyper-resorption of the alveolar bone in Hertwig's epithelial root sheath (HERS) of molars in both RANKTg mice and controls. This is done through the immuno-detection of matrical, epithelial and cellular proliferation proteins with histological, histoenzymology and inmunohistochemical techniques. Osteoclastic hiperactivity in alveolar bone does not alter the root structure and integrity of molars in RANKTg mice; the acceleration in root formation does not alter the HERS integrity. An area of cellular hyper-proliferation in the apical follicular tissue of HERS was found, which could regulate root growth in response to osteoclastic activity. The overexpressed RANK produces an inhibition of amelogenin expression at 5 days of age, suggesting an indirect regulation of these cells by RANK/RANKL. Exploring other molecular factors expressed in HERS, and the related engram, would make possible the use of new therapies for the control of osseous and inflammatory pathologies during root formation.

Las alteraciones en el balance de la actividad osteoblástica-osteoclástica (osteopetrosis, osteolisis) tienen un impacto en el desarrollo dental. La activación de la vía sobre la osteoclastogénesis RANK/RANKL/OPG en ratones RANKTg produce una aceleración de la erupción de los dientes y elongación de las raíces, lo que sugiere que esta vía podría controlar la velocidad de formación de los dientes. El objetivo de este estudio consiste en evaluar el efecto de la hiperactividad osteoclástica en la formación de las raíces de los molares en ratones RANKTg. Se realizó un estudio histológico descriptivo y comparativo del impacto de la hiper-reabsorción del hueso alveolar sobre la vaina epitelial radicular (de Hertwig - HERS) de molares en ratones RANKTg y controles. Se realizó la inmuno-detección de la proliferación matricial, epitelial y celular de proteínas, combinada con técnicas histológicas, inmunohistoquímicas e histoenzimológicas. La hiperactividad osteoclástica en el hueso alveolar no altera la estructura de la raíz dentaria y la integridad de los molares en ratones RANKTg; la aceleración de la formación de la raíz no altera la integridad de la misma. Se encontró un área de hiper-proliferación celular en el tejido folicular apical del HERS, que podría regular el crecimiento de la raíz en respuesta a la actividad osteoclástica. La sobreexpresión en los RANK produce una inhibición de la expresión de amelogenina a los 5 días de edad, lo que sugiere una regulación indirecta de estas células por RANK/RANKL. La exploración de otros factores moleculares expresados en HERS, y el engrama relacionado, haría posible el uso de nuevas terapias para el control de patologías óseas e inflamatorias durante la formación de la raíz dentaria.

Porphyromonas gingivalis decreases osteoblast proliferation through IL-6-RANKL/OPG and MMP-9/TIMPs pathways.

Background: Porphyromonas gingivalis, an important periodontal pathogen, is closely associated with inflammatory alveolar bone resorption. This bacterium exerts its pathogenic effect indirectly through multiple virulence factors, such as lipopolysaccharides, fimbriae, and proteases. Another possible pathogenic path may be through a direct interaction with the host's soft and hard tissues (e.g., alveolar bone), which could lead to periodontitis. Aims and Objectives: The aim of the present study was to investigate the direct effect of live and heat-inactivated P gingivalis on bone resorption, using an in vitro osteoblast culture model. Results: Optical microscopy and 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide MTT assay revealed that live P gingivalis induced osteoblast detachment and reduced their proliferation. This effect was specific to live bacteria and was dependent on their concentration. Live P gingivalis increased IL-6 mRNA expression and protein production and downregulated RANKL and OPG mRNA expression. The effect of live P gingivalis on bone resorption was strengthened by an increase in MMP-9 expression and its activity. This increase was accompanied by an increase in TIMP-1 and TIMP-2 mRNA expression and protein production by osteoblasts infected with live P gingivalis. Conclusion: Overall, the results suggest that direct contact of P gingivalis with osteoblasts induces bone resorption through an inflammatory pathway that involves IL-6, RANKL/OPG, and MMP-9/TIMPs.

Agregado de trióxido mineral (MTA) e resposta imune: da imunidade inata à reabsorção óssea periapical / Mineral trioxide aggregate (MTA) and immune response: from innate immunity to periapical bone resorption

O agregado de trióxido mineral (MTA), pode ser um cimento retro-obturador utilizado em regiões inflamadas e/ou infectadas, deve ser biocompatível e não interferir negativamente na resposta imune periapical. Sendo essa resposta imune um papel protetor, prevenindo a disseminação de infecções, as implicações clínicas de suas alterações precisam ser estudadas. Nesse contexto, nosso objetivo foi observar o papel do MTA na imunidade inata, adaptativa e na reabsorção óssea. A atividade de macrófagos M1 e M2 peritoneais, na presença do MTA, foi objeto de nosso estudo na imunidade inata. Foram analisadas a viabilidade e aderência celular, a fagocitose de Saccharomyces boulardii, a produção de espécies reativas de oxigênio (ROI) e de nitrogênio (NO), assim como a atividade da arginase. A produção de IgG em resposta ao Fusobacterium nucleatum, a proliferação e produção de citocinas por células T pré-imunes estimuladas por anti-TCR e anti-CD28 e por células T de memória reativas ao F. nucleatum e ao Peptostreptococus anaerobius, na presença do MTA, foram analisadas no estudo da resposta imune adaptativa. Por último, a influência do MTA na osteoclastogênese medida por RANKL e a atividade desses osteoclastos também foram pesquisadas. Observou-se que o MTA não afetou nem a atividade antibacteriana, nem a cicatricial dos macrófagos M1 e M2. A produção de IgG ao F. necleatum em MTA foi estimulada em níveis comparáveis aos grupos imunizados com F. nucleatum em adjuvante de Freund a adjuvante de hidróxido de alumínio. O MTA estimulou a proliferação das células T pré-imunes estimuladas com anti-TCR e anti-CD 28, elevou a produção das citocinas TNF, RANKL e IFN-y, além de diminuir a produção de IL-10, por essas células. O MTA reduziu a proliferação das células T de memória antígeno específica...