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1.
Clín. investig. arterioscler. (Ed. impr.) ; 32(1): 33-42, ene.-feb. 2020. graf, ilus
Artigo em Espanhol | IBECS | ID: ibc-187006

RESUMO

La osteoporosis es una enfermedad esquelética sistémica, caracterizada por baja masa ósea y deterioro en la microarquitectura del tejido óseo, que origina un aumento de la fragilidad ósea y, en consecuencia, mayor susceptibilidad a fracturas. Es la enfermedad metabólica ósea más frecuente en nuestra población, y las fracturas resultantes de la osteoporosis son cada vez más comunes. Por otro lado, la calcificación vascular es un factor de riesgo reconocido de morbimortalidad cardiovascular, que históricamente era considerada como un proceso pasivo y degenerativo. Sin embargo, en la actualidad se reconoce como un proceso activo que tiene características histopatológicas, de composición mineral y de mecanismos de iniciación y desarrollo propias de la formación del hueso. Paradójicamente, los pacientes con osteoporosis muestran con frecuencia calcificaciones vasculares. Tradicionalmente se han considerado como procesos independientes relacionados con la edad, aunque estudios epidemiológicos recientes han evidenciado que existe una estrecha relación entre la pérdida de masa ósea y la calcificación vascular, independiente de la edad. De hecho, ambas entidades comparten factores de riesgo y mecanismos fisiopatológicos. Entre ellos destacan la relación entre proteínas de origen óseo, como la osteopontina y la osteoprotegerina, con la patología vascular, y el sistema intercelular proteico RANK/RANKL/OPG y la vía de señalización Wnt. Los mecanismos vinculados en ambas patologías deben considerarse en las decisiones clínicas, dado que los tratamientos para la osteoporosis podrían tener efectos imprevistos en la calcificación vascular, y a la inversa. En definitiva, una mejor comprensión de la relación entre ambas entidades puede contribuir a plantear estrategias para disminuir la prevalencia creciente de calcificación vascular y osteoporosis en la población que envejece


Osteoporosis is a systemic skeletal disease, characterised by low bone mass and deterioration in the micro-architecture of bone tissue, which causes increased bone fragility and consequently greater susceptibility to fractures. It is the most frequent metabolic bone disease in our population, and fractures resulting from osteoporosis are becoming more common. Furthermore, vascular calcification is a recognised risk factor of cardiovascular morbidity and mortality that historically has been considered a passive and degenerative process. However, it is currently recognised as an active process, which has histopathological characteristics, mineral composition and initiation and development mechanisms characteristic of bone formation. Paradoxically, patients with osteoporosis frequently show vascular calcifications. Traditionally, they have been considered as independent processes related to age, although more recent epidemiological studies have shown that there is a close relationship between the loss of bone mass and vascular calcification, regardless of age. In fact, both conditions share risk factors and pathophysiological mechanisms. These include the relationship between proteins of bone origin, such as osteopontin and osteoprotegerin (OPG), with vascular pathology, and the intercellular protein system RANK/RANKL/OPG and the Wnt signalling pathway. The mechanisms linked in both pathologies should be considered in clinical decisions, given that treatments for osteoporosis could have unforeseen effects on vascular calcification, and viceversa. In short, a better understanding of the relationship between both entities can help in proposing strategies to reduce the increasing prevalence of vascular calcification and osteoporosis in the aging population


Assuntos
Humanos , Osteoporose/etiologia , Calcificação Vascular/etiologia , Fatores de Risco , Doenças Cardiovasculares/epidemiologia , Osteoporose/fisiopatologia , Calcificação Vascular/fisiopatologia , Calcificação Vascular/classificação , Cálcio/uso terapêutico , Osteoclastos/metabolismo , beta Catenina
2.
Rev. osteoporos. metab. miner. (Internet) ; 11(2): 39-45, abr.-jun. 2019. graf, ilus
Artigo em Espanhol | IBECS | ID: ibc-188335

RESUMO

La activación de la señalización de Wnt/β‐catenina en células del linaje osteoblástico conduce a un aumento en la masa ósea a través de un mecanismo dual: por una parte, aumentando la osteoblastogénesis, y por otra, disminuyendo la os‐teoclastogénesis. El predominio de un mecanismo sobre otro depende del estado madurativo del osteoblasto en el que produzca la acumulación de β‐catenina. La activación de la señalización de Wnt/β‐catenina en células del linaje osteo‐clástico y sus posibles efectos en la regulación de la masa ósea es menos conocida. Estudios previos han demostrado que la ablación condicional de β‐catenina en los osteoclastos induce una disminución de la masa ósea asociada a un aumento de los osteoclastos, y este hecho se ha atribuido a un incremento de la osteoclastogénesis. Sin embargo, no se han evaluado otras posibilidades alternativas como que una disminución de la apoptosis normal de los osteoclastos pueda también contribuir al mayor número de los mismos. En este trabajo, para obtener información sobre este hecho, generamos ratones en los que la β‐catenina se eliminó selectivamente de las células del linaje de monocito/macrófago utilizando un alelo flanqueado de la β‐catenina (Catnbf) junto con la línea de deleción LisozimaMCre (LysMCre). El análisis tridimensional de los huesos de los ratones Catnbf/f; LysMrevelaron una disminución significativa del grosor de la cortical femoral, mientras que el hueso trabecular vertebral no se vio afectado. Este fenotipo se asoció con un mayor número de osteoclastos en la superficie ósea. El número de osteoclastos en los cultivos procedentes de los ratones Catnbf/f; LysMfuedos veces mayor que en los cultivos obtenidos de los ratones control. La administración de WNT3a atenuó la formación de osteoclastos inducida por M‐CSF y RANKL in vitro. Además, WNT3a promovió la apoptosis de osteoclastos, y este efecto fue contrarrestado, tanto por la presencia de DKK1 como por la ausencia de β‐catenina. En conjunto, estos resultados apoyan un efecto autónomo celular de la β‐catenina en el osteoclasto, y proporcionan evidencia convincente del papel proapoptótico de β‐catenina en estas células


The activation of Wnt/β‐catenin signaling in cells of the osteoblastic lineage leads to an increase in bone mass through a dual mechanism: increasing osteoblastogenesis and decreasing osteoclastogenesis. The predominance of one mechanism over another depends on the maturational state of the osteoblast in which β‐catenin accumulation occurs. The activation of Wnt/β‐catenin signaling in cells of the osteoclastic lineage and its possible effects on the regulation of bone mass is less known. Previous studies have shown that conditional ablation of β‐catenin in osteoclasts induces a decrease in bone mass associated with an increase in osteoclasts, and this fact has been attributed to an increase in osteoclastogenesis. However, other alternative possibilities have not been evaluated, such as that a decrease in the normal osteoclastapoptosis may also contribute to the greater number of osteoclasts. In this paper, to obtain information about this fact, we generated mice in which β‐catenin was selectively eliminated from cells of the monocyte/macrophage lineage usingan allele flanked by β‐catenin (Catnbf) together with the deletion line LisozimaMCre (LysMCre). The three‐dimensional analysis of the bones of the Catnbf/f;LysMmice revealed a significant decrease in the thickness of the femoral cortex, while the trabecular bone of the vertebrae was not affected. This phenotype was associated with a greater number ofosteoclasts on the bone surface. The number of osteoclasts in the cultures from the Catnbf/f;LysMmice was twice as high as in the cultures obtained from the control mice. The administration of WNT3a attenuated the osteoclast formation induced by M‐CSF and RANKL in vitro. In addition, WNT3a promoted apoptosis of osteoclasts, and this effect was counteracted, both by the presence of DKK1 and by the absence of β‐catenin. Taken together, these results support a cellular autonomous effect of β‐catenin in the osteoclast, and provide convincing evidence of the proapoptotic role of β‐cateninin these cells


Assuntos
Animais , Camundongos , Apoptose , Osteoclastos , Proteína Wnt3A/metabolismo , Fator Estimulador de Colônias de Macrófagos/metabolismo , NF-kappa B/metabolismo , Fenótipo , Reação em Cadeia da Polimerase em Tempo Real , Western Blotting , Modelos Animais de Doenças
3.
Rev. clín. med. fam ; 12(2): 101-104, jun. 2019. ilus
Artigo em Espanhol | IBECS | ID: ibc-186264

RESUMO

La hipercalcemia es un hallazgo casual frecuente en el ámbito de la Atención Primaria, así como en los servicios de Urgencias. Valores poco elevados de calcemia o una instauración gradual de la misma suelen pasar clínicamente desapercibidos, por lo que su diagnóstico en pacientes asintomáticos es, con frecuencia, incidental. Nuestro objetivo principal en el diagnóstico diferencial de la hipercalcemia es determinar el mecanismo subyacente, sabiendo que el hiperparatiroidismo primario (HPP), junto con las neoplasias malignas, es responsable de hasta el 90 % de los casos; dichas entidades deben diferenciarse temprano para proporcionar al paciente un tratamiento óptimo y un pronóstico preciso. En nuestro trabajo presentamos el caso clínico de una mujer de 87 años, con antecedentes de hipercalcemia asintomática sostenida, que consulta por dolor e impotencia funcional no traumática del brazo izquierdo. En la prueba de imagen se observó una fractura del húmero proximal izquierdo sobre una estructura ósea alterada con grandes áreas quísticas "en sacabocados", entidad que recibe el nombre de osteítis fibrosa quística y que, aunque poco frecuente, es específica del HPP; en este caso, y tras completar el estudio, se vio que era debido a un adenoma paratiroideo único, responsable de hasta el 85 % de los casos del HPP. El único tratamiento definitivo, la paratiroidectomía, fue rechazado por la paciente, en quien se inició así tratamiento farmacológico, presentando hoy en día una buena evolución clínico-analítica. Las recomendaciones para los pacientes que no se someten a cirugía paratiroidea incluyen el control de las concentraciones séricas de calcio y densitometría ósea anuales


Hypercalcemia is a common chance finding in the primary care setting, as well as in emergency services. Low values of calcemia or its gradual establishment usually go clinically unnoticed, so the diagnosis is often incidental in asymptomatic patients. Our main objective in the differential diagnosis of hypercalcemia is to determine the underlying mechanism, knowing that primary hyperparathyroidism (PHPT) together with malignant neoplasms are responsible for up to 90% of the cases; these conditions must be differentiated early to provide the patient with optimal treatment and accurate prognosis. In our work, we present the clinical case of an 87-year-old woman with a history of sustained asymptomatic hypercalcemia, who presents with pain and non-traumatic functional deficit of the left arm. The imaging test showed a left proximal humerus fracture on an altered bone structure with large "punched-out" cystic areas, an entity that is called osteitis fibrosa cystica and that, although rare, is specific to PHPT; in this case, and after completing the study, it was seen that it was due to a parathyroid adenoma, responsible for up to 85% of cases of PHPT. The only definitive treatment, parathyroidectomy, was rejected by the patient. Therefore pharmacological treatment was initiated, presenting a good clinical-analytical evolution. Recommendations for patients who do not undergo parathyroid surgery include annual monitoring of serum calcium concentrations and bone densitometry


Assuntos
Humanos , Feminino , Idoso de 80 Anos ou mais , Osteíte Fibrosa Cística/diagnóstico , Hipercalcemia/diagnóstico , Hiperparatireoidismo Primário/complicações , Neoplasias das Paratireoides/diagnóstico , Atenção Primária à Saúde , Adenoma/diagnóstico , Achados Incidentais , Osteoclastos/efeitos dos fármacos , Denosumab/uso terapêutico , Difosfonatos/uso terapêutico , Conservadores da Densidade Óssea/uso terapêutico
5.
J. physiol. biochem ; 74(1): 3-8, feb. 2018. graf
Artigo em Inglês | IBECS | ID: ibc-178912

RESUMO

The taste receptor type 1 (TAS1R) family of heterotrimeric G protein-coupled receptors participates in monitoring energy and nutrient status. TAS1R member 3 (TAS1R3) is a bi-functional protein that recognizes amino acids such as L-glycine and L-glutamate or sweet molecules such as sucrose and fructose when dimerized with TAS1R member 1 (TAS1R1) or TAS1R member 2 (TAS1R2), respectively. It was recently reported that deletion of TAS1R3 expression in Tas1R3 mutant mice leads to increased cortical bone mass but the underlying cellular mechanism leading to this phenotype remains unclear. Here, we independently corroborate the increased thickness of cortical bone in femurs of 20-week-old male Tas1R3 mutant mice and confirm that Tas1R3 is expressed in the bone environment. Tas1R3 is expressed in undifferentiated bone marrow stromal cells (BMSCs) in vitro and its expression is maintained during BMP2-induced osteogenic differentiation. However, levels of the bone formation marker procollagen type I N-terminal propeptide (PINP) are unchanged in the serum of 20-week-old Tas1R3 mutant mice as compared to controls. In contrast, levels of the bone resorption marker collagen type I C-telopeptide are reduced greater than 60% in Tas1R3 mutant mice. Consistent with this, Tas1R3 and its putative signaling partner Tas1R2 are expressed in primary osteoclasts and their expression levels positively correlate with differentiation status. Collectively, these findings suggest that high bone mass in Tas1R3 mutant mice is due to uncoupled bone remodeling with reduced osteoclast function and provide rationale for future experiments examining the cell-type-dependent role for TAS1R family members in nutrient sensing in postnatal bone remodeling


No disponible


Assuntos
Animais , Masculino , Reabsorção Óssea/metabolismo , Osso Cortical/metabolismo , Regulação da Expressão Gênica no Desenvolvimento , Células-Tronco Mesenquimais/metabolismo , Osteoblastos , Osteoclastos/metabolismo , Osteogênese , Receptores Acoplados a Proteínas-G/metabolismo , Biomarcadores/metabolismo , Reabsorção Óssea/imunologia , Reabsorção Óssea/patologia , Catepsina K , Linhagem Celular , Osso Cortical , Células-Tronco Mesenquimais/citologia , Camundongos Endogâmicos C57BL , Camundongos Knockout , Camundongos Mutantes
6.
Reumatol. clín. (Barc.) ; 13(6): 352-353, nov.-dic. 2017. ilus
Artigo em Inglês | IBECS | ID: ibc-167211

RESUMO

Cherubism is a rare disorder with autosomal dominant inheritance. It is classified as a benign fibro-osseous lesions and may involve either facial bone. Its typical dentofacial deformities are caused by mutations in the SH3BP2 gene. The protein encoded by SH3BP2 had a significant role in the regulation of osteoblasts and osteoclasts. Accordingly with the radiological findings, differential diagnoses includes fibrous dysplasia, giant cell granuloma, osteosarcoma, juvenile ossifying fibroma, fibrous osteoma, odontogenic cyst and hyperparathyroidism. The aim of the present report is twofold. First, we examine the importance of the proper management of these cases. Second, we describe this rare syndrome with the goal of proposing suitable treatments (AU)


El querubismo es una enfermedad rara. Presenta herencia autosómica dominante y es clasificada como una enfermedad fibroósea benigna. Las deformidades típicas de esta dolencia se deben a la alteración del gen SH3BP2 y pueden afectar a cualquier hueso del macizo facial. La proteína codificada por este gen es fundamental para el correcto funcionamiento de osteoblastos y osteoclastos. El diagnóstico diferencial debe incluir: displasia fibrosa, granuloma de células gigantes, osteosarcoma, fibroma osificante juvenil, fibroma osteoide e hiperparatiroidismo (AU)


Assuntos
Humanos , Masculino , Criança , Querubismo/diagnóstico , Querubismo/patologia , Atrofia Óptica Autossômica Dominante/complicações , Fibroma Ossificante/complicações , Fibroma Ossificante/diagnóstico , Assimetria Facial/complicações , Diagnóstico Diferencial , Osteoclastos , Cirurgia Bucal/métodos , Radiografia Panorâmica/métodos , Cistos Ósseos/complicações , Células Gigantes/citologia , Células Gigantes/patologia
8.
Rev. osteoporos. metab. miner. (Internet) ; 9(1): 38-49, ene.-mar. 2017. tab, ilus
Artigo em Espanhol | IBECS | ID: ibc-162870

RESUMO

La osteoporosis es una enfermedad esquelética sistémica caracterizada por disminución de la densidad mineral ósea con alteraciones de la microarquitectura del hueso y aumento del riesgo de fractura. Se ha demostrado que depende de procesos fisiológicos y secundarios a otras patologías como son las enfermedades reumáticas, e incluso asociado al uso de glucocorticoides siendo esta la causa más frecuente de osteoporosis asociada a fármacos, y que a su vez representa una problemática de gran magnitud en la actualidad. Debido a esto, se presenta esta revisión con el fin de recalcar la importancia clínica de la osteoporosis en las enfermedades reumáticas e inducidas por glucocorticoides (AU)


Osteoporosis is a systemic skeletal disease characterized by low bone mineral density, changes in bone microarchitecture and increased risk of fracture. It has been shown that depends on physiological processes and secondary to other pathologies and associated with the use of glucocorticoids, the latest being the most common cause of osteoporosis associated to drugs, this may be represent a great magnitude public health issue. This review is presented in order to emphasize the clinical importance of osteoporosis in rheumatic diseases and glucocorticoid-induced osteoporosis (AU)


Assuntos
Humanos , Doenças Reumáticas/induzido quimicamente , Doenças Reumáticas/epidemiologia , Osteoporose/induzido quimicamente , Fraturas Ósseas/complicações , Vitamina D/uso terapêutico , Cálcio/uso terapêutico , Densidade Óssea , Osteoclastos , Artrite Reumatoide/induzido quimicamente , Artrite Reumatoide/complicações , Espondilite Anquilosante/complicações
9.
Rev. osteoporos. metab. miner. (Internet) ; 8(1): 5-14, ene.-mar. 2016. ilus, tab, graf
Artigo em Espanhol | IBECS | ID: ibc-151228

RESUMO

Objetivos: Identificar microRNAs (miRNAs) diferencialmente expresados en muestras óseas con fractura osteoporótica respecto a huesos sanos. Material y métodos: Se extrajo RNA total a partir de hueso trabecular fresco del cuello femoral de mujeres sometidas a reemplazo de cadera, ya sea debido a fractura osteoporótica (n=6) o por artrosis en ausencia de osteoporosis (según la DMO) (n=6). Las muestras se hibridaron en un array de miRNAs y se realizaron diagramas de PCA y de mapa de calor. Para la comparación de los niveles de expresión, se fijó como significativo un umbral de cambio de >1,5 veces y un valor p <0,05 en la t de Student (corregido para múltiples pruebas). Resultados: Tanto los análisis de PCA como el mapa de calor mostraron una agrupación de las muestras según si eran de fractura o no. Se detectaron 790 miRNAs en las muestras de hueso, 82 de los cuales estaban alterados en las muestras osteoporóticas. Tras la validación en otro panel de 6 muestras osteoporóticas y 6 no osteoporóticas mediante PCR a tiempo real de los miRNAs más significativos, y para los que existía un ensayo disponible, se confirmaron los miRNAs miR-320a y miR-22-3p. Estos dos miRNAs se detectaron en cultivos de osteoblastos primarios, aunque no mantenían el mismo patrón de expresión que en las muestras de hueso total. Conclusiones: Hemos demostrado que existen diferencias en la expresión de miRNAs en muestras con fractura osteoporótica, lo que abre nuevas perspectivas para la investigación y diseño de nuevas terapias (AU)


Objectives: To identify microRNAs (miRNAs) differentially expressed in bone samples with osteoporotic fracture compared with healthy bones. Methods: Total RNA was extracted from fresh trabecular bone of the femoral neck of women undergoing hip replacement surgery, either because to osteoporotic fracture (n=6) or in the absence of osteoarthritis osteoporosis (based on BMD) (n=6). The samples were hybridized on an array of miRNAs and PCA diagrams and heat map were made. To compare expression levels, >1.5 times and a value p<0.05 Student's T test (corrected for multiple testing) was set as a threshold of significant change. Results: Both PCA analysis and the heat map showed a samples grouping whether there was fracture or not. 790 were detected miRNAs in bone samples, 82 of which were altered in the osteoporotic samples. After validation in another panel of 6 samples 6 osteoporotic and non-osteoporotic by PCR real time of the most significant miRNAs, and for which there was a test available, the miRNAs, miR-320a and miR-22-3p were confirmed. These two miRNAs were detected in cultures of primary osteoblasts, although they did not maintain the same pattern of expression in total bone samples. Conclusions: We have shown that there are differences in the expression of miRNAs in samples with osteoporotic fracture. This opens prospects for research and design of new therapies (AU)


Assuntos
Humanos , MicroRNAs/genética , Perfilação da Expressão Gênica , Osteoporose/genética , Fraturas por Osteoporose/genética , Osteoblastos/fisiologia , Osteoclastos/fisiologia
10.
Med. oral patol. oral cir. bucal (Internet) ; 20(6): e651-e656, nov. 2015. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-144695

RESUMO

Background: The aim of this study was to evaluate the effects of long and short term systemic usage of royal jelly on bone formation in the expanded maxillary suture in a rat model. Material and Methods: Twenty eight Wistar albino rats were randomly divided into 4 equal groups: Control (C); Only Expansion (OE), Royal Jelly (RJ) group, Royal Jelly was given to rats by oral gavage only during the expansion and retention period; Royal Jelly plus Nursery (RJN) group, Royal Jelly was given to rats by oral gavage during their nursery phase of 40 days and during the retention period. After the 5 day expansion period was completed, the rats underwent 12 days of mechanical retention. All rats were sacrificed in same time. Histological examination was performed to determine the number of osteoclasts, number of osteoblasts, number of capillaries, inflammatory cell infiltration, and new bone formation. Results: New bone formation, number of osteoclasts, number of osteoblasts, and the number of capillaries in the expanded maxillary sutures were higher in the RJ and RJN groups than in the other groups. Statistical analysis also demonstrated that new bone formation and the number of osteoblasts was also highest in the RJN group. Conclusions: The systemic administration of Royal Jelly in conjunction with rapid maxillary expansion may increase the quality of regenerated bone (AU)


Assuntos
Animais , Feminino , Masculino , Ratos , Maxila/patologia , Maxila , Osteogênese/fisiologia , Modelos Animais , Mel , Oclusão Dentária , Osteoclastos/fisiologia , Reabsorção Óssea , Fenômenos Fisiológicos Dentários
11.
Ars pharm ; 56(3): 131-140, jul.-sept. 2015.
Artigo em Inglês | IBECS | ID: ibc-144106

RESUMO

Objectives. Given the relationship between chronic periodontitis and high levels of oxidative stress, this review aims to clarify what role can played the dietary intake of different antioxidants in maintaining a healthy periodontium and in reducing chronic periodontitis risk, as well as possible use of dietary therapies based on them for this disease treatment. Methods. The database of the National Library of Medicine, Washington, DC (MEDLINE PubMed) was used and all the studies in animals and humans are on the subject of interest in English writing online available from inception of the database until May 2015 were collected. Results. Antioxidants analyzed in this regard include vitamin C, vitamin A, carotenoids and some polyphenols, and coenzyme Q; as well as minerals iron, copper and zinc that are constituents of antioxidant enzymes. Still, there is a paucity of studies with few human studies, mostly observational. Among the various antioxidants, vitamin E and polyphenols seem to have more evidence for its beneficial effect, but in general the studies are insufficient to rule out or establish what antioxidants are useful and which are not. Conclusions. Overall, the data presented indicate that dietary antioxidants are beneficial for periodontal health, at least under certain circumstances. However more studies are needed to establish the relationship between chronic periodontitis and each specific anti-oxidant and to design useful dietary interventions for this disease management


Objetivos. Dada la relación existente entre periodontitis crónica y altos niveles de estrés oxidativo, esta revisión pretende clarificar qué papel puede desempeñar la ingesta de los diferentes antioxidantes de la dieta en el mantenimiento de un periodonto saludable y en la reducción del riesgo de padecer periodontitis crónica, así como el posible uso de terapias dietéticas basadas en estos para el tratamiento de dicha enfermedad. Métodos. Se utilizó la base de datos de la National Library of Medicine, Washington, DC (MEDLINE: PubMed) y todos los estudios en animales y humanos tratando el tema de interés escritos en inglés disponibles online desde la creación de la base de datos hasta Mayo de 2015 fueron recopilados. Resultados. Los antioxidantes analizados a este respecto incluyen a la vitamina C, la vitamina A, algunos carotenoides y polifenoles, y el coenzima Q; así como los minerales, hierro, cobre y zinc que forman parte de enzimas antioxidantes. Aun así hay una escasez generalizada de estudios con pocos estudios en humanos, la mayoría de tipo observacional. Entre los diferentes antioxidantes, la vitamina E y los polifenoles parecen ser los que más evidencias a favor de su efecto beneficioso suman, pero en general los estudios son insuficientes para descartar o establecer qué antioxidantes son útiles y cuáles no. Conclusiones. En general, los datos presentados indicarían que los antioxidantes de la dieta resultan beneficiosos para la salud periodontal, al menos bajo ciertas circunstancias. Sin embargo se necesitan más estudios para establecer la relación entre la periodontitis crónica y cada antioxidante concreto así como para diseñar intervenciones dietéticas útiles en la gestión de esta enfermedad


Assuntos
Animais , Humanos , Camundongos , Coelhos , Ratos , Periodontite Crônica/dietoterapia , Periodontite Crônica/prevenção & controle , Periodontite Crônica/etiologia , Gengivite/patologia , Perda de Dente/patologia , Espécies Reativas de Oxigênio , Estresse Oxidativo , Osteoclastos , Antioxidantes/uso terapêutico , Vitaminas na Dieta/uso terapêutico , Vitamina A/uso terapêutico , Carotenoides/uso terapêutico , Ácido Ascórbico/uso terapêutico , Vitamina E/uso terapêutico , Cobre/uso terapêutico , Zinco/uso terapêutico , Polifenóis/uso terapêutico , Ubiquinona/uso terapêutico , Ferro na Dieta/uso terapêutico , Terapia Nutricional
15.
SEMERGEN, Soc. Esp. Med. Rural Gen. (Ed. impr.) ; 40(3): e47-e50, abr. 2014. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-122153

RESUMO

La picnodisostosis es una enfermedad rara, producida por una disfunción de los osteoclastos, debida a una mutación en el gen de la catepsina K. Presentamos un caso de un paciente adulto joven con dicho síndrome que tras una caída de baja energía presenta una fractura atípica de tibia, al acudir a urgencias se observan unas alteraciones óseas predisponentes a la fractura. Al poco tiempo sufre la misma fractura en la otra tibia. Debido a las condiciones características de la picnodisostosis para el tratamiento de dicha fractura requirió un abordaje no convencional para una fractura diafisaria de tibia (placa de osteosíntesis), asociado a un mayor tiempo consolidación. Finalmente el caso se resolvió de forma satisfactoria (AU)


Pycnodysostosis is a rare disease caused by a dysfunction of the osteoclasts due to a mutation in the cathepsin K gene. We present a case of a young adult patient with the above mentioned syndrome, who suffered an atypical fracture of the tibia after a low energy fall. Some bone changes that could have predisposed the fracture were observed when examined in the Emergency Department. Not long afterwards he suffered the same type of fracture in another tibia. Due to the conditions typical of the pycnodysostosis, the above mentioned fracture required an unconventional approach for this mid-shaft tibial fracture (osteosynthesis plate), combined with a longer consolidation time. The case was finally resolved satisfactorily (AU)


Assuntos
Humanos , Masculino , Adulto , Picnodisostose/diagnóstico , Fraturas Ósseas/etiologia , Osteoclastos/fisiologia , Reabsorção Óssea/fisiopatologia , Catepsina K/genética , Mutação/genética
16.
Med. oral patol. oral cir. bucal (Internet) ; 19(2): 106-111, mar. 2014. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-121348

RESUMO

Bisphosphonates is a group of inorganic pyrophosphates analogues that suppress bone resorption by inducing osteoclast inactivation, being frequently used for management of diseases affecting bone metabolism, bone metastases and bone tumors. However, since 2003 many cases describing the presence of necrotic bone exposures in the jaws have been described in patients receiving these drugs, what represent a significant complication of bisphosphonates treatment. The overall incidence of bisphosphonate-related osteonecrosis of the jaws is low, ranging from 0.7% to 12%, mainly observed in those patients receiving intravenously treatment. Osteonecrosis of the jaws associated to oral bisphosphonate, particularly alendronate, has also been reported by a number of authors. Considering that alendronate is one of the most used drug worldwide, specially for treatment of osteoporosis, a better understanding of osteonecrosis of the jaws related to its use and how to manage these patients is extremely important. Therefore, in the current manuscript the authors aim to review the most important topics related to this pathological presentation (AU)


Assuntos
Humanos , /diagnóstico , Alendronato/efeitos adversos , Difosfonatos/efeitos adversos , Fatores de Risco , Osteoclastos , Osteoprotegerina/farmacocinética
17.
Arch. esp. urol. (Ed. impr.) ; 66(5): 463-474, jun. 2013. tab, ilus
Artigo em Espanhol | IBECS | ID: ibc-113260

RESUMO

Las metástasis óseas son complicaciones frecuentes y a menudo desvastadoras de los pacientes con cáncer. Recientemente se han producido avances significativos en nuestra comprensión de los mecanismos moleculares responsables de metástasis tanto osteolíticas como osteoblásticas. El uso de las “OMICAS” y la disponibilidad de modelos animales preclínicos de metástasis óseas adecuados han permitido la identificación de los factores producidos por el tumor o por el estroma en respuesta al tumor. Este tipo de estudios deberían resultar en una disminución de las morbilidades esqueléticas graves asociadas con el cáncer de próstata metastásico y pueden en el futuro mejorar la supervivencia general. En esta revisión, se resumirá las dianas moleculares en las metástasis óseas de nueva generación (AU)


Bone metastases are a frequent and devastating complication in cancer patients. Recently, significant advances in our understanding of the molecular mechanisms responsible for both osteolytic and osteoblastic bone metastases have occurred. The use of OMICS and the availability of appropriate preclinical animal models of bone metastasis have permitted the identification of factors produced by the tumor or by the host stroma in response to the tumor. These types of studies should result in a decrease of the serious skeletal morbidities associated with metastatic prostate cancer and may in the future improve overall survival. In this review the next generation of molecular targets in bone metastasis will be summarized (AU)


Assuntos
Humanos , Patologia Molecular/métodos , Neoplasias Ósseas/secundário , Metástase Neoplásica/patologia , Biologia Molecular/tendências , Osteoclastos , Osteoblastos
18.
Med. oral patol. oral cir. bucal (Internet) ; 18(2): 351-355, mar. 2013. tab
Artigo em Inglês | IBECS | ID: ibc-112409

RESUMO

Introduction: The purpose of this study was to investigate the effect of pregnancy on orthodontic tooth movement in Wistar rats. Material and Methods: Forty eight female three-month old Wistar rats with an average weight of 250±25 gr were selected and randomly divided into two experimental (pregnant) and control groups (non-pregnant). Maxillary central incisors were tipped distally by insertion of springs exerting 30g force. Two, seven and fourteen days after spring insertion animals were sacrificed. Then the mesioincisal distance between maxillary incisors were measured. Subsequently, histological sections were prepared to count osteoclasts under a light microscope. The data on the extent of orthodontic tooth movement, and the number of osteoclasts were analyzed by independent sample t-test. Results: The results indicated that 2,7 and 14 days after force application there was no significant difference inorthodontic tooth movement between experimental and control groups (p>0.05). The number of osteoclasts were significantly lower in the experimental group 7 and 14 days after spring insertion (p<0.05).Conclusion: Pregnancy may decrease the amount of tooth movement in the linear phase but it is not statistically significant. The number of osteoclasts is significantly decreased during pregnancy (AU)


Assuntos
Animais , Feminino , Gravidez , Ratos , Movimento Mesial dos Dentes/diagnóstico , Osteoclastos , Complicações na Gravidez
19.
Med. oral patol. oral cir. bucal (Internet) ; 17(3): 367-370, mayo 2012. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-103465

RESUMO

Objectives: To determine whether there is a relationship between the total BP dose administered and the variations in serum CTX concentration. Study design: The study included 50 patients requiring dental implant surgery and treated with oral BPs, seen in an Oral Surgery and Implantology Unit between January 2007 and June 2009. The patients were divided into two groups: those in which the medication was not suspended before obtaining the laboratory test sample, and those patients referred from other dental clinics in which BPs was suspended before reporting to our Unit. The total drug dosage administered and the total dose per kilogram body weight were evaluated for comparison with serum CTX. The data obtained were correlated to the osteonecrosis risk table developed by Marx et al. in 2007.Results: There were no significant differences between the two groups in relation to the total administered dose and the dose in mg/kg b.w. Likewise, in both groups no relationship was observed between the serum CTX value and the total administered dose or the dose in mg/kg b.w. No differences were found between the two patient groups regarding chemical osteonecrosis risk based on the criteria of Marx et al Conclusions: No relationship was observed between the oral BP dose administered (total dose or expressed in mg/kg b.w.) and serum CTX concentration, and suspension of the medication did not influence the serum CTX levels (AU)


No disponible


Assuntos
Humanos , /diagnóstico , Difosfonatos/efeitos adversos , Osteoclastos/ultraestrutura , Reabsorção Óssea/induzido quimicamente , Colágeno Tipo I
20.
J. physiol. biochem ; 68(1): 129-139, mar. 2012.
Artigo em Inglês | IBECS | ID: ibc-122385

RESUMO

No disponible


The 26S proteasome is a key component of the ubiquitin-proteasome system, a process responsible for the majority of cellular protein degradation. The function of the proteasomal ubiquitin receptor hRpn13, a component of the 26S proteasome, is not completely understood. To investigate the role of hRpn13 in the ubiquitin-proteasome system in osteoblasts, the effects of suppressing and overexpressing the hRpn13 gene on proliferation, differentiation, and function of human osteoblast-like MG63 cells were examined. After knockdown of hRpn13 by small interfering RNA, changes in osteoblast proliferation were evaluated by methyl-thiazolyl-tetrazolium assay. There was an increase in markers for osteoblast proliferation, specifically alkaline phosphatase activity, and elevated protein levels of osteocalcin, proliferating cell nuclear antigen (PCNA), and ubiquitin. Furthermore, hRpn13 knockdown also resulted in a decrease in the ratio between the gene expressions of RANKL and OPG, key players in the pathogenesis of bone diseases that influence the normal balance between bone formation and resorption. In contrast, overexpression of hRpn13 inhibited the proliferation of MG63 cells, and decreased alkaline phosphatase activity as well as protein levels of osteocalcin, PCNA, and ubiquitin while the ratio of RANKL to OPG expression increased. To confirm the function of hRpn13 in the ubiquitin-proteasome pathway, osteoblast proliferation enhancement and ubiquitin accumulation after hRpn2 knockdown was assessed. The results suggest that overexpression of hRpn13 negatively influences proliferation and osteogenic differentiation in MG63 cells. The evidence implies that hRpn13 modulates the influence of osteoblasts on osteoclasts by controlling the stability of regulatory proteins in osteoblasts. In summary, overexpression of hRpn13 promoted the activity of the ubiquitin-proteasome system (AU)


Assuntos
Humanos , Complexo de Endopeptidases do Proteassoma/fisiologia , Ubiquitinação/fisiologia , Osteoblastos/fisiologia , Osteoclastos/fisiologia , Proteínas Reguladoras de Apoptose/fisiologia , Imunoglobulina M/fisiologia
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