ALEXANDRE POVOA BARBOSA
Projetos de Pesquisa
Unidades Organizacionais
LIM/17 - Laboratório de Investigação em Reumatologia, Hospital das Clínicas, Faculdade de Medicina
5 resultados
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- Increased bone resorption by long-term cigarette smoke exposure in animal model(2021) JUNQUEIRA, Jader Joel Machado; LOURENCO, Juliana Dias; SILVA, Kaique Rodrigues da; JORGETTI, Vanda; VIEIRA, Rodolfo P.; ARAUJO, Amanda Aparecida de; ANGELIS, Katia De; CORREIA, Aristides Tadeu; ALVES, Luan Henrique Vasconcelos; TIBERIO, Iolanda de Fatima Lopes Calvo; BARBOSA, Alexandre Povoa; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosIntroduction: Clinical and experimental studies have been attesting the deleterious effects of smoking mainly due to the stimulation of osteoclastogenesis and inhibition of osteoblastogenesis. However the physiological mechanisms that can explain these changes are not fully understood. Aims: To evaluate the trabecular bone resorption effect caused by long-term exposure to cigarette smoke and the action of cytokines and reactive oxygen species involved in this process. Methods: Sixty young adult C57BL/6 mice were allocated to two groups: control, 30 animals exposed to filtered air for 1, 3 and 6 months; and smoke, 30 animals exposed to cigarette smoke for 1, 3 and 6 months. Femoral and tibial extraction was performed to evaluate the bone mineral matrix, bone cytokines (Receptor activator of nuclear factor-kappa B ligand -RANKL and Osteoprotegerin -OPG) and oxidative stress markers (Thiobarbituric acid reactive substances -Tbars). Results: Exposure to cigarette smoke (CS) generated changes in bone structural parameters in the 6th month of follow-up, demonstrating an evident bone loss; reduction in OPG/RANKL ratio from the 3rd month on and increase in Tbars in the first month, both closely related to the increase in osteoclastogenic activity and bone resorption. Conclusion: These findings reinforce the importance of CS-induced oxidative stress in bone compromising the bone cellular activities with a consequent impairment in bone turn over and changes in bone structure.
- Smoking induces increased apoptosis in osteoblasts: changes in bone matrix organic components(2023) KOHLER, Julia Benini; SILVA, Alex Ferreira da; FARIAS, Walleson Alves; SAMPAIO, Barbara Fialho Carvalho; NEVES, Marco Aurelio Silveiro; LIMA, Leandro Gregorut; LOURENCO, Juliana Dias; MOREIRA, Alyne Riani; BARBOSA, Alexandre Povoa; TIBERIO, Iolanda de Fatima Lopes Calvo; TEODORO, Walcy Rosolia; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosClinical studies demonstrate the impact of smoking on bone tissue fragility and higher incidence of fractures. However, it is not totally understood which physiological mechanisms could be involved in these events. Previously, we showed important changes in bone tissue components in experimental model of cigarette smoke (CS) exposure. CS exposure induces worsening in bone mineralization and a decrease in collagen type I deposition, leading to bone fragility. Considering that the majority of clinical studies described bone structural changes by radiographic images, in this study we performed analyses ""in situ"" using tissue samples from smokers, former smokers and non-smokers to better understand how the increase in inflammatory mediators induced by smoking exposure could interfere in bone cells activity leading bone structural changes. We observed increased levels of IL-1 beta, IL-6 and TNF-alpha in bone tissue homogenates with a concomitant increase in osteoblast apoptosis in smokers and former smokers compared with non-smokers. Histological changes in both smokers and former smokers were characterized by reduction in collagen type I. Only in smokers, it was observed decrease in trabecular area, suggesting increased bone resorption and increase in collagen type V. These results showed that osteoblasts apoptosis in association with increased bone resorption leads bone structural changes in smokers.
- The deleterious effects of smoking in bone mineralization and fibrillar matrix composition(2020) BARBOSA, Alexandre Povoa; LOURENCO, Juliana Dias; JUNQUEIRA, Jader Joel Machado; FRANCA, Silva Larissa Emidio de; MARTINS, Janaina S.; OLIVEIRA JUNIOR, Manoel Carneiro; BEGALLI, Isadora; VELOSA, Ana Paula Pereira; OLIVO, Clarice Rosa; BASTOS, Thiago Bernardes; JORGETTI, Vanda; PAULA, Vieira Rodolfo de; TEODORO, Walcy Rosolia; LOPES, Fernanda D. T. Q. S.Introduction: This study aimed to verify the effects of cigarette smoke exposure in bone mineralization and fibrillar matrix composition as well as in bone healing after tibial fracture induction. Methods: C57Bl/6 Mice were assigned according to exposure and surgery: C room air; F room air and tibia open osteotomy; CS cigarette smoke; FCS cigarette smoke and tibia open osteotomy. In order to study fracture healing we performed, under anesthesia, a bone injury through a tibial shaft osteotomy. Bone samples were obtained to evaluate bone histomorphometry, trabecular morphology and volume, trabecular collagen types composition and presence of inflammatory cytokines and growth factors. Results: CS exposure significantly reduced the thickness of bone trabeculae associated with decrease in mineralizing surface and mineral deposition rate, leading a lower bone formation rate and longer mineralization time. Resorption surface and osteoclastic surface were greater in the CS group, attesting increased resorptive action. There was a decrease in type I collagen deposition and genes expression in the CS and FCS groups compared to C group and in contrast there was an increase in type V collagen deposition and genes expression in the CS, FC and FSC groups compared to C group. Also, CS exposure induced a decrease in bone forming cytokines and an increase in inflammatory associated cytokines, and these changes were intensified under fracture conditions. Conclusion: Cigarette smoke exposure alters bone matrix composition and worsens bone mineralization, leading to bone fragility by increasing collagen V synthesis and deposition and impairing collagen I fibril forming and assembling. And these deleterious effects contributed to the worsening in fracture healing after tibia osteotomy.
- Decreased Bone Type I Collagen in the Early Stages of Chronic Obstructive Pulmonary Disease (COPD)(2020) JUNQUEIRA, Jader Joel Machado; LOURENCO, Juliana Dias; SILVA, Kaique Rodrigues da; CERVILHA, Daniela Aparecida de Brito; SILVEIRA, Lizandre Keren Ramos da; CORREIA, Aristides Tadeu; SILVA, Larissa Emidio de Franca; TEODORO, Walcy Rosolia; TIBERIO, Iolanda de Fatima Lopes Calvo; BARBOSA, Alexandre Povoa; LOPES, Fernanda Degobbi Tenorio Quirino dos SantosSmoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) and is known to have deleterious effects on bone metabolism. However, the effects on bone collagen matrix during the development of COPD are unclear. The aim of this study was to evaluate the temporal effect of cigarette smoke exposure on bone type I collagen during COPD development in a cigarette smoke-induced model. C57BL/6 mice were allocated to three groups: control (C), animals exposed to filtered air for 1, 3 and 6 months; cigarette smoke (S), animals exposed to cigarette smoke for 1, 3 and 6 months; provisional smoking (PS), animals exposed to cigarette smoke for 3 months, followed by another 3 months of filtered air exposure. Evaluation of the respiratory mechanics and alveolar enlargement were performed. Femoral and tibial extraction was also performed to evaluate the type I collagen by immunofluorescence andCOL1A1gene expression. Exposure to cigarette smoke led to an alveolar enlargement and progressive reduction in lung tissue resistance and elastance, progressive reduction of type I collagen and reduction inCOL1A1gene expression. Although we did not observe any improvement in the functional and histological parameters in the provisional smoking group, we detected an increase inCOL1A1gene expression. A worsening in bone collagen matrix is part of the initial physiopathological events during COPD development and the smoking cessation induced an evident recovery ofCOL1A1expression, possibly to attempt at tissue repair.
conferenceObject Smoking effects in bone tissue in patients with advanced stages of osteoarthritis(2022) KOHLER, Julia; FERREIRA, Alex; NUNES, Walleson; FIALHO, Barbara; NEVES, Marco Aurelio; LIMA, Leandro; TEODORO, Walcy; PEREIRA, Rosa; TIBERIO, Iolanda; BARBOSA, Alexandre; LOPES, Fernanda Degobbi