Several studies have established an association between diabetes and alterations in bone metabolism; however, the underlying mechanism is not well established. Although zinc is recognized as a potential preventive agent against diabetes-induced bone loss, there is no evidence demonstrating its effect in chronic diabetic conditions. This study evaluated the effects of zinc supplementation in a chronic (90 days) type 1 diabetes-induced bone-loss model. Male Wistar rats were distributed in three groups: control, type 1 diabetes mellitus (T1DM), and T1DM plus zinc supplementation (T1DMS). Serum biochemical analysis; tibia histomorphometric, biomechanical, and collagen-content analyses; and femur mRNA expression were evaluated. Relative to T1DM, the zinc-supplemented group showed increased histomorphometric parameters such as TbWi and BAr and decreased TbSp, increased biomechanical parameters (maximum load, stiffness, ultimate strain, and Young’s modulus), and increased type I collagen content. Interestingly, similar values for these parameters were observed between the T1DMS and control groups. These results demonstrate the protective effect of zinc on the maintenance of bone strength and flexibility. In addition, downregulation of OPG, COL1A, and MMP-9 genes was observed in T1DMS, and the anabolic effects of zinc were evidenced by increased OC expression and serum ALP activity, both related to osteoblastogenesis, demonstrating a positive effect on bone formation. In contrast, T1DM showed excessive bone loss, observed through reduced histomorphometric and biomechanical parameters, characterizing diabetes-associated bone loss. The bone loss was also observed through upregulation of OPG, COL1A, and MMP-9 genes. In conclusion, zinc showed a positive effect on the maintenance of bone architecture and biomechanical parameters. Indeed, OC upregulation and control of expression of OPG, COL1A, and MMP-9 mRNAs, even in chronic hyperglycemia, support an anabolic and protective effect of zinc under chronic diabetic conditions. Furthermore, these results indicate that zinc supplementation could act as a complementary therapy in chronic T1DM.
BackgroundThe purpose of this study is to examine current beliefs about the use, the clinical importance, the theoretical fundamentals and the utilization criteria of therapeutic ultrasound (TUS) among physical therapists on the clinical practice in orthopedic and sports physiotherapy in Brazil.MethodsA brief survey was developed based on previous studies and was sent to 55 physical therapists with advanced competency in orthopedics and sports physiotherapy. The questions addressed general topics about the professional profile and ultrasound usage and dosage.ResultsOur data show the wide availability and frequent use of TUS in this sample of physical therapists. TUS is used in distinct musculoskeletal injuries and/or disorders in both acute and chronic conditions. Muscles, tendons and ligaments represented the major structures where TUS is used. Questions on the basic theory of TUS demonstrated a lack of knowledge of the ultrasound physiological effects as well as its interaction with biological tissues and TUS absolute contraindication.ConclusionA Brazilian profile about the US usage and dosage in orthopedic and sports physiotherapy is presented and highlights the need for a continuous upgrading process and further research into its effects.
Type 1 diabetes mellitus (T1DM) is associated with several skeletal alterations, particularly in conditions of poor glycaemic control. Insulin therapy is the major conservative treatment for T1DM; however, the effects of this hormone on bone markers of T1DM rats are limited, and the regulatory mechanisms remain elusive. Therefore, the evaluation of molecular and non-molecular parameters in a chronic animal model of T1DM-induced bone loss, treated with and without insulin, may help in elucidating the insulin mechanisms. Male Wistar rats were assigned into three groups: control, T1DM (T1DM rats induced with streptozotocin [STZ] at 40 mg/kg intravenously) and T1DM plus insulin therapy (T1DMI). After 8 weeks, we evaluated the serum biochemical, tibia histomorphometric and biomechanical parameters, as well as the gene expression of the receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG) and osteocalcin (OC) of femur mRNA. Compared with T1DM, the T1DMI group showed less bone loss, which was revealed by the increased trabecular width (TbWi, p < 0.001) and trabecular bone area (BAr, p < 0.01), reduced trabecular separation (TbSp, p < 0.01) and increased Young's modulus (p < 0.05). Moreover, molecular analyses indicated that the expression of OPG and OC was up-regulated (p < 0.001 and p < 0.05, respectively). In summary, the up-regulation of OPG and OC in the T1DMI group supports an anabolic effect of insulin, which was demonstrated by the maintenance of bone architecture and flexibility. These results suggest that insulin therapy may prevent T1DM-induced bone loss via the effects on the bone formation.
Purpose To examine healing adaptations over 17 weeks post Achilles tendon (AT) rupture in the injured region (IR) compared to an uninjured region (UIR) of the AT. Methods Twenty-four rats were subjected to a complete right-sided AT rupture, while the left side served as a control. ATs were harvested at 1, 2, 8 and 17 weeks post-rupture and stained with antibodies speciic to Collagen type I (Col I) and II (Col II) as well as Alcian Blue and Picrosirius Red staining techniques. Histopathological changes, proteoglycan content, collagen alignment and immunoexpression were assessed. Results Both regions examined, IR and UIR, exhibited over weeks 1-17 similar healing adaptations of increasing collagen alignment, decreasing Col I immunoexpression, as well as increasing proteoglycan content and Col II occurrence. Increased proteoglycan content was found already at week 2 in the UIR, while it irst increased at week 8 in the IR. The area positive to Col II was increased compared to controls at week 8 in the UIR, whereas it irst raised at week 17 in the IR. Collagen disorganization successively declined to reach control levels at week 17 in the UIR, but was still higher in the IR. Conclusion This study demonstrated that uninjured areas of the AT remote from the rupture site also undergo pronounced remodeling, although with time-span diferences relative to injured AT portions. These changes including the pathologic heterotopic mineralization and chondrogenic diferentiation observed in both regions may have implications in the choice of rehabilitation regimes in order to prevent secondary rupture.
The aim of this study was to compare the treatment effects of laser photobiomodulation (LPBM) therapy and aerobic exercise on the biomechanical properties, tissue morphology and the expression of tendon matrix molecules during early remodeling of Achilles tendon (AT) injury in diabetic rats. Animals were randomly assigned to five groups: injured non diabetic (I, n = 15), injured diabetic (ID, n = 15), injured diabetic plus LPBM (IDL, n = 16), injured diabetic plus aerobic exercise (IDE, n = 16) and injured diabetic plus aerobic exercise and LPBM (IDEAL, n = 17). Type 1 diabetes was induced via a single intravenous injection of Streptozotocin at a dose of 40 mg/kg. A partial tenotomy was performed in the right AT. LPBM was performed with an indium-gallium-aluminum-phosphide 660 nm 10 mW laser device (spot size 0.04 cm2, power density 250 mW/cm2, irradiation duration 16 s, energy 0.16 J, energy density 4 J/cm2) on alternate days for a total of 9 sessions over 3 weeks (total energy 1.44 J), using a stationary contact technique to a single point over the dorsal aspect of the AT. Moderate aerobic exercise was performed on a motorized treadmill (velocity 9 m/min for 60 minutes). At 3 weeks post-injury, biomechanical analyzes as well as assessment of fibroblast number and orientation were performed. Collagen 1 (Col1) and 3 (Col3) and matrix metalloproteinases (MMPs) -3 and 13 protein distributions were studied by immunohistochemistry; while Col1 and Col3 and MMP-2 and 9 gene expression were assessed by quantitative RT-PCR (qRT-PCR). IDEAL exhibited significant increases in several biomechanical parameters in comparison to the other groups. Moreover, IDEAL presented stronger Col1 immunoreactivity when compared to ID, and weaker Col3 immunoreactivity than IDE. Both IDL and IDEAL demonstrated weaker expression of MMP-3 in comparison to I, while IDL presented no expression of MMP-13 when compared to ID. ID, IDL and IDE showed an increased number of fibroblasts in comparison to I, while IDEAL decreased the number of these cells in comparison to ID and IDE. IDL and IDEAL groups exhibited decreased angular dispersion among the fibroblasts when compared to I. The gene expression results showed that IDE demonstrated a downregulation in Col1 mRNA expression in comparison to I and ID. IDEAL demonstrated upregulation of Col1 mRNA expression when compared to IDL or IDE alone and increased MMP-2 expression when compared to IDL and IDE. MMP-9 expression was upregulated in IDEAL when compared to I, IDL and IDE. Our results suggest a beneficial interaction of combining both treatment strategies i.e., aerobic exercise and LPBM, on the biomechanical properties, tissue morphology and the expression of matrix molecules in diabetic tendons.
<div>Introdução: Embora seja o mais forte dentre os tendões humanos, o tendão calcâneo (TC) é comumente afetado por condições patológicas e/ou traumáticas. Apesar da prevalência e tratamento complexo, a patomecânica da tendinopatia do calcâneo continua desconhecida. Equipamentos capazes de mensurar as propriedades biomecânicas de TCs são indispensáveis em estudos que visam elucidar fatores responsáveis pela tendinopatia ou que influenciem o reparo tecidual. Objetivo: Desenvolver um dispositivo, de baixo custo, acoplado a célula de carga para avaliação biomecânica de TCs de ratos, alcançando reprodutibilidade de resultados em conformidade com a literatura. Metodologia: Após calibração do sistema (relação entre Tensão de saída e Força), seis TCs controle</div><div>e seis TCs previamente lesionados foram extraídos de ratos Wistar, anexados ao dispositivo e submetidos à sobrecarga gradual até o ponto de ruptura total. Foram analisados a força máxima (N), distensão máxima (mm), coeficiente de rigidez (N/mm) e energia absorvida no ponto de ruptura (N.mm). Resultados: Os TCs lesionados demonstraram menor força máxima (27,15 ± 6,67 N) em comparação aos controles (41,02 ± 10,19 N). Ainda, exibiram redução significativa na rigidez (controle 20,37 ± 6,61; lesionados 12,99 ± 2,22 N/mm). Não se observou diferença na distensão máxima e energia absorvida entre os grupos. Conclusão: Os dados obtidos verificam a confiabilidade do sistema, o qual constitui uma ferramenta eficiente para investigação das propriedades mecânicas de TCs em modelos de tendinopatia e reparo tecidual.</div>
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