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Literatura académica sobre el tema "Bone Diabetes"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 1 de febrero de 2022

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Artículos de revistas sobre el tema "Bone Diabetes"

Krakauer, J. C., M. J. McKenna, N. F. Buderer, D. S. Rao, F. W. Whitehouse y A. M. Parfitt. "Bone loss and bone turnover in diabetes". Diabetes 44, n.º 7 (1 de julio de 1995): 775–82. http://dx.doi.org/10.2337/diabetes.44.7.775.

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Piscitelli, Prisco, Cosimo Neglia, Antonella Vigilanza y Annamaria Colao. "Diabetes and bone". Current Opinion in Endocrinology, Diabetes and Obesity 22, n.º 6 (diciembre de 2015): 439–45. http://dx.doi.org/10.1097/med.0000000000000203.

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Heilmeier, Ursula y Janina Patsch. "Diabetes and Bone". Seminars in Musculoskeletal Radiology 20, n.º 03 (14 de octubre de 2016): 300–304. http://dx.doi.org/10.1055/s-0036-1592366.

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Pietschmann, P., J. M. Patsch y G. Schernthaner. "Diabetes and Bone". Hormone and Metabolic Research 42, n.º 11 (13 de agosto de 2010): 763–68. http://dx.doi.org/10.1055/s-0030-1262825.

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Hull, Beatrice y Nichole R. Smith. "Diabetes and Bone". American Journal of the Medical Sciences 351, n.º 4 (abril de 2016): 356–60. http://dx.doi.org/10.1016/j.amjms.2016.02.010.

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Hygum, Katrine, Jakob Starup-Linde y Bente L. Langdahl. "Diabetes and bone". Osteoporosis and Sarcopenia 5, n.º 2 (junio de 2019): 29–37. http://dx.doi.org/10.1016/j.afos.2019.05.001.

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Schwartz, A. "Diabetes and bone". Bone 44 (junio de 2009): S210. http://dx.doi.org/10.1016/j.bone.2009.03.038.

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Ferrari, Serge. "Diabetes and Bone". Calcified Tissue International 100, n.º 2 (febrero de 2017): 107–8. http://dx.doi.org/10.1007/s00223-017-0234-y.

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Deeba, Farah, Sidra Younis, Nida Qureshi, Tahmina Mustafa, Nadia Iqbal y Saira Hussain. "Effect of Diabetes Mellitus and Anti-Diabetic Drugs on Bone Health-A Review". Journal of Bioresource Management 8, n.º 2 (26 de mayo de 2021): 131–48. http://dx.doi.org/10.35691/jbm.1202.0187.

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Osteoporosis and diabetes mellitus (DM) are widespread diseases and have a significant health burden. Type-1 diabetes mellitus (T1DM) and Type-2 diabetes mellitus (T2DM) are associated with an increased bone fracture. In T1DM, the increased risk of bone fracture is associated with low bone mass. In patients with T2DM, the risk of fracture of the bone is increased due to low quality of bone, despite increased bone mineral density (BMD). In type 2 diabetic patients, bone fragility depends on the quality of bone instead of a reduction in bone mass. Thiazolidinediones (TZD) cause differentiation of adipocytes and inhibit differentiation of osteoblast and bone marrow stromal stem cells (BMSC). In this review, we have described the effect of anti-diabetic drugs and diabetes mellitus on bone health and our finding shows that sulfonylureas and metformin have no negative effect on bone health and protect bones against fractures.

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Krakauer, J. C., M. J. Mckenna, N. Fenn Buderer, D. S. Rao, F. W. Whitehouse y A. M. Parfitt. "Bone Loss and Bone Turnover in Diabetes". Diabetes 44, n.º 7 (1 de julio de 1995): 775–82. http://dx.doi.org/10.2337/diab.44.7.775.

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Tesis sobre el tema "Bone Diabetes"

Retzepi, Maria. "The effect of experimental diabetes on guided bone regeneration". Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/18575/.

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The aim of the present PhD thesis was to investigate the impact of uncontrolled and controlled experimental diabetes on the neo-osteogenesis and bone regeneration potential following Guided Bone Regeneration (GBR). Wistar strain rats (n=128) were allocated in three experimental groups: a) streptozotocin-induced, uncontrolled diabetes; b) systemic insulin controlled diabetes; c) systemic health. The impact of the diabetic status on the neo-osteogenesis and on the bone regeneration potential were evaluated histometrically in GBR treated models of de novo mandibular bone formation and regeneration of critical size calvarial defects respectively. Genome-wide microarray analysis was conducted in tissue samples obtained from GBR treated calvarial defects during the early healing stages. Following application of the GBR therapeutic principle, significant neo-osteogenesis and regeneration of critical size osseous defects were observed histologically and morphometrically, even in the presence of uncontrolled diabetes. Nonetheless, the diabetic status was associated with lower outcome predictability, which was improved via systemic insulin mediated glycaemic control. Uncontrolled diabetes compromised the initial stages of intramembranous bone regeneration following GBR, as evidenced by aberrations in fibrin mesh organisation, inflammatory and mesenchymal cells influx and woven bone formation. In parallel, the uncontrolled diabetic condition featured downregulation of genes encoding chemoattractants and inflammatory mediators during the inflammatory phase of the GBR healing process. Further, pathways related to cell division, energy production and osteogenesis were underexpressed during the proliferative phase, while the NF-kB and Wnt signalling pathways were misregulated. The insulin controlled diabetic state enhanced granulation tissue formation and osteogenesis and upregulated genes encoded growth factors and for extracellular matrix proteins during the early healing phases. It is suggested that, although experimental diabetes may compromise the initial stages of osteogenesis, GBR treatment can provide an environment permissive for significant, even though delayed, bone formation. Insulin mediated glycaemic control may enhance the bone regeneration potential in the diabetic status. Genome-wide expression profiling revealed perturbed pathways in GBR healing depending on the metabolic status, which may be applied in the design of novel therapeutic strategies for the reconstruction of osseous defects in diabetic patients.

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Rees, S. M. "Bone density and neuropathy in type 2 diabetes mellitus". Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419549.

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Mansur, Sity Aishah. "Extrapancreatic actions of incretin-based therapies on bone in diabetes mellitus". Thesis, Ulster University, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.694218.

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Diabetes mellitus is correlated with modifications in bone micro architectural and mechanical strength, leading to increased bone fragility. The in cretin hormones, with a classical effect to increase insulin secretion following food ingestion, are now postulated to have important direct effects on bone. As such, glucose-dependent insulinotropic polypeptide (GIP) has dual actions on bone cells; enhancing boneforming activity of osteoblasts and suppressing bone resorption by osteoclasts. The sister incretin of GIP, glucagon-like peptide-l (GLP-I), is also suspected to directly influence bone health in a beneficial manner, although mechanism are less clear at present. The physiological actions of incretins are attenuated by dipeptidyl peptidase (DPP-4) activity and it is speculated that introduction of DPP-4 inhibitor may also positively affect quality of the skeleton. As such, this thesis evaluates the potential beneficial effects of a DPP-4 resistant GIP analogue, namely [D-Ala2]GIP, on osteoblastic-derived, SaOS-2 cells, and also preliminary in vivo studies on the impact of genetic deficiencies of GIPRs and GLP-IRs on bone mineral density and content. Further studies characterised the beneficial effects of incretin-based therapies on metabolic control, bone microstructure and bone mechanical integrity in animal models of pharmacologically-, genetically- and environmentally-induced diabetes. GIP and related stable analogue increased bone-forming biomarkers in SaOS-2 cells and importantly, [D-Ala2]GIP was shown to be more potent than native GIP. Knockout mouse studies revealed that both GIPR and GLP-IR signaling are important for optimum bone mass. All diabetic mouse models displayed reduced bone mass, altered bone micromorphology and impairment of bone mechanical strength, similar to the human situation, confirming their appropriateness. The incretin-based therapeutics, [D-Ala2]GIP and Liraglutide, in streptozotocin-diabetic significantly increased bone matrix properties, indicating recovery of bone strength at the tissue level. The beneficial effects of administration of [D-Ala2]GIPoxyntomodulin on bone health in db/db mice were more prominent as the Oxm analogue did not only improve bone strength at tissue level, but also at whole-bone level. These modifications were independent of metabolic status. Twice-daily Exendin-4 therapy improved glycaemic control and increased work required to resist bone fracture in high-fat fed mice. It was also established that Sitagliptin had neutral effects on bone microstructure and mechanical strength in high-fat mice.

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Urbina, Princess. "Bone Morphogenetic Protein-7 Attenuates Inflammation and Apoptosis and Improves Cardiac Function in Diabetes". Master's thesis, University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5716.

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Bone Morphogenetic Protein-7 (BMP-7) belongs to the transforming growth factor-β (TGFβ) family of cytokines has is known to have potent anti-inflammatory properties. It has been used in patients to treat osteoporosis clinically and has been reported to treat diabetic nephropathy in murine models. Moreover, studies show that inflammation is up-regulated in patients with pre-diabetes (PD). We, therefore, hypothesize that the administration of BMP-7 will attenuate inflammation in the heart of Streptozotocin (STZ)-induced PD mice. In this study, we divided C57Bl/6 mice into three groups: CONTROL, PD, and PD+BMP-7. CONTROL mice received intraperitoneal (i.p.) injections of Sodium Citrate Buffer while PD and PD+BMP-7 groups received i.p. injections of Streptozotocin (STZ) for two days. In addition, PD+BMP-7 mice received intravenous injections (i.v.) of BMP-7 (200µg/kg) on the last day of STZ injection and for the following two days. Animals were sacrificed 21 days post last injection and examined for levels of oxidative stress, inflammatory immune response, apoptosis, fibrosis and cardiac function. Our results indicate significant glucose intolerance in PD mice (p<0.05), which was attenuated in the PD+BMP-7 group (p<0.05). We also observed increased oxidative stress (p<0.001) and secretion of pro-inflammatory cytokines (p<0.05), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), in PD mice as compared with the controls. PD+BMP-7 mice revealed significant up-regulation of M2 macrophages (p<0.05) and secretion of anti-inflammatory cytokines (p<0.05), interleukin-10 (IL-10) and interleukin-1RA (IL-1RA), as compared to PD mice. This was observed with a concomitant down-regulation of pro-inflammatory cytokines, IL-6 and TNF-α, as compared to the PD group. Moreover, we observed significantly increased cardiac apoptosis and fibrosis in PD mice (p<0.001) as compared to the control group. These observations, however, were down-regulated upon treatment with BMP-7. Lastly, analysis of echocardiograms revealed significantly depressed cardiac function in PD mice as compared with controls, while the PD+BMP-7 group presented improved cardiac function compared to PD mice. In conclusion, our data suggest that treatment with BMP-7 is effective in alleviating cardiac inflammation, inhibiting apoptosis, blunting cardiac remodeling and improving cardiac function in the hearts of STZ-induced PD mice. This reveals the potential of BMP-7 as a therapy in PD patients who present an increased inflammatory immune response.
M.S.
Masters
Molecular Biology and Microbiology
Medicine
Molecular and Microbiology

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Singh, Dhruvaraj Kailashnath. "Clinical studies in diabetic vasculopathy to assess interactions between blood, bone and kidney". Thesis, University of Hertfordshire, 2010. http://hdl.handle.net/2299/4186.

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Diabetic vasculopathy (DV) is the most important consequence of chronic hyperglycemia in patients with diabetes mellitus (DM). This thesis explores the interaction of blood, bone and kidney in the pathogenesis of DV by i) reviewing the current understanding of pathogenesis of macrovascular and microvascular diseases in DM to identify gaps in literature and generate hypotheses relating to various facets of DV ii) undertaking a series of prospective studies to examine these hypotheses iii) analysing the findings and integrating any new information obtained from the clinical studies into the current knowledge base and iv) generating hypotheses upon which future work might be based. The literature search was carried out with the aim of understanding current concepts of pathogenesis of DV and its potential modulators. The original reviews resulting from this process are presented in chapters 2 to 4. A series of pilot studies reported in chapters 7 to 11, were then carried out to interrogate hypotheses originating from this process. The first study was carried out in healthy individuals to define the biological variation of potential modulators of DV, namely erythropoietin (EPO), parathyroid hormone, 25 hydroxyvitamin D and 1, 25-dihydroxyvitamin D to facilitate the design and interpretation of subsequent studies. It revealed a wide biological variation of these modulators in the healthy population thus,emphasizing the need to have a control group in the subsequent study population. To examine whether tubulointerstitial dysfunction occurs before the onset of microalbuminuria, a measurement of the above mentioned parameters was carried out along with markers of tubulointerstitial injury in patients with type 1 and type 2 DM without microalbuminuria and in non-diabetic controls. It was found that tubulointerstitial dysfunction with low levels of EPO and 1, 25-dihydroxyvitamin D and higher excretion of tubular injury markers, occurs before the onset of microalbuminuria. Subsequently, diabetic and nondiabetic chronic kidney disease (CKD) patients with EPO deficiency anaemia were examined to study the effects of EPO therapy on the excretion of tubular injury markers. However, in these patient groups, we were unable to demonstrate an effect of EPO therapy on the markers of tubular injury in spite of a beneficial haematological response. To examine whether vascular calcification (VC) and bone mineral density (BMD) were linked in patients with diabetes mellitus and to explore their relationship to modulators of DV, an assessment of VC and BMD was undertaken in patients with type 2 DM with different degrees of proteinuria and normoalbuminuria. VC was assessed by CT scan and BMD by a DEXA scan. Modulators of DV were measured including serum Osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-b-ligand (RANKL). The findings were i) a high prevalence of VC and osteopenia in normoalbuminuric type 2 DM patients with normal serum creatinine ii) a weak inverse relationship between VC and osteopenia iii) proteinuric patients had worse VC but not osteopenia iv) weak relationships between OPG levels and both VC and osteopenia, masked by age in multivariate analysis. The final study examined the relationship between modulators of DV, including OPG and RANKL, and the degree of CKD. It was found that abnormalities of OPG and RANKL occur before the onset of microalbuminuria and progress with deterioration of renal function. Compared to nondiabetics, DM patients have higher OPG levels in the predialysis phase and lower levels in haemodialysis phase, a phenomenon that might indicate endothelial exhaustion in dialysis patients with DM. The derangements associated with DV seem to occur earlier than previously thought. Further work is required to untangle these complexities and to define the contribution of factors such as the adverse blood milieu, the vasculature, abnormal bone and mineral metabolism, and early tubulointerstitial damage. The findings from the studies reported here may help in the formulation of new hypotheses, which might contribute to future work in this area.

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Stabley, John Nathan. "Relationship between autonomic nervous system function and bone mineral density in type 1 diabetic individuals". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 65 p, 2006. http://proquest.umi.com/pqdweb?did=1203584531&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Al-Qarakhli, Ahmed. "Altered bone cell biology associated with Type Two Diabetes Mellitus : consequences for periodontal disease". Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/112980/.

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Periodontitis is a widely spread disease, affecting about 80% of the worldwide population, resulting in teeth loss, a heavy impact on patients in terms of function and aesthetic. Type 2 Diabetes Mellitus (T2DM) is described to be linked to the exacerbation of periodontitis and delayed healing. This link between these two diseases, however, is not fully evaluated and the mechanisms are yet to be fully elucidated. Osteopontin (OPN) is described to inhibit mineral crystal formation. Herein, it has been hypothesized that increased OPN in diabetic healing bone may be the causative factor of delayed healing in periodontitis and subsequent deterioration, leading to teeth loss. This project aims to gain a greater understanding of the effect of high glucose (HG) levels on mesenchymal stem cells (MSCs) and macrophages, their ability to synthesise OPN and hence, its effects on MSCs to synthesise new bone tissue. Further, the influence of Porphyromonas gingivalis lipopolysaccharides (Pg-LPS) on these cells was analyzed, in an attempt to create a model to study the healing in the presence of periodontitis and T2DM. Investigating the MSCs isolated from the rat compact bone (CB-MSCs) during the growth in culture, revealed two main populations; a heterogenous population appeared with predominantly mature characteristics at PD15. This population then demonstrated a change in its heterogeneity and became more immature in nature at PD50. These two main populations differed in their growth rate and capability of osteodifferentiation. HG environments exerted significant decreases in osteogenic differentiation on PD15, but not PD50. Addition of pg-LPS showed inhibitory effects on osteodifferentiation on PD15 cells more than PD50. Conversely, in the combined presence of HG and pg-LPS, PD50 showed a significant decrease in osteodifferentiation. OPN levels demonstrated a gradual decrease in CB-MSCs in both normal and HG conditions. Investigating OPN levels secreted by macrophages, however, revealed interesting results. Synergistic effects of both HG and pg-LPS exhibited a significant increase in OPN levels in both pro-inflammatory M1 macrophages and in repair related M2 macrophages. In conclusion, HG was mainly reported to inhibit osteogenic differentiation of the mature cell population, whereas the immature population was found to be affected by combined pg-LPS and HG. OPN levels in HG conditions were shown to decrease along the osteodifferentiation period. However, macrophages showed increase secretion of OPN by the synergistic effects of both pg-LPS and HG in both M1 and M2 and by pg-LPS effects in M2 macrophages. These outcomes as far as we are aware, are novel and disclose a new mechanism of bone resorption in the case of T2DM patients concurrently with periodontal disease.

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Berchieri, Carolina Bragiola [UNESP]. "Avaliação da densidade mineral óssea e os fatores a ela associados em indivíduos adultos com Diabetes Mellitus". Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/92167.

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O esqueleto é um dos maiores sistemas do corpo humano e é responsável pela manutenção da estrutura corporal e pelo armazenamento de minerais e proteínas, sendo a massa óssea determinada pela formação e reabsorção óssea. A osteoporose é um distúrbio osteometabólico crônico, multifatorial, relacionado à perda progressiva de massa óssea, geralmente de progressão assintomática até a ocorrência de fraturas. Caracteriza-se pela diminuição da densidade mineral óssea (DMO), com deterioração da microarquitetura óssea, que leva a um aumento da fragilidade esquelética e do risco de fraturas. As principais manifestações clínicas são as fraturas, sendo mais freqüentes as de vértebras, fêmur e antebraço. Desde 1949, quando Albright e Reifeinstein relataram a ocorrência de osteoporose em pacientes com diabetes (DM) de longa duração e mal-controlados, vários outros trabalhos foram publicados sobre o assunto, permanecendo não estabelecido o papel do DM como um fator de risco para osteoporose e fraturas ósseas. Avaliar a DMO e os possíveis fatores envolvidos em sua manutenção e formação, em adultos jovens com DM 1 e DM 2, comparando-os a um grupo controle homogêneo quanto à idade, gênero e índice de massa corpórea (IMC). Constituíram-se 2 grupos, sendo o primeiro de indivíduos com diabetes, subdividido em 25 indivíduos DM 1 e 25 indivíduos DM 2. O segundo grupo foi determinado como controle, composto por 18 indivíduos, os quais não apresentavam DM ou outras doenças que pudessem interferir no metabolismo ósseo e cuja faixa etária, gênero e IMC foram semelhantes aos diabéticos, compondo assim um grupo homogêneo. Os critérios de inclusão para os DM foram: idade entre 20 e 50 anos, tempo de diagnóstico do DM ≥5 anos, estar em acompanhamento ambulatorial, sem...
The skeleton is one of the largest systems in the human body and it is responsible for the maintenance of the body structure and also the storage of minerals and proteins. The bone mass is determined by the bone formation and reabsorption. Osteoporosis is a osteometabolic chronic multifactor disturb, related to progressive loss of bone mass, usually of asymptomatic progression until the occurrence of fractures. It is characterized by the decrease of the bone mineral density (BMD), with deterioration of the bone microarchitecture, which leads to a raise of the bone fragility and the risk of fractures. The main clinical manifestations are the fractures, more commonly on lumbar spine, femoral neck and forearm. Since 1949 when Albright & Reifeinstein described the occurrence of osteoporosis on long-term diabetic patients with poor metabolic control, many other studies were developed in this issue, remaining not well established the role of diabetes (DM) as a risk factor for osteoporosis and bone fractures. Assess the BMD and the possible factors involved in its maintenance and formation, in young type 1 and 2 diabetic adults, comparing them to a control group, alike on age, gender and body mass index (BMI). Two groups were established, the first one with type 1 (DM 1) and type 2 (DM 2) diabetic patients (25 individuals each) and the second one the control group, with 18 individuals without DM or any other disease which could affect bone metabolism. Age, gender and BMI were in parallel with the diabetic group characteristics, establishing a homogeneous group. Inclusion criteria for diabetic patients were: age between 20 and 50 years, diagnosis time ≥5 years, in actual clinical follow up, without further complications due to diabetes, not in use of drugs or having any disease which could interfere on bone metabolism, and non-pregnant or menopause women. A protocol was ...(Complete abstract click electronic access below)

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Abdalrahaman, Naiemh. "The assessment of bone health in young women with childhood-onset type one diabetes mellitus". Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8413/.

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The risk of hip fracture in people with type one diabetes mellitus (T1DM) is reported to be 7 to 12 times greater than in those without T1DM, and this increased risk is evident in both children and young adults. This fracture risk is higher than expected bone mineral density (BMD) measurements, which indicates the likelihood that other skeletal factors, not captured by DXA, may contribute toward increased fracture risk. There is increasing evidence that alteration in trabecular bone microarchitecture and increased bone marrow adiposity (BMA) are causes for excess skeletal fragility, yet these data are lacking in people with T1DM. Recent technological advances in magnetic resonance imaging (MRI) have allowed the quantification of trabecular bone architecture. In addition, MRI can quantify the amount of intra-abdominal fat, and magnetic resonance spectroscopy (MRS) can also be used to assess BMA. These advances may enhance our understanding of the underlying causes of diabetic osteopathy which may lead to improved fracture risk predictors and preventive measures in patients with T1DM beyond that provided by dual energy x-ray absorptiometry (DXA). The overall objective of this thesis was to improve the understanding of the bone pathology of young adult women with childhood-onset T1DM by using high resolution MRI. A cross-sectional study was first carried out to assess trabecular bone microarchitecture of the tibia, vertebral BMA and abdominal adiposity in patients with childhood onset T1DM (n=30) compared with healthy controls (n=28). Additionally, the biochemical markers of bone turnover, adiposity and GH/IGF-1 axis (IGF-1, IGFBP3, and ALS) were examined to evaluate the underlying mechanism that might result in bone deficit in this group of people. We found that young women with childhood onset T1DM had reduced apparent trabecular bone volume (appBV/TV) and apparent trabecular number (appTbN) and greater apparent trabecular separation (appTbSp) than women without T1DM. Interestingly, these differences remained significant after adjustment for multiple confounders. Furthermore, these abnormalities were markedly obvious in those with microvascular complication compared with those without microvascular complication. Although women with T1DM had greater abdominal adiposity compared with healthy controls, there was no significant difference in BMA between the groups. However, BMA showed positive significant association with current glycaemic control (r= 0.45, p=0.02). Women with T1DM had lower bone turnover and decreased GH/IGF axis compared with healthy controls. Osteocalcin and ALS were negatively correlated with trabecular separation in women with T1DM. III Next, a one-year prospective study was conducted in a subset (n=28) of the participants involved in the cross-sectional study. The aim of this study was to compare one year changes in trabecular bone microarchitecture and BMA in women with and without T1DM. Additionally, the study aimed to evaluate the effect of glycaemic control on these changes over this period. After adjustment for relevant confounders, the cases (n=17) had a lower median appTbN and a higher median appTbSp at baseline and 12 months compared with healthy controls (n=11). Although the sample size was small at follow-up, the trabecular bone deficits were clearly noticeable in those with retinopathy compared with those without retinopathy. Similarly, there was no difference in median BMA which was 26.2% (12.1, 62.1) and 22.4% (9.6, 41.9) in cases and controls, respectively (p=0.57). Additionally, over the 12 month period, there was no significant change in MRI-measured parameters in cases or in controls, and no differences in the change of these variables between the two groups. Mixed model effect analysis showed that age was a negative predictor of percent changes of appBV/TV, appTbN and appTbSp in both cases and controls (p=0.02, p=0.02, p=0.002, respectively). Interestingly, there was a strong correlation between change in HbA1c and change in BMA (r=0.8; p=0.002). In the third study, we aimed to assess adiposity-based determinants of bone mineral density and bone microarchitecture in healthy young women and women with T1DM. Additionally, we aimed to compare the feasibility of using DXA and MRI-measured bone parameters to differentiate women with and without T1DM. In addition to high resolution MRI we used DXA scans to measure BMD and body composition from the same participants (n=26) involved in the longitudinal study. Vertebral BMA was positively correlated with VAT. Additionally, we demonstrated evidence of an inverse association of vertebral BMA and DXA-measured bone parameters of femoral neck, lumbar spine and total body independent of demographics and body composition in healthy young women and women with T1DM. These finding support the hypothesis that BMA is linked with low bone density, and may contribute to excess bone fragility. Moreover, this study suggested that MRI-measured trabecular bone measurements were able to differentiate between T1DM with and without microvascular complication compared with DXA-measured BMD. In summary, differences in MRI-measured trabecular microarchitecture parameters identified in this body of work provide preliminary explanations for elevated fracture risk in young women with childhood onset T1DM. Additionally, these findings provide potential insight into a number of possible underlying mechanisms of diabetic osteopathy.

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Yusop, Norhayati. "Altered biological responsiveness of cells regulating intramembraneous bone repair associated with Type 2 Diabetes Mellitus". Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/75468/.

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The successful outcome from implant procedure relies heavily on the integration between the implant and the surrounding bone tissues. Besides, Type 2 Diabetes Mellitus (T2DM), which is linked with delay of osseointegration and reduction of bone-implant interface, further compromises the success rate of implant in diabetic patients. Apart from hyperglycaemia, the precise mechanism of diabetes influence on bone repair associated with dental implants is not completely understood. Nevertheless, the transforming growth factor-β1 (TGF-β1) has been indicated to increase healing processes, by exerting the stimulatory role on mesenchymal stem cells (MSCs) and macrophage populations during the inflammatory stage of bone repair. Moreover, the bioavailability of growth factors has been associated with the functional role of SLRPs, particularly biglycan and decorin. However, the responsiveness of each relevant bone-repair cell and biomolecule during bone repair in a diabetic environment has not been fully evaluated. On the other hand, the in vivo osseointegration of implant in T2DM animal models,investigated in respect to the expression of TGF-β1 by MSCs, demonstrated statistically significant differences in TGF-β1 labelled between the young diabetic and the control groups. Besides, the in vitro assessment demonstrated alterations for TGF-β1 expression and synthesis by osteoprogenitor cells, macrophages populations,between cells with different proliferative states, and prior hyperglycaemic-induction. Moreover, hyperglycaemia altered osteogenic and adipogenic differentiation capacities in MSCs. The data also suggested that hyperglycaemia induced lower proliferative capacity in MSCs, which led to significant changes in growth factor and proteoglycans bioactivity in bone repair. Hence, the data gathered from both in vivo and in vitro experiments suggested the potential association of MSCs proliferative stage with bioavailability of TGF-β1 and proteoglycans sequestration in the extracellular matrix compartment. Apart from that, the inter-dependent relationship observed between the osseointegration biomolecules directly exerted a synergical impact on the capability of MSCs to form osteoblast and further stimulate bone formation in order to induce bone-healing processes. Thus, the original contribution of this study to the field of reparative medicine is the novel identification and the characterisation of key biological components in both cellular and molecular bone repairs; the osteoprogenitor cell populations, as well as the macrophages, in relation to hyperglycaemia that directly influences growth factors, signalling the role of proteoglycans during the bone repair processes in T2DM. Collectively, the evidence gathered within this study is highly valuable to assist in elucidating the relevant therapeutic target to accelerate bone repair processes in T2DM patients. Keywords: diabetes, osseointegration, hyperglycaemia, bone, growth factors.

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Libros sobre el tema "Bone Diabetes"

Lecka-Czernik, Beata y John L. Fowlkes, eds. Diabetic Bone Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-16402-1.

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Török, M. Estée, Fiona J. Cooke y Ed Moran. Bone and joint infections. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0022.

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This chapter provides an overview of inflammations of the joint space and bones, such as arthritis and bursitis, including osteomyelitis and bone destruction and formation of sequestra. The chapter also includes prosthetic joint infections such as hip and knee replacements. It also describes diabetic foot infections, defined as any inframalleolar infection in a patient with diabetes mellitus. Infections include paronychia, cellulitis, myositis, abscesses, necrotizing fasciitis, septic arthritis, tendonitis, and osteomyelitis.

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Tan, Meng Hee. Diabetes Mellitus: Impact on Bone, Dental and Musculoskeletal Health. Elsevier Science & Technology Books, 2020.

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Lecka-Czernik, Beata y John L. Fowlkes. Diabetic Bone Disease: Basic and Translational Research and Clinical Applications. Springer, 2015.

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Lecka-Czernik, Beata y John L. Fowlkes. Diabetic Bone Disease: Basic and Translational Research and Clinical Applications. Springer, 2016.

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Chiu, Sai-Wing Andrew. Vanadium treatment prevents bone loss and maintains bone quality in a combined osteoporosis and diabetes rat model. 2006.

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Facchini, Diana Maria. The effects of vanadium on bone quality in rat models of diabetes and postmenopausal osteoporosis. 2005.

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Facchini, Diana Maria. The effects of vanadium on bone quality in rat models of diabetes and postmenopausal osteoporosis. 2005.

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Fox, Grenville, Nicholas Hoque y Timothy Watts. Metabolic problems and jaundice. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198703952.003.0013.

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This chapter covers problems of glycaemic control in neonates (including investigation and management of hypoglycaemia and hyperglycaemia); management of babies of women with diabetes (infant of the diabetic mother); the physiological basis and rational approach to the treatment of metabolic acidosis in the newborn; the presentation, investigation, and management of inborn errors of metabolism presenting in the newborn; and metabolic bone disease (also known as osteopenia or rickets of prematurity). There is an overview of the investigation and treatment of neonatal jaundice, including physiological jaundice, aetiology, and investigation of non-physiological jaundice and aims of treatment of this; with guidelines for the use of phototherapy, exchange transfusion, and intravenous immunoglobulin. The importance of assessment of prolonged jaundice with reference to conjugated hyperbilirubinaemia is also covered in this section.

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Steiner, Lisa A. Osteomyelitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0049.

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Osteomyelitis is an infectious process that affects any part of the bone, including the periosteum, the cortex, or the marrow. It most often occurs in the lower extremities and can be an acute, subacute, or chronic process. Osteomyelitis is often characterized as a consequence of a contiguous spread or hematogenous spread of bacterial infection or as a consequence of vascular insufficiency. Chronic osteomyelitis can be associated with significant bone necrosis, sometimes requiring months to years of treatment with antibiotics or even surgical debridement. Consultation with the orthopedic service (or spine service for vertebral osteomyelitis) should be considered. Vascular service consultation should also occur if there is a concern for osteomyelitis in the foot of a patient with diabetes mellitus. These patients often require admission to the hospital for follow-up.

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Capítulos de libros sobre el tema "Bone Diabetes"

Starup-Linde, Jakob y Søren Gregersen. "Bone and Diabetes". En Endocrinology, 411–36. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36694-0_13.

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Palermo, Andrea, Anda Mihaela Naciu, Gaia Tabacco, Luca D’Onofrio y Nicola Napoli. "Bone and Diabetes". En Multidisciplinary Approach to Osteoporosis, 153–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75110-8_10.

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Starup-Linde, Jakob y Søren Gregersen. "Bone and Diabetes". En Endocrinology, 1–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-27316-7_13-1.

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Starup-Linde, Jakob y Søren Gregersen. "Bone and Diabetes". En Endocrinology, 1–26. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-27316-7_13-2.

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Starup-Linde, Jakob y Søren Gregersen. "Bone and Diabetes". En Endocrinology, 411–36. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-44433-8_13.

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Amir, Gail. "Bone Repair in Diabetes". En Principles of Bone Regeneration, 59–66. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2059-0_5.

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Leslie, William D. y Stephen Hough. "Fracture Risk Assessment in Diabetes". En Diabetic Bone Disease, 45–69. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-16402-1_3.

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Rejnmark, Lars. "A Bone Perspective". En Pharmacotherapy of Diabetes: New Developments, 267–69. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-69737-6_26.

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Xiao, E., Yingying Wu y Dana T. Graves. "Impact of Diabetes on Periodontal Disease". En Diabetic Bone Disease, 95–112. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-16402-1_5.

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Grey, Andrew y Nicola Dalbeth. "Bone and Rheumatic Disorders in Diabetes". En Textbook of Diabetes, 773–88. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924853.ch53.

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Actas de conferencias sobre el tema "Bone Diabetes"

Sherrod, Brandon, Shawn Gilbert, Krista Casazza y Alan Eberhardt. "Design of a Torsion Tester for Measuring Murine Bone Properties for Studies on the Effects of Diabetes and Obesity". En ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14412.

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Conditions such as diabetes and obesity have been found to affect the mechanical integrity of bone. Studies have shown that diabetic rodent models exhibit lower levels of new bone formation during fracture healing 1, lower bone mineral density (BMD) 2, and increased risk of fracture 3. There are differences, however, in the bone integrity of bone samples from type I and type II diabetics, which is most likely due to obesity 2. Findings from research on obesity’s effects on bone integrity have been controversial; although there is an increase in bone mineral density (BMD) with increasing body mass index (BMI) and a decrease in fracture incidence in the central body regions in obese women compared to healthy weight women due to soft tissue padding, there is an increase in fracture incidence at extremeties 4. Other studies have shown that while cortical bone strength may not be adversely affected by high-fat diets, cancellous bone BMD and mechanical strength was significantly lower in high-fat diet mice than low-fat diet mice 5. In addition, extreme obesity has been associated with lower BMD despite the general trend of increased BMD with higher BMI 6.

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McNulty, M., T. Castaño-Martinez, C. Morrison, A. Schürmann y T. Laeger. "FGF21, not GCN2, contributes to cortical bone remodeling due to protein and methionine restriction". En Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727563.

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Hanouchine, Nassima, Salah Ouhadj y Chafia Dahou-Makhloufi. "FRI0471 BONE QUALITY ASSESSMENT IN PATIENTS WITH TYPE 2 DIABETES MELLITUS". En Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7199.

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Hidaka, Kazuhiro y Yoshiki Kuroda. "458 Epidemiological study between type 2 diabetes and bone mineral density". En 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.107.

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Mohsin, S., J. J. Sunny, K. Menon y S. Kaimala. "THU0496 Skeletal deficit due to altered bone quality in type 1 diabetes mellitus". En Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.1957.

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Fazullina, Olga y Vadim Klimontov. "Modeling the Risk of Decrease in Bone Mineral Density in Men with Type 2 Diabetes". En 2019 International Multi-Conference on Engineering, Computer and Information Sciences (SIBIRCON). IEEE, 2019. http://dx.doi.org/10.1109/sibircon48586.2019.8958320.

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Wang, Wei, Bingbing Jiang, Shandong Ye y Liting Qian. "Risk Factor Analysis of Bone Mineral Density Based on Feature Selection in Type 2 Diabetes". En 2018 IEEE International Conference on Big Knowledge (ICBK). IEEE, 2018. http://dx.doi.org/10.1109/icbk.2018.00037.

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Woo, D. G., Q. J. Lee, W. P. Park, C. Y. Ko, D. Lim, H. S. Kim y B. Y. Lee. "Relationship Between Obesity and Osteopenia in Lumbar Spines of Rats Using Mechanical and Morphological Studies". En ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192537.

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Obesity (OB) and osteopenia (OP), grave consequences for human health, quality of life, and even the efficiency of the labor force and economy, are two common complex diseases. Two public health problems have exploded in prevalence over the past decade [1]. OB, now a major epidemic in the developed world and frequent among elderly subjects, is a condition of excessive body fat that causes or exacerbates several risk of developing non-insulin dependent diabetes mellitus, cardiovascular disease, cancer and other diseases [2]. OP is defined as a systemic skeletal disease caused by low bone mass and microstructural deterioration of the bone.

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"Bone remodeling in men with type 2 diabetes: is it just the same thing as in women?" En Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-268.

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Fazullina, Olga N. y Maksim V. Dashkin. "Bone remodeling in men with type 2 diabetes: is it just the same thing as in women?" En 2020 Cognitive Sciences, Genomics and Bioinformatics (CSGB). IEEE, 2020. http://dx.doi.org/10.1109/csgb51356.2020.9214749.

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