Academic literature on the topic 'Diabetic bone fractures'
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Journal articles on the topic "Diabetic bone fractures"
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Cain, Jarrett D., Michelle Titunick, Patricia McLaughlin, and Ian Zagon. "Effects of Local Opioid Antagonist on Diabetic Fracture Rat Model." Foot & Ankle Orthopaedics 3, no. 3 (July 1, 2018): 2473011418S0017. http://dx.doi.org/10.1177/2473011418s00178.
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Category: Diabetes Introduction/Purpose: Complications associated with the diabetes include increased incidence of fracture healing, delayed fracture healing, delayed osteoblasts cell replication, decreased angiogenesis, migration and/or osteoblast cell differentiation. The cellular events involved in bone healing are adversely affected by diabetes; however, can be modulated by the Opioid Growth Factor (OGF)–OGF receptor (OGFr) is an inhibitory peptide that downregulates DNA synthesis in a tissue nonspecific manner. Diabetes is associated with elevated serum levels of OGF and dysregulation of the OGFr leading to multiple complications related to healing, sensitivity, and regeneration. This study explores the presence and function of the OGF-OGFr axis in bone tissue from type 1 diabetic rats examining intact and fractured femurs during early phases of the repair process Methods: Seven-week-old Sprague Dawley rats were injected with streptozotocin (40mg/kg i.p.) to induce T1D; other rats received buffer only and served as controls. After one month, hyperglycemia rats underwent surgery to produce a fracture at the distal third of the femur. Four diabetic rats received opioid antagoinist (naltrexone) and calcium sulfate and all remaining rats received calcium sulfate with water only. X-rays were taken immediately after surgery and after rats were euthanized on post-surgery; femur and tibia were collected for protein isolation, western blot analysis along with frozen or paraffin-embedded for histological analysis Results: Immunofluorescence indicated approximately 90% increase in opioid growth factor receptor expression in diabetic femurs compared to age-matched normal femurs. Western Blotting also suggested an increase in the receptor protein in diabetic bones relative to normal bone. TRAP staining for osteoclasts was greater in control and opioid antagonist-treated diabetic fractures when compared to the number of osteoclasts in vehicle-treated diabetic fractured femurs. Safranin O stained sections revealed approximately more bone in opioid growth receptor antagonist-treated diabetic bone fractures than in vehicle-treated bone fractures Conclusion: These data support our hypothesis that expression levels of OGFr are dysregulated in the bone of diabetic patients leading to complications in bone healing. Moreover, modulation of the OGF-OGFr pathway with receptor antagonists restored some aspects of bone healing. With further study, these preliminary results support the role of the OGF-OGFr axis in treatment of diabetic bone healing. New therapies to target dysregulation of the OGF-OGFr regulatory pathway in diabetes would provide a safe and effective disease-modifying treatment for delayed bone healing.
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Ilic, Jana, and Branka Kovacev. "Diabetic osteopathy." Medical review 58, no. 3-4 (2005): 147–52. http://dx.doi.org/10.2298/mpns0504147i.
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Introduction. The aim of this study was to point out some dilemmas about the existence and pathogenesis of primary diabetic osteopathy as a separate entity, based on currently available studies. Expert disagreements are present not only about the occurrence of generalized osteopathy with diabetic disease, but also about direct relationship between metabolic diabetes control and bone metabolism and influence of disease duration and sex on bone changes. Pathogenesis of diabetic osteopathy Decreased bone formation is the basic mechanism leading to decreased bone mass. Biochemical markers showed no clear connection with bone density measurement. Insulin and insulin-like growth factor (IGF) affect bone metabolism. Osteopathy in patients with diabetic disease-type 1 Some clinical studies have shown that patients with diabetic disease-type 1 have a mild decrease in bone mass, while others have not presented such results. Osteopathy in patients with diabetic disease-type2 In patients with diabetic disease-type 2 the risk for osteopathy is even less defined. Patients treated with oral hypoglycemics present with higher decrease of bone mass has than patients treated with insulin therapy. This could partly be explained by anabolic effects of insulin on bones. Bone fractures in patients with diabetic disease Literature data are contradictory concerning the occurrence of bone fractures in diabetic patients. A survey of bone fracture occurrence in diabetic patients was performed in "Veljko Vlahovic Medical Center" in Vrbas and it included a group of 100 patients with diabetic disease. The results show that 12 patients had some fractures: mostly females in postmenopause, aged and with secondary insulin-dependent diabetes and most frequently arm fractures. Considering contradictory literature data, further longitudinal studies are necessary. .
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Deeba, Farah, Sidra Younis, Nida Qureshi, Tahmina Mustafa, Nadia Iqbal, and Saira Hussain. "Effect of Diabetes Mellitus and Anti-Diabetic Drugs on Bone Health-A Review." Journal of Bioresource Management 8, no. 2 (May 26, 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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Akhtar, Muhammad Mahmood, Abdulaziz Saad Alghamdi, Abdulrahman Mohammed Alshehri, Hussain Zaki Alfaraj, Abdullah Mohammed Alshamrani, Anoud Abdulrazzag Althagafi, Elaf Abdulqader Bahanshel, et al. "Bone and mineral disorders among Saudi diabetics." International Journal Of Community Medicine And Public Health 8, no. 5 (April 27, 2021): 2605. http://dx.doi.org/10.18203/2394-6040.ijcmph20211797.
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Increasing bone and mineral changes which caused by both diabetes type 1 and type 2 can raise fracture risks for a period of time during illness and low blood sugar levels. The connection between diabetes and bone fragility is further complicated by the variable effects on the skeleton by various diabetic medications. Diabetic patients are at a higher risk of bone and mineral density alterations, osteoporosis and fragility fractures. Diabetic patients are often susceptible to develop various conditions due to malnutrition, uncontrolled blood sugar and lack of proper follow up regiment. Diabetics should be tested for osteoporosis risk and given effective prevention strategies. Preventing osteoporosis would require interventions such as sufficient vitamin D and calcium intake, physical exercise and exposure to sunlight.
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Watson, Luke, Xi Zhe Chen, Aideen E. Ryan, Áine Fleming, Aoife Carbin, Lisa O’Flynn, Paul G. Loftus, et al. "Administration of Human Non-Diabetic Mesenchymal Stromal Cells to a Murine Model of Diabetic Fracture Repair: A Pilot Study." Cells 9, no. 6 (June 3, 2020): 1394. http://dx.doi.org/10.3390/cells9061394.
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Individuals living with type 1 diabetes mellitus may experience an increased risk of long bone fracture. These fractures are often slow to heal, resulting in delayed reunion or non-union. It is reasonable to theorize that the underlying cause of these diabetes-associated osteopathies is faulty repair dynamics as a result of compromised bone marrow progenitor cell function. Here it was hypothesized that the administration of non-diabetic, human adult bone marrow-derived mesenchymal stromal cells (MSCs) would enhance diabetic fracture healing. Human MSCs were locally introduced to femur fractures in streptozotocin-induced diabetic mice, and the quality of de novo bone was assessed eight weeks later. Biodistribution analysis demonstrated that the cells remained in situ for three days following administration. Bone bridging was evident in all animals. However, a large reparative callus was retained, indicating non-union. µCT analysis elucidated comparable callus dimensions, bone mineral density, bone volume/total volume, and volume of mature bone in all groups that received cells as compared to the saline-treated controls. Four-point bending evaluation of flexural strength, flexural modulus, and total energy to re-fracture did not indicate a statistically significant change as a result of cellular administration. An ex vivo lymphocytic proliferation recall assay indicated that the xenogeneic administration of human cells did not result in an immune response by the murine recipient. Due to this dataset, the administration of non-diabetic bone marrow-derived MSCs did not support fracture healing in this pilot study.
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Al-Hariri, Mohammed. "Sweet Bones: The Pathogenesis of Bone Alteration in Diabetes." Journal of Diabetes Research 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/6969040.
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Diabetic patients have increased fracture risk. The pathogenesis underlying the status of bone alterations in diabetes mellitus is not completely understood but is multifactorial. The major deficits appear to be related to a deficit in mineralized surface area, a decrement in the rate of mineral apposition, deceased osteoid surface, depressed osteoblast activity, and decreased numbers of osteoclasts due to abnormal insulin signaling pathway. Other prominent features of diabetes mellitus are an increased urinary excretion of calcium and magnesium, accumulation of advanced glycation end products, and oxidative stress leading to sweet bones (altered bone’s strength, metabolism, and structure). Every diabetic patient should be assessed for risk factors for fractures and osteoporosis. The pathogenesis of the bone alterations in diabetes mellitus as well as their molecular mechanisms needs further study.
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Lee, Eun-Jung, Woojin Na, Min-Kyung Kang, Yun-Ho Kim, Dong-Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, et al. "Hydroxycoumarin Scopoletin Inhibits Bone Loss through Enhancing Induction of Bone Turnover Markers in a Mouse Model of Type 2 Diabetes." Biomedicines 9, no. 6 (June 7, 2021): 648. http://dx.doi.org/10.3390/biomedicines9060648.
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Diabetes induces bone deterioration, which leads to increased risk of fracture, osteopenia, and osteoporosis. Thus, diabetes-associated bone fragility has been recognized as a diabetic complication. However, the pathophysiological effects of hyperglycemia on bone turnover remain unclear. Literature evidence demonstrates that anti-diabetic medications increase the risk of fractures in individuals with type 2 diabetes. Scopoletin is a naturally occurring hydroxycoumarin potentially exhibiting anti-inflammatory and antioxidant activities and ameliorating insulin resistance as an anti-diabetic agent. However, little is known regarding the effects of scopoletin on the impairment of bone remodeling that is caused by diabetes. The aim of this study was to identify that scopoletin was capable of inhibiting the impairment of bone remodeling and turnover in a mouse model of type 2 diabetes. Submicromolar scopoletin accelerated the formation TRAP-positive multinucleated osteoclasts (40.0 vs. 105.1%) and actin ring structures impaired by 33 mM glucose. Further, 1–20 μM scopoletin enhanced bone resorption and the induction of matrix-degrading enzymes in diabetic osteoclasts. The oral administration of 10 mg/kg scopoletin elevated serum RANKL/OPG ratio and osteocalcin level reduced in db/db mice along with an increase in BMD by ~6–14%; however, it was not effective in lowering blood glucose and hemoglobin glycation. In addition, the supplementation of scopoletin elevated the formation of trabecular bones and collagen fibers in femoral epiphysis and metaphysis with a thicker epiphyseal plate and cortical bones. Furthermore, 1–20 μM scopoletin enhanced ALP activity (4.39 vs. 7.02 nmol p-nitrophenyl phosphate/min/mg protein) and deposits of mineralized bone nodules in cultured osteoblasts reduced by 33 mM glucose. The treatment of diabetic osteoblasts with scopoletin stimulated the cellular induction of BMP-2 and osteopontin and Runx2 transcription. Accordingly, the administration of scopoletin protected mice from type 2 diabetes-associated bone loss through boosting bone remodeling via the robust induction of bone turnover markers of both osteoclasts and osteoblasts. These findings suggest that scopoletin could be a potential osteoprotective agent for the treatment of diabetes-associated bone loss and fractures.
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Gougoulias, Nikolaos, Hesham Oshba, Apostolos Dimitroulias, Anthony Sakellariou, and Alexander Wee. "Ankle fractures in diabetic patients." EFORT Open Reviews 5, no. 8 (August 2020): 457–63. http://dx.doi.org/10.1302/2058-5241.5.200025.
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Surgical complications are more common in patients with complicated diabetes (presence of inner organ failure, neuropathy). Of all patients undergoing ankle fracture fixation, approximately 13% are diabetic and 2% have complicated diabetes mellitus. Non-operative management of ankle fractures in patients with complicated diabetes results in an even higher rate of complications. Insufficient stability of ankle fractures (treated operatively, or non-operatively) can trigger Charcot neuroarthropathy, and result in bone loss, deformity, ulceration, and the need for amputation. Rigid fixation is recommended. Hindfoot arthrodesis (as primary procedure or after failed ankle fracture management) can salvage the limb in approximately 80% of patients. Early protected weight bearing can be allowed, provided rigid fixation without deformity has been achieved. Cite this article: EFORT Open Rev 2020;5:457-463. DOI: 10.1302/2058-5241.5.200025
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Safarova, S. S. "Pathogenetic aspects of bone metabolism in diabetes mellitus." Clinical Medicine (Russian Journal) 96, no. 8 (December 20, 2018): 707–12. http://dx.doi.org/10.18821/0023-2149-2018-96-8-707-712.
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Metabolic disorders caused by diabetes affect bone remodeling, alter the structure and reduce the strength of bone tissue, leading to the development of diabetic osteopathy. However, between diabetes mellitus (DM) type 1 and 2 there are noticeable differences in the effect on the bone structure, which is obviously due to the different cellular and molecular mechanisms of these processes. The density of bone tissue with DM typel decreases, which leads to an increase in the risk of fractures by 7 times. With DM type 2, bone mineral density is moderately elevated, which is expected to lead to a decrease in the incidence of osteoporotic fractures, but in fact, this index is approximately doubled. Pathophysiological mechanisms underlying osteoporotic changes in diabetes mellitus are complex and included hyperglycemia, oxidative stress and accumulation of advanced glycation endproducts that alter the properties of collagen, increase fatty infiltration of the bone marrow, release inflammatory factors and adipokines from visceral adipose tissue and potentially change the function osteoblasts. Additional factors are, some antidiabetic drugs that directly affect the metabolism of bones and minerals (such as thiazolidinediones), as well as an increased tendency to fall due to micro- and macroangiopathies, all contribute to an increased risk of low-fracture fractures in patients with diabetes mellitus.
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Jackuliak, Peter, and Juraj Payer. "Osteoporosis, Fractures, and Diabetes." International Journal of Endocrinology 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/820615.
Full textAbstract:
It is well established that osteoporosis and diabetes are prevalent diseases with significant associated morbidity and mortality. Patients with diabetes mellitus have an increased risk of bone fractures. In type 1 diabetes, the risk is increased by ∼6 times and is due to low bone mass. Despite increased bone mineral density (BMD), in patients with type 2 diabetes the risk is increased (which is about twice the risk in the general population) due to the inferior quality of bone. Bone fragility in type 2 diabetes, which is not reflected by bone mineral density, depends on bone quality deterioration rather than bone mass reduction. Thus, surrogate markers and examination methods are needed to replace the insensitivity of BMD in assessing fracture risks of T2DM patients. One of these methods can be trabecular bone score. The aim of the paper is to present the present state of scientific knowledge about the osteoporosis risk in diabetic patient. The review also discusses the possibility of problematic using the study conclusions in real clinical practice.
Dissertations / Theses on the topic "Diabetic bone fractures"
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Guo, Qidong. "Healing of bone fracture in type 1 diabetic rat models : a potential gene therapy using bone morphogenetic protein." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/8946b0c7-d4b0-4d59-bbcb-ca914643673d.
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Räkel, Agnès. "Importance of diabetes as a risk factor for fractures after solid organ transplantation." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112348.
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Background. Diabetes seems to be associated with an increased risk of fractures in the general population. We aimed to determine whether pre-transplant diabetes increases the risk of fractures among patients receiving solid organ transplantation.Methods. We conducted a nested case-control study in a cohort of subjects 18 years and older who received a first solid organ transplantation in Quebec between January 1st 1986 and July 31st 2005, and who were covered by the RAMQ drug plan at least 1 year before the transplantation and 3 months after the date of discharge from the transplantation hospitalization. Cases were subjects from the cohort who had sustained a fracture between the date of discharge from the hospitalization for transplantation and the end of the study period or the patient's death. The fracture date was the case index date. All incidental fractures were included except fractures of the skull, phalanges of the hand and foot, multiple fractures and pathological fractures, and were identified by medical service claims. Controls were matched to cases on the type of organ transplanted and on the date of the transplantation (+/- 3 months). Crude and adjusted odds ratios (OR) were obtained with univariate and multivariate conditional logistic regression models.
Results. The study included 238 cases and 873 controls. Pre-transplant diabetes was present in 30% of the cases and 22% of the controls (crude OR: 2.16, 95% CI: 1.7--2.8). After adjusting for potential confounders, pre-transplantation diabetes remained a significant risk factor for fractures (adjusted OR: 1.94, 95% CI: 1.5--2.6).
Conclusion. Pre-transplant diabetes appeared to significantly increase post-transplant fractures among adults receiving solid organ transplantation.
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Davidson, Melissa Anne. "A Pharmacovigilance Approach for Assessing Cardiovascular, Osteological, and Carcinogenic Risk Associated with Thiazolidinedione Drugs Used in the Treatment of Type 2 Diabetes Mellitus." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38062.
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Diabetes is a chronic and debilitating disease that affects nearly half a billion people worldwide with the vast majority of diabetics suffering from Type 2 diabetes mellitus (T2DM), a disease characterized by insulin insensitivity that often requires pharmacotherapy to effectively maintain target blood sugar levels. The thiazolidinedione (TZD) class of drugs consists of oral hypoglycaemic agents used alone or in combination with other antidiabetic drugs to treat T2DM. The drugs within this class, which include rosiglitazone and pioglitazone, were originally heralded as providing novel first and second-line treatment of T2DM with glycaemic control and physiological effects comparable to, and in some cases, better than, first-line treatments such as metformin. However, over time they have also been associated with adverse cardiovascular, osteological, and carcinogenic effects in some, but not all clinical trials, observational studies, and meta-analyses. Given the conflicting evidence to date on the safety of TZD drugs, their role in the treatment of T2DM continues to be debated and epidemiological gaps remain. The objectives of this doctoral research are fourfold: 1) to conduct an in-depth review of the epidemiology of TZD pharmacotherapy including pharmacokinetics and modes of action, the results of previous studies investigating health risks and benefits associated with TZD treatment, and new and future uses for this class of drugs; 2) to determine whether diabetic patients treated with TZDs are at increased risk of adverse cardiovascular outcomes; 3) to assess whether TZD pharmacotherapy is associated with an increased risk of bone fractures and whether risks differ depending on fracture site and patient sex; and, 4) to investigate associations between TZD use and risk of bladder cancer. Specific research questions were investigated using nested case-control analyses designed to capture incident users of antidiabetic drugs and electronic health data from Cerner Health Facts®, an electronic medical record database that stores time-stamped patient records from more than 480 contributing hospitals throughout the United States. Findings from this work are reported in a series of manuscripts, including a published review paper. Key findings include: 1) TZD use was associated with an increased risk of incident myocardial infarction and congestive heart failure compared to never use of TZD drugs with a trend towards a potential early treatment effect within the first year of exposure to pioglitazone; 2) TZD use was associated with an increased risk of closed bone fractures among Type 2 diabetics with use of pioglitazone or rosiglitazone associated with an increased risk across multiple fracture sites in women, but only rosiglitazone use in men and only at peripheral fracture sites; 3) use of either pioglitazone or rosiglitazone were associated with an increased risk of incident bladder cancer compared to never users, however, a low number of bladder cancer cases resulted in underpowered analyses; and, 4) insulin use in a hospital setting may replace a patient's normal course of antidiabetic therapy which, when combined with other potential sources of bias in traditional nested case-control studies using hospital-based data, may lead to overestimation or underestimation of adverse health risks associated with non-insulin antidiabetic therapies. Although these findings warrant replication, the results of the research contained within this dissertation suggest that caution should be exercised when prescribing diabetic patients TZD drugs if they have cardiovascular, osteological, or carcinogenic risk factors. Additional pharmacovigilance studies should also continue to strive to better understand the health risks related to TZD therapy, especially as new therapeutic roles for TZDs in the prevention and treatment of some cancers, inflammatory diseases, and other conditions in non-diabetic populations are being explored.
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Wispel, Juliana. "AVALIAÇÃO DAS CONCENTRAÇÕES PLASMÁTICAS DE STWEAK NO DIABETES MELLITUS E FRATURAS ÓSSEAS EM MULHERES NA PÓS MENOPAUSA." Universidade Federal de Santa Maria, 2015. http://repositorio.ufsm.br/handle/1/5864.
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Osteoporosis is defined as an osteometabolic disease characterized by the reduction of
bone mineral density (BMD) and micro-architectural deterioration, leading to enhanced bone
fragility and increased susceptibility to fractures. Chronic inflammation affecting bone resorption
and/or bone formation is an important mechanism in the hystopathology of osteoporosis. In
this regard, several inflammatory markers are associated in special, tumor necrosis factor alpha
(TNFα). Recent evidence from the literature pointed out that other members of the TNF superfamily,
the tumor necrosis factor TNF-like weak inducer of apoptosis (TWEAK), in its soluble
bioactive form (sTWEAK), has been related with diverse endocrine metabolic disarrangements
such as diabetes mellitus or metabolic syndrome. Thus, we hypothesized a possible association
between sTWEAK plasma levels and bone fractures and diabetes mellitus in post menopausal
women.
This was a cross sectional study nested in a cohort of 1057 post menopausal women
outpatients attending the UBS, Unidades Básicas de Saúde, of Santa Maria. We used data
from 52 individuals recruited who reported major bone fractures. For the control group, we
aleatory recruited 110 individuals without the history of major bone fractures. All subjects
in this study proceeded to a standard questionnaire about clinical data and were submitted to
anthropometry evaluation. Blood samples were obtained for the biochemical profile consisting
in fast glucose, total cholesterol, TG, HDL, LDL, creatinine, albumin, calcium and phosphorus
in serum. sTWEAK concentration was established by ELISA. Assimetric variables were logN
transformed. Student T test or Mann-Whitney test were used to comparison of data between
two groups. For statistical analysis that form more than two groups were employed ANOVA or
Chi quadrate and Fisher s test.
An statistical significant reduction (p=0.002) of sTWEAK (log transformed) was observed
in diabetes mellitus (DM) subjects in comparison to non-diabetics. There was no differences
in the plasma levels of sTWEAK when the history of major bone fractures was analysed.
Even when stratified for DM and fractures, Ln sTWEAK remained consistently reduced in the
group of individuals with DM without fractures against non-diabetics no-fractures women (p
<0.01).
Findings from this study indicated that plasma levels of sTWEAK was not related with
bone fragility in post menopausal women population. Nevertheless, low plasma levels of this
biomarker were associated with diabetes mellitus, as previously described in the literature.A osteoporose é um transtorno osteometabólico caracterizado pela diminuição da densidade mineral óssea (DMO) e deterioração de sua microarquitetura com o consequente aumento da fragilidade do osso e suscetibilidade à fraturas. A fisiopatologia dessa doença tem a inflamação crônica como importante mecanismo no aumento da reabsorção e redução da formação óssea. Entre os marcadores inflamatórios associados à osteoporose destacam-se aqueles do grupo dos fatores de necrose tumoral, em particular, o fator de necrose tumoral alfa (TNFα). Evidências recentes da literatura observaram que um outro membro da mesma família, o TNFlike weak inducer of apoptosis (TWEAK), em sua forma solúvel (sTWEAK), foi relacionado com a presença de outros distúrbios endócrino metabólicos, tais como diabetes mellitus (DM) e síndrome metabólica. Com base nisso, testamos a hipótese de associação entre sTWEAK e fraturas ósseas maiores, e também DM, em mulheres na pós menopausa. Este é um estudo transversal que partiu de uma coorte de 1057 pacientes na pós menopausa que consultam nas Unidades Básicas de Saúde da cidade de Santa Maria-RS. Foram recrutadas 52 pacientes com histórico de fraturas ósseas maiores e, para o grupo controle, escolhidas aleatoriamente 110 pacientes sem história de fraturas ósseas. Todos os indivíduos do estudo responderam a um questionário padronizado sobre a sua história clínica além de serem submetidos a avaliação antropométrica e exames bioquímicos (glicose de jejum, colesterol total, triglicerídeos, HDL, LDL, creatinina, albumina, cálcio e fósforo). Os níveis plasmáticos de sTWEAK foram avaliados pelo método de ELISA. As variáveis com distribuição assimétrica foram submetidas à transformação para o seu logaritmo natural e então comparadas. Para a análise estatística entre dois grupos foi feita a utilização dos testes T de Student ou Mann-Whitney. Para mais de dois grupos foram empregados ANOVA ou os testes de Chi Quadrado ou Fisher. Foi observada redução significativa (p=0.002) dos valores do sTWEAK (transformado para logN) nos indivíduos com DM em comparação com os sem DM. Não houveram diferenças quando analisado somente o histórico de fraturas. Estratificando a população em subgrupos de acordo com o critério de existência de fratura reportada ou de diagnóstico de DM, permaneceu somente a diferença entre os grupos com DM sem fratura e sem DM sem fratura (p<0.01). Os achados indicam que na população de mulheres na pós menopausa com e sem história de fraturas ósseas maiores, os níveis plasmáticos de sTWEAK não tem associação com a fragilidade óssea. Entretanto, níveis baixos deste biomarcador estão associados com o diagnóstico de DM, como reportado na literatura.
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Sung, Yu-Ting, and 宋鈺婷. "Research on Bone Fracture Risk with Dipeptidyl peptidase-4 inhibitors in Patients with Diabetes Mellitus." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/56b839.
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Maratová, Klára. "Vliv sérových hladin 25-hydroxycholekalciferolu na muskuloskeletální systém u dětí se zánětlivým střevním onemocněním." Doctoral thesis, 2020. http://www.nusl.cz/ntk/nusl-435288.
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The effect of serum 25-hydroxycholekalciferol levels on musculoskeletal system in children with inflammatory bowel disease Background: Low bone mineral density and osteoporosis represent severe secondary complications that can be a result of childhood chronic disease. According to Frost's mechanostat theory impaired muscle functions may contribute to the changes observed on the skeleton. Aims: The aim of this study was to: 1) evaluate parameters of bone mineral density, bone geometry and dynamic muscle functions in children and adolescent with chronic disease - inflammatory bowel disease (IBD) and type 1 diabetes (T1D); 2) evaluate a possible effect of vitamin D deficiency and vitamin D supplementation or duration of the disease on the musculoskeletal unit; 3) determine clinical or laboratory predictors of muscle and bone parameters. Methods: The study was divided into two substudies according to the diagnosis. Seventy patients with IBD (median age 13.8 years) were included in one study, fifty-five of which completed all of the planned procedures. During the study, IBD patients were supplemented with 2000 IU/d of vitamin D. In the second study 95 patients with T1D were included (median age 16.4 years). BMD and bone geometry of non-dominant tibia was evaluated using peripheral quantitative computed...
Books on the topic "Diabetic bone fractures"
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Heckman, JD. Instructional course lectures v.42. American Acadamy of Orthopedic Surgeons, 1993.
Find full textBook chapters on the topic "Diabetic bone fractures"
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Leslie, William D., and Stephen Hough. "Fracture Risk Assessment in Diabetes." In 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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Yamada, Shinsuke, and Masaaki Inaba. "Diabetes and Bone." In Osteoporotic Fracture and Systemic Skeletal Disorders, 283–95. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-5613-2_18.
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Yousefzadeh, Nasibeh, Sajad Jeddi, Khosrow Kashfi, and Asghar Ghasemi. "Role of Nitric Oxide in Type 2 Diabetes-Induced Osteoporosis." In The Role of Nitric Oxide in Type 2 Diabetes, 161–89. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010011.
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Osteoporosis affects 200 million people worldwide. Osteoporosis in subjects with diabetes is called diabetoporosis, and type 2 diabetes (T2D) contributes to and aggravates osteoporotic fractures. Hyperglycemia, insulin resistance, bone vasculature impairment, increased inflammation, oxidative stress, and bone marrow adiposity contribute to a higher incidence of osteoporotic fractures in T2D. Decreased nitric oxide (NO) bioavailability due to lower endothelial NO synthase (eNOS)-derived NO and higher inducible NOS (iNOS)-derived NO is one of the main mechanisms of the diabetoporosis. Available data indicates that T2D increases osteoclast-mediated bone resorption and decreases osteoblast-mediated bone formation, mediated in part by reducing eNOS-derived NO and increasing iNOS-derived NO. NO donors delay osteoporosis and decrease osteoporotic fractures in subjects with T2D, suggesting the potential therapeutic implication of NO-based interventions for diabetoporosis.
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Miller, Paul D., and Michael Pazianas. "Bones and the Kidney." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 699–706. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0086.
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Management of osteoporosis in patients with chronic kidney disease (CKD) is often very challenging and it should consider the pathophysiology of both disorders. Patients with stage 4–5 CKD are especially at very high risk for fragility fractures and secondary increase in mortality. Discriminating between osteoporosis and CKD-MBD is best accomplished with quantitative bone histomorphometry but biochemical markers of bone turnover, especially intact parathyroid hormone (PTH) and bone-specific alkaline phosphatase, also may be helpful. The one renal bone disease where antiresorptive osteoporosis therapies would be potentially unsafe is idiopathic renal adynamic bone disease. The two renal bone diseases where an osteoporosis pharmacological agent would not be advised are osteomalacia and primary hyperparathyroid bone disease which can be excluded by defining the underlying cause of a high bone-specific alkaline phosphatase or defining the cause of a very high intact PTH. If a stage 4–5 CKD patient with fragility fractures is felt to have osteoporosis as the major underlying metabolic bone disease causing fractures, FDA approved pharmacological agents for the treatment of osteoporosis can be beneficial on or off label.
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Watts, Laura M., Bernard Freudenthal, J. H. Duncan Bassett, and Graham R. Williams. "Thyroid Disorders and Bone Disease." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 739–50. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0089.
Full textAbstract:
Thyroid hormones have important effects on bone that are mediated by thyroid hormone receptor alpha. Hypothyroidism in children causes growth retardation and delayed bone age, whereas juvenile thyrotoxicosis accelerates growth and skeletal maturation. In adults, hyperthyroidism increases bone resorption and formation disproportionately and results in high bone turnover osteoporosis and an increased susceptibility to fracture. Thus, thyroid hormones stimulate anabolic responses during skeletal growth but have catabolic effects in adults. Overt thyrotoxicosis, subclinical hyperthyroidism, and overtreatment of hypothyroid patients with thyroxine all result in bone loss and varying degrees of osteoporosis and susceptibility to fracture. Furthermore, population studies demonstrate that thyroid status within the upper normal reference range is associated with low bone mass and an increased risk of fracture. Taken together, it is evident that thyroid hormones are essential for skeletal growth and adult bone maintenance, and the skeleton remains exquisitely sensitive to thyroid hormones throughout life.
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Eastell, Richard. "Osteoporosis." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 727–38. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0088.
Full textAbstract:
Osteoporosis is an important public health problem. It is defined in the individual by a low bone mineral density and a high risk of fracture. It is a consequence of a low peak bone mass or accelerated bone loss, or both. Oestrogen deficiency and ageing are important causes of accelerated bone loss as are a number of drugs and diseases. Treatments for osteoporosis are effective at reducing the risk of further fracture and these include drugs that work by inhibiting bone resorption or stimulating bone formation. Bisphosphonates are the drugs most commonly used for osteoporosis and most guidelines recommend a drug holiday after treatment for 5 years.
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Cheung, Moira S., Apostolos I. Gogakos, J. H. Duncan Bassett, and Graham R. Williams. "Thyroid disorders and bone disease." In Oxford Textbook of Endocrinology and Diabetes, 712–20. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0465.
Full textAbstract:
Osteoporosis is defined as a bone mineral density (BMD) of 2.5 or more standard deviations below that of a young adult (T score ≤ −2.5). It is characterized by reduced bone mass, low BMD, deterioration of bone microarchitecture, and an increased susceptibility to fragility fracture. The prevalence of postmenopausal osteoporosis increases with age from 6% at 50 years of age to over 50% at age 80 and the lifetime incidence of fracture for a 50 year old in the UK is 40% for women and 13% for men. Osteoporosis is a worldwide public health burden that costs an estimated £1.7 billion in the UK, $15 billion in the USA, and £32 billion in Europe per annum (see Chapter 4.7).
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Prince, R. L. "Bone disease in older people." In Oxford Textbook of Endocrinology and Diabetes, 1526–34. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0146.
Full textAbstract:
Bone disease is a common problem in the elderly, and its clinical manifestation are a major preventable public health problem. The disorders of the skeleton have been classified in a variety of ways, an approach which tends to restrict understanding of the clinical problem in a particular patient. Frequently, several separate disorders coexist, each contributing to impairment of bone form or function, and each requiring a separate intervention. The major categories of disorder are osteoporosis, too little bone within the bone, osteomalacia, impaired mineralization of bone matrix, and infiltration of bone with cancer cells. Each represents a distinct pathological processes that results in abnormal bone structure and function, which may present as bone pain and/or fracture.
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Mazziotti, Gherardo, Andrea Giustina, Ernesto Canalis, and John P. Bilezikian. "Glucocorticoid-induced osteoporosis." In Oxford Textbook of Endocrinology and Diabetes, 754–59. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0497.
Full textAbstract:
Synthetic glucocorticoids are used in a wide variety of disorders including autoimmune, pulmonary, and gastrointestinal diseases, as well as in patients following organ transplantation and with malignancies. Although the indications for glucocorticoids in these various conditions are clear, their use is fraught with a host of potential side effects. In particular, glucocorticoids are detrimental to bone and glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis (1). Despite the fact that glucocorticoids can cause bone loss and fractures, many patients receiving or initiating long-term glucocorticoid therapy are not evaluated for their skeletal health. Furthermore, patients often do not receive specific preventive or therapeutic agents when indicated. New knowledge of the pathophysiological mechanisms underlying GIO has been accompanied by the availability of effective strategies to prevent and treat GIO (1).
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Paschou, Stavroula A., Panagiotis Anagnostis, and Dimitrios G. Goulis. "Female Hypogonadism." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 1351–58. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0163.
Full textAbstract:
Menopause marks the permanent cessation of menstruation and the transition to the non-reproductive stage of a woman’s life, after completion of 12 months of amenorrhoea or immediately after bilateral oophorectomy. The purpose of this chapter is to provide current knowledge regarding the different stages preceding and following the final menstrual period, the physiology of the endocrine changes occurring during the menopausal transition, the clinical manifestations, diagnosis, and differential diagnoses, as well as the pros and cons of its medical management. Hormone replacement therapy (HRT) is the treatment of choice for most. Additionally, it may be considered for osteoporosis treatment and fracture risk reduction, but only for women who present with VMS. In cases of hysterectomy, oestrogen-only formulations should be used, whereas for women with intact uterus progestogen needs to be added to counteract the harmful effects of oestrogen on the endometrium. Postmenopausal women should also be managed with lifestyle interventions, including diet, exercise, smoking cessation, and decrease in alcohol consumption, with a particular focus on bone and cardiovascular health. Alternatively, drug or non-pharmaceutical therapies may be considered for the alleviation of VMS in cases, when HRT is contraindicated. The ultimate goal of the healthcare providers should be an integrated plan for the postmenopausal women, bearing in mind that most of them will spend more than one-third of their lifespan in menopausal status.
Conference papers on the topic "Diabetic bone fractures"
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Sherrod, Brandon, Shawn Gilbert, Krista Casazza, and Alan Eberhardt. "Design of a Torsion Tester for Measuring Murine Bone Properties for Studies on the Effects of Diabetes and Obesity." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14412.
Full textAbstract:
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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Sheikh, Abdul Q., Andrei Kogan, and Daria A. Narmoneva. "Electromagnetic Field Mediates Capillary-Like Network Formation via MAPK/ERK Signaling Cascade." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206710.
Full textAbstract:
Abnormal angiogenesis (formation of capillaries) plays an important role in the impaired diabetic wound healing and has emerged as a new target area for therapeutic interventions. Pulsed magnetic field therapy, which was initially used for healing of bone fractures, has been recently introduced as a potential therapy to treat diabetic and chronic wounds [1], although the mechanisms responsible for improved healing are still unclear. Electromagnetic fields (EMF) have been shown to act as a directional cues in cellular responses such as migration and activations of several signal transduction cascades [2]. Recent literature delineates an important role of GHz EMF (i.e., with an oscillation period of a fraction of a nanosecond) in inducing rapid and sustained phosphorylation of mitrogen-activated kinase and extracellular-signal-regulated kinase (MAPK/ERK) [3]. Recent studies have also implicated MAP kinase in mediating the phosphorylation of Connexin-43 (Cx43) that accompanies regulation of cell-cell communication via connexin gap junctions [4]. Importantly, both MAPK/ERK pathway and Cx43 signaling are involved in the process of angiogenesis [5,6]. Therefore, the goal of this study was to test the hypothesis that high-frequency (7.5GHz) EMFs promote angiogenesis in vitro via MAPK/ERK and/or Cx43 signaling. We used a custom-built EMF exposure setup and a self-assembling peptide nanoscaffold as a controlled angiogenic microenvironment [7] to quantify the effect of EMF on capillary formation and underlying cellular responses.