Journal articles on the topic 'Diabetic bone fractures'
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1
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.
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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.
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Yalochkina, Tatiana O., and Zhanna E. Belaya. "Fragility fractures and bone remodeling in type 2 diabetes mellitus." Obesity and metabolism 14, no. 3 (November 13, 2017): 11–18. http://dx.doi.org/10.14341/omet2017311-18.
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Fracture risk is significantly increased in both type 1 and type 2 diabetes and individuals with diabetes experience worse fracture outcomes compared to normoglycemic individuals. Patients with T1DM have decreased bone mineral density (BMD), whereas patients with T2DM demonstrate increased BMD compared to healthy control. The latest studies show increased incidence of low-traumatic fractures in patients with T2DM instead of high bone mineral density (BMD). The risk of osteoporotic fractures in patients with T2DM can be explained by disease complications and increased risk of falls and consequent trauma. However, the most important cause of bone fragility in T2DM is the deterioration in bone microarchitecture, the mechanism of which is not completely understood. High BMD in patients with T2DM does not allow us to use dual-energy X-ray-absorptiometry as a gold standard test for diagnosticsof osteoporosis. Consequently,new risk factors and diagnostic algorithm as well as treatment strategy should be developed for patients with T2DM. In addition to this, some researchers considered that the group of T2DM is geterogenous and physicians might face patients with osteoporosis and mild diabetes that add very little to bone fragility; patients with osteoporosis and moderate or severe diabetes which also affects bone tissue diabetoosteoporosis; and patients without osteoporosis but severe diabetes which cause bone tissue deterioration with the development of diabetic bone disease. New diagnostic tools and algorithm and new experimental research are needed for better understanding bone deterioration in patients with T2DM. This review summarizes our current knowledge on fracture rate, risk factors for fractures and causes of bone deterioration in subjects with T2DM.
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Russo, Giuseppina T., Annalisa Giandalia, Elisabetta L. Romeo, Morabito Nunziata, Marco Muscianisi, Maria Concetta Ruffo, Antonino Catalano, and Domenico Cucinotta. "Fracture Risk in Type 2 Diabetes: Current Perspectives and Gender Differences." International Journal of Endocrinology 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/1615735.
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Type 2 diabetes mellitus (T2DM) is associated with an increased risk of osteoporotic fractures, resulting in disabilities and increased mortality. The pathophysiological mechanisms linking diabetes to osteoporosis have not been fully explained, but alterations in bone structure and quality are well described in diabetic subjects, likely due to a combination of different factors. Insulin deficiency and dysfunction, obesity and hyperinsulinemia, altered level of oestrogen, leptin, and adiponectin as well as diabetes-related complications, especially peripheral neuropathy, orthostatic hypotension, or reduced vision due to retinopathy may all be associated with an impairment in bone metabolism and with the increased risk of fractures. Finally, medications commonly used in the treatment of T2DM may have an impact on bone metabolism and on fracture risk, particularly in postmenopausal women. When considering the impact of hypoglycaemic drugs on bone, it is important to balance their potential direct effects on bone quality with the risk of falling-related fractures due to the associated hypoglycaemic risk. In this review, experimental and clinical evidence connecting bone metabolism and fracture risk to T2DM is discussed, with particular emphasis on hypoglycaemic treatments and gender-specific implications.
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Olarte, Oscar Rosero, and Mauricio Alvarez Andrade. "Underlying Mechanisms Between Diabetes Mellitus and Osteoporosis." US Endocrinology 14, no. 2 (2018): 65. http://dx.doi.org/10.17925/use.2018.14.2.65.
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Several studies have linked diabetes mellitus with an increased risk of bone fractures. Patients with type 1 diabetes have lower bone mineral density and patients with type 2 diabetes have an increased risk of fracture despite normal or high bone mineral density, measured by dual energy x-ray absorptiometry. Different mechanisms have been proposed in the pathophysiology of bone disease in diabetic patients. The mechanisms involved include microvasculature changes, advanced glycation end products accumulation, and altered osteoblast–osteoclast function with increased sclerostin, decreased insulin-like growth factor 1 (IGF1), decreased osteocalcin, and other molecular alterations, leading to a decrease in bone turnover and altered bone quality. Other factors, such as increased risk of falls related to diabetic neuropathy and diabetic retinopathy have also been proposed. Different diagnostic methods have been described for the study of bone disease in patients with diabetes, due to the lack of correlation between bone mineral density measured by dual x-ray absorptiometry and the fracture risk in this group of patients. These methods include the evaluation of bone turnover markers, the FRAX score, the trabecular bone score, and the evaluation of microarchitecture with high-resolution peripheral quantitative tomography. This editorial provides a short overview of the underlying mechanisms between diabetes mellitus and osteoporosis, and the diagnostic methods used to evaluate these patients.
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Hughes, Jessica, Jonathan Hughes, Kindyle Brennan, Yolanda Munoz Maldonado, and Daniel Stahl. "Relationship Between Hemoglobin A1c Value and Bone Healing in Diabetic Ankle Fractures Treated Operatively versus Non-operatively." Foot & Ankle Orthopaedics 3, no. 3 (July 1, 2018): 2473011418S0025. http://dx.doi.org/10.1177/2473011418s00253.
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Category: Ankle Introduction/Purpose: Diabetic ankle fractures create unique challenges to fracture management, such as impaired wound / bone healing and increased infection rate. There is inconclusive evidence regarding a specific hemoglobin A1c (A1c) value or glucose level at which the risk of adverse outcomes increases. The aim of this study was to evaluate the A1c level at which the rate of nonunion and other major complications significantly increased in diabetic ankle fractures treated operatively (Op) and non-operatively (Nonop). Methods: This is a retrospective cohort study of diabetic ankle fractures treated Op or NonOp with at least 3 months follow up and a hemoglobin A1c value within 90 days of injury. A query of electronic medical records was performed to identify all patients 18 years of age or older with a diagnosis of diabetes and who underwent Op or NonOp management as the initial treatment of an ankle fracture between January 1, 2004 and December 31, 2014 within a single health system. Union was defined as callus formation at 3 of 4 cortices on radiographs, while nonunion was defined as lack of fracture healing at 6 months based on radiographs of the injured ankle. Multivariable logistic regression analysis was performed to explore demographic, injury-related, and management-related risk factors that influence nonunion and major complications. Results: A total of 243 ankle fractures (130 Op, 113 NonOp) were identified. Nine patients in the NonOp group failed nonoperative management and required surgical fixation. There were 51 patients that developed nonunion/malunions (19 Op, 32 NonOp). Patients with diabetic neuropathy or nephropathy had significantly higher risk of nonunion. In both groups, length of immobilization greater than 12 weeks was a significant predictor of nonunion. There was no A1c level nor preinjury glucose level at which there was significantly increased rate of nonunion or deep infections in either treatment group. However, A1c was a predictor of wound complications at 3 months postoperative in the Op group with an odds ratio of 1.26. There was no significant difference in wound complications at 3 months between treatment groups. Conclusion: While no specific A1c value or glucose level demonstrated a significant rise in fracture nonunion, this study found that diabetic neuropathy and diabetic nephropathy play a significant role in fracture healing. However, hemoglobin A1c was found to be a predictor of wound complications at 3 months postoperative. Additionally, the data suggested a longer duration of immobilization may negatively impact fracture union. These results highlight the complexity of treating diabetic ankle fractures and suggest prolonged immobilization may not be beneficial for this subpopulation.
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A Asseri, Khalid, Yahya I. Asiri, Ali Alqahtani, Krishnaraju Venkatesan, Noohu Abdulla Khan, Sirajudeen Shaik Alavudeen, Ester Mary Pappiya, et al. "Herba Epimedii extraction overcome Rosiglitazone induced bone loss in diabetic rats." International Journal of Current Research in Chemistry and Pharmaceutical sciences 8, no. 9 (September 3, 2021): 7–14. http://dx.doi.org/10.22192/ijcrcps.2021.08.09.002.
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Diabetes mellitus patients are more prone to suffer from bone fractures. Herba Epimedii has been demonstrated to be an osteoporosis reducer in the past. However, it is yet uncertain if Herba Epimedii may protect diabetic rats from bone loss when co-administered with rosiglitazone (RSG). This study examines the impact of Herba Epimedii on bone oxidative stress and turnover markers in diabetic rats co-treated with rosiglitazone (RSG). Streptozotocin (STZ) causes diabetics. Wistar albino rats were placed into five groups, each with six rats: control (vehicle therapy), Streptozotocin (diabetes) group, Herba Epimedii group, Rosiglitazone, and Rosiglitazone +Herba Epimedii. Each medication was given by gastric gavage once a day for 35 days. Insulin, oxidative stress, and bone turnover markers were measured in the blood using ELISA assays. Insulin and osteocalcin levels were significantly higher in diabetic rats administered Herba Epimedii than in diabetic control rats. Herba Epimedii may be able to prevent diabetic osteoporosis in RSG-treated diabetic rats by enhancing osteogenesis and lowering bone oxidative stress. The utility of Herba Epimedii as an osteoporosis therapy in diabetic individuals is supported by these findings. Keywords: Herba Epimedii, Diabetes, Osteoporosis, Rosiglitazone
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Yue, James J., and Randall E. Marcus. "The Role of Internal Fixation in the Treatment of Jones Fractures in Diabetics." Foot & Ankle International 17, no. 9 (September 1996): 559–62. http://dx.doi.org/10.1177/107110079601700909.
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The purpose of this study was to evaluate the treatment of fractures of the proximal fifth metatarsal at the junction of the metaphysis and diaphysis (i.e., Jones fracture) in diabetics. Open reduction and internal fixation with bone grafting resulted in clinical and radiographic union 8 weeks after surgery in patients treated with either immediate or delayed open reduction and internal fixation. Open reduction and internal fixation with autologous bone grafting is an effective treatment regimen in the diabetic patient with a Jones fracture. An initial trial of casting can be attempted without any apparent deleterious effects on secondary open reduction and internal fixation.
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Siddapur, Priyanka R., Anuradha B. Patil, and Varsha S. Borde. "Comparison of Bone Mineral Density, T-Scores and Serum Zinc between Diabetic and Non Diabetic Postmenopausal Women with Osteoporosis." Journal of Laboratory Physicians 7, no. 01 (January 2015): 043–48. http://dx.doi.org/10.4103/0974-2727.151681.
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ABSTRACT Context: Postmenopausal osteoporosis is a public health problem. Diabetics are at increased risk of osteoporosis-related fractures. Zinc (Zn) has a role in collagen metabolism, and its levels are altered in diabetes. Aims: The aim was to compare bone mineral density (BMD), T-score and serum Zn between diabetic and nondiabetic postmenopausal women with osteoporosis to see if they influence increased fracture risk in diabetes. Settings and Design: It is a cross-sectional study conducted at Department of Biochemistry, Jawaharlal Nehru Medical College, Belgaum. Materials and Methods: Thirty type 2 diabetic and 30 age-matched (aged 45-75 years) nondiabetic Dual energy X-ray absorptiometry (DEXA) confirmed postmenopausal osteoporotics were included from January 2011 to March 2012. Serum Zn was analyzed by atomic absorption spectrophotometry. Statistical Analysis Used: Mean and standard deviation of the parameters of the two groups were computed and compared by unpaired Student's t-test. Relationship between variables was measured by Karl Pearson's correlation co-efficient. A statistical significance is set at 5% level of significance (P < 0.05). Results: T-score was significantly higher in diabetics compared with nondiabetics(−2.84 ± 0.42 vs. −3.22 ± 0.74) P < 0.05. BMD and serum Zn of diabetics showed a significant positive correlation with body mass index (BMI). Conclusions: Type 2 diabetic postmenopausal osteoporotics have a higher T-score than the nondiabetics. High BMI in type-2 diabetes mellitus (T2DM) may contribute to high BMD and may be a protective factor against zincuria. Increased fracture risk in T2DM could be due to other factors like poor bone quality due to hyperglycemia rather than BMD. Strict glycemic control is of paramount importance.
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Fontaine, Javier La, Nathan A. Hunt, Stacey Curry, Tyler Kearney, Daniel Jupiter, Naohiro Shibuya, and Lawrence A. Lavery. "Fracture Healing and Biomarker Expression in a Diabetic Zucker Rat Model." Journal of the American Podiatric Medical Association 104, no. 5 (September 1, 2014): 428–33. http://dx.doi.org/10.7547/0003-0538-104.5.428.
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Background Persons with diabetes have a higher incidence of fractures compared with persons without diabetes. However, there is little published information concerning the deleterious effect of late-stage diabetes on fracture healing. There are no studies using animal models that evaluate the effect of advanced diabetes on fracture healing. The purpose of our study was to evaluate cytokine expression, specifically macrophage inflammatory protein 1 (MIP-1) and vascular endothelial growth factor, in fracture healing in a type 2 diabetes rat model. Methods We evaluated biomarker expression after femur fracture using a rat model. The two groups consisted of 24 Zucker diabetic rats (study group) and 12 Zucker lean rats (control group). An independent reviewer was used to assess delayed union. We evaluated serum samples 2, 4, 7, and 14 days after surgery for MIP-1, vascular endothelial growth factor, leptin, and other cytokine levels. Results At 3 weeks, Kaplan-Meier estimates showed that 45.8% of femur fractures in Zucker diabetic rats had healed, whereas 81.8% of those in Zucker lean rats had healed (P = .02). A logistic regression model to predict fast healing that included the three cytokines and diabetes status showed that the only factor achieving significance was MIP-1α. Vascular endothelial growth factor was the only biomarker to show significance compared with delayed healing. Conclusions These results confirm significant differences in biomarker expression between diabetic and nondiabetic rats during bone healing. The key factors for bone healing may appear early in the healing process, whereas differences in diabetes versus nondiabetes are seen later in the healing process. Increased levels of MIP-1α were associated with the likelihood of delayed healing.
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Zhukouskaya, Volha V., Alla P. Shepelkevich, and Iacopo Chiodini. "Bone Health in Type 1 Diabetes: Where We Are Now and How We Should Proceed." Advances in Endocrinology 2014 (June 25, 2014): 1–12. http://dx.doi.org/10.1155/2014/982129.
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Type 1 diabetes (T1D) is autoimmune disease with chronic hyperglycaemic state. Besides diabetic retinopathy, nephropathy, and neuropathy, T1D is characterized by poor bone health. The reduced bone mineralization and quality/strength, due to hyperglycemia, hypoinsulinemia, autoimmune inflammation, low levels of insulin growth factor-1 (IGF-1), and vitamin D, lead to vertebral/hip fractures. Young age of T1D manifestation, chronic poor glycemic control, high daily insulin dose, low BMI, reduced renal function, and the presence of complications can be helpful in identifying T1D patients at risk of reduced bone mineral density. Although risk factors for fracture risk are still unknown, chronic poor glycemic control and presence of diabetic complications might raise the suspicion of elevated fracture risk in T1D. In the presence of the risk factors, the assessment of bone mineral density by dual-energy X-ray absorptiometry and the search of asymptomatic vertebral fracture by lateral X-ray radiography of thorax-lumbar spine should be recommended. The improvement of glycemic control may have a beneficial effect on bone in T1D. Several experiments showed promising results on using anabolic pharmacological agents (recombinant IGF-1 and parathyroid hormone) in diabetic rodents with bone disorder. Randomized clinical trials are needed in order to test the possible use of bone anabolic therapies in humans with T1D.
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Guo, Yan, Yingfang Wang, Feng Chen, Jiabei Wang, and Difei Wang. "Assessment of Risk Factors for Fractures in Patients with Type 2 Diabetes over 60 Years Old: A Cross-Sectional Study from Northeast China." Journal of Diabetes Research 2020 (January 28, 2020): 1–8. http://dx.doi.org/10.1155/2020/1508258.
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Aims. Previous evidence has demonstrated an increased fracture risk among the population with type 2 diabetes mellitus (T2DM). This study investigated the prevalence of bone fractures in elderly subjects (with and without type 2 diabetes) and identified any fracture risk factors, especially the risk factors for common known fractures in particular diabetic populations. Methods. This cross-sectional study was conducted with community-dwelling people over 60 years old in nine communities from the city of Shenyang, which is the capital of Northeast China’s Liaoning Province. A total of 3430 elderly adults (2201 females, mean±standard deviation age 68.16±6.1 years; 1229 males, 69.16±6.7 years) were included. Our study measured the heel bone mineral density (BMD) and used the timed “up and go” (TUG) test and other indicators. In addition, we performed logistic regression analysis to explore the risk factors for fractures in the general population and the diabetic population and to analyze the differences. Results. The results revealed that a total of 201 elderly persons (5.8%), with an average age of 70.05±6.54 years, suffered from a history of fragility fractures, which affected more females (74.6%) than males (p=0.001). The prevalence of fractures in the T2DM population was 7.3%, which was much higher than the 5.2% in non-T2DM population (p<0.05). In the non-T2DM population, the BMD was lower and the TUG time was longer in the fracture group than in the nonfracture group (p<0.001). However, in the T2DM population, the BMD and TUG values were similar between the fracture group and the nonfracture group (p>0.05). Logistic regression analysis showed that the female sex (OR 1.835), TUG time>10.2 s (OR 1.602), and T‐score≤−2.5 (OR 1.750) were independent risk factors for fragility fractures in the non-T2DM population, but they were not risk factors in the T2DM population. Conclusions. This study found that low BMD and slow TUG time were independent risk factors for fractures in non-T2DM patients, while no associations were found in the T2DM population. Patients with T2DM have a higher risk for fractures even when they have sufficient BMD and a short TUG time. TUG and BMD underestimated the risk for fractures in the T2DM population.
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Asseri, Khalid A., Yahya I. Asiri, Ali Alqahtani, Krishnaraju Venkatesan, Noohu Abdulla Khan, Vigneshwaran Easwaran, Ester Mary Pappiya, et al. "Radix Dipsaci extract protects against Rosiglitazone induced bone loss." International Journal of Current Research in Chemistry and Pharmaceutical sciences 8, no. 9 (September 3, 2021): 15–21. http://dx.doi.org/10.22192/ijcrcps.2021.08.09.003.
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The dried root of Dipsacus asperoides is known as Radix Dipsaci extract(RDE). It's a kidney-toning herbal medication with a lengthy track record of safe usage in the treatment of bone fractures and joint disorders. The drug rosiglitazone (RSG) causes an imbalance in bone remodelling, which results in increased apoptotic death of osteogenic cells and decreased bone production. The goal of this study was to investigate the effects of RDE on RSGinduced bone loss in diabetic rats in a systematic way. Five groups of six Wistar albino rats were studied: control (vehicle therapy), Streptozotocin (diabetes) group, RDE group, Rosiglitazone, and Rosiglitazone +RDE group. Insulin, oxidative stress, and bone turnover markers in the blood were all detected using ELISA tests. When compared to diabetic control rats, RDE therapy significantly raised insulin and osteocalcin levels. RDE may be able to prevent diabetic osteoporosis by boosting osteogenesis and lowering oxidative stress in the bone.These findings support the use of RDE as a bone loss inhibiting in diabetics. Well-designed clinical trials are likely to yield further scientific evidence on its bone-protective effects and safety. Keywords: Radix Dipsaci, Diabetic osteoporosis, Rosiglitazone.
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O'Neill, Elizabeth. "Diabetic Skeletal Health and Potential Benefits of Exercise." Journal of Clinical Exercise Physiology 8, no. 3 (September 1, 2019): 108–14. http://dx.doi.org/10.31189/2165-6193-8.3.108.
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ABSTRACT Bone tissue undergoes continual remodeling through resorption and formation. The balance between these 2 activities is critical to optimizing bone mineral density (BMD) and the biomechanical integrity of the tissue, thereby reducing fractures. There is increasing evidence that diabetes negatively alters the cellular activity of bone tissue and reduces bone quality resulting in an increased risk of fractures. The mechanisms by which diabetes impacts bone are not completely understood; however, insulin, hyperglycemia, and glycation appear to influence skeletal regulation. This review will explore the influence of diabetes mellitus on bone as well as examine the potential methods by which exercise can serve as a nonpharmacological method to optimize bone health in persons with diabetes.
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Zhang, Wei, Jing Luo, Huanli Shi, Chen Wang, Xinxin Fu, and Xiaomei Li. "Analysis of bone metabolism mechanisms in postmenopausal females with type 2 diabetes and DKK1 gene polymorphisms and the effects of polymer nanomaterials on wound infection in patients." Materials Express 11, no. 7 (July 1, 2021): 1109–15. http://dx.doi.org/10.1166/mex.2021.1985.
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Diabetic patients are prone to abnormal bone metabolism. Menopausal women exhibit reduced estrogen secretion and bone absorption exceeds the rate of bone formation. Therefore, postmenopausal women with diabetes are even more likely to suffer from osteoporosis. Identifying the specific mechanism of abnormal bone metabolism in diabetic menopausal women will help reduce the risk of bone fractures. This study explored the specific mechanisms of bone metabolism disorders in menopausal women with type 2 diabetes in relation to genetic polymorphisms. We found that the distribution frequency of the CA genotype and A allele at the rs1373004 locus of the DKK1 gene in menopausal women with diabetes and abnormal bone mass were significantly lower compared with that in normal bone. The distribution of the GG genotype at the rs1528877 locus was also less frequent compared with those exhibiting normal bone mass. This suggests that the genotype and allele frequency distribution in the DKK1 gene at rs1373004 and RS1528877 in postmenopausal T2DM women is associated with glucose metabolism and bone metabolism. To analyze the efficacy of polylactic acid (PLA)/gelatin nanofibers on T2DM patients with infectious fractures, we compared various aspects of wound healing in patients treated with conventional therapy versus PLA/gelatin nanofibers. The results indicated that the number of days required for wound healing and the frequency of incisions in patients treated with PLA/gelatin nanofibers were significantly lower compared with those treated with conventional therapy (P < 0.05). The wound healing rate of patients treated with PLA/gelatin nanofibers was significantly higher compared with that of patients treated with conventional therapy on days 7, 14, 21, and 28 of treatment. Our findings indicate that PLA/gelatin nanofiber treatment can significantly promote fracture wound healing.
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Elmedani, Sarah, Steven Douedi, Khin Zin, Raquel Ong, and Jennifer Cheng. "A Rare Presentation of Non-Traumatic Recurring Bone Fractures in Adult Patient With Juvenile Onset Hypophosphatasia." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A178. http://dx.doi.org/10.1210/jendso/bvab048.360.
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Abstract Background: Hypophosphatasia is a rare metabolic bone disease caused by mutations in the tissue-nonspecific alkaline (TNSALP) phosphatase gene. The disease is typically diagnosed in children but may be seen in adults with premature loss of adult teeth, poor bone healing, recurrent bone fractures, and limited mobility due to chronic pain. Clinical case: A 48-year-old female with Juvenile Onset hypophosphatasia and diabetes mellitus type 2 who presented to the endocrine clinic for diabetes mellitus. She had a telemedicine visit because she was not able to come to the office due to her recent rib fracture and pain. She had multiple fractures since she was 16-years-old with multiple fractures in her toes. She later developed a femur fracture when 20 years old and second at 28-years-old in the other femur. She was tested for juvenile hypophosphatasia and the diagnosis was confirmed. She received no treatment at that time. She subsequently had recurrent non-traumatic rib fractures that interfered with daily life. She is unable to exercise due to her frequent fractures and consequently having poor diabetic control. She has family history of brother with femur fracture. Labs showed decreased alkaline phosphatase (<5 normal: 38–126 U/L), elevated vitamin B6 levels (2296.2: normal 20–125 nmol/L) normal vitamin D (33: normal 30–100 ng/mL) and calcium levels. Chest x-ray showed multiple rib fractures with different healing stages. Dexa scan was also done and was normal to age with lowest Z-score being 8.2. Patient was started on Asfotase Alfa (an enzyme replacement therapy that contains the active site of TNSALP). Conclusion: This case illustrates the debilitating effects of hypophosphatasia and importance of recognizing previously untreated adult patients with hypophosphatasia. Many patients have very late diagnosis and suffer severe complications in their adulthood. Although this disease is rare, recognizing the symptoms of juvenile onset hypophosphatasia can help initiate early treatment to decrease these complications. Hypophosphatasia should be considered as a differential diagnosis in adults with multiple fractures and decreased alkaline phosphatase.
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Kanazawa, Ippei, Toru Yamaguchi, Masahiro Yamamoto, Mika Yamauchi, Shozo Yano, and Toshitsugu Sugimoto. "Relationships between serum adiponectin levels versus bone mineral density, bone metabolic markers, and vertebral fractures in type 2 diabetes mellitus." European Journal of Endocrinology 160, no. 2 (February 2009): 265–73. http://dx.doi.org/10.1530/eje-08-0642.
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BackgroundAlthough, adiponectin might be associated with bone metabolism, the relationships between serum adiponectin and bone mineral density (BMD) as well as vertebral fracture in type 2 diabetes are still unclear.Objective and methodsWe investigated the relationships between each of serum total and high molecular weight (HMW) adiponectin versus BMD, bone markers, and the presence of vertebral fractures in a total of 231 men and 170 post-menopausal women with type 2 diabetes.ResultsMultiple regression analysis adjusted for age, duration of diabetes, BMI, serum creatinine, and HbA1c showed that serum total adiponectin was negatively correlated with BMD at the total, lumbar spine, and femoral neck (r=−0.165, P<0.05; r=−0.187, P<0.05; and r=−0.136, P<0.05 respectively) and positively with urinary N-terminal cross-linked telopeptide of type-I collagen in men (r=0.148, P<0.05), and that serum HMW adiponectin was negatively correlated with BMD at the lumbar spine (r=−0.146, P<0.05). Multivariate logistic regression analysis adjusted for the parameters described above showed that total adiponectin was associated with the presence of vertebral fractures in men (odds ratio (OR)=1.396, 95% confidential interval (CI) 1.020–1.911 per s.d. increase, P<0.05), and both total and HMW adiponectin were associated with moderate or severe vertebral fractures (OR=1.709, 95% CI 1.048–2.787 per s.d. increase, P<0.05 and OR=1.810, 95% CI 1.112–2.946 per s.d. increase, P<0.05 respectively), but not in post-menopausal women.ConclusionsSerum adiponectin could be associated with BMD and turnover and clinically useful for assessing the risk of vertebral fractures in type 2 diabetic men.
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NURULLINA, G. M., G. I. AKHMADULLINA, O. V. KRASNOPEROVA, M. M. ALEKSEEVA, O. V. ALEKSANDROVA, and A. V. CHERNOVA. "RISK FACTORS OF LOW-ENERGY FRACTURES IN PATIENTS WITH TYPE 2 DIABETES MELLITUS." Kuban Scientific Medical Bulletin 25, no. 4 (October 3, 2018): 115–23. http://dx.doi.org/10.25207/1608-6228-2018-25-4-115-123.
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Osteoporosis is a metabolic disease of the bone tissue, which is characterized by a violation of the qualitative (microarchitecture change) and quantitative characteristics (decreased bone mass) of the skeleton, and, as a result, lowenergy fractures. The medical and social significance of osteoporosis is due to its consequences: fractures of the femoral neck, vertebral bodies, radius and other large bones of the skeleton, which significantly reduces the quality of patients’ lives and entails significant financial costs for treatment and rehabilitation. Prevalence of diabetes mellitus (DM) significantly increases in all countries of the world, including the Russian Federation. Diabetes and osteoporosis were considered to be individual diseases for a long time. In many prospective large-scale studies it was proved that patients with T2DM have a greater risk of falls and fractures in contrast with the overall population. Despite the increased risk of fractures in diabetic patients, there is still no risk stratification in these patients. The link between the classic risk factors of osteoporotic fractures (such as chronic intake of glucocorticoids, use of alcohol, tobacco, etc.) and the occurrence of fractures is similar in patients with both T2DM and without it. However, it is necessary to take into account other characteristics of diabetes. The specific risk factors of fractures in T2DM patients are duration of the diabetes for more than 10 years, diabetes decompensation, the severity of diabetes, obesity, the frequency of falls, hypoglycemia, insulin, thiazolidinedione, exenatide, sulfonylureas, canagliflozin therapy, and, most likely, the reduction of 25 (OH) vitamin D, functional hypoparathyroidism, the increase of sclerostin, pentosidine, decreased bone mineral density (BMD) of the hip.
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Bharadwaj, Pratishttha, Avijit Mazumder, Saumya Das, Himanshu Singh, Nashra, and Shruti Dhasmana. "A Critical Analysis of Relationship and Management of Sweet Bones in Insulin-Dependent Diabetes Mellitus." International Journal of Pharmaceutical Sciences and Nanotechnology(IJPSN) 15, no. 6 (December 12, 2022): 6245–57. http://dx.doi.org/10.37285/ijpsn.2022.15.6.7.
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Due to the increased risk of encountering several bone deformities as a result of insulin-dependent diabetes mellitus (Type 1 diabetes), it has become obligatory to study this relationship among them so that such conditions of skeletal complications might be detected and treated at a much earlier stage. Type 1 diabetic patients have ameliorated bone mineral density and bone turnover, thus increasing the risk of individuals suffering from fractures. The mechanism behind bone deformities is multifactorial and not completely understood yet. The major factors responsible are less amount of osteoclasts and decreased activity of osteoblasts due to deviated insulin signaling pathway. Other eminent factors involved are oxidative stress, elevated levels of calcium and magnesium in urine, and the build-up of advanced glycation end products. These eminent factors lead to the formation of sweet bones. Sweet bone is a name given collectively to the altered structure, strength, and metabolism of bones. This study will help the researchers to understand and maintain good lifestyle practices. Educating the patients about avoiding other diabetic complications, regular consumption of calcium and vitamin D, along with maintaining proper serum glucose levels are the major steps to be taken primarily in treating bone loss due to type 1 diabetes.
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Alqahtani, Ali, Khalid A. Asseri, Yahya I. Asiri, Krishnaraju Venkatesan, Noohu Abdulla Khan, Sirajudeen Shaik Alavudeen, Ester Mary Pappiya, et al. "Rhizoma Drynariae protects against Canaglifloxacin induced bone loss." International Journal of Current Research in Chemistry and Pharmaceutical sciences 8, no. 9 (September 3, 2021): 22–28. http://dx.doi.org/10.22192/ijcrcps.2021.08.09.004.
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Osteoporosis is a condition marked by a loss of bone mass and degradation of the bone microstructure, both of which lead to increased fragility and consequent fragility fractures, particularly in the elderly. Rhizoma Drynariae (DRE) is one of the most often used herbal remedies for osteoporosis therapy. Transdermal drug administration is a well- established new method for drug delivery that offers numerous benefits over conventional routes. Wistar albino rats were split into five groups of six rats each: vehicle control, diabeticgroup, DRE group, Canagliflozin (CGF), and CGF + DRE group. Each medication was given by gastric gavage once a day for 35 days. The drug canagliflozin appears to raise the risk of fractur. When compared to the control group, DRE treatment increased bone strength at the femoral diaphysis in osteoporotic fractures in rats by increasing ultimate load and stiffness. The goal of this study is to investigate the anti-osteoporosis effects of DRE in diabetic rats co-treated with CGF. Blood glucose levels and bone mineral density (BMD) were measured. According to the data, DRE produced a significant increase in bone amount. DRE may help prevent and cure diabetic osteoporosis by increasing bone mineral density, according to one study. Keywords: Rhizoma Drynariae Diabetic osteoporosis, Streptozotocin induced diabetes, Canagliflozin
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Mohsin, Sahar, Suneesh Kaimala, Jens Jolly Sunny, Ernest Adeghate, and Eric Mensah Brown. "Type 2 Diabetes Mellitus Increases the Risk to Hip Fracture in Postmenopausal Osteoporosis by Deteriorating the Trabecular Bone Microarchitecture and Bone Mass." Journal of Diabetes Research 2019 (November 7, 2019): 1–10. http://dx.doi.org/10.1155/2019/3876957.
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T2DM is linked to an increase in the fracture rate as compared to the nondiabetic population even with normal or raised bone mineral density (BMD). Hence, bone quality plays an important role in the pathogenesis of skeletal fragility due to T2DM. This study analyzed the changes in the trabecular bone microstructure due to T2DM at various time points in ovariectomized and nonovariectomized rats. Animals were divided into four groups: (I) control (sham), (II) diabetic (sham), (III) ovariectomized, and (IV) ovariectomized with diabetes. The trabecular microarchitecture of the femoral head was characterized using a micro-CT. The differences between the groups were analyzed at 8, 10, and 14 weeks of the onset of T2DM using a two-way analysis of variance and by post hoc multiple comparisons. The diabetic group with and without ovariectomies demonstrated a significant increase in trabecular separation and a decrease in bone volume fraction, trabecular number, and thickness. BMD decreased in ovariectomized diabetic animals at 14 weeks of the onset of T2DM. No significant change was found in connectivity density and degree of anisotropy among groups. The structural model index suggested a change towards a weaker rod-like microstructure in diabetic animals. The data obtained suggested that T2DM affects the trabecular structure within a rat’s femoral heads negatively and changes are most significant at a longer duration of T2DM, increasing the risk to hip fractures.
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Lee, Eun-Jung, Min-Kyung Kang, Yun-Ho Kim, Dong Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, Su Yeon Oh, Woojin Na, and Young-Hee Kang. "Coumarin Ameliorates Impaired Bone Turnover by Inhibiting the Formation of Advanced Glycation End Products in Diabetic Osteoblasts and Osteoclasts." Biomolecules 10, no. 7 (July 15, 2020): 1052. http://dx.doi.org/10.3390/biom10071052.
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Accumulating evidence demonstrates that the risk of osteoporotic fractures increases in patients with diabetes mellitus. Thus, diabetes-induced bone fragility has recently been recognized as a diabetic complication. As the fracture risk is independent of the reduction in bone mineral density, deterioration in bone quality may be the main cause of bone fragility. Coumarin exists naturally in many plants as phenylpropanoids and is present in tonka beans in significantly high concentrations. This study investigated whether coumarin ameliorated the impaired bone turnover and remodeling under diabetic condition. The in vitro study employed murine macrophage Raw 264.7 cells differentiated to multinucleated osteoclasts with receptor activator of nuclear factor-κΒ ligand (RANKL) in the presence of 33 mM glucose and 1–20 μM coumarin for five days. In addition, osteoblastic MC3T3-E1 cells were exposed to 33 mM glucose for up to 21 days in the presence of 1–20 μM coumarin. High glucose diminished tartrate-resistant acid phosphatase activity and bone resorption in RANKL-differentiated osteoclasts, accompanying a reduction of cathepsin K induction and actin ring formation. In contrast, coumarin reversed the defective osteoclastogenesis in diabetic osteoclasts. Furthermore, high glucose diminished alkaline phosphatase activity and collagen type 1 induction of osteoblasts, which was strongly enhanced by submicromolar levels of coumarin to diabetic cells. Furthermore, coumarin restored the induction of RANK and osteoprotegerin in osteoclasts and osteoblasts under glucotoxic condition, indicating a tight coupling of osteoclastogenesis and osteoblastogenesis. Coumarin ameliorated the impaired bone turnover and remodeling in diabetic osteoblasts and osteoclasts by suppressing the interaction between advanced glycation end product (AGE) and its receptor (RAGE). Therefore, coumarin may restore optimal bone turnover of osteoclasts and osteoblasts by disrupting the hyperglycemia-mediated AGE–RAGE interaction.
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Masajtis-Zagajewska, Anna, Tomasz Hołub, Katarzyna Pęczek, Agnieszka Makówka, and Michał Nowicki. "Different Effects of Empagliflozin on Markers of Mineral-Bone Metabolism in Diabetic and Non-Diabetic Patients with Stage 3 Chronic Kidney Disease." Medicina 57, no. 12 (December 11, 2021): 1352. http://dx.doi.org/10.3390/medicina57121352.
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Background and objectives: Treatment with sodium–glucose co-transporter 2 (SGLT2) inhibitors decrease tubular reabsorption of phosphate, which may explain the reduction of bone mineral density and an excess of bone fractures observed in some studies with this class of drugs. Since an increased risk of bone fractures may also be a result of diabetes itself, our study aimed to compare the effect of empagliflozin on the markers of mineral-bone metabolism between diabetic (DKD) and non-diabetic (ND-CKD) patients with stage 3 chronic kidney disease (CKD). Materials and Methods: Forty-two patients with stage 3 CKD and A2 albuminuria, including 18 with DKD and 24 ND-CKD, were investigated. All subjects received 10 mg empagliflozin for 7 days. Serum calcium, phosphate, parathormone (PTH), calcitriol, bone alkaline phosphatase (BAP), FGF-23 and urine calcium, phosphate, albumin and the renal tubular maximum reabsorption rate of phosphate to the glomerular filtration rate (TmP-GFR) were measured before and after empagliflozin administration. Differences in biomarkers response to empagliflozin between DKD and ND-CKD were the main measures of outcome. Results: There was a significant increase of PTH, FGF-23 and phosphate in DKD but not in ND-CKD whereas BAP and TmP/GFR did not change in either group. The reduction of albuminuria was only significant in ND-CKD. Conclusions: The effect of SGLT2 inhibitor on serum mineral and bone markers and on albuminuria in patients with CKD may be differently modified by the presence of diabetes mellitus.
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Valkusz, Zsuzsanna. "Diabetes and osteoporosis." Orvosi Hetilap 152, no. 29 (July 2011): 1161–66. http://dx.doi.org/10.1556/oh.2011.29154.
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Over the last decades a considerable amount of data has accumulated to indicate that metabolic and endocrine alterations of diabetes affect bone quantity and quality. These skeletal changes may increase the risk of bone fracture. There is strong evidence that in type 1 diabetes the decreased bone mass, lack of insulin and insulin-like growth factor-1, dysregulation of adipokines, and increased levels of proinflammatory cytokines are in the background of fragility fractures. In type 2 diabetes hyperinsulinemia, insulin resistance and increased body weight may result in an increase of bone mass; however, accumulation of advanced glycation end products within the bone collagen driven by glucotoxicity may increase the cortical porosity. There is a higher incidence of falls resulting from diabetes-related co-morbidities such as diabetic retinopathy, peripheral neuropathy, hypoglycemic episodes and sometimes from the medications. Vitamin D deficiency has special impact on glucose metabolism and the prevalence of diabetes. Vitamin D supplementation in childhood can decrease incidence of type 1 diabetes by 80%. The effect of thiazolidinediones, glucagon-like peptide-1 agonists and metformin, agents for treatment of diabetes open a new connection between bone, carbohydrate and fat metabolism. Orv. Hetil., 2011, 152, 1161–1166.
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Eun-Jung, Lee, and Young-Hee Kang. "Coumarin Boosts Optimal Bone Remodeling Through Blocking AGE-RAGE Interaction in Diabetic Osteoblasts and Osteoclasts." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 395. http://dx.doi.org/10.1093/cdn/nzaa045_028.
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Abstract Objectives Accumulating evidence has shown that the risk of osteoporotic fractures is increased in patients with diabetes mellitus despite normal or high bone mineral density. Thus, diabetes-induced bone fragility has been recently recognized as a diabetic complication. Because the fracture risk is independent of the reduction in bone mineral density, deterioration of the bone quality may be the main cause of bone fragility. Coumarin is naturally found in many plants as phenylpropanoids and present in tonka beans at notably high concentrations. The purpose of this study was to identify that hyperglycemia-mediated advanced glycation end-product (AGE) resulted in impaired bone remodeling and to examine whether coumarin was capable of preventing diabetic osteoporosis through boosting bone remodeling. Methods The in vitro study employed osteoblastic MC3T3-E1 cells that were exposed to 33 mM glucose for 6 days in the presence of 1–20 μM coumarin. Alkaline phosphatase (ALP) activity was quantitatively determined in osteoblastic cells by using stable p-nitrophenyl phosphate. In addition, murine macrophage Raw 264.7 cells were differentiated to multi-nucleated osteoclasts with receptor activator of nuclear factor-κΒ ligand (RANKL) in 33 mM glucose and 1–20 μM coumarin for 5 days. Results High glucose attenuated the ALP activity of osteoblastic cells, which was enhanced by treating 1–20 μM coumarin to cells. On the other hand, 33 mM glucose diminished TRAP and bone resorption activity in RANKL-differentiated osteoclasts, indicating that osteoclast activation was impaired under diabetic conditions. On the contrary, coumarin elevated osteoclastic differentiation and activation. In addition, coumarin ameliorated aberrant bone remodeling in osteoblasts and osteoclasts evoked by AGE. Together, coumarin improved bone remodeling impaired in diabetic osteoblasts and osteoclasts though suppressing interaction of AGE and its receptor. Conclusions These findings suggest the possibility that coumarin might be a potential agent for the treatment of diabetic osteoporosis. Funding Sources This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (2019R1A2C1003218).
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Mahajan, Neetin P., Kunal Chaudhari, Pritam Talukder, Kartik Pande, and Ravikumar Dadhaniya. "Study of the post operative outcome in orthopeadic management in cases of high HBA1c diabetic patients-a case series." International Journal of Research in Medical Sciences 10, no. 3 (February 25, 2022): 723. http://dx.doi.org/10.18203/2320-6012.ijrms20220526.
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Elderly diabetic patients are at risk of poor fracture healing in post-traumatic fracture seven due to trivial low energy falls and chronic pathological bone involvement. Glycated haemoglobins are haemoglobins with an attached sugar moiety. HbA1c is the predominant fraction of HbA1 and gives an estimate of the blood sugar levels of an individual over the last three months. Here we present a case series of 3 elderly patients who came to us with post traumatic fractures or chronic bone pathologies and very high HBA1C values (>10%) who required operative orthopaedics management. The injuries were adequately managed with splintage and operative procedures after proper control of the patients’ blood sugars levels. Postoperatively mobilization was challenging. Orthopaedic chronic bone pathologies and post traumatic limb fractures with uncontrolled sugar and very high HBa1c are very difficult to treat. Postoperatively patients are at a very high risk of infection, poor suture healing, risk of repeat fracture, osteoporosis, etc which often results into functional outcome being hampered. Proper counselling by operating surgeon, physiotherapy and postoperative rehabilitation with the help of relatives and assisting devices with strict preoperative and post operative sugar control provides good outcome. In cases of trauma in old age, one should always thoroughly examine and screen for comorbidities such as hypertension and diabetes using reliable markers such as HBa1c levels. So that early appropriate treatment and mobilization can be done with good functional outcome.
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Sandru, Florica, Mara Carsote, Mihai Cristian Dumitrascu, Simona Elena Albu, and Ana Valea. "Glucocorticoids and Trabecular Bone Score." Journal of Medicine and Life 13, no. 4 (October 2020): 449–53. http://dx.doi.org/10.25122/jml-2019-0131.
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TBS (Trabecular Bone Score) is the latest tool for clinicians to evaluate bone micro-architecture based on a pixel greyscale, which is provided by lumbar dual-energy X-ray absorptiometry (DXA). Its use enhances fracture prediction in addition to DXA-BMD (Bone Mineral Density). This is independent of fracture risk assessment (FRAX) and DXA results. We present a narrative review regarding the connection between TBS and Glucocorticoids (GC), either as a drug used for different conditions or as a tumor-produced endogenous excess. TBS is a better discriminator for GC-induced vertebral fractures compared to DXA-BMD. This aspect is similarly available for patients with osteoporosis diagnosed by DXA. TBS is inversely correlated with the cumulative dose of GC (systemic or inhaled), with disease duration, and positively correlated with respiratory function in patients with asthma. Low TBS values are found in females with a T-score at the hip within the osteoporosis range, with diabetes mellitus, or who use GC. Lumbar TBS is a screening tool in menopausal women with type 2 diabetes mellitus. TBS is an independent parameter that provides information regarding skeleton deterioration in diabetic patients receiving GC therapy in a manner complementary to DXA-BMD. TBS might become an essential step regarding the adrenalectomy decision in patients with adrenal incidentaloma in whom autonomous cortisol secretion might damage bone micro-architecture. TBS currently represents a standard tool of fracture risk evaluation in patients receiving GC therapy or with endogenous Cushing’s syndrome, a tool easy to be applied by different practitioners since GCs are largely used
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Schulze, Sabine, Christin Neuber, Stephanie Möller, Ute Hempel, Lorenz C. Hofbauer, Klaus-Dieter Schaser, Jens Pietzsch, and Stefan Rammelt. "Impact of Sulfated Hyaluronan on Bone Metabolism in Diabetic Charcot Neuroarthropathy and Degenerative Arthritis." International Journal of Molecular Sciences 23, no. 23 (December 2, 2022): 15146. http://dx.doi.org/10.3390/ijms232315146.
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Bone in diabetes mellitus is characterized by an altered microarchitecture caused by abnormal metabolism of bone cells. Together with diabetic neuropathy, this is associated with serious complications including impaired bone healing culminating in complicated fractures and dislocations, especially in the lower extremities, so-called Charcot neuroarthropathy (CN). The underlying mechanisms are not yet fully understood, and treatment of CN is challenging. Several in vitro and in vivo investigations have suggested positive effects on bone regeneration by modifying biomaterials with sulfated glycosaminoglycans (sGAG). Recent findings described a beneficial effect of sGAG for bone healing in diabetic animal models compared to healthy animals. We therefore aimed at studying the effects of low- and high-sulfated hyaluronan derivatives on osteoclast markers as well as gene expression patterns of osteoclasts and osteoblasts from patients with diabetic CN compared to non-diabetic patients with arthritis at the foot and ankle. Exposure to sulfated hyaluronan (sHA) derivatives reduced the exaggerated calcium phosphate resorption as well as the expression of genes associated with bone resorption in both groups, but more pronounced in patients with CN. Moreover, sHA derivatives reduced the release of pro-inflammatory cytokines in osteoclasts of patients with CN. The effects of sHA on osteoblasts differed only marginally between patients with CN and non-diabetic patients with arthritis. These results suggest balancing effects of sHA on osteoclastic bone resorption parameters in diabetes.
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Zheng, Hongxing, Shanshan Qi, and Chen Chen. "Salidroside Improves Bone Histomorphology and Prevents Bone Loss in Ovariectomized Diabetic Rats by Upregulating the OPG/RANKL Ratio." Molecules 23, no. 9 (September 19, 2018): 2398. http://dx.doi.org/10.3390/molecules23092398.
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Postmenopausal diabetic women have a high risk of fractures. Salidroside has preventive effects on estrogen deficiency-induced osteoporosis and has hypoglycemic effects on diabetes in rats. However, whether salidroside inhibits bone loss in postmenopausal diabetic patients is still unknown. Here, we established a rat model of osteoporosis to investigate the protective effects of salidroside on bone loss induced by ovariectomy combined with diabetes, also investigating the underlying mechanisms. Two-month-old female Sprague-Dawley rats were divided into three equal groups (10 rats in each group): control group (with sham operation, treated with drug vehicle); OVX/T1DM group (ovariectomized diabetic rats); OVX/T1DM-SAL group, comprising ovariectomized diabetic rats treated with salidroside (20 mg/kg body weight) by gavage. The results showed that after 60 consecutive days of treatment, the bone mineral density (BMD) of OVX/T1DM-SAL increased significantly compared with the OVX/T1DM group (p < 0.01). The level of serum bone turnover markers, including alkaline phosphatase (ALP), cross linked c-telopeptide of type I collagen (CTX-1), osteocalcin, N-terminal propeptide of type I procollagen (PINP), and tartrate-resistant acid phosphatase 5b (TRACP 5b) were all increased in the OVX/T1DM group compared with the control (p < 0.01), and those were decreased by salidroside treatment. Meanwhile, the bone histopathological changes were also attenuated, and the bone marrow adipogenesis was inhibited in salidroside treated rats. Moreover, protein and mRNA ratio of bone osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL) was upregulated in ovariectomized diabetic rats by salidroside treatment. The results above indicated that the protective effect of salidroside on bone loss induced by ovariectomy and diabetes was mainly due to its ability to suppress bone turnover, inhibit bone marrow adipogenesis, and up-regulate the OPG/RANKL ratio.
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Radugin, F. M., and T. L. Karonova. "Bone metabolism in diabetes mellitus: focus on vitamin K2." Osteoporosis and Bone Diseases 24, no. 3 (February 15, 2022): 11–18. http://dx.doi.org/10.14341/osteo12929.
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Diabetes mellitus (DM) type 2 is reported to be among the most common diseases both worldwide and in Russian Federation, whereby chronic implications that develop under hyperglycemia pose a serious socioeconomic problem. Besides of classic microvascular complications like diabetic retinopathy, nephropathy and polyneuropathy it’s recently worthy of note the presence of high fracture risk in DM type 2 even in normal bone mass density, known as “diaporosis” or “diabetoporosis” considered as another DM complication. It is well known that osteoporosis is reported to be widespread disease as same as DM type 2 and likewise is a widely abundant in older age that makes their combination is really possible in a single patient. Taking into account high social value and disability due to osteoporotic fractures and chronic DM type 2 complications it becomes necessary to continue physiologic and biochemical basis investigations of bone formation and remodeling and pathogenesis of osteoporosis development in the context of chronic hyperglycemia. One of the fairly new factors which the experts believe it is link between impaired glucose metabolism and bone remodeling is osteocalcin which concentration is dependent on vitamin K2 maintenance considered as a potential agent in osteoporotic fractures prevention. In this review current information on vitamin K2 influence on bone status and possibility of using this nutrient in clinical practice in the focus on patients with DM will be covered.
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Fraser, Lisa-Ann, Alexandra Papaioannou, Jonathan D. Adachi, Jinhui Ma, and Lehana Thabane. "Risk Factors for Fracture in Diabetes: The Canadian Multicentre Osteoporosis Study." ISRN Epidemiology 2013 (December 2, 2013): 1–6. http://dx.doi.org/10.5402/2013/249874.
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Objective. Individuals with diabetes have been found to be at increased risk of nontraumatic fracture. However, within the diabetic population, how to distinguish who is at the highest risk and warranting therapy has remained elusive. Design. Cross-sectional analysis of a national population-based cohort study. Patients. Men and women over the age of 50 with diabetes from across Canada. Measurements. Logistic regression analysis to identify diabetes specific factors associated with a history of one or more non-traumatic fractures. Results. Six hundred and six individuals with diabetes with a mean age of 69 years were examined. Thirty percent had a history of non-traumatic fracture. Macrovascular diseases in the form of stroke or TIA, as well as hypertension, were found to be independently associated with fragility fracture. Other, more traditional, clinical risk factors were also associated with fracture, including increased age, female gender, rheumatoid arthritis, family history of osteoporosis, and decreased bone mineral density. Conclusions. In this cohort of Canadians with diabetes, those with rheumatoid arthritis, a family history of osteoporosis, female gender, increased age, decreased BMD, cerebrovascular disease, or hypertension were more likely to have had a non-traumatic fracture. These risk factors may be important to clinicians when identifying which of their diabetic patients are at highest risk of fracture and in need of preventative therapies.
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Klöting, Nora, Niels Follak, and Ingrid Klöting. "Is there an autoimmune process in bone? Gene expression studies in diabetic and nondiabetic BB rats as well as BB rat-related and -unrelated rat strains." Physiological Genomics 24, no. 1 (January 2006): 59–64. http://dx.doi.org/10.1152/physiolgenomics.00094.2005.
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It is well known that type 1 diabetes is associated with a decrease in bone mass and delayed healing of fractures in human and in animal models of type 1 diabetes. Using well- and poorly compensated diabetic BB/O(ttawa) K(arlsburg) rats spontaneously developing insulin-dependent type 1 diabetes, it was recently shown that, in contrast to all other tissues studied, bone is most influenced by metabolic state and seems to be regulated in a manner different from other organs. Therefore, we studied the expression of additional genes ( Bmp-1, Bmp-4, Vegf, Bglap, Il-1b, Infg, Tnfa, Calca, Sp1, Yy1) in bone of nondiabetic BB rats compared with newly diagnosed and well- and poorly compensated diabetic rats as well as two nondiabetes-prone congenic BB.SHR rats, BB rat-related (WOKW) and -unrelated rat strains (F344). Six males of each group were euthanized, the tibial bone was removed, and total RNA was extracted, transcribed in complementary DNA, and used for real-time PCR. In a comparison of nondiabetic with diabetic groups, the relative gene expression was reduced by >80% in newly diagnosed and in well-compensated diabetic BB/OK rats. The gene expression in poorly compensated rats increased significantly in 7 of 10 genes and was comparable with those of nondiabetic BB/OK rats. In a comparison of gene expression between diabetes-prone BB/OK and nondiabetes-prone BB.1K, BB.4S, WOKW, and F344 rats, there were no significant differences between newly diagnosed and well-compensated BB/OK diabetic rats and nondiabetic BB.1K, BB.4S, WOKW, and F344 rats. On the basis of these findings, we concluded that spontaneous diabetes influences bone gene expression in BB/OK rats, which may be attributed to the genetically determined autoimmune process not only affecting pancreatic β-cells but also bone formation and resorption.
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Khaleel, Emad Elias, and Hussein Hadi Atiyah. "Evaluation of Diabetic Patients’ Knowledge to Cutoff Osteoporosis at Diabetes Center in Duhok City." Pakistan Journal of Medical and Health Sciences 16, no. 3 (March 31, 2022): 586–89. http://dx.doi.org/10.53350/pjmhs22163586.
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Background: Patients with T1DM had two to six fold greater of fractures hazard compared to healthy individuals, with the dangerous being highest in T1DM females. In a recent study examining the factors that influence bone break hazards in T1DM adult persons, about 50% of the participants said they had at least one fracture after being diagnosed with diabetes. With comparison of non-diabetic persons, those with T2DM get a 1.2- to 3-fold high prevalence of breakage, especially hip fractures and moreover forearm and leg fracture. Break incidence appear higher in people with a BMI of less than 30 kg/m2 comparing to obese people, and does not appear to differentiate much by gender. Longer duration of diabetes, poor levels of physical activity, sugar and systemically corticosteroid usage, and advancing ages are all linked to an increased fracture risk in T2DM patients. Falls are another cause of fractures, particularly in diabetic women. Aims: The present study conducted to evaluate the patients’ knowledge to put off osteoporosis among a sample from a diabetes center in Duhok city. Methodology: A descriptive design aimed to evaluate diabetic patients’ knowledge from 25 November 2020 to 26 June 2021. In order to get reliable data and a representative sample, a nonprobability (accidental) sample of 27 patients were selected from the diabetes center of Azadi teaching hospital in Duhok city. The statistical data analysis approaches used in order to analyze and assess the results of the study under the application of the statistical package (SPSS) ver. (22.0). Descriptive statistical data analysis and inferential data analysis were used to analyze the finding of the present study Results: The finding of the present study shows female were more than male, constituted 19 (70.4%). The distribution of the gender variable is coincident in the study, as it is high of females, age was between (50- 60) and constituted 12 (44.4%). With regard to the marital status, most of the participants were married and constituted 23(85.2%). Regarding the educational level, most of the participants do not read and write (illiterate) and constituted 12 (44.4%). Most of the participants had low knowledge score of Relative sufficiency coefficient (RS%) less than (33.34) about osteoporosis. Conclusion: Most of the participants were suffer from type two diabetes mellitus and most of them who visit a diabetes center had minimum knowledge toward osteoporosis. Instructional programs with a large sample should be designed for all diabetic patients with both types of diabetes to improve their knowledge about osteoporosis.
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Issa, Claire, Mira S. Zantout, and Sami T. Azar. "Osteoporosis in Men with Diabetes Mellitus." Journal of Osteoporosis 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/651867.
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Osteoporosis is more common in women than in men. The prevalence in men is not defined yet; however it is becoming much more recognized as its prevalence and impact have become explicable. It is estimated that around 1% of bone mineral density is lost in men every year. Studies show that secondary osteoporosis is the major cause thus, making it important to define the disorders associated with male osteoporosis. Diabetes is a risk factor for bone fractures. In male patients with diabetes measures should be undertaken such as encouraging exercise, assuring adequate calcium and vitamin D intake, and treating diabetic complications.
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Safarova, S. S., and S. S. Safarova. "BONE REMODELING MARKERS AS PREDICTORS OF BONE METABOLIC CHANGES IN MALES WITH DIABETIC OSTEOPATHY." Rheumatology Science and Practice 58, no. 3 (June 24, 2020): 290–93. http://dx.doi.org/10.14412/1995-4484-2020-290-293.
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Diabetic osteopathy is one of the little studied complications of diabetes mellitus (DM), which leads to common lowtrauma fractures and, as a consequence, disability and death. The level of insulin is connected with bone functional and morphological changes followed by decreased bone mineral density (BMD) in the early stages of diabetic osteopathy. Objective: to study bone morphofunctional properties in males with type 1 and 2 DM (T1DM and T2DM). Subjects and methods. Examinations were made in 41 male patients with T1DM and 52 male patients with T2DM without a history of fractures. Their age varied from 40 to 70 years (mean age, 55.8±0.7 years and 58.4±0.9 years, respectively). A control group consisted of 34 patients (mean age, 55.9±0.9 years) without a history of DM. Patients with other endocrine disorders, end-stage complications, or chronic liver and kidney diseases were excluded from the investigation. BMD was determined by dual-energy X-ray absorptiometry (DXA). Serum bone remodeling markers (procollagen type 1 amino-terminal propeptide and C-terminal telopeptide), as well as 25(OH)D, parathyrin, insulin, glycated hemoglobin (HbA1c), and electrolytes (Ca2+, P+) were evaluated. Results and discussion. An association of BMD with renal function, HbA1c, and body mass index was observed in patients with T2DM. In the T1MD group, BMD was closely related to insulin deficiency and was significantly lower than that in the control group. In patients with vitamin D deficiency, BMD was significantly lower than in those with normal vitamin D levels (p<0.05). The patients with T1DM displayed both a decrease in BMD (p<0.05) and a pronounced change in the levels of bone markers (p<0.05). Those with T2DM had impaired bone remodeling processes, which was determined by the level of these markers (p<0.05) and observed in the presence of normal BMD due to the complex pathophysiology of the underlying disease. Conclusion. Vitamin D deficiency, insufficient and decreased insulin sensitivity, hyperglycemia, and overweight are important causes of osteopathy in patients with DM. The markers of bone remodeling may become promising indicators for diagnosing osteopathy, but additional studies are needed to elaborate recommendations for their use in routine practice in order to predict and prevent this complication of DM.
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Yan, Pijun, Yong Xu, Zhihong Zhang, Jianhua Zhu, Ying Miao, Chenlin Gao, and Qin Wan. "Association of Circulating Omentin-1 with Osteoporosis in a Chinese Type 2 Diabetic Population." Mediators of Inflammation 2020 (October 15, 2020): 1–16. http://dx.doi.org/10.1155/2020/9389720.
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Aims. Omentin-1, a newly identified adipokine, has been demonstrated to be associated with bone metabolism, but the results have been inconsistent. Moreover, the potential relationship of circulating omentin-1 with diabetic osteoporosis has never been reported. This study is intended for studying the association between circulating omentin-1, bone mineral density (BMD), prior fragility fractures, and other bone metabolic-related parameters. Methods. Circulating omentin-1 levels were measured in 172 patients with type 2 diabetes mellitus (T2DM), and participants were divided into the normal BMD group ( n = 52 ), the osteopenia group ( n = 66 ), and the osteoporosis group ( n = 54 ). The relationship between circulating omentin-1 and diabetic osteoporosis and other parameters was analyzed. Results. Circulating omentin-1 was significantly higher in the osteoporosis group than in the normal group and in the osteopenia group (both P < 0.05 ). Circulating omentin-1 levels were correlated significantly and positively with sex; high-density lipoprotein cholesterol; apolipoprotein A; and prevalence of prior fragility fractures, diabetic nephropathy, and retinopathy; they were correlated negatively with diastolic blood pressure, triglyceride, hemoglobin, atherogenic index of plasma, osteoporosis self-assessment tool for Asians, BMD at different skeletal sites, and corresponding T scores, irrespective of age, sex, and body mass index ( P < 0.01 or P < 0.05 ). Moreover, circulating omentin-1 was an independent decisive factor for the presence of osteoporosis only in women after multivariate adjustment (odds ratio: 1.069; 95% confidence interval: 1.003-1.139; P < 0.05 ). Lastly, the analysis of receiver operating characteristic curves revealed that the best cutoff value for circulating omentin-1 to predict diabetic osteoporosis was 15.37 ng/mL (sensitivity: 71.7%; specificity: 58.5%) in female subjects. Conclusions. High levels of circulating omentin-1 may be associated with the development of osteoporosis in female diabetic subjects and may be a potential biomarker for diabetic osteoporosis in women.
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Sain Safarova, Sain Safarova. "RISK FACTORS FOR THE DEVELOPMENT OF OSTEOPOROSIS IN TYPE 2 DIABETES MELLITUS IN POST-MENOPAUSAL PERIOD." INTERNATIONAL JOURNAL OF INNOVATIVE MEDICINE & HEALTHCARE 01, no. 01 (April 1, 2022): 34–38. http://dx.doi.org/10.55858/ijimh01012022-34.
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ABSTRACT Women with type 2 diabetes mellitus (T2DM) are at a significantly higher risk of fractures, even with normal or elevated bone mineral density (BMD). It was found that in the general population among women, the incidence of osteoporosis is more than 30% in the menopausal period and 43.3% among postmenopausal women, while among people with type 2 diabetes it reaches 75%. An aggravating risk factor in this case is the period of transition of patients with diabetes to postmenopausal age. DM, already predisposing to osteoporotic processes, is aggravated by postmenopausal osteoporosis. Comorbid exacerbation of these processes, which have different mechanisms of action on the bone structure, exacerbates changes in bone characteristics. At the same time, for DM, the most characteristic is a violation of the structure of the cortical bone, mainly the femoral neck and peripheral skeleton, and in postmenopausal osteoporosis, mainly trabecular tissue is damaged, with a predominant lesion of the vertebrae. However, the pathogenetic mechanisms of this influence remain poorly understood. Objective: to evaluate the features of changes in BMD in the lumbar spine and proximal femur in patients with type 2 DM aggravated by postmenopausal osteoporosis. Methods: A total of 96 postmenopausal women with T2DM and 32 control women without diabetes were assessed for bone mineral density (BMD, using dual energy X-ray absorptiometry), biochemical bone markers β-isomerized C-terminal telopeptides (β-CTx) and total procollagen type 1 amino-terminal propeptide (P1NP) and glucose metabolism. Results: In patients with type 2 diabetes When comparing the indicators of phosphorus-calcium metabolism and bone density, a fairly high degree of correlation was found only between the indicators of bone mineral density and ionized calcium (r = -0.321; p = 0.03), as well as between the BMD of the LI-LIV zone and beta-CTx marker (r = -0.436; p = 0.006), which indicates increased bone resorption. At the same time, starting from the state of diabetes subcompensation, bone tissue resorption significantly and significantly increased bone resorption (increased levels of beta-CTx) in 76% of patients and reduced bone mineral density. Conclusion: Our data support the ability of the beta-CTx marker to detect differences in the risk of osteoporotic fractures in postmenopausal women with T2DM compared with non-diabetic controls. The activity of total alkaline phosphatase does not reflect the essence of metabolic changes in bone tissue in diabetes mellitus. It should be noted that in patients suffering from type 2 diabetes, osteopenic syndrome depends not so much on age as on the duration of the disease, the degree of compensation of the glycemic profile. Also, the higher the HbA1c level in women with diabetes, the lower the bone density of the lumbar spine. Assessment of the state of bone mineral density and indicators of its metabolism in postmenopausal women with diabetes will allow timely detection of changes in bone remodeling and contribute to the prevention of fractures, including such a severe injury as a fracture of the femoral neck. Keywords: osteoporosis, diabetes mellitus type 2, post menopause.
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Picke, Ann-Kristin, Graeme Campbell, Nicola Napoli, Lorenz C. Hofbauer, and Martina Rauner. "Update on the impact of type 2 diabetes mellitus on bone metabolism and material properties." Endocrine Connections 8, no. 3 (March 2019): R55—R70. http://dx.doi.org/10.1530/ec-18-0456.
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The prevalence of type 2 diabetes mellitus (T2DM) is increasing worldwide, especially as a result of our aging society, high caloric intake and sedentary lifestyle. Besides the well-known complications of T2DM on the cardiovascular system, the eyes, kidneys and nerves, bone strength is also impaired in diabetic patients. Patients with T2DM have a 40–70% increased risk for fractures, despite having a normal to increased bone mineral density, suggesting that other factors besides bone quantity must account for increased bone fragility. This review summarizes the current knowledge on the complex effects of T2DM on bone including effects on bone cells, bone material properties and other endocrine systems that subsequently affect bone, discusses the effects of T2DM medications on bone and concludes with a model identifying factors that may contribute to poor bone quality and increased bone fragility in T2DM.
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Caffarelli, Carla, Maria Dea Tomai Pitinca, Antonella A. Refaie, Elisa Giglio, Fiorella Anna Lombardi, and Stefano Gonnelli. "LBODP055 Discrimination Effectiveness Of Radiofrequency Echographic Multispectrometry As Non Invasive Method For Osteoporosis Diagnosis Applied To Elderly Women With Type 2 Diabetes." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A274. http://dx.doi.org/10.1210/jendso/bvac150.565.
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Abstract Type 2 diabetes mellitus (T2DM) is associated with an increased risk of fracture, although bone mineral density (BMD) is unaltered or higher in diabetic patients, measured by Dual-energy X-ray absorptiometry (DXA). This paradox could be explained from compromise bone microarchitecture that induce abnormal bone cell function and matrix structure, with increased osteoblast apoptosis, diminished osteoblast differentiation, and enhanced osteoclast-mediated bone resorption.1 In this context, a non-invasive method for assessing the bone density and quality on the axial reference sites (lumbar spine and proximal femur) called Radiofrequency Echographic Multi Spectrometry (REMS), has been introduced and clinically validated. This study aimed to evaluate whether the use of the REMS technique may improve the identification of osteoporosis in T2DM patients. A cohort of ABOUT 100 elderly women with T2DM and mean age 70.5 (± 7.6) years, and 100 healthy age-matched controls underwent DXA and REMS scans on the same anatomical sites (lumbar spine and proximal femur). DXA measurements were all higher in T2DM than controls; instead, all REMS measurements were lower in T2DM than controls. Moreover, the percentage of T2DM women classified as "osteoporotic", on the basis of BMDREMS was markedly higher with respect to those classified by BMDDXA (47. 0% vs 28. 0%, respectively). On the contrary, the percentage of T2DM women classified as osteopenic or normal by BMDDXA was higher with respect by BMDREMS (48.8% and 23.2% vs 38.6% and 14.5%, respectively). T2DM women with fragility fractures presented lower values of both BMDDXA and BMDREMS at the lumbar spine with respect to those without fractures; however, the difference was significant only for BMDREMS (p<0. 05). In conclusion, BMDDXA, as expected, were higher in women with T2DM, while BMDREMS were lower in women with T2DM with respect to controls. Therefore, the data suggest that REMS could be a good diagnostic tool in demonstrating the diabetes-associated bone disease, due to its ability to assess bone quality2 and that may represent a useful approach to enhance the diagnosis of osteoporosis in patients with T2DM.1. Sanches, C. P., et al. The impact of type 2 diabetes on bone metabolism. Diabetol. Metab. Syndr. 9, 1-7 (2017).2. Adami, G. et al. Radiofrequency echographic multi spectrometry for the prediction of incident fragility fractures: A 5-year follow-up study. Bone 134, 115297 (2020). Presentation: No date and time listed
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Deng, Xiangqun, Min Xu, Moyu Shen, and Jinluo Cheng. "Effects of Type 2 Diabetic Serum on Proliferation and Osteogenic Differentiation of Mesenchymal Stem Cells." Journal of Diabetes Research 2018 (June 5, 2018): 1–9. http://dx.doi.org/10.1155/2018/5765478.
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Diabetic patients have an increased risk of osteoporosis-associated fractures. However, the results of most studies of the effects of diabetes on bone mass in patients with type 2 diabetes (T2DM) have been contradictory. To clarify these conflicting findings, we investigated the effects of diabetic serum on the proliferation and osteogenic differentiation of mesenchymal stem cells (MSCs). We used human sera from subjects with different levels of glycemic control to culture the MSCs and induce osteogenic differentiation. The rate of MSC proliferation differed when MSCs were cultured with sera from diabetic subjects with different levels of hyperglycemia. Hyperglycemic sera promoted MSC proliferation to some extent, but all the diabetic sera inhibited the differentiation of MSCs to osteoblasts. The effects of type 2 diabetic sera on the proliferation and osteogenic differentiation of MSCs are closely related to glycemic control. Our data demonstrate the importance of stratifying the study population according to glycemic control in clinical research into diabetic osteoporosis.
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Jones, Jared M., Phillip R. Worts, and Aaron J. Guyer. "Comparison of Diabetic and Non-Diabetic Individuals Outcomes Following Ankle ORIF Surgery Based on Physical Therapy Start Times." Foot & Ankle Orthopaedics 7, no. 4 (October 2022): 2473011421S0071. http://dx.doi.org/10.1177/2473011421s00712.
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Category: Ankle; Trauma Introduction/Purpose: The surgical correction of ankle fractures are one of the most common orthopedic procedures performed and about 13% of individuals undergoing these procedure are classified as diabetic. Diabetes, as a disease, impairs fracture healing due to decreased bone quality and cardiometabolic dysfunction. The use of early mobilization following ankle surSgery has improved post-operative outcomes in the 'healthy' populations; however, early mobilization or early physical therapy initiation in the diabetic populations has not been elucidated. Methods: Surgical correction CPT codes for ankle fracture were used to identify eligible patients followed by a retrospective chart review to confirm diagnosis and procedure(s) as well as collection of demographic information and pertinent medical history. Patient cases were examined over a two year period. Once the inclusion criteria was met, 209 unique patients were included in the analyses. Patients were grouped by diabetes status and early (i.e., <=8 weeks) or late mobilization (i.e., days post- op until physical therapy referral). Generalized linear models and a series Chi-squared tests, Fisher's Exact tests, one-way ANOVAs, and Mann Whitney U Tests were used to assess recovery duration, fracture healing, time to PT referral, medical history, and demographic information. Results: The diabetic group in our study was significantly older [60 (IQR:18) vs. 58 (26) years; p = 0.019] and had a higher BMI [34(8) vs. 29(10); p = 0.041] compared to our non-diabetic group but there were no differences in the proportions for sex or the fracture type by diabetic status. The non-diabetic group displayed a quicker fracture healing time [86(35) vs. 111(45) days; p = 0.04] but there were no differences in recovery duration or days until physical therapy was prescribed. The GLM analysis performed with recovery duration (i.e., time to medical clearance) found that late mobilization was a significant predictor (p < 0.001) of recovery duration but not diabetic diagnosis (p = 0.738). Conclusion: There appears to be a different demographic profile for diabetic patients experiencing an ankle fracture when compared to non-diabetic patients. The delay in physical therapy referral and presumably early mobilization appears to be the strongest predictor of recovery duration. Future research should utilize randomized controlled trials to determine if early mobilization is safe and effective at facilitating quicker fracture healing and recovery following the surgical correction of an ankle fracture in diabetic patients.
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Kaur, Kawalpreet, Gurpreet Kaur Gill, and Ravi Kumar Dhawan. "Effect of Hyperglycemia on Impairment of Calcium Metabolism in T2DM." International Journal of Health Sciences and Research 12, no. 11 (November 8, 2022): 86–93. http://dx.doi.org/10.52403/ijhsr.20221113.
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Background: T2DM or type 2 diabetes mellitus is mostly related to the growing incidence of reduction in bone mineral density with increased porosity and susceptibility to fractures. Diabetes mellitus eventually compromise bone quality through production of advanced glycation products and misalignment of collagen fibrils, thereby culminating in reduction of bone strength. The underlying cellular mechanisms are related to suppression of osteoblast-induced bone formation and calcium accretion, as well as enhancement of osteoclast- induced bone resorption. Objectives: The aim of the present study was to evaluate the effect of high glucose level on the impairment of calcium metabolism in diabetes mellitus patients and to study the inter- relationship between diabetes mellitus and calcium metabolism. The linked association between them would be helpful to support public health policy markers and practioners. Materials and Methods: Total 100 samples were collected from Government Civil Hospital, Lopoke (Amritsar) with age group of 35-60 years having duration of diabetes more than 5 years. Blood and urine samples were analysed for biochemical parameters such as serum fasting glucose, alkaline phosphatase (ALP), albumin, vitamin D, phosphorus and calcium. Urine samples were also analysed to examine the excretion of phosphorus and calcium. Results: Decreased levels of serum calcium, albumin, vitamin D in serum along with elevated urinary calcium were observed in type 2 diabetic patients. Conclusion: From the study it has revealed that in the diabetic patients the calcium metabolism has been affected by the hyperglycemic state of the body. Hence, it is well established that effect of hyperglycemia on calcium metabolism is a risk factor for the development of osteoporosis in diabetic patients. Key words: Diabetes mellitus, Insulin, Osteoporosis, Calcium, Phosphorus, Vitamin D.