Journal articles: 'Bone fragility'

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Napoli, Nicola. "Osteoporosis/bone fragility." Journal of Gerontology and Geriatrics 69, no. 4 (December 2021): 265–68. http://dx.doi.org/10.36150/2499-6564-n456.

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Heaney, Robert P. "Osteoporotic Bone Fragility." JAMA 261, no. 20 (May 26, 1989): 2986. http://dx.doi.org/10.1001/jama.1989.03420200076041.

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Burr, David B. "Microdamage and bone fragility." Current Opinion in Orthopaedics 12, no. 5 (October 2001): 365–70. http://dx.doi.org/10.1097/00001433-200110000-00001.

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Seeman, Ego. "Loading and bone fragility." Journal of Bone and Mineral Metabolism 23, S1 (January 2005): 23–29. http://dx.doi.org/10.1007/bf03026319.

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Robinson, Marie-Eve, and Frank Rauch. "Mendelian bone fragility disorders." Bone 126 (September 2019): 11–17. http://dx.doi.org/10.1016/j.bone.2019.04.021.

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Lane, Nancy E., and Wei Yao. "Glucocorticoid-induced bone fragility." Annals of the New York Academy of Sciences 1192, no. 1 (April 2010): 81–83. http://dx.doi.org/10.1111/j.1749-6632.2009.05228.x.

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Schaffler, Mitchell. "Fatigue and bone fragility." Calcified Tissue International 53, S1 (February 1993): S67. http://dx.doi.org/10.1007/bf01673405.

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Mondillo, Caterina. "Bone fragility in sarcoidosis." International Journal of Bone Fragility 3, no. 3 (June 1, 2023): 36–40. http://dx.doi.org/10.57582/ijbf.230301.036.

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Purpose: Few studies have suggested that sarcoidosis may be associated with low bone mineral density (BMD) and fragility fractures. However, studies on bone mineral loss or fractures in sarcoidosis are conflicting. This study aimed to evaluate: 1) the history of fragility fractures in patients with sarcoidosis; 2) the correlation of bone fragility with severity of sarcoidosis disease. Methods: We selected 252 sarcoidosis patients (54.7 ± 12.1 years) and age- and sex-matched healthy controls. We evaluated BMD at the lumbar spine (BMD-LS), femoral neck, and total hip (BMD-TH), and also the occurrence of any fracture. Forced expiratory volume in one second, forced vital capacity, and diffusion capacity for carbon monoxide (DLCO) were also assessed. Results: BMD T-scores were lower in sarcoidosis patients than in healthy controls, but the difference was statistically significant only for BMD-LS (p < 0.01) and BMD-TH (p < 0.05). Moreover, BMD-LS and BMD-TH values were significantly associated with DLCO (%) (p < 0.05). The prevalence of fragility fracture was higher in patients with sarcoidosis than in controls (30.6% vs. 12.3%). The sarcoidosis patients with a higher number of vertebral fractures (>3) also showed reduced values on pulmonary function test parameters, particularly DLCO (%). Conclusions: This study shows that fragility fractures are significantly more frequent in patients with sarcoidosis than in control subjects. Furthermore, a greater number of vertebral fractures was linked to worse pulmonary function tests.

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Marini, Francesca, Francesca Giusti, Teresa Iantomasi, and Maria Luisa Brandi. "Congenital Metabolic Bone Disorders as a Cause of Bone Fragility." International Journal of Molecular Sciences 22, no. 19 (September 24, 2021): 10281. http://dx.doi.org/10.3390/ijms221910281.

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Bone fragility is a pathological condition caused by altered homeostasis of the mineralized bone mass with deterioration of the microarchitecture of the bone tissue, which results in a reduction of bone strength and an increased risk of fracture, even in the absence of high-impact trauma. The most common cause of bone fragility is primary osteoporosis in the elderly. However, bone fragility can manifest at any age, within the context of a wide spectrum of congenital rare bone metabolic diseases in which the inherited genetic defect alters correct bone modeling and remodeling at different points and aspects of bone synthesis and/or bone resorption, leading to defective bone tissue highly prone to long bone bowing, stress fractures and pseudofractures, and/or fragility fractures. To date, over 100 different Mendelian-inherited metabolic bone disorders have been identified and included in the OMIM database, associated with germinal heterozygote, compound heterozygote, or homozygote mutations, affecting over 80 different genes involved in the regulation of bone and mineral metabolism. This manuscript reviews clinical bone phenotypes, and the associated bone fragility in rare congenital metabolic bone disorders, following a disease taxonomic classification based on deranged bone metabolic activity.

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Bala, Yohann, Roger Zebaze, and Ego Seeman. "Role of cortical bone in bone fragility." Current Opinion in Rheumatology 27, no. 4 (July 2015): 406–13. http://dx.doi.org/10.1097/bor.0000000000000183.

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Moosa, Shahida. "Perinatal lethal osteogenesis imperfecta." South African Journal of Radiology 16, no. 4 (November 28, 2012): 141–42. http://dx.doi.org/10.4102/sajr.v16i4.261.

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Osteogenesis imperfecta (OI) is a heterogeneous group of genetic bone disorders that are characterised by decreased bone mass, increased bone fragility and susceptibility to fractures. The severe, perinatal lethal form (Type II) (OMIM 166210) is characterised by bone fragility, with perinatal fractures, severe bowing of long bones, undermineralisation, and death in the perinatal period owing to respiratory insufficiency. The overall prevalence of OI Type II is unknown. There are three subtypes of OI Type II (A, B and C) that are characterised by different radiological features, and may be caused by different genetic faults. Two fetuses with OI Type IIA are presented.

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Merlotti, Daniela, Christian Mingiano, Roberto Valenti, Guido Cavati, Marco Calabrese, Filippo Pirrotta, Simone Bianciardi, Alberto Palazzuoli, and Luigi Gennari. "Bone Fragility in Gastrointestinal Disorders." International Journal of Molecular Sciences 23, no. 5 (February 28, 2022): 2713. http://dx.doi.org/10.3390/ijms23052713.

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Osteoporosis is a common systemic disease of the skeleton, characterized by compromised bone mass and strength, consequently leading to an increased risk of fragility fractures. In women, the disease mainly occurs due to the menopausal fall in estrogen levels, leading to an imbalance between bone resorption and bone formation and, consequently, to bone loss and bone fragility. Moreover, osteoporosis may affect men and may occur as a sequela to different diseases or even to their treatments. Despite their wide prevalence in the general population, the skeletal implications of many gastrointestinal diseases have been poorly investigated and their potential contribution to bone fragility is often underestimated in clinical practice. However, proper functioning of the gastrointestinal system appears essential for the skeleton, allowing correct absorption of calcium, vitamins, or other nutrients relevant to bone, preserving the gastrointestinal barrier function, and maintaining an optimal endocrine-metabolic balance, so that it is very likely that most chronic diseases of the gastrointestinal tract, and even gastrointestinal dysbiosis, may have profound implications for bone health. In this manuscript, we provide an updated and critical revision of the role of major gastrointestinal disorders in the pathogenesis of osteoporosis and fragility fractures.

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Radin, Eric L. "Current Concepts of Bone Fragility." Journal of Bone & Joint Surgery 69, no. 3 (March 1987): 477–78. http://dx.doi.org/10.2106/00004623-198769030-00025.

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Bouxsein, Mary L., and David Karasik. "Bone geometry and skeletal fragility." Current Osteoporosis Reports 4, no. 2 (June 2006): 49–56. http://dx.doi.org/10.1007/s11914-006-0002-9.

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Schwartz, Ann V., and Deborah E. Sellmeyer. "Diabetes, fracture, and bone fragility." Current Osteoporosis Reports 5, no. 3 (September 2007): 105–11. http://dx.doi.org/10.1007/s11914-007-0025-x.

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Briot, K., P. Geusens, I. Em Bultink, W. F. Lems, and C. Roux. "Inflammatory diseases and bone fragility." Osteoporosis International 28, no. 12 (September 15, 2017): 3301–14. http://dx.doi.org/10.1007/s00198-017-4189-7.

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Kanazawa, Ippei, and Toshitsugu Sugimoto. "Diabetes Mellitus-induced Bone Fragility." Internal Medicine 57, no. 19 (October 1, 2018): 2773–85. http://dx.doi.org/10.2169/internalmedicine.0905-18.

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Fujita, Takuo. "Calcitonin on osteoporotic bone fragility." Calcified Tissue International 47, no. 4 (October 1990): 256. http://dx.doi.org/10.1007/bf02555928.

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Moretti, Antimo, Sara Liguori, Marco Paoletta, Silvia Migliaccio, Giuseppe Toro, Francesca Gimigliano, and Giovanni Iolascon. "Bone fragility during the COVID-19 pandemic: the role of macro- and micronutrients." Therapeutic Advances in Musculoskeletal Disease 15 (January 2023): 1759720X2311582. http://dx.doi.org/10.1177/1759720x231158200.

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Bone fragility is the susceptibility to fracture due to poor bone strength. This condition is usually associated with aging, comorbidities, disability, poor quality of life, and increased mortality. International guidelines for the management of patients with bone fragility include a nutritional approach, mainly aiming at optimal protein, calcium, and vitamin D intakes. Several biomechanical features of the skeleton, such as bone mineral density (BMD), trabecular and cortical microarchitecture, seem to be positively influenced by micro- and macronutrient intake. Patients with major fragility fractures are usually poor consumers of dairy products, fruit, and vegetables as well as of nutrients modulating gut microbiota. The COVID-19 pandemic has further aggravated the health status of patients with skeletal fragility, also in terms of unhealthy dietary patterns that might adversely affect bone health. In this narrative review, we discuss the role of macro- and micronutrients in patients with bone fragility during the COVID-19 pandemic.

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Iolascon, Giovanni, Marco Paoletta, Sara Liguori, Francesca Gimigliano, and Antimo Moretti. "Bone fragility: conceptual framework, therapeutic implications, and COVID-19-related issues." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2211334. http://dx.doi.org/10.1177/1759720x221133429.

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Bone fragility is the susceptibility to fracture even for common loads because of structural, architectural, or material alterations of bone tissue that result in poor bone strength. In osteoporosis, quantitative and qualitative changes in density, geometry, and micro-architecture modify the internal stress state predisposing to fragility fractures. Bone fragility substantially depends on the structural behavior related to the size and shape of the bone characterized by different responses in the load–deformation curve and on the material behavior that reflects the intrinsic material properties of the bone itself, such as yield and fatigue. From a clinical perspective, the measurement of bone density by DXA remains the gold standard for defining the risk of fragility fracture in all population groups. However, non-quantitative parameters, such as macro-architecture, geometry, tissue material properties, and microcracks accumulation can modify the bone’s mechanical strength. This review provides an overview of the role of different contributors to bone fragility and how these factors might be influenced by the use of anti-osteoporotic drugs and by the COVID-19 pandemic.

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Chavassieux, P., E. Seeman, and P. D. Delmas. "Insights into Material and Structural Basis of Bone Fragility from Diseases Associated with Fractures: How Determinants of the Biomechanical Properties of Bone Are Compromised by Disease." Endocrine Reviews 28, no. 2 (December 19, 2006): 151–64. http://dx.doi.org/10.1210/er.2006-0029.

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Minimal trauma fractures in bone diseases are the result of bone fragility. Rather than considering bone fragility as being the result of a reduced amount of bone, we recognize that bone fragility is the result of changes in the material and structural properties of bone. A better understanding of the contribution of each component of the material composition and structure and how these interact to maintain whole bone strength is obtained by the study of metabolic bone diseases. Disorders of collagen (osteogenesis imperfecta and Paget’s disease of bone), mineral content, composition and distribution (fluorosis and osteomalacia); diseases of high remodeling (postmenopausal osteoporosis, hyperparathyroidism, and hyperthyroidism) and low remodeling (osteopetrosis, pycnodysostosis); and other diseases (idiopathic male osteoporosis, corticosteroid-induced osteoporosis) produce abnormalities in the material composition and structure that lead to bone fragility. Observations in patients and in animal models provide insights on the biomechanical consequences of these illnesses and the nature of the qualities of bone that determine its strength.

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Caffarelli, Carla, Antonella Al Refaie, Caterina Mondillo, Michela De Vita, Leonardo Baldassini, Giuseppe Valacchi, and Stefano Gonnelli. "Bone Fracture in Rett Syndrome: Mechanisms and Prevention Strategies." Children 10, no. 12 (November 27, 2023): 1861. http://dx.doi.org/10.3390/children10121861.

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The present study aimed to evaluate the burden and management of fragility fractures in subjects with Rett syndrome. We searched all relevant medical literature from 1 January 1986 to 30 June 2023 for studies under the search term “Rett syndrome and fracture”. The fracture frequency ranges from a minimum of 13.9% to a maximum of 36.1%. The majority of such fractures occur in lower limb bones and are associated with low bone mineral density. Anticonvulsant use, joint contractures, immobilization, low physical activity, poor nutrition, the genotype, and lower calcium and vitamin D intakes all significantly impair skeletal maturation and bone mass accrual in Rett syndrome patients, making them more susceptible to fragility fractures. This review summarizes the knowledge on risk factors for fragility fracture in patients with Rett syndrome and suggests a possible diagnostic and therapeutic care pathway for improving low bone mineral density and reducing the risk of fragility fractures. The optimization of physical activity, along with adequate nutrition and the intake of calcium and vitamin D supplements, should be recommended. In addition, subjects with Rett syndrome and a history of fracture should consider using bisphosphonates.

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Wool, Nathan K., Shannon Wilson, Alexander C. M. Chong, and Bradley R. Dart. "Bone Health Improvement Protocol." Kansas Journal of Medicine 10, no. 3 (August 1, 2017): 62–66. http://dx.doi.org/10.17161/kjm.v10i3.8659.

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Introduction. Metabolic bone disease is a malady that causessignificant morbidity and mortality to a patient who has sustaineda fragility fracture. There is currently no protocol toprevent secondary fragility fracture at our institution. The objectiveof this study was to create an appropriate protocol forimplementing clinical pathways for physicians to diagnose andtreat osteoporosis and fragility fractures by educating patients. Methods. A multidisciplinary team created an appropriateprotocol that could be implemented in an inpatient setting.A thorough literature review was conducted to evaluatepotential barriers and efficacious methods of protocol design. Results. A bone health improvement protocol was developed.Any patient over the age of 50 who sustains a fracture from lowenergy trauma, such as a fall from standing or less, should beconsidered to place into this protocol. These patients receivededucation on metabolic bone disease, a prescription for highdose vitamin D therapy, and laboratory testing to determinethe etiology of their metabolic bone disease. Continuity of careof these patients with their primary care provider was providedfor further management of their metabolic bone disease andevaluation of their disease after discharged from the hospital. Conclusion. Comprehensive secondary prevention should consistof osteoporosis assessment and treatment together with afall risk assessment. With this protocol, secondary fragility fracturespotentially could be prevented. KS J Med 2017;10(3):62-66.

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Sihota, Praveer, Ram Naresh Yadav, Ruban Dhaliwal, Jagadeesh Chandra Bose, Vandana Dhiman, Deepak Neradi, Shailesh Karn, et al. "Investigation of Mechanical, Material, and Compositional Determinants of Human Trabecular Bone Quality in Type 2 Diabetes." Journal of Clinical Endocrinology & Metabolism 106, no. 5 (January 21, 2021): e2271-e2289. http://dx.doi.org/10.1210/clinem/dgab027.

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Abstract Context Increased bone fragility and reduced energy absorption to fracture associated with type 2 diabetes (T2D) cannot be explained by bone mineral density alone. This study, for the first time, reports on alterations in bone tissue’s material properties obtained from individuals with diabetes and known fragility fracture status. Objective To investigate the role of T2D in altering biomechanical, microstructural, and compositional properties of bone in individuals with fragility fracture. Methods Femoral head bone tissue specimens were collected from patients who underwent replacement surgery for fragility hip fracture. Trabecular bone quality parameters were compared in samples of 2 groups, nondiabetic (n = 40) and diabetic (n = 30), with a mean duration of disease 7.5 ± 2.8 years. Results No significant difference was observed in aBMD between the groups. Bone volume fraction (BV/TV) was lower in the diabetic group due to fewer and thinner trabeculae. The apparent-level toughness and postyield energy were lower in those with diabetes. Tissue-level (nanoindentation) modulus and hardness were lower in this group. Compositional differences in the diabetic group included lower mineral:matrix, wider mineral crystals, and bone collagen modifications—higher total fluorescent advanced glycation end-products (fAGEs), higher nonenzymatic cross-link ratio (NE-xLR), and altered secondary structure (amide bands). There was a strong inverse correlation between NE-xLR and postyield strain, fAGEs and postyield energy, and fAGEs and toughness. Conclusion The current study is novel in examining bone tissue in T2D following first hip fragility fracture. Our findings provide evidence of hyperglycemia’s detrimental effects on trabecular bone quality at multiple scales leading to lower energy absorption and toughness indicative of increased propensity to bone fragility.

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Lacativa, Paulo Gustavo S., and Maria Lucia F. de Farias. "Office practice of osteoporosis evaluation." Arquivos Brasileiros de Endocrinologia & Metabologia 50, no. 4 (August 2006): 674–84. http://dx.doi.org/10.1590/s0004-27302006000400013.

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Osteoporosis is a metabolic disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk. Bone fragility depends on bone density, turnover and microarchitectural features, such as relative trabecular volume, spacing, number and connectivity. Previous fragility fractures increase the fracture risk irrespective of bone density. Other risk factors must also be considered as many fractures occur in patients with osteopenia on densitometry. On the other hand, the diagnosis of osteoporosis and increased fracture risk should not be based on densitometric data alone when young populations such as men below 65 years, premenopausal women, adolescents and children are considered.

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Nguyen, Chi-Duc, Vincent Morel, Adeline Pierache, Georges Lion, Bernard Cortet, René-Marc Flipo, Valérie Canva-Delcambre, and Julien Paccou. "Bone and joint complications in patients with hereditary hemochromatosis: a cross-sectional study of 93 patients." Therapeutic Advances in Musculoskeletal Disease 12 (January 2020): 1759720X2093940. http://dx.doi.org/10.1177/1759720x20939405.

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Background: The aim of this study was to determine the frequency and characteristics of bone and joint complications, specifically bone fragility, joint replacement surgery, and arthropathy, in hereditary hemochromatosis (HH) and related factors. Methods: This study was a cross-sectional observational study of 93 patients with HH. Radiographs of the hands, wrists, knees, and ankles were scored for joint space narrowing, erosions and cysts, osteophytes, and chondrocalcinosis. Prevalent (vertebral and non-vertebral) fragility fractures were recorded and bone mineral density (BMD) was systematically evaluated by dual energy X-ray absorptiometry. Bone fragility was defined as (i) a T-score ⩽ −2.5 at any site with or without a prevalent fragility fracture, or (ii) a T-score between −1.0 and −2.5 at any site and a prevalent fragility fracture. Results: The mean age of the patients was 60.0 (11.2) years, and 58.0% of them were men. The frequency of radiographic MCP2–3 arthropathy was 37.6% (95% CI 0.28–0.48). Radiographic MCP2–3 arthropathy was independently associated with older age [OR 1.17 (1.09–1.26) per year, p < 0.0001], male sex [OR 3.89 (1.17–12.97), p = 0.027] and C282Y+/+ genotype [OR 4.78 (1.46–15.68), p = 0.010]. The frequency of joint replacement surgery was 12.9% (95% CI 0.07–0.21). The frequency of bone fragility was 20.4% (95% CI 0.13–0.30). Bone fragility was independently associated with hepatic cirrhosis [OR 8.20 (1.74–38.68), p = 0.008]. Discussion: Radiographic MCP2–3 arthropathy was found to occur in 37.6% of patients with HH. The association observed between this form of arthropathy and C282Y homozygosity, male sex, and older age suggests that demographic characteristics and genetic background are likely to be major determinants of this joint disorder and play a more important role than severity of iron overload. Bone fragility was observed in a fifth of the patients with HH, independently of genetic background and severity of iron overload, and was strongly associated with hepatic cirrhosis. Conclusion: Future investigations should focus on pathogenesis and early identification of patients at risk of developing bone and joint complications secondary to HH.

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Eller-Vainicher, C., E. Cairoli, G. Grassi, F. Grassi, A. Catalano, D. Merlotti, A. Falchetti, A. Gaudio, I. Chiodini, and L. Gennari. "Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility." Journal of Diabetes Research 2020 (May 23, 2020): 1–18. http://dx.doi.org/10.1155/2020/7608964.

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Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of bone fragility fractures compared to nondiabetic subjects. This increased fracture risk may occur despite normal or even increased values of bone mineral density (BMD), and poor bone quality is suggested to contribute to skeletal fragility in this population. These concepts explain why the only evaluation of BMD could not be considered an adequate tool for evaluating the risk of fracture in the individual T2DM patient. Unfortunately, nowadays, the bone quality could not be reliably evaluated in the routine clinical practice. On the other hand, getting further insight on the pathogenesis of T2DM-related bone fragility could consent to ameliorate both the detection of the patients at risk for fracture and their appropriate treatment. The pathophysiological mechanisms underlying the increased risk of fragility fractures in a T2DM population are complex. Indeed, in T2DM, bone health is negatively affected by several factors, such as inflammatory cytokines, muscle-derived hormones, incretins, hydrogen sulfide (H2S) production and cortisol secretion, peripheral activation, and sensitivity. All these factors may alter bone formation and resorption, collagen formation, and bone marrow adiposity, ultimately leading to reduced bone strength. Additional factors such as hypoglycemia and the consequent increased propensity for falls and the direct effects on bone and mineral metabolism of certain antidiabetic medications may contribute to the increased fracture risk in this population. The purpose of this review is to summarize the literature evidence that faces the pathophysiological mechanisms underlying bone fragility in T2DM patients.

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Ciardo, D., P. Pisani, F. A. Lombardi, R. Franchini, F. Conversano, and S. Casciaro. "POS0163 INCIDENT FRACTURE RISK PREDICTION USING THE FRAGILITY SCORE CALCULATED BY LUMBAR SPINE RADIOFREQUENCY ECHOGRAPHIC MULTI SPECTROMETRY (REMS) SCANS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 294.2–294. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2311.

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Background:The main consequence of osteoporosis is the occurrence of fractures due to bone fragility, with important sequelae in terms of disability and mortality. It has been already demonstrated that the information about bone mass density (BMD) alone is not sufficient to predict the risk of fragility fractures, since several fractures occur in patients with normal BMD [1].The Fragility Score is a parameter that allows to estimate skeletal fragility thanks to a trans-abdominal ultrasound scan performed with Radiofrequency Echographic Multi Spectrometry (REMS) technology. It is calculated by comparing the results of the spectral analysis of the patient’s raw ultrasound signals with reference models representative of fragile and non-fragile bones [2]. It is a dimensionless parameter, which can vary from 0 to 100, in proportion to the degree of fragility, independently from BMD.Objectives:This study aims to evaluate the effectiveness of Fragility Score, measured during a bone densitometry exam performed with REMS technology at lumbar spine, in identifying patients at risk of incident osteoporotic fractures at a follow-up period of 5 years.Methods:Caucasian women with age between 30 and 90 were scanned with spinal REMS and DXA. The incidence of osteoporotic fractures was assessed during a follow-up period of 5 years. The ability of the Fragility Score to discriminate between patients with and without incident fragility fractures was subsequently evaluated and compared with the discriminatory ability of the T-score calculated with DXA and with REMS.Results:Overall, 533 women (median age: 60 years; interquartile range [IQR]: 54-66 years) completed the follow-up (median 42 months; IQR: 35-56 months), during which 73 patients had sustained an incident fracture.Both median REMS and DXA measured T-score values were significantly lower in fractured patients than for non-fractured ones, conversely, REMS Fragility Score was significantly higher (Table 1).Table 1.Analysis of T-score values calculated with REMS and DXA and Fragility Score calculated with REMS. Median values and interquartile ranges (IQR) are reported. The p-value is derived from the Mann-Whitney test.Patients without incident fragility fracturePatients with incident fragility fracturep-valueT-score DXA[median (IQR)]-1.9 (-2.7 to -1.0)-2.6 (-3.3 to -1.7)0.0001T-score REMS[median (IQR)]-2.0 (-2.8 to -1.1)-2.7 (-3.5 to -1.9)<0.0001Fragility Score[median (IQR)]29.9 (25.7 to 36.2)53.0 (34.2 to 62.5)<0.0001By evaluating the capability to discriminate patients with/without fragility fractures, the Fragility Score obtained a value of the ROC area under the curve (AUC) of 0.80, higher than the AUC of the REMS T-score (0.66) and of the T-score DXA (0.64), and the difference was statistically significant (Figure 1).Figure 1.ROC curve comparison of Fragility Score, REMS and DXA T-score values in the classification of patients with incident fragility fractures.Furthermore, the correlation between the Fragility Score and the T-score values was low, with Pearson correlation coefficient r=-0.19 between Fragility Score and DXA T-score and -0.18 between the Fragility Score and the REMS T-score.Conclusion:The Fragility Score was found to be an effective tool for the prediction of fracture risk in a population of Caucasian women, with performances superior to those of the T-score values. Therefore, this tool presents a high potential as an effective diagnostic tool for the early identification and subsequent early treatment of bone fragility.References:[1]Diez Perez A et al. Aging Clin Exp Res 2019; 31(10):1375-1389.[2]Pisani P et al. Measurement 2017; 101:243–249.Disclosure of Interests:None declared

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Mjöberg, Bengt, Einar Hellquist, Hans Mallmin, and Ulf Lindh. "Aluminum, Alzheimer's disease and bone fragility." Acta Orthopaedica Scandinavica 68, no. 6 (January 1997): 511–14. http://dx.doi.org/10.3109/17453679708999016.

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Paschalis, Eleftherios P., Elizabeth Shane, George Lyritis, Grigoris Skarantavos, Richard Mendelsohn, and Adele L. Boskey. "Bone Fragility and Collagen Cross-Links." Journal of Bone and Mineral Research 19, no. 12 (August 30, 2004): 2000–2004. http://dx.doi.org/10.1359/jbmr.040820.

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Kontulainen, Saija Annukka, Chantal Elizabeth Kawalilak, James Duncan Johnston, and Donald Alexander Bailey. "Prevention of Osteoporosis and Bone Fragility." American Journal of Lifestyle Medicine 7, no. 6 (May 9, 2013): 405–17. http://dx.doi.org/10.1177/1559827613487664.

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Fyhrie, David P., and Blaine A. Christiansen. "Bone Material Properties and Skeletal Fragility." Calcified Tissue International 97, no. 3 (May 5, 2015): 213–28. http://dx.doi.org/10.1007/s00223-015-9997-1.

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Cohen-Solal, Martine. "Physiopathology and Characterization of Bone Fragility." Osteoporosis and Sarcopenia 4, no. 4 (December 2018): S4. http://dx.doi.org/10.1016/j.afos.2018.11.013.

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Samuel, Jitin, Rohit Khanna, and Xiaodu Wang. "Perspective: Ultrastructural Origins of Bone Fragility." Osteology and Rheumatology – Open Journal 1, no. 1 (July 20, 2016): 1–3. http://dx.doi.org/10.17140/orhoj-1-101.

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Bone fragility fractures due to deteriorated tissue quality are a major healthcare concern in the healthcare of elderly who are at particularly high risk of bone fractures. Thus, identifying and treating patients at risk is critical in sustaining a healthy life style for the elderly.

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Bisson, Sarah-Kim, Roth-Visal Ung, and Fabrice Mac-Way. "Role of the Wnt/β-Catenin Pathway in Renal Osteodystrophy." International Journal of Endocrinology 2018 (2018): 1–15. http://dx.doi.org/10.1155/2018/5893514.

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Vascular calcification and bone fragility are common and interrelated health problems that affect chronic kidney disease (CKD) patients. Bone fragility, which leads to higher risk of fracture and mortality, arises from the abnormal bone remodeling and mineralization that are seen in chronic kidney disease. Recently, sclerostin and Dickkopf-related protein 1 were suggested to play a significant role in CKD-related bone disease as they are known inhibitors of the Wnt pathway, thus preventing bone formation. This review focuses on new knowledge about the Wnt pathway in bone, how its function is affected by chronic kidney disease and how this affects bone structure. Expression of components and inhibitors of the Wnt pathway has been shown to be affected by the loss of kidney function, and a better understanding of the bone effects of Wnt pathway inhibitors could allow the development of new therapies to prevent bone fragility in this population.

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Caetano-Lopes, J., I. Aleixo, A. Rodrigues, I. P. Perpetuo, D. Fernandes, A. Lopes, A. Pena, et al. "Bone cell activity influences bone fragility and fracture risk." Annals of the Rheumatic Diseases 69, Suppl 2 (March 1, 2010): A20—A21. http://dx.doi.org/10.1136/ard.2010.129593m.

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Fonseca, Hélder, Daniel Moreira-Gonçalves, Hans-Joachim Appell Coriolano, and José Alberto Duarte. "Bone Quality: The Determinants of Bone Strength and Fragility." Sports Medicine 44, no. 1 (October 3, 2013): 37–53. http://dx.doi.org/10.1007/s40279-013-0100-7.

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Thurner, Philipp J., Carol G. Chen, Sophi Ionova-Martin, Luling Sun, Adam Harman, Alexandra Porter, Joel W. Ager, Robert O. Ritchie, and Tamara Alliston. "Osteopontin deficiency increases bone fragility but preserves bone mass." Bone 46, no. 6 (June 2010): 1564–73. http://dx.doi.org/10.1016/j.bone.2010.02.014.

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Heaney, Robert P. "Bone Mass, Bone Fragility, and the Decision to Treat." JAMA 280, no. 24 (December 23, 1998): 2119. http://dx.doi.org/10.1001/jama.280.24.2119.

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Agten, Christoph A., Stephen Honig, Punam K. Saha, Ravinder Regatte, and Gregory Chang. "Subchondral bone microarchitecture analysis in the proximal tibia at 7-T MRI." Acta Radiologica 59, no. 6 (September 12, 2017): 716–22. http://dx.doi.org/10.1177/0284185117732098.

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Background Bone remodels in response to mechanical loads and osteoporosis results from impaired ability of bone to remodel. Bone microarchitecture analysis provides information on bone quality beyond bone mineral density (BMD). Purpose To compare subchondral bone microarchitecture parameters in the medial and lateral tibia plateau in individuals with and without fragility fractures. Material and Methods Twelve female patients (mean age = 58 ± 15 years; six with and six without previous fragility fractures) were examined with dual-energy X-ray absorptiometry (DXA) and 7-T magnetic resonance imaging (MRI) of the proximal tibia. A transverse high-resolution three-dimensional fast low-angle shot sequence was acquired (0.234 × 0.234 × 1 mm). Digital topological analysis (DTA) was applied to the medial and lateral subchondral bone of the proximal tibia. The following DTA-based bone microarchitecture parameters were assessed: apparent bone volume; trabecular thickness; profile-edge-density (trabecular bone erosion parameter); profile-interior-density (intact trabecular rods parameter); plate-to-rod ratio; and erosion index. We compared femoral neck T-scores and bone microarchitecture parameters between patients with and without fragility fracture. Results There was no statistical significant difference in femoral neck T-scores between individuals with and without fracture (–2.4 ± 0.9 vs. −1.8 ± 0.7, P = 0.282). Apparent bone volume in the medial compartment was lower in patients with previous fragility fracture (0.295 ± 0.022 vs. 0.317 ± 0.009; P = 0.016). Profile-edge-density, a trabecular bone erosion parameter, was higher in patients with previous fragility fracture in the medial (0.008 ± 0.003 vs. 0.005 ± 0.001) and lateral compartment (0.008 ± 0.002 vs. 0.005 ± 0.001); both P = 0.025. Other DTA parameters did not differ between groups. Conclusion 7-T MRI and DTA permit detection of subtle changes in subchondral bone quality when differences in BMD are not evident.

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Iwasaki, Yoshiko, Junichiro James Kazama, and Masafumi Fukagawa. "Molecular Abnormalities Underlying Bone Fragility in Chronic Kidney Disease." BioMed Research International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/3485785.

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Prevention of bone fractures is one goal of therapy for patients with chronic kidney disease-mineral and bone disorder (CKD-MBD), as indicated by the Kidney Disease: Improving Global Outcomes guidelines. CKD patients, including those on hemodialysis, are at higher risk for fractures and fracture-related death compared to people with normal kidney function. However, few clinicians focus on this issue as it is very difficult to estimate bone fragility. Additionally, uremia-related bone fragility has a more complicated pathological process compared to osteoporosis. There are many uremia-associated factors that contribute to bone fragility, including severe secondary hyperparathyroidism, skeletal resistance to parathyroid hormone, and bone mineralization disorders. Uremia also aggravates bone volume loss, disarranges microarchitecture, and increases the deterioration of material properties of bone through abnormal bone cells or excess oxidative stress. In this review, we outline the prevalence of fractures, the interaction of CKD-MBD with osteoporosis in CKD patients, and discuss possible factors that exacerbate the mechanical properties of bone.

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El-Gazzar, Ahmed, and Wolfgang Högler. "Mechanisms of Bone Fragility: From Osteogenesis Imperfecta to Secondary Osteoporosis." International Journal of Molecular Sciences 22, no. 2 (January 10, 2021): 625. http://dx.doi.org/10.3390/ijms22020625.

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Bone material strength is determined by several factors, such as bone mass, matrix composition, mineralization, architecture and shape. From a clinical perspective, bone fragility is classified as primary (i.e., genetic and rare) or secondary (i.e., acquired and common) osteoporosis. Understanding the mechanism of rare genetic bone fragility disorders not only advances medical knowledge on rare diseases, it may open doors for drug development for more common disorders (i.e., postmenopausal osteoporosis). In this review, we highlight the main disease mechanisms underlying the development of human bone fragility associated with low bone mass known to date. The pathways we focus on are type I collagen processing, WNT-signaling, TGF-ß signaling, the RANKL-RANK system and the osteocyte mechanosensing pathway. We demonstrate how the discovery of most of these pathways has led to targeted, pathway-specific treatments.

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El-Gazzar, Ahmed, and Wolfgang Högler. "Mechanisms of Bone Fragility: From Osteogenesis Imperfecta to Secondary Osteoporosis." International Journal of Molecular Sciences 22, no. 2 (January 10, 2021): 625. http://dx.doi.org/10.3390/ijms22020625.

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Bone material strength is determined by several factors, such as bone mass, matrix composition, mineralization, architecture and shape. From a clinical perspective, bone fragility is classified as primary (i.e., genetic and rare) or secondary (i.e., acquired and common) osteoporosis. Understanding the mechanism of rare genetic bone fragility disorders not only advances medical knowledge on rare diseases, it may open doors for drug development for more common disorders (i.e., postmenopausal osteoporosis). In this review, we highlight the main disease mechanisms underlying the development of human bone fragility associated with low bone mass known to date. The pathways we focus on are type I collagen processing, WNT-signaling, TGF-ß signaling, the RANKL-RANK system and the osteocyte mechanosensing pathway. We demonstrate how the discovery of most of these pathways has led to targeted, pathway-specific treatments.

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Jadžić, Jelena, and Marija Đurić. "Structural basis of increased bone fragility in aged individuals: Multi-scale perspective." Medicinska istrazivanja 57, no. 1 (2024): 67–74. http://dx.doi.org/10.5937/medi57-45170.

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Numerous epidemiological studies have shown that increased bone fragility and a higher risk of fractures are present in the aged, which reduces their quality of life and represents a significant socio-economic burden for the healthcare system. However, morphological and structural determinants underlying increased bone fragility have yet to be fully explained. This paper aimed to provide an overview of modern studies that dealt with determinants of increased bone fragility, analyzing different hierarchical levels of bone tissue organization (macro-, micro-, and nano-levels) in aged individuals and individuals with chronic comorbidities (mainly in individuals with chronic liver disease, renal disorders, and type 2 diabetes mellitus). Also, variable frequency of fractures at different skeletal sites in aged persons and individuals with chronic diseases was shown, indicating that aging-related bone loss is not a uniform process. A complete understanding of the spatial pattern of impaired bone quality can aid in the targeted evaluation of individualized fracture risk. Establishing a firm connection between the results of the clinical assessment of bone status and the analysis of numerous structural and mechanical bone properties (on various hierarchical levels) can represent a solid base for developing adequate guidelines and algorithms for prevention and treatment of increased bone fragility in aged individuals and individuals with chronic diseases.

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Martínez-Montoro, José Ignacio, Beatriz García-Fontana, Cristina García-Fontana, and Manuel Muñoz-Torres. "Evaluation of Quality and Bone Microstructure Alterations in Patients with Type 2 Diabetes: A Narrative Review." Journal of Clinical Medicine 11, no. 8 (April 14, 2022): 2206. http://dx.doi.org/10.3390/jcm11082206.

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Bone fragility is a common complication in subjects with type 2 diabetes mellitus (T2DM). However, traditional techniques for the evaluation of bone fragility, such as dual-energy X-ray absorptiometry (DXA), do not perform well in this population. Moreover, the Fracture Risk Assessment Tool (FRAX) usually underestimates fracture risk in T2DM. Importantly, novel technologies for the assessment of one microarchitecture in patients with T2DM, such as the trabecular bone score (TBS), high-resolution peripheral quantitative computed tomography (HR-pQCT), and microindentation, are emerging. Furthermore, different serum and urine bone biomarkers may also be useful for the evaluation of bone quality in T2DM. Hence, in this article, we summarize the limitations of conventional tools for the evaluation of bone fragility and review the current evidence on novel approaches for the assessment of quality and bone microstructure alterations in patients with T2DM.

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Dei, Metella, and Claudia Succu. "Bone fragility in young people: significant anamnestic elements." International Journal of Bone Fragility 4, no. 1 (September 2, 2024): 11–15. http://dx.doi.org/10.57582/ijbf.240401.011.

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Various factors are known to interfere with gain in bone density and structure during growth and development. Bone status in childhood has been shown to be a predictor of bone mass in young adulthood. This concise review aims to discuss the main factors that can influence peak bone mass during growth and development, and whether they may be predictors of future bone fragility risk, useful for physicians taking care of children and adolescents. KEY WORDS: Children and adolescent bone health, peak bone mass, predictors of bone fragility, osteoporosis prevention.

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André, Grégoire, Antoine Chretien, Antoine Demoulin, Mélanie Beersaerts, Pierre-Louis Docquier, and Catherine Behets. "Col1A-2 Mutation in Osteogenesis Imperfecta Mice Contributes to Long Bone Fragility by Modifying Cell-Matrix Organization." International Journal of Molecular Sciences 24, no. 23 (November 30, 2023): 17010. http://dx.doi.org/10.3390/ijms242317010.

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Osteogenesis imperfecta (OI) is a rare congenital bone dysplasia generally caused by a mutation of one of the type I collagen genes and characterized by low bone mass, numerous fractures, and bone deformities. The collagen organization and osteocyte lacuna arrangement were investigated in the long bones of 17-week-old wildtype (WT, n = 17) and osteogenesis imperfecta mice (OIM, n = 16) that is a validated model of severe human OI in order to assess their possible role in bone fragility. Fractures were counted after in vivo scanning at weeks 5, 11, and 17. Humerus, femur, and tibia diaphyses from both groups were analyzed ex vivo with pQCT, polarized and ordinary light histology, and Nano-CT. The fractures observed in the OIM were more numerous in the humerus and femur than in the tibia, whereas the quantitative bone parameters were altered in different ways among these bones. Collagen fiber organization appeared disrupted, with a lower birefringence in OIM than WT bones, whereas the osteocyte lacunae were more numerous, more spherical, and not aligned in a lamellar pattern. These modifications, which are typical of immature and less mechanically competent bone, attest to the reciprocal alteration of collagen matrix and osteocyte lacuna organization in the OIM, thereby contributing to bone fragility.

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Amanullah, Md Farid, BP Shrestha, GP Khanal, NK Karna, S. Ansari, and K. Ahmad. "Evaluation of association of fragility fracture and bone mineral density in Nepalese population." Nepal Journal of Medical Sciences 2, no. 2 (October 17, 2013): 130–34. http://dx.doi.org/10.3126/njms.v2i2.8956.

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Background: Fragility fractures are one of the major health problems. Many factors are associated with it some of which are modifiable and some are not. If we know the value of T-score at which fragility fracture occurs and associated factors responsible for fragility fracture than we will be able to control this burden to the society. The objective of this study is to determine association between fragility fracture and bone mineral density (BMD) using bone densitometry and to know the value of T-score at which fragility fracture occurs. Methods: Patients presenting to B.P. Koirala Institute of Health Sciences with fragility fracture of distal end of radius, fracture around hip and vertebral fractures were included in the study to know the value of T-score at which fragility fracture occurs and their associated risk factor. Patients less than 50 years of age, high energy trauma fracture and pathological fractures were excluded from the study. Results: We found that being multipara, smoking, alcohol consumption, post-hysterectomized patients and steroid intake had significant association with fragility fracture. There was no association with religion, geographic location, associated medical illness, age, sex, associated injury and site of injury. Conclusion: The patients with risk factor for fragility fracture like smoking, alcohol consumption, multipara women, post-hysterectomized women and those who are on long term steroid therapy should undergo BMD test and the value at -3.254 are prone to fragility fracture and should be treated accordingly. Nepal Journal of Medical Sciences | Volume 02 | Number 02 | July-December 2013 | Page 130-134 DOI: http://dx.doi.org/10.3126/njms.v2i2.8956

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Ravikumar A S, Pradeep H, and Appu G. Pillai. "Humerus nail for tibial reconstruction in adolescent with osteogenesis imperfecta – A rare surgical case report." Indian Journal of Orthopaedics Surgery 8, no. 3 (September 15, 2022): 236–39. http://dx.doi.org/10.18231/j.ijos.2022.042.

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Osteogenesis Imperfecta (OI) is a rare connective tissue disorder known for excessive bone fragility caused by collagen mutations. The common orthopaedic problems related to bone fragility include frequent multiple bone fractures, progressive deformity of long bones leading to impaired ambulation. Surgical correction of long bone deformities in OI is conventionally done using distraction osteogenesis (illizarov fixator), elastic intramedullary nailing, rigid extramedullary fixation using plates, after osteotomy. Intramedullary fixation appears to be an ideal choice for correction of recurrent deformity in the long bone and the devices used previously include telescoping rods, single or dual non-elongating nails (rush nail, TENS). Recently in a case report of 3 individual patients, a humerus nail has been used to reconstruct femur in adolescents with OI. We report a case of humerus nailing for reconstruction of tibia in an adolescent OI male with excellent outcomes which is first of its kind and not reported previously by any other authors.

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Jbebli, Elhem, Samar Rhayem, Amdouni Rim, Faten Fedhila, and Monia Khemiri. "Difficulties in Managing Multifactorial Osteoporosis in an Adolescent with Demyelinating Neuropathy." International Journal of Current Research and Review 16, no. 18 (2024): 07–09. http://dx.doi.org/10.31782/ijcrr.2024.161802.

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Introduction: Secondary osteoporosis is rare in children/adolescents. Delays in the specific management of risk factors for bone fragility can lead to a silent loss of bone mass and an increased risk of early osteoporosis. We reported a case of a teenage girl with multifactorial bone fragility complicating a chronic neuropathy treated between 2021 and 2024. Case Report: A 15-year-old girl patient has been under observation for demyelinating sensorimotor neuropathy since the neonatal period. The condition was complicated by multiple skeletal deformities that have required surgical treatment. Bone fragility was noted intraoperatively. The etiologic diagnosis favored a multifactorial origin, including neurological, endocrine, nutritional, and mechanical factors. Treatment of the offending factors was inadequate. Osteoporosis was diagnosed in the presence of a zscore for bone densitometry below -2 standard deviation and multiple long bone fractures. The specific treatment of osteoporosis was limited by the lack of pediatric approval for most molecules. After a two-year course of symptomatic then specific treatment, there was a favorable clinical response and partial improvement in osteodensitometry. Conclusion: This clinical case illustrates the difficulty of managing multifactorial bone fragility leading to osteoporosis in a girl with chronic neuropathy, in terms of managing the incriminating factors and prescribing bisphosphonates.

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Journal articles on the topic 'Bone fragility'

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