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Books on the topic 'Bone fragility'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 April 2025

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1

Uhthoff, Hans K., ed. Current Concepts of Bone Fragility. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70709-4.

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2

1925-, Uhthoff Hans K., Stahl Elvira, and Applied Basic Science Course (12th : 1985 : Ottawa, Ont.), eds. Current concepts of bone fragility. Berlin: Springer-Verlag, 1986.

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3

Culbert, Ainsley Amanda. Studies of the molecular basis of bone fragility in individuals with osteogenesis imperfecta. Manchester: University of Manchester, 1996.

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4

Evans, E. P. Credit quality spreads, bond market efficiency and financial fragility. London: LSE Financial Markets Group, 1990.

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5

Uhthoff, Hans K., and Elvira Stahl. Current Concepts of Bone Fragility. Springer London, Limited, 2011.

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6

Uhthoff, Hans K., and Elvira Stahl. Current Concepts of Bone Fragility. Springer London, Limited, 2012.

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7

Current Concepts of Bone Fragility. Springer, 1986.

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8

Uhthoff, Hans K. Current Concepts of Bone Fragility. Island Press, 1986.

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9

Javaid, Kassim. Osteoporosis and fragility fracture. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0275.

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Osteoporosis is defined as a systemic bone disease with reduction in both bone density and microarchitectural integrity, resulting in an increase in fragility fracture risk. It is a multifactorial disease which, through effects on bone formation and resorption, reduces the peak bone mass achieved during early adulthood and increases the rate of bone loss in later adulthood. Osteoporosis is clinically silent until a fragility fracture occurs. There are 3 million patients with osteoporosis in the UK, with over 200 000 fractures per year and 80 000 hip fractures. This chapter addresses the causes, clinical features, diagnosis, and management of osteoporosis.

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10

Lappe, Joan Marie. RISK FACTORS FOR BONE FRAGILITY: A LONGITUDINAL STUDY. 1992.

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11

Foster, Helen, and Paul A. Brogan, eds. Bone diseases, skeletal dysplasias, disorders of collagen. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199592630.003.0005.

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Metabolic bone diseases 330Skeletal dysplasias 333The osteochondroses 343Heritable disorders of connective tissue 346• Principal features are bone fragility and low bone mass leading to fractures and bone deformity with growth retardation.• Ligamentous laxity, dentinogenesis imperfecta, and blue scleral hue are variable features. 90% of OI dominantly inherited due to defects in the type ↑ collagen genes ...

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12

Price, Susan. Genetic bone and joint disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0276.

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Genetic conditions affecting the skeleton and supporting structures are individually rare and heterogeneous. This chapter presents an approach to assessing patients with suspected skeletal dysplasia, osteogenesis imperfecta, Marfan syndrome, and Ehlers–Danlos syndrome. Skeletal dysplasias are caused by abnormalities of bone growth and modelling; the commonest non-lethal type is achondroplasia, with an incidence of 1/10 000 to 1/30 000. The typical presentation of osteogenesis imperfecta is with multiple fractures, sometimes prenatally. There may be associated short stature, bone deformity, dentogenesis imperfecta, blue sclera, and hearing loss. Most patients with osteogenesis imperfecta have mutations in COL1A1 or COL1A2. Marfan syndrome is a connective tissue disease with a pattern of symptoms related to the presence of fibrillin in tissues. Typically, affected individuals are of tall, thin stature, with long fingers and toes (arachnodactyly), a pectus deformity, and scoliosis. Between 66% and 91% of individuals with Marfan syndrome have a mutation in fibrillin-1 (FBN1; locus: 15q21). All forms of Ehlers–Danlos syndrome present with variable thinning and fragility of skin, leading to easy bruising and poor scar formation. There is skin and joint laxity. In severe forms, blood vessels and internal organs are affected.

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13

Rowe, Elisabeth Jane. Can a growth hormone-derived peptide (AOD9604) prevent bone loss and fragility in a rat model of osteoporosis? 2007.

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14

Kakascik, Aimee G. Osteogenesis Imperfecta. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0061.

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Osteogenesis imperfecta (OI) is a genetic disorder that affects collagen formation and ultimately leads to increased bone fragility. The fragile nature of the bones leads to fractures, even from seemingly normal patient care. Affected patients are at the highest risk for unintentional fractures during perioperative care. There are several different types of OI. Type I is the most common. With the different types come varying degrees of severity. Types II and III are the more severe forms. The classic clinical triad seen in OI is blue sclerae, multiple fractures, and conductive hearing loss. The patient may have other systemic involvement beyond the fragile musculoskeletal system. It is imperative that the anesthesiologist be well-versed in the natural history and perioperative management of patients with OI in order to optimize care and minimize complications.

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15

Magliano, Malgorzata. Osteoporosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.010006.

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♦ Osteoporotic fractures affect one in two women and one in five men over the age of 50♦ Previous fragility fracture increases future fracture risk and should prompt further assessment and treatment♦ Clinical risk factors in combination with bone mineral density measurement allow identifying patients at risk♦ Screening for secondary causes of osteoporosis is important, particularly in men and younger women♦ Patients at high risk for future fracture should be offered appropriate treatment. Bisphosphonates together with adequate calcium and vitamin D supplementation constitute first-line therapy♦ Compliance with treatment and clinical response need to be monitored.

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16

Hill, Uta, Jane Ashbrook, and Charles Haworth. Metabolic and musculoskeletal effects of cystic fibrosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0009.

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This chapter provides a comprehensive update on the prevention, recognition, and treatment of low bone mineral density in people with CF. As life expectancy improves, the extra-pulmonary complications of CF are becoming increasingly important to quality of life. Up to 25 per cent of CF patients have reduced bone mineral density in adulthood, leading to the development of fragility fractures which cause pain, thereby interfering with airway clearance and predisposing to pulmonary infection. Osteoporosis can be a relative contraindication for lung transplantation. Other important musculoskeletal issues including CF arthropathy, growth, and urinary incontinence are covered. CF arthropathy is a non-erosive episodic sero-negative arthritis, often difficult to treat and which may require specialist input. Urinary incontinence is common girls and women with CF and has a negative impact on quality of life and ability to complete therapies. The pathophysiology and management of urinary incontinence are discussed.

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17

Bell, Tanvir K. Musculoskeletal Complications of HIV. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0043.

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Vitamin D levels have been observed to be low in HIV-infected patients. If replacement of low vitamin D is warranted, supplementation is done with vitamin D2 or D3. HIV-infected patients may be at higher risk for osteopenia, osteoporosis, and fragility fractures. Tenofovir alafenamide has been shown to produce less bone loss compared to tenofovir disoproxil fumarate. Muscle disorders can be debilitating in HIV-infected patients. Myopathies can have a range of presentation from myalgias to rhabdomyolysis. HIV myopathy is a rare proximal muscle disorder that can occur in HIV-infected patients. Antiretroviral drugs, including zidovudine and raltegravir, can cause myopathy and elevated creatine kinase.

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18

Friedlaender, Gary E., and Jason A. Lowe. Osteoporosis and Fragility Fractures, an Issue of Orthopedic Clinics. Elsevier, 2013.

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