Books on the topic 'Osteoarthritis Risk factors'
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1
Prescott, Vanessa. A picture of osteoarthritis in Australia. Canberra: Australian Institute of Health and Welfare, 2007.
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2
Prescott, Vanessa. A picture of osteoarthritis in Australia. Canberra: Australian Institute of Health and Welfare, 2007.
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3
Doherty, Michael. Osteoarthritis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0266.
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Osteoarthritis (OA) is a disorder of synovial joints and is characterized by the combination of focal hyaline cartilage loss and accompanying subchondral bone remodelling and marginal new bone formation (osteophyte). It has genetic, constitutional, and environmental risk factors and presents a spectrum of clinical phenotypes and outcomes. OA commonly affects just one region (e.g. knee OA, hip OA). However, multiple hand interphalangeal joint OA, usually accompanied by posterolateral firm swellings (nodes), is a marker for a tendency towards polyarticular ‘generalized nodal OA’.
4
Abhishek, Abhishek, and Michael Doherty. Epidemiology and risk factors for calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0048.
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Calcium pyrophosphate crystal deposition (CPPD) is rare in younger adults but becomes increasingly common over the age of 55 years, especially at the knee. Ageing and osteoarthritis (OA) are the main attributable risk factors. Hyperparathyroidism, hypomagnesaemia, haemochromatosis, and hypophosphatasia are other less common risk factors. Rare families with familial CPPD have been reported from many different parts of the world, and mainly present as young-onset polyarticular CPPD. Recent studies suggest that CPPD occurs as the result of a generalized constitutional predisposition and may also associate with low cortical bone mineral density. Previous meniscectomy, joint injury, and constitutional knee malalignment are local biomechanical risk factors specifically for knee chondrocalcinosis. Although associated with OA, current evidence suggests that CPPD does not associate with development or progression of OA.
5
Vincent, Tonia L., and Linda Troeberg. Pathogenesis of osteoarthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0138.
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Understanding pathogenic mechanism in disease is critical for development of targeted therapeutic strategies. Although there are, at this time, only a handful of experimental approaches for treating osteoarthritis (OA), until 10 years ago this disease was almost universally considered an unmodifiable condition. Emerging data during this time, largely fuelled by studies in rodent models, has completely changed the paradigm of disease pathogenesis and has for the first time, generated novel, realistic targets for this highly prevalent and disabling condition. These targets include the aggrecanases, members of the ADAMTS family, and collagenases, which together are critical for the early breakdown of the extracellular matrix of cartilage. Some recent success has also been demonstrated by targeting bone in disease. Development of pain in OA is complex and likely arises from different tissues at different stages of disease. In the following section we describe the pathological features of OA, and discuss the evolution of theories of OA pathogenesis and factors that have limited mechanistic clarity in this disease. We summarize the molecular pathways that are now known to be active in disease, and consider how these identified molecular pathways could be linked to known epidemiological risk factors. We finish by discussing possible future therapeutic strategies that will emerge from these discoveries and the current limitations in implementing new therapies in OA.
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Doherty, Michael, Johannes Bijlsma, Nigel Arden, David J. Hunter, and Nicola Dalbeth. Introduction: what is osteoarthritis? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0001.
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This brief introductory chapter summarizes some of the key clinical and structural features of osteoarthritis (OA) and highlights some general observations and concepts concerning the nature of OA. General observations include the preservation of OA throughout human evolution; the occurrence of OA in many other animals; the dynamic, metabolically active nature of OA pathophysiology; the fact that most OA never associates with symptoms or functional impairment; and the good outcome in many cases of symptomatic OA. Such observations support the concept of OA as the inherent repair process of synovial joints, which can be triggered by a range of diverse insults and in which all the joint tissues are involved. Aetiologically, OA is a common complex disorder with recognized genetic, constitutional, and environmental risk factors, and these may combine in multiple ways to cause marked variation in phenotypic presentation and in some instances ‘joint failure’ with associated symptoms and disability. Within the spectrum of OA are some discrete subsets, the best defined being nodal generalized OA. However, in many people OA does not fit neatly into one type and its phenotypic characteristics may change as it evolves. Two striking associations of OA are with ageing and with crystal deposition, especially calcium crystals but also urate crystals, and there are a number of possible mechanisms to explain these.
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Doherty, Michael, David J. Hunter, Hans Bijlsma, Nigel Arden, and Nicola Dalbeth, eds. Oxford Textbook of Osteoarthritis and Crystal Arthropathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.001.0001.
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The Oxford Textbook of Osteoarthritis and Crystal Arthropathy provides full coverage of joint failure, and includes detailed sections on epidemiology, risk factors, clinical assessment, and investigations. There are also new in-depth sections on gout and other crystal arthropathies. Clinically relevant and easily understandable overviews of basic science, including pathology and pain physiology, along with critical appraisal of current guidelines, make this a highly valuable resource. Significant coverage is also given to patient education and the involvement of the patient in management planning.
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L, Sutton Amy, ed. Arthritis sourcebook: Basic consumer health information about the risk factors, symptoms, diagnosis, and treatment of osteoarthritis, rheumatoid arthritis, juvenile arthritis, gout, infectious ... 3rd ed. Detroit, MI: Omnigraphics, 2010.
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9
Dekker, Joost, Daniel Bossen, Jasmijn Holla, Mariëtte de Rooij, Cindy Veenhof, and Marike van der Leeden. Psychological strategies in osteoarthritis of the knee or hip. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0025.
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Characteristic clinical presentations of osteoarthritis (OA) include pain and activity limitations. These presentations are dependent on psychological processes. The literature reviewed in this chapter leads to the following conclusions: (1) symptoms of depression, anxiety, and fatigue are more prevalent among patients with OA than among the general population. Recently, a depressive mood phenotype has been identified in knee OA. (2) Symptoms of depression, anxiety, and fatigue, as well as other psychological variables are established risk factors for future worsening of pain and activity limitations. (3) Psychological interventions such as depression care and pain coping skills training have been demonstrated to improve pain and activity limitations, as well as psychological outcomes. Self-management may have beneficial effects, although there is clearly room for improvement. Interventions combining psychological interventions with exercise therapy have been shown to be effective; improved outcome over exercise therapy alone stills needs to be demonstrated. (4) Psychological interventions are effective in improving exercise adherence and promoting physical activity. Overall, it can be concluded that the psychological approach towards OA is fruitful: the psychological approach has resulted in substantial contributions to the understanding and management of clinical presentations of OA, including pain and activity limitations.
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Runhaar, Jos, and Sita M. A. Bierma-Zeinstra. Lifestyle. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0012.
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Modern lifestyles put a great burden on the human musculoskeletal system. Since 1980, the worldwide prevalence of obesity has tripled in many European countries. Obesity is known to affect both weight-bearing and non-weight-bearing joints due to a combination of mechanical overload and systemic inflammation. On the other hand, both to combat the obesity pandemic and to increase or maintain the quality of life, physical activity and sports are encouraged next to a healthy diet. Although both have a positive influence on cardiovascular risk factors, physical activity and especially sporting activities do lead to increased loading of the active joints and increased risk for joint injuries, which might lead to osteoarthritis development. This chapter provides an overview of the current knowledge on lifestyle risk factors for the development and progression of osteoarthritis as published in recent systematic reviews, complemented with several narrative reviews.
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Calisoff, Randy L., and David R. Walega. Chronic Knee Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0010.
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Chronic knee pain affects 27 million people in the United States and is a leading cause of disability. Seventy percent of the population 65 years or older will have knee pain with radiographic evidence of osteoarthritis, and 12% will have clinical symptoms of osteoarthritis. Chronic knee pain after total knee replacement ranges from 10% to 20%. Patellofemoral pain syndrome (PFPS) refers to anterior knee pain exacerbated with knee joint loading activities (squatting, kneeling, prolonged sitting, ascending/descending stairs). PFPS is a clinical diagnosis, and treatment is directed toward pain alleviation and restoration of proper biomechanics. Pes anserine syndrome is common in runners, athletes, and individuals with osteoarthritis of the knee. Other risk factors include: female sex and a history of diabetes mellitus, obesity, or arthritis. Knowledge of the common knee pain etiologies, as well as key clinical manifestations, physical exam findings, differential diagnosis, and treatment options for each is important for pain specialists.
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Valdes, Ana M. Genetics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0009.
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Epidemiological studies have demonstrated that osteoarthritis (OA) is a complex trait with numerous environmental and genetic risk factors. A great deal of effort has been spent elucidating these risk factors and progress has been made. It is clear however that the causes behind OA development and progression continue to remain largely elusive. Identification of those genes that, in conjunction with environmental factors, predispose to OA severity will lead to a better understanding of the mechanisms underlying disease development and thus promote improved health strategies for prevention. An understanding of the molecular signalling pathways involved in the initiation and progression of the disease will improve clinical diagnosis and help identify improved, tailored treatment regimens. This chapter focuses on these issues, exploring the heritability of OA, known genetic risk factors, and specific traits and outcomes studied in the genetics of OA.
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Roddy, Edward, and Michael Doherty. Calcium pyrophosphate crystal deposition (CPPD). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0142.
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Calcium pyrophosphate crystal deposition (CPPD) in articular cartilage is a common age-related phenomenon. Recent important advances in our understanding of the pathophysiology of pyrophosphate metabolism include the identification of a mutation within the ANK gene which associates with familial CPPD, and elucidation of the interleukin-1β (IL-1β)-dependent mechanisms by which crystals invoke an inflammatory response. Risk factors for CPPD include age, prior joint damage and osteoarthritis, genetic factors, and occasionally metabolic diseases (hyperparathyroidism, haemochromatosis, hypomagnesaemia, and hypophosphatasia). CPPD is commonly asymptomatic or may present as osteoarthritis with CPPD, acute calcium pyrophosphate (CPP) crystal arthritis, or chronic CPP crystal inflammatory arthritis. Although radiographic chondrocalcinosis is often taken to be synonymous with CPPD, other calcium crystals can also have this appearance and definitive diagnosis requires identification of CPP crystals by compensated polarized light microscopy of aspirated synovial fluid. Recently, the ultrasonographic appearances of CPPD have been described. Treatment of CPPD is targeted to the clinical presentation. Acute CPP crystal arthritis is treated by aspiration and injection of glucocorticosteroid, local ice packs, non-steroidal anti-inflammatory drugs (NSAIDS), low-dose colchicine, oral or parenteral glucocorticosteroids, or adrenocorticotrophic hormone (ACTH). Treatment of osteoarthritis with CPPD is very similar to the treatment of osteoarthritis alone. There is no specific therapy for chronic CPP crystal inflammatory arthritis: options include NSAID, low-dose colchicine, low-dose glucocorticosteroid, methotrexate, and hydroxychloroquine. Recommendations for the management of CPPD are derived from a small evidence base and largely based on clinical experience and extrapolation from gout. Further research into diagnosis and management including novel treatment strategies such as IL-1β blockade is much needed.
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Walsh, David A. Contextual aspects of pain: why does the patient hurt? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0014.
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The context in which osteoarthritis (OA) pain is experienced moderates and, to an extent, mediates its severity and impact. Context is both internal to the patient (e.g. genes, gender, age, comorbidities, psychological distress, and catastrophizing), and a consequence of external factors (e.g. social, healthcare, and work environment). Context influences how people report their pain, and also how the nervous system processes nociceptive information. Treatment contexts moderate and mediate therapeutic effectiveness, dependent on treatment expectations, beliefs, and risk evaluation. Uptake of treatments, both in primary and secondary care, is further influenced by the contexts in which they are offered. Understanding the nature and consequences of context helps explain heterogeneity between different people with OA pain, and opens avenues for potentially powerful interventions that could improve their quality of life. Context can be adjusted through the clinician–patient relationship and by targeting risk factors for poor outcome. Concurrent weight reduction, and psychological and physiotherapeutic interventions illustrate the use of combination therapy to address multiple contextual aspects of OA pain.
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Arden, Nigel, and Michael C. Nevitt. Epidemiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0008.
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Despite the impact of osteoarthritis (OA) on patients and the health service, OA remains an elusive condition to define and treat. Traditionally, OA has been diagnosed using radiographs and more recently magnetic resonance imaging; however, the last 20 years of research have changed our thinking about the disease and its treatment. We know today that OA takes up to 10–15 years to develop, has a range of risk factors, and that there is a considerable discordance between symptoms and structural signs, such that new classifications and definitions are moving away from structural criteria to combined structure and pain definitions. This chapter reviews the definition and classification of OA and its prevalence, incidence, and natural history.
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Aspden, Richard, and Jenny Gregory. Morphology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0011.
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The study of joint morphology can help us to understand the risk factors for osteoarthritis (OA), how it progresses, and aids in developing imaging biomarkers for study of the disease. OA results in gross structural changes in affected joints. Growth of osteophytes, deformation of joint components, and loss of joint space where cartilage has broken down are all characteristics of the disorder. Certain bone shapes as well as malalignment predispose people to future OA, or may be a marker for early OA. Geometrical measures, such as the alpha angle or Wiberg’s CE angle, used to be the primary tool for investigating morphology. In recent years, however, statistical shape modelling (SSM) has become increasingly popular. SSM can be used with any imaging modality and has been successfully applied to a number of musculoskeletal conditions. It uses sets of landmark points denoting the anatomy of one or more bones to generate new variables (modes) that describe and quantify the shape variation in a set of images via principal components analysis. With the aid of automated search algorithms for point placement, the use of SSMs is expanding and provides a valuable and versatile tool for exploration of bone and joint morphometry. Whilst the majority of research has focused on hip and knee OA, this chapter provides an overview of joint morphology through the whole skeleton and how it has helped our ability to understand and quantify the risk and progression of osteoarthritis.
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Henriksen, Marius, Robin Christensen, Berit L. Heitmann, and Henning Bliddal. Weight loss. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0023.
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Obesity is widely acknowledged as a risk factor for both the incidence and progression of osteoarthritis. Loss of at least 10% of body weight is recognized as a cornerstone in the management of obese patients with osteoarthritis, and can lead to significant improvement in symptoms, pain relief, physical function, and health-related quality of life. However, questions still remain surrounding optimal management and whether structural disease progression can be arrested. Given the significant health, social, and economic burden of osteoarthritis, especially in obese patients, it is imperative to advance our knowledge of osteoarthritis and obesity, and apply this to improve care and outcomes. This chapter overviews what is known about osteoarthritis, obesity, and weight loss and discusses current key challenges in management and maintenance of weight loss for overweight and obese individuals with osteoarthritis.
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Brand, Caroline A., and Ilana N. Ackerman. Delivery (organization and outcome). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0036.
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This chapter considers the organization and delivery of care for osteoarthritis (OA) within the broader context of chronic condition management, and with a specific focus on the current OA literature. It describes factors that have influenced healthcare reforms for people with chronic conditions such as OA, and the development and characteristics of chronic condition models of care. The chapter also examines existing models of care for OA, which are commonly multidisciplinary in nature and situated within primary care, community care, or secondary/tertiary care settings. It summarizes current evidence for the effectiveness and cost-effectiveness of OA models of care, acknowledging that limited data are available regarding access and efficiency outcomes. Barriers to the successful development, implementation, and sustainability of OA models of care are discussed, as well as enablers that could facilitate the success of models of care. The chapter also presents points to consider when planning the implementation and evaluation of models of care, such as the development of a program logic, use of theoretical models or frameworks, and careful selection of appropriate research designs (including mixed-methods approaches). Finally, it considers future challenges for OA models of care, particularly the rise of multi-morbidity among patient populations that will necessitate integrated chronic condition management rather than stand-alone OA services. Future models of care may require the design of specific OA modules that can be integrated with generic chronic condition models that address risk behaviour modification and optimize self-management and mental health outcomes.
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Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards, and Cyrus Cooper. Environment. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0038.
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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.
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Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards, and Cyrus Cooper. Environment. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0038_update_001.
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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.
21
Manek, Nisha J., and George Muñoz. Common Rheumatic Diseases in the Elderly. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0022.
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With increasing longevity, the prevalence and impact of rheumatic diseases are projected to rise dramatically in the coming decades. Common rheumatic diseases such as osteoarthritis typically arise among the elderly. For diseases such as rheumatoid arthritis and gout, patients diagnosed at earlier ages carry the burden into their later years. Gout is associated both with comorbid conditions whose prevalence rises with age as well as with medications commonly prescribed in older people. These factors, along with the unique challenges associated with optimal diagnosis and treatment of arthritides in the elderly, suggest we can expect a “perfect storm” of health challenges for older patients and their health care providers. The chapter reviews the most common rheumatic diseases in geriatric patients and the evidence base for complementary and integrative therapies. In most cases, a multidisciplinary approach is beneficial.
22
Bannwarth, Bernard, and Francis Berenbaum. Systemic analgesics (including paracetamol and opioids). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0029.
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Apart from non-steroidal anti-inflammatory drugs (NSAIDs), there are only two categories of systemic analgesics, namely paracetamol (acetaminophen) and opioids, that are currently available worldwide for clinical use. Paracetamol is poorly effective in relieving pain and improving function in patients with symptomatic osteoarthritis (OA). Furthermore, its safety profile is less favourable than classically thought. In fact, there is evidence paracetamol acts as a weak inhibitor of the cyclooxygenase enzymes. Given that paracetamol poses a lower risk of severe adverse events than NSAIDs while being better tolerated than opioids, it is usually considered as the first-line systemic analgesic for OA. Commonly prescribed opioids are primarily agonists of the mu receptors, thereby producing similar desirable (analgesia) and untoward effects. Meta-analyses of short-term clinical trials showed that, on average, the modest clinical benefits of opioids did not outweigh the side effects in patients with knee or hip OA. Accordingly, most current guidelines support the use of opioids for selected OA patients only (e.g. patients who have not had an adequate response to other treatment modalities and are not candidates for total joint arthroplasty). In view of the limited efficacy and/or potential harms of available analgesics, particular attention was paid to novel painkillers, especially nerve growth factor (NGF) antagonists. Although these agents provided clinically meaningful improvements in pain and physical function in patients with hip or knee OA, they lead to severe side effects, including rapidly destructive arthropathies and neuropathies. Thus, if approved for marketing, NGF antagonists would be reserved for selected and well-defined patients with OA.