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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Osteoarthritis &#40;OA&#41; is the most common rheumatic pathology and classically is associated with ageing&#46; Prevalence studies demonstrate that most individuals above 65 years present evidence of this pathology&#44; giving an idea of its enormous social impact&#46; Global estimates are that 9&#46;6&#37; of men and 18&#46;0&#37; of women over 60 have symptomatic OA&#46; OA is the first cause of permanent job incapacity&#59; it is one of the most frequent causes of incapacity in the elderly&#44; and also one of the most common reasons for primary care visits&#46; Between 2002 and 2007&#44; OA moved from the twelfth to the sixth leading cause of years lost by disability or morbidity &#40;World Health Organization &#40;WHO&#41; data&#41;&#46; US studies confirm that OA is responsible of 4 million hospitalizations and the loss of 68 million labour days per year&#46; Given the current rate&#47;tempo of population ageing&#44; it is estimated that the number of people who suffer from this disease will double in the next three decades&#46; Moreover&#44; they estimate the costs of an OA patient &#40;drugs&#44; medical visits&#44; radiographies&#44; etc&#46;&#41; at around 2000<span class="elsevierStyleHsp" style=""></span>dollars&#47;year&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">However&#44; although the social&#44; economic and health impact of OA is very high&#44; therapies are symptomatic and pursue only pain alleviation&#44; but have no effect on slowing down the progression of the disease&#46; At least three causes could explain the actual limitation of treating the OA progression&#46; One is the classical OA definition&#46; Although OA has a multifactorial aetiology&#44; for a long time it has been primarily associated with the breakdown of cartilage in joints&#46; A classical definition of OA is referred as a degenerative joint disease involving cartilage degradation&#44; synovial inflammation and subchondral bone sclerosis&#46; Nevertheless&#44; according to our actual knowledge any definition of OA must include degradation of the articular cartilage&#44; thickening of the subchondral bone&#44; osteophyte formation&#44; variable degrees of synovial inflammation&#44; degeneration of ligaments and&#44; in the knee&#44; the menisci&#44; and hypertrophy of the joint capsule&#46; There can also be changes in periarticular muscles&#44; nerves&#44; bursa&#44; and local fat pads that may contribute to OA or the symptoms of OA&#46; The findings of pathological changes in all of the joint tissues are the impetus for considering OA as a disease of the joint as an organ&#44; resulting in an organic dysfunction or joint failure&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Another explanation is regarding the diagnostic criteria of OA&#46; Currently&#44; the diagnosis of OA relies on the description of pain symptoms&#44; stiffness in the affected joints&#44; and radiography&#44; used as the reference technique for determining the grade of joint destruction&#46; Nevertheless&#44; X-ray offers only indirect information about the state of the cartilage&#44; such as narrowing of the joint space or the appearance of bony spurs &#40;osteophytes&#41;&#46; Moreover&#44; this procedure lacks sensitivity in detection of slight changes in the joint&#44; making it necessary to wait for several years in order to obtain feasible information about the progression of the disease&#46; Thus&#44; efficient strategies in detecting early phases of OA are essential for the development of new OA modifying therapies and for the evaluation of therapeutic answers&#46; These include the standardization of imaging techniques &#40;magnetic resonance imaging &#40;MRI&#41; and ultra-sound &#40;US&#41;&#41; and the identification of early biomarkers and molecular players of OA&#46; Both MRI and US are more sensitive than radiography in detection of cartilage degradation&#44; sinovitis&#44; subchondral bone modifications and any damaged tissue in the joint&#46; In the past few years&#44; new approaches in OA research such as genomic&#44; proteomic and metabolomic technologies are increasing the number of potential molecular biomarkers for the diagnosis and prognosis of OA&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Some of these biomarkers &#40;after clinical qualification&#41; in combination with the OA risk factors such as ageing&#44; heredity&#44; obesity&#44; and mechanical influences&#44; including joint injury or joint overuse could be parameters to define an index to predict the risk of developing OA similar to the cardiovascular index or FRAX&#46; All of these new approaches must help us with diagnosis of early OA &#40;symptomatic and asymptomatic OA&#41;&#44; and early diagnosis will permit earlier treatment to modify the course of this disease&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Finally&#44; OA has been considered and it has been treated as a unique disease&#44; without taking into account the different OA phenotypes&#46; Given our current understanding of OA pathogenesis this concept must change&#46; OA is emerging as a disease that has a variety of phenotypes including metabolic&#44; age-related&#44; inflammatory&#44; hormonal and injury-related phenotypes&#46; In addition&#44; although in some cases the patients present a clear phenotype&#44;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> in some patients the phenotype is overlapped&#46; From all phenotypes the metabolic phenotype is demonstrating high interest among the scientific community&#46; Evidence from both epidemiological and biological studies support the concept of metabolic OA&#44; defined as a broad clinical phenotype that includes obesity-related OA&#46; Interestingly&#44; studies have demonstrated associations linking OA to several components of the metabolic syndrome&#44; such as hypertension and type 2 diabetes&#44; independently from obesity or any of the other known risk factors for OA&#46; Thus&#44; it is clear that if we want to improve the health of patients with OA&#44; we must treat each OA phenotype with an appropriate therapy&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In conclusion&#44; OA is a prevalent&#44; disabling disease&#44; involving an organ &#40;the joint&#41;&#44; resulting in an organic dysfunction or joint failure that currently lacks disease-modifying treatments&#46; The ability to detect early OA as well as to characterize the OA phenotypes are crucial for understanding the disease process&#44; identifying potential disease-modifying treatments&#44; and evaluating the effectiveness of new therapies&#46;</p></span>"
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Editorial
Osteoarthritis: Something is moving
Artrosis: algo se mueve
Francisco J. Blanco
Servicio de Reumatología, INIBIC-Hospital Universitario A Coruña, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Osteoarthritis &#40;OA&#41; is the most common rheumatic pathology and classically is associated with ageing&#46; Prevalence studies demonstrate that most individuals above 65 years present evidence of this pathology&#44; giving an idea of its enormous social impact&#46; Global estimates are that 9&#46;6&#37; of men and 18&#46;0&#37; of women over 60 have symptomatic OA&#46; OA is the first cause of permanent job incapacity&#59; it is one of the most frequent causes of incapacity in the elderly&#44; and also one of the most common reasons for primary care visits&#46; Between 2002 and 2007&#44; OA moved from the twelfth to the sixth leading cause of years lost by disability or morbidity &#40;World Health Organization &#40;WHO&#41; data&#41;&#46; US studies confirm that OA is responsible of 4 million hospitalizations and the loss of 68 million labour days per year&#46; Given the current rate&#47;tempo of population ageing&#44; it is estimated that the number of people who suffer from this disease will double in the next three decades&#46; Moreover&#44; they estimate the costs of an OA patient &#40;drugs&#44; medical visits&#44; radiographies&#44; etc&#46;&#41; at around 2000<span class="elsevierStyleHsp" style=""></span>dollars&#47;year&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">However&#44; although the social&#44; economic and health impact of OA is very high&#44; therapies are symptomatic and pursue only pain alleviation&#44; but have no effect on slowing down the progression of the disease&#46; At least three causes could explain the actual limitation of treating the OA progression&#46; One is the classical OA definition&#46; Although OA has a multifactorial aetiology&#44; for a long time it has been primarily associated with the breakdown of cartilage in joints&#46; A classical definition of OA is referred as a degenerative joint disease involving cartilage degradation&#44; synovial inflammation and subchondral bone sclerosis&#46; Nevertheless&#44; according to our actual knowledge any definition of OA must include degradation of the articular cartilage&#44; thickening of the subchondral bone&#44; osteophyte formation&#44; variable degrees of synovial inflammation&#44; degeneration of ligaments and&#44; in the knee&#44; the menisci&#44; and hypertrophy of the joint capsule&#46; There can also be changes in periarticular muscles&#44; nerves&#44; bursa&#44; and local fat pads that may contribute to OA or the symptoms of OA&#46; The findings of pathological changes in all of the joint tissues are the impetus for considering OA as a disease of the joint as an organ&#44; resulting in an organic dysfunction or joint failure&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Another explanation is regarding the diagnostic criteria of OA&#46; Currently&#44; the diagnosis of OA relies on the description of pain symptoms&#44; stiffness in the affected joints&#44; and radiography&#44; used as the reference technique for determining the grade of joint destruction&#46; Nevertheless&#44; X-ray offers only indirect information about the state of the cartilage&#44; such as narrowing of the joint space or the appearance of bony spurs &#40;osteophytes&#41;&#46; Moreover&#44; this procedure lacks sensitivity in detection of slight changes in the joint&#44; making it necessary to wait for several years in order to obtain feasible information about the progression of the disease&#46; Thus&#44; efficient strategies in detecting early phases of OA are essential for the development of new OA modifying therapies and for the evaluation of therapeutic answers&#46; These include the standardization of imaging techniques &#40;magnetic resonance imaging &#40;MRI&#41; and ultra-sound &#40;US&#41;&#41; and the identification of early biomarkers and molecular players of OA&#46; Both MRI and US are more sensitive than radiography in detection of cartilage degradation&#44; sinovitis&#44; subchondral bone modifications and any damaged tissue in the joint&#46; In the past few years&#44; new approaches in OA research such as genomic&#44; proteomic and metabolomic technologies are increasing the number of potential molecular biomarkers for the diagnosis and prognosis of OA&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Some of these biomarkers &#40;after clinical qualification&#41; in combination with the OA risk factors such as ageing&#44; heredity&#44; obesity&#44; and mechanical influences&#44; including joint injury or joint overuse could be parameters to define an index to predict the risk of developing OA similar to the cardiovascular index or FRAX&#46; All of these new approaches must help us with diagnosis of early OA &#40;symptomatic and asymptomatic OA&#41;&#44; and early diagnosis will permit earlier treatment to modify the course of this disease&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Finally&#44; OA has been considered and it has been treated as a unique disease&#44; without taking into account the different OA phenotypes&#46; Given our current understanding of OA pathogenesis this concept must change&#46; OA is emerging as a disease that has a variety of phenotypes including metabolic&#44; age-related&#44; inflammatory&#44; hormonal and injury-related phenotypes&#46; In addition&#44; although in some cases the patients present a clear phenotype&#44;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> in some patients the phenotype is overlapped&#46; From all phenotypes the metabolic phenotype is demonstrating high interest among the scientific community&#46; Evidence from both epidemiological and biological studies support the concept of metabolic OA&#44; defined as a broad clinical phenotype that includes obesity-related OA&#46; Interestingly&#44; studies have demonstrated associations linking OA to several components of the metabolic syndrome&#44; such as hypertension and type 2 diabetes&#44; independently from obesity or any of the other known risk factors for OA&#46; Thus&#44; it is clear that if we want to improve the health of patients with OA&#44; we must treat each OA phenotype with an appropriate therapy&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In conclusion&#44; OA is a prevalent&#44; disabling disease&#44; involving an organ &#40;the joint&#41;&#44; resulting in an organic dysfunction or joint failure that currently lacks disease-modifying treatments&#46; The ability to detect early OA as well as to characterize the OA phenotypes are crucial for understanding the disease process&#44; identifying potential disease-modifying treatments&#44; and evaluating the effectiveness of new therapies&#46;</p></span>"
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2016 Julio 21 7 28
2016 Junio 0 6 6
2016 Abril 0 15 15
2016 Marzo 0 15 15
2016 Enero 0 21 21
2015 Diciembre 3 0 3
2015 Noviembre 1 22 23
2015 Octubre 1 16 17
2015 Septiembre 1 0 1
2015 Agosto 2 0 2
2015 Julio 29 9 38
2015 Junio 34 14 48
2015 Mayo 50 31 81
2015 Abril 44 17 61
2015 Marzo 31 16 47
2015 Febrero 42 0 42
2015 Enero 29 1 30
2014 Diciembre 39 0 39
2014 Noviembre 30 1 31
2014 Octubre 29 0 29
2014 Septiembre 31 0 31
2014 Agosto 42 0 42
2014 Julio 35 0 35
2014 Junio 61 0 61
2014 Mayo 41 0 41
2014 Abril 65 0 65
2014 Marzo 117 40 157
2014 Febrero 213 119 332
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