2012
DOI: 10.1038/nrrheum.2012.80
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Mechanisms and targets of angiogenesis and nerve growth in osteoarthritis

Abstract: During osteoarthritis (OA), angiogenesis is increased in the synovium, osteophytes and menisci and leads to ossification in osteophytes and the deep layers of articular cartilage. Angiogenic and antiangiogenic factors might both be upregulated in the osteoarthritic joint; however, vascular growth predominates, and the articular cartilage loses its resistance to vascularization. In addition, blood vessel growth is increased at--and disrupts--the osteochondral junction. Angiogenesis in this location is dependent… Show more

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Cited by 437 publications
(400 citation statements)
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“…One possible mechanism of the first immediate improvement is that decreasing abnormal blood flow somehow reduced the accompanying sensory nerve stimulation. It is already known that inflammation leads to angiogenesis and sensory nerve growth along new blood vessels in osteoarthritic joints [13]. In the immunohistochemical analysis, neovessels and accompanying nerve growth have been reported in synovium [14] and fat pads [15,16] of osteoarthritic joints.…”
Section: Discussionmentioning
confidence: 97%
“…One possible mechanism of the first immediate improvement is that decreasing abnormal blood flow somehow reduced the accompanying sensory nerve stimulation. It is already known that inflammation leads to angiogenesis and sensory nerve growth along new blood vessels in osteoarthritic joints [13]. In the immunohistochemical analysis, neovessels and accompanying nerve growth have been reported in synovium [14] and fat pads [15,16] of osteoarthritic joints.…”
Section: Discussionmentioning
confidence: 97%
“…The presence of these reactions in both cohorts is noteworthy because these reactions have been implicated in the development of pain. Specifically, increased vascularization (angiogenesis) and sensory nerve growth are closely linked processes [5,24]; and tissue necrosis or cell death results in the release of proinflammatory cytokines and other factors that initiate persistent pain by directly activating nociceptive sensory neurons [6,38]. Both reactions can lead to maladaptive plasticity and neural disease states, which raises the question whether these tissue responses contributed to neuropathic pain in both fixed-and mobile-bearing L-TDR patients.…”
Section: Discussionmentioning
confidence: 99%
“…Ангиогенез -процесс образования новых крове-носных сосудов в органе или ткани -также может уча-ствовать в формировании боли, поскольку рост крове-носных сосудов и сенсорных нейронов является инте-гративным процессом [39]. Повышение активности ан-гиогенеза у больных ОА наблюдали при росте остеофи-тов [40], в суставном хряще [28], синовии [41] и мениске [42].…”
unclassified
“…Повышение активности ан-гиогенеза у больных ОА наблюдали при росте остеофи-тов [40], в суставном хряще [28], синовии [41] и мениске [42]. Проангиогенными факторами, которые продуци-руются хондроцитами, синовиоцитами, а также в суб-хондральной кости и костном мозге, внутри сустава, при ОА являются простагландины, окись азота, цитоки-ны, хемокины и факторы роста, ключевым из которых является сосудистый эндотелиальный фактор роста (СЭФР) [39]. При этом суставной хрящ при ОА менее устойчив к ангиогенезу в связи с потерей протеоглика-нов, синтезом коллагенов типов I и X вокруг врастаю-щих сосудов, что представляет собой фенотипический сдвиг от хряща к костеобразованию после прорастания сосудов [43].…”
unclassified
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