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Endothelial dysfunction and tendinopathy: how far have we come?
Symptomatic tendon tears are one of the most important causes of pain and joint dysfunction. Among the intrinsic causes, vascularization recently gained a major role. Endothelial function is indeed a key factor, as well as vascular tone and thrombotic factors, in the regulation of vascular homeostas...
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Published in: | Musculoskeletal surgery 2013-12, Vol.97 (3), p.199-209 |
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description | Symptomatic tendon tears are one of the most important causes of pain and joint dysfunction. Among the intrinsic causes, vascularization recently gained a major role. Endothelial function is indeed a key factor, as well as vascular tone and thrombotic factors, in the regulation of vascular homeostasis and the composition of vascular wall. In this review, we studied systematically whether there is a relationship between endothelial dysfunction and tendinopathy. A literature search was performed using the isolated or combined keywords endothelial dysfunction and tendon,’ ‘nitric oxide (NO) and tendinopathy,’ and ‘endothelial dysfunction in tendon healing.’ We identified 21 published studies. Of the selected studies, 9 were in vivo studies, 2 focusing on animals and 7 on humans, while 12 reported about in vitro evaluations, where 7 were carried out on humans and 5 on animals. The evidence about a direct relationship between tendinopathy and endothelial dysfunction is still poor. As recent studies have shown, there is no significant improvement in clinical and functional assessments after treatment with NO in patients suffering from tendinopathy in different locations. No significant differences were identified in the outcomes reported for experiment group when compared with controls treated with conventional surgical procedures or rehabilitation programs. Nitric oxide could be a marker to quantify the response of the endothelium to mechanical stress or hypoxia indicating the final balance between vasodilatating and vasoconstricting factors and their effects, but more ad stronger evidence is still needed to fully support this practice. |
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Among the intrinsic causes, vascularization recently gained a major role. Endothelial function is indeed a key factor, as well as vascular tone and thrombotic factors, in the regulation of vascular homeostasis and the composition of vascular wall. In this review, we studied systematically whether there is a relationship between endothelial dysfunction and tendinopathy. A literature search was performed using the isolated or combined keywords endothelial dysfunction and tendon,’ ‘nitric oxide (NO) and tendinopathy,’ and ‘endothelial dysfunction in tendon healing.’ We identified 21 published studies. Of the selected studies, 9 were in vivo studies, 2 focusing on animals and 7 on humans, while 12 reported about in vitro evaluations, where 7 were carried out on humans and 5 on animals. The evidence about a direct relationship between tendinopathy and endothelial dysfunction is still poor. As recent studies have shown, there is no significant improvement in clinical and functional assessments after treatment with NO in patients suffering from tendinopathy in different locations. No significant differences were identified in the outcomes reported for experiment group when compared with controls treated with conventional surgical procedures or rehabilitation programs. Nitric oxide could be a marker to quantify the response of the endothelium to mechanical stress or hypoxia indicating the final balance between vasodilatating and vasoconstricting factors and their effects, but more ad stronger evidence is still needed to fully support this practice.</description><identifier>ISSN: 2035-5106</identifier><identifier>EISSN: 2035-5114</identifier><identifier>DOI: 10.1007/s12306-013-0295-7</identifier><identifier>PMID: 23907599</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Aging ; Animals ; Apoptosis ; Biomarkers ; Cumulative Trauma Disorders - physiopathology ; Endothelium ; Endothelium, Vascular - physiopathology ; Enzyme Induction - drug effects ; Humans ; Inflammation ; Isoenzymes - genetics ; Isoenzymes - metabolism ; Medicine ; Medicine & Public Health ; Mice, Knockout ; Nitric oxide ; Nitric Oxide - blood ; Nitric Oxide - physiology ; Nitric Oxide - therapeutic use ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase - metabolism ; Nitroglycerin - pharmacology ; Nitroglycerin - therapeutic use ; Orthopedics ; Oxidative Stress - drug effects ; Rats ; Reactive Oxygen Species - metabolism ; Review ; RNA, Messenger - biosynthesis ; Surgical Orthopedics ; Tendinopathy - drug therapy ; Tendinopathy - etiology ; Tendinopathy - physiopathology ; Tendinopathy - rehabilitation ; Vasoconstriction - physiology ; Vasodilation - physiology</subject><ispartof>Musculoskeletal surgery, 2013-12, Vol.97 (3), p.199-209</ispartof><rights>Istituto Ortopedico Rizzoli 2013</rights><rights>COPYRIGHT 2013 Springer</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3977-6f98f48da28e4f775f43cfbf7fdbca10cfce7d174043cc4aec27a1fd072939cb3</citedby><cites>FETCH-LOGICAL-c3977-6f98f48da28e4f775f43cfbf7fdbca10cfce7d174043cc4aec27a1fd072939cb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23907599$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Papalia, R.</creatorcontrib><creatorcontrib>Moro, L.</creatorcontrib><creatorcontrib>Franceschi, F.</creatorcontrib><creatorcontrib>Albo, E.</creatorcontrib><creatorcontrib>D’Adamio, S.</creatorcontrib><creatorcontrib>Di Martino, A.</creatorcontrib><creatorcontrib>Vadalà, G.</creatorcontrib><creatorcontrib>Faldini, C.</creatorcontrib><creatorcontrib>Denaro, V.</creatorcontrib><title>Endothelial dysfunction and tendinopathy: how far have we come?</title><title>Musculoskeletal surgery</title><addtitle>Musculoskelet Surg</addtitle><addtitle>Musculoskelet Surg</addtitle><description>Symptomatic tendon tears are one of the most important causes of pain and joint dysfunction. Among the intrinsic causes, vascularization recently gained a major role. Endothelial function is indeed a key factor, as well as vascular tone and thrombotic factors, in the regulation of vascular homeostasis and the composition of vascular wall. In this review, we studied systematically whether there is a relationship between endothelial dysfunction and tendinopathy. A literature search was performed using the isolated or combined keywords endothelial dysfunction and tendon,’ ‘nitric oxide (NO) and tendinopathy,’ and ‘endothelial dysfunction in tendon healing.’ We identified 21 published studies. Of the selected studies, 9 were in vivo studies, 2 focusing on animals and 7 on humans, while 12 reported about in vitro evaluations, where 7 were carried out on humans and 5 on animals. The evidence about a direct relationship between tendinopathy and endothelial dysfunction is still poor. As recent studies have shown, there is no significant improvement in clinical and functional assessments after treatment with NO in patients suffering from tendinopathy in different locations. No significant differences were identified in the outcomes reported for experiment group when compared with controls treated with conventional surgical procedures or rehabilitation programs. Nitric oxide could be a marker to quantify the response of the endothelium to mechanical stress or hypoxia indicating the final balance between vasodilatating and vasoconstricting factors and their effects, but more ad stronger evidence is still needed to fully support this practice.</description><subject>Aging</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers</subject><subject>Cumulative Trauma Disorders - physiopathology</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Enzyme Induction - drug effects</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Isoenzymes - genetics</subject><subject>Isoenzymes - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice, Knockout</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - blood</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide - therapeutic use</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitroglycerin - pharmacology</subject><subject>Nitroglycerin - therapeutic use</subject><subject>Orthopedics</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Review</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Surgical Orthopedics</subject><subject>Tendinopathy - drug therapy</subject><subject>Tendinopathy - etiology</subject><subject>Tendinopathy - physiopathology</subject><subject>Tendinopathy - rehabilitation</subject><subject>Vasoconstriction - physiology</subject><subject>Vasodilation - physiology</subject><issn>2035-5106</issn><issn>2035-5114</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp1kUtLAzEQx4Movj-AF1nwvHXy2M3GSyniCwQveg5pHu2WblKTraXf3ki1KihzyDDz-08y-SN0hmGAAfhlwoRCXQKmJRBRlXwHHRKgVVlhzHa3OdQH6CilGUDNmkrsowNCBfBKiEM0vPEm9FM7b9W8MOvkll73bfCF8qborTetDwvVT9dXxTSsCqdiMVVvtljZQofODk_QnlPzZE8_z2P0cnvzfH1fPj7dPVyPHktNBedl7UTjWGMUaSxznFeOUe3Gjjsz1gqDdtpygzmDXNdMWU24ws4AJ4IKPabH6GIzdxHD69KmXs7CMvp8pcSsxtBkknxTEzW3svUu9FHprk1ajjiuGKeAcaYGf1A5jO1aHbx1ba7_EuCNQMeQUrROLmLbqbiWGOSHE3LjhMxOyA8nJM-a888HL8edNVvF19dngGyAlFt-YuOPjf6d-g67ZpGX</recordid><startdate>201312</startdate><enddate>201312</enddate><creator>Papalia, R.</creator><creator>Moro, L.</creator><creator>Franceschi, F.</creator><creator>Albo, E.</creator><creator>D’Adamio, S.</creator><creator>Di Martino, A.</creator><creator>Vadalà, G.</creator><creator>Faldini, C.</creator><creator>Denaro, V.</creator><general>Springer Milan</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>201312</creationdate><title>Endothelial dysfunction and tendinopathy: how far have we come?</title><author>Papalia, R. ; 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Among the intrinsic causes, vascularization recently gained a major role. Endothelial function is indeed a key factor, as well as vascular tone and thrombotic factors, in the regulation of vascular homeostasis and the composition of vascular wall. In this review, we studied systematically whether there is a relationship between endothelial dysfunction and tendinopathy. A literature search was performed using the isolated or combined keywords endothelial dysfunction and tendon,’ ‘nitric oxide (NO) and tendinopathy,’ and ‘endothelial dysfunction in tendon healing.’ We identified 21 published studies. Of the selected studies, 9 were in vivo studies, 2 focusing on animals and 7 on humans, while 12 reported about in vitro evaluations, where 7 were carried out on humans and 5 on animals. The evidence about a direct relationship between tendinopathy and endothelial dysfunction is still poor. As recent studies have shown, there is no significant improvement in clinical and functional assessments after treatment with NO in patients suffering from tendinopathy in different locations. No significant differences were identified in the outcomes reported for experiment group when compared with controls treated with conventional surgical procedures or rehabilitation programs. Nitric oxide could be a marker to quantify the response of the endothelium to mechanical stress or hypoxia indicating the final balance between vasodilatating and vasoconstricting factors and their effects, but more ad stronger evidence is still needed to fully support this practice.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>23907599</pmid><doi>10.1007/s12306-013-0295-7</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aging Animals Apoptosis Biomarkers Cumulative Trauma Disorders - physiopathology Endothelium Endothelium, Vascular - physiopathology Enzyme Induction - drug effects Humans Inflammation Isoenzymes - genetics Isoenzymes - metabolism Medicine Medicine & Public Health Mice, Knockout Nitric oxide Nitric Oxide - blood Nitric Oxide - physiology Nitric Oxide - therapeutic use Nitric Oxide Synthase - genetics Nitric Oxide Synthase - metabolism Nitroglycerin - pharmacology Nitroglycerin - therapeutic use Orthopedics Oxidative Stress - drug effects Rats Reactive Oxygen Species - metabolism Review RNA, Messenger - biosynthesis Surgical Orthopedics Tendinopathy - drug therapy Tendinopathy - etiology Tendinopathy - physiopathology Tendinopathy - rehabilitation Vasoconstriction - physiology Vasodilation - physiology |
title | Endothelial dysfunction and tendinopathy: how far have we come? |
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