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dc.contributor.authorWixted, John J.
dc.contributor.authorFanning, Paul J.
dc.contributor.authorRothkopf, Ian
dc.contributor.authorStein, Gary S.
dc.contributor.authorLian, Jane B.
dc.date2022-08-11T08:10:08.000
dc.date.accessioned2022-08-23T16:56:39Z
dc.date.available2022-08-23T16:56:39Z
dc.date.issued2010-08-26
dc.date.submitted2011-05-26
dc.identifier.citationJ Orthop Trauma. 2010 Sep;24(9):539-42. <a href="http://dx.doi.org/10.1097/BOT.0b013e3181f17b33">Link to article on publisher's site</a>
dc.identifier.issn0890-5339 (Linking)
dc.identifier.doi10.1097/BOT.0b013e3181f17b33
dc.identifier.pmid20736790
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42976
dc.description.abstractNot all fractures heal well or rapidly in the adult skeleton, and basic scientists and clinicians continue to search for ways to make fractures heal more predictably. It is a fundamental tenet of orthopaedics that skeletal injury is followed by inflammation and that this inflammatory response is the first stage in a sequence of events that culminate in skeletal repair. Modulating this response can affect the inflammatory stage and in turn subsequent stages that are required for healing. Literally dozens of studies in animals dating back to the 1970s have investigated the effects of commonly used anti-inflammatory medications on prostaglandin synthesis and fracture repair with strikingly uniform results. More recently, investigators have begun examining other means of modulating the early inflammatory stages after fracture in an effort to enhance fracture healing. This article reviews recent investigations into the potential role of leukotrienes as negative regulators of fracture healing and potential pharmacologic use of medications that block this effect.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20736790&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1097/BOT.0b013e3181f17b33
dc.subjectAnimals
dc.subjectArachidonic Acid
dc.subjectCartilage, Articular
dc.subjectChondrogenesis
dc.subjectEicosanoids
dc.subjectFracture Healing
dc.subjectFractures, Bone
dc.subjectHumans
dc.subjectInflammation
dc.subjectInflammation Mediators
dc.subjectLeukotriene Antagonists
dc.subjectLeukotrienes
dc.subjectOrthopedics
dc.subjectRehabilitation and Therapy
dc.titleArachidonic acid, eicosanoids, and fracture repair
dc.typeJournal Article
dc.source.journaltitleJournal of orthopaedic trauma
dc.source.volume24
dc.source.issue9
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/ortho_pp/18
dc.identifier.contextkey2032256
html.description.abstract<p>Not all fractures heal well or rapidly in the adult skeleton, and basic scientists and clinicians continue to search for ways to make fractures heal more predictably. It is a fundamental tenet of orthopaedics that skeletal injury is followed by inflammation and that this inflammatory response is the first stage in a sequence of events that culminate in skeletal repair. Modulating this response can affect the inflammatory stage and in turn subsequent stages that are required for healing. Literally dozens of studies in animals dating back to the 1970s have investigated the effects of commonly used anti-inflammatory medications on prostaglandin synthesis and fracture repair with strikingly uniform results. More recently, investigators have begun examining other means of modulating the early inflammatory stages after fracture in an effort to enhance fracture healing. This article reviews recent investigations into the potential role of leukotrienes as negative regulators of fracture healing and potential pharmacologic use of medications that block this effect.</p>
dc.identifier.submissionpathortho_pp/18
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentDepartment of Orthopedics and Physical Rehabilitation
dc.source.pages539-42


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