Source:http://linkedlifedata.com/resource/pubmed/id/17936170
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2007-10-15
|
| pubmed:abstractText |
Inflammation in JIA results from the interaction of myeloid, lymphoid, and stromal cells, cartilage destruction, bone erosion, and debility. These cells and the mediators they release cause cartilage destruction, bone erosion, and debility. Neutrophils are thought to mediate much of the actual destruction within a joint; however, many cases of JIA are not associated with boney erosions, but there is significant inflammation caused by the cellular infiltrate and the proliferation of synoviocytes. NSAIDs address many of the non-cell-dependent aspects of inflammation. Disease-modifying drugs are required for resistant or progressive disease. These agents are effective in modifying the cellular interactions that perpetuate inflammation. In particular, TNFalpha inhibitors impair cell migration into the joint and reduce macrophage functions.
|
| pubmed:commentsCorrections | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:status |
PubMed-not-MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0889-857X
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
33
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
365-88
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
Inflammation in juvenile idiopathic arthritis.
|
| pubmed:affiliation |
University of Pennsylvania School of Medicine, Division of Allergy and Immunology, Children's Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, PA 19104, USA. sullivak@mail.upenn.edu
|
| pubmed:publicationType |
Journal Article
|