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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
12
|
| pubmed:dateCreated |
1999-4-1
|
| pubmed:abstractText |
Periodontal disease is a significant cause of tooth loss in humans and is one of the most prevalent diseases associated with bone loss. Following bacterial colonization, the gingiva becomes inflamed and, in some cases, progresses to destruction of alveolar bone. To investigate the temporal movement of inflammatory cells toward alveolar bone and the role of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in this process, studies were carried out in a Macaca fascicularis primate model of experimental periodontitis. IL-1 and TNF activity was inhibited by local application of soluble receptors to IL-1 and TNF by injection into interdental papillae. The results indicate that following induction of experimental periodontitis, the front of inflammatory cells progresses toward alveolar bone and is associated with osteoclast formation. These processes are inhibited by blockers to IL-1 and TNF. These studies suggest that the conversion from gingivitis to periodontitis is directly associated with the movement of an inflammatory infiltrate toward alveolar bone, and that this activity is at least partially dependent upon IL-1 and/ or TNF.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
D
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0022-3492
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
69
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1419-25
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:9926773-Alveolar Bone Loss,
pubmed-meshheading:9926773-Alveolar Process,
pubmed-meshheading:9926773-Animals,
pubmed-meshheading:9926773-Cell Movement,
pubmed-meshheading:9926773-Disease Models, Animal,
pubmed-meshheading:9926773-Disease Progression,
pubmed-meshheading:9926773-Epithelium,
pubmed-meshheading:9926773-Gingivitis,
pubmed-meshheading:9926773-Humans,
pubmed-meshheading:9926773-Interleukin-1,
pubmed-meshheading:9926773-Leukocytes, Mononuclear,
pubmed-meshheading:9926773-Macaca fascicularis,
pubmed-meshheading:9926773-Neutrophils,
pubmed-meshheading:9926773-Osteoclasts,
pubmed-meshheading:9926773-Periodontitis,
pubmed-meshheading:9926773-Porphyromonas gingivalis,
pubmed-meshheading:9926773-Receptors, Interleukin-1,
pubmed-meshheading:9926773-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:9926773-Tooth Loss,
pubmed-meshheading:9926773-Tumor Necrosis Factor-alpha
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Interleukin-1 and tumor necrosis factor antagonists inhibit the progression of inflammatory cell infiltration toward alveolar bone in experimental periodontitis.
|
| pubmed:affiliation |
Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, MA 02218, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|