ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2011
PI3Kγ deletion reduces variability in the in vivo osteolytic response induced by orthopaedic wear particles.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Innate immunity sensors participating in pathophysiology of joint diseases: a brief overview.Journal of long-term effects of medical implants · 2014Article
- Local effect of IL-4 delivery on polyethylene particle induced osteolysis in the murine calvarium.Journal of biomedical materials research. Part A · 2013Article
- Direct subcutaneous injection of polyethylene particles over the murine calvaria results in dramatic osteolysis.International orthopaedics · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Orthopedic wear particles activate a number of intracellular signaling pathways associated with inflammation in macrophages and we have previously shown that the phosphoinositol-3-kinase (PI3K)/Akt pathway is one of the signal transduction pathways that mediates the in vitro activation of macrophages by orthopedic wear particles. Since PI3Kγ is primarily responsible for PI3K activity during inflammation, we hypothesized that PI3Kγ mediates particle-induced osteolysis in vivo. Our results do not strongly support the hypothesis that PI3Kγ regulates the overall amount of particle-induced osteolysis in the murine calvarial model. However, our results strongly support the conclusion that variability in the amount of particle-induced osteolysis between individual mice is reduced in the PI3Kγ(-/-) mice. These results suggest that PI3Kγ contributes to osteolysis to different degrees in individual mice and that the mice, and patients, that are most susceptible to osteolysis may be so, in part, due to an increased contribution from PI3Kγ.
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Registered trials
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