Abstract:
:Inflammation plays a key role in excessive bone loss in conditions such as rheumatoid arthritis and periodontitis. An important paradigm in immunology is that inflammatory factors activate feedback inhibition mechanisms to restrain inflammation and limit associated tissue damage. We hypothesized that inflammatory factors would activate similar feedback mechanisms to restrain bone loss in inflammatory settings. We have identified three mechanisms that inhibit osteoclastogenesis and are induced by inflammatory factors such as toll-like receptor ligands and cytokines; downregulation of expression of costimulatory molecules such as TREM-2; induction of shedding, and thereby inactivation of the M-CSF receptor c-Fms, leading to decreased RANK transcription; and induction of transcriptional repressors such as interferon regulatory factor 8. It is likely that these mechanisms work in a complementary and cooperative manner to fine tune the extent of osteoclastogenesis in inflammatory settings, and their augmentation may represent an alternative therapeutic approach to suppress bone resorption.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Ivashkiv LB,Zhao B,Park-Min KH,Takami Mdoi
10.1111/j.1749-6632.2011.06217.xsubject
Has Abstractpub_date
2011-11-01 00:00:00pages
88-94eissn
0077-8923issn
1749-6632journal_volume
1237pub_type
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