Publication: Chondrocyte-like apoptosis in temporomandibular joint disc internal derangement as a repair-limiting mechanism. An in vivo study
Loading...
Date
2009
Authors
Loreto, C. ; Musumeci, G. ; Leonardi, R.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
Temporomandibular joint internal
derangement (TMJ ID) is characterised by disc
displacement and degenerative tissue changes involving
an active cellular response, with cell phenotype
transformation from fibroblast-like to fibrochondrocyte
and, eventually, to chondrocyte-like, possibly as a
response to abnormal loading. However, only small
patches of chondral tissue are detected in TMJ discs with
ID. We decided to explore the reasons for such
incomplete tissue change, postulating an involvement of
the apoptosis process.
Twenty-one discs removed from 19 patients with
TMJ ID were processed for TRAIL and DR5 immunohistochemical
localisation, and subjected to the TUNEL
assay.
Overexpression of DR5 receptor and its ligand
(TRAIL) in chondrocyte-like cells suggested activation
of programmed cell death, as also demonstrated by
TUNEL-positive cells.
The data suggest a failed adaptive response to disc
displacement through chondroid metaplasia. The
apoptotic death of chondrocyte-like cells, which is at
least partly regulated by TRAIL and its death receptor,
appears to underpin the failed disc repair, eventually
leading to its perforation.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.