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Título: Chondrocyte-like apoptosis in temporomandibular joint disc internal derangement as a repair-limiting mechanism. An in vivo study
Fecha de publicación: 2009
Editorial: Murcia : F. Hernández
ISSN: 0213-3911
Materias relacionadas: 616 - Patología. Medicina clínica. Oncología
Palabras clave: Internal derangement
Temporomandibular joint disc
Resumen: 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.
Autor/es principal/es: Loreto, C.
Musumeci, G.
Leonardi, R.
Forma parte de: Histology and histopathology
URI: http://hdl.handle.net/10201/35995
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 6
Derechos: info:eu-repo/semantics/openAccess
Aparece en las colecciones:Vol.24, nº3 (2009)

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