Title

Apoptosis in Displaced Temporomandibular Joint Disc with and without Reduction: An Immunohistochemical Study

Document Type

Article

Language

eng

Publication Date

1-4-2011

Publisher

Wiley

Source Publication

Journal of Oral Pathology & Medicine

Source ISSN

0904-2542

Abstract

Internal derangement (ID) of the temporomandibular joint (TMJ) is due to an abnormal relationship of the articular disc to the mandibular condyle, glenoid fossa and articular eminence. The two most common types of internal derangement are anterior disc displacement with (ADDwR) and without reduction (ADDwoR). Disc displacement is associated with degenerative tissue changes. The histological features of discs from patients with TMJ ID reflect a general remodelling caused by abnormal loading. A correlation has been demonstrated between TMJ ID and apoptosis. Few investigations have addressed the role of apoptosis or caspase activity in TMJ ID. The apoptosis activation process was studied in different areas of discs from 18 patients with ID (both ADDwR and ADDwoR) and four cadavers (controls), with emphasis on the expression of caspase 3, whose activation makes the death process irreversible. The results showed a greater proportion of caspase 3‐positive cells in ADDwR and ADDwoR than in control discs. Immunopositivity also varied between disc areas; in particular, in ADDwoR sections labelled cells were significantly more numerous (P <0.01) in the posterior disc attachment than in the anterior and intermediate bands. In addition, a significantly greater proportion of labelled cells was seen in the anterior (+) and intermediate (++) band of ADDwR compared with ADDwoR discs both bands (P <0.05). These data suggest the importance of programmed cell death in the progression of TMJ ID.

Comments

Journal of Oral Pathology & Medicine, Vol 40, No. 1 (January 2011): 103-110. DOI.

Louis Eduardo Almeida was affiliated with Center for Health and Biological Sciences, Pontifical Catholic, University of Panarà, Curitibe, Brazil at the time of publication.

Share

COinS