Document Type

Article

Language

eng

Publication Date

1-2014

Publisher

Wiley

Source Publication

Journal of Oral Pathology & Medicine

Source ISSN

0904-2542

Abstract

Background

Apoptosis is a programme of cell death which does not induce an inflammatory response. Recent previous research has suggested a correlation between temporomandibular internal derangement and apoptosis. Fas ligand (FasL) is an apoptosis‐inducing factor, known to trigger apoptosis through distinct signal pathways. This study aims to examine, by immunohistochemistry, the expression of FasL in temporomandibular joint (TMJ) articular discs of patients with anterior disc displacement with reduction (ADDwR) and without reduction (ADDwoR) in patients with and without osteoarthrosis (OA).

Methods

Forty‐two (n = 42) TMJ articular discs were divided into two cut‐offs: (i) 8 control, 17 ADDwR, 17 ADDwoR, and (ii) without OA (n = 25) and with OA (n = 17). The area of immunostaining was compared statistically between groups (P < 0.05).

Results

Statistically significant differences were found in the expression of FasL in TMJ discs between the three groups (P = 0.001). ADDwR presented significant higher FasL expression when compared with ADDwoR (P < 0.001). Significant higher FasL expression was observed in the group without OA (P = 0.001). All patients without OA presented ADDwR, while all the patients with OA presented ADDwoR.

Conclusion

A higher area of in situ immunostaining of FasL was found in temporomandibular discs with reduction, which is the less severe condition. Moreover, a reduced expression of FasL in the discs of patients with osteoarthrosis was found, suggesting that some aspects of apoptosis might underlie the progression of TMJ disorders.

Comments

Accepted version. Journal of Oral Pathology & Medicine, Vol. 43, No. 1 (January 2014): 69-75. DOI. © 1999-2019 John Wiley & Sons, Inc. Used with permission.

Luis Eduardo Almeida was affiliated with School of Health and Biosciences, Pontifícia Universidade Católica do Paraná (PUCPR), Curitiba, Brazil at the time of publication.

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