Apoptosis in displaced temporomandibular joint disc with and without reduction: an immunohistochemical study

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.

Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice

“…Apoptosis is known to be responsible for disc tissue degeneration correlated with the severity of disc pathologic processes (Caltabiano, et al, 2013; Leonardi et al,2010; Loreto et al, 2011). We therefore conducted Tunel assay to determine if there is any alteration in cell apoptosis in the disc.…”

Expression of endoplasmic reticulum stress protein in rabbit condyle cartilage following anterior disk displacement

“…Sustained excessive joint loading associated with TMD is considered to be a risk factor for osteoarthritis (OA) development by promoting chondrocytes apoptosis . Previous researches have demonstrated the correlation between TMD and apoptosis . However, the signaling pathways that trigger apoptosis of chondrocytes during the development of TMD are still unknown.…”

The Role of Intrinsic Pathway in Apoptosis Activation and Progression in Peyronie’s Disease

“…This complex hydrolyzes adenosine triphosphate to cleave and activate caspase 9. The initiator caspase 9 then cleaves and activates the executioner caspases 3, 6, and 7, resulting in cell apoptosis [14, 17]. The antiapoptotic proteins bcl-2 and bcl-XL inhibit cytochrome C release [18].…”