CD44 standard form (CD44H) expression and distribution in dysfunctional human temporomandibular joint discs

被引:10
作者
Leonardi, R
Villari, L
Piacentini, C
Bernasconi, G
Baciliero, U
Travali, S
机构
[1] Univ Catania, Ist Patol Gen, I-95124 Catania, Italy
[2] Univ Catania, Cattedra Ortognatodonzia, I-95124 Catania, Italy
[3] Univ Catania, Ist Anat Patol, I-95124 Catania, Italy
[4] Univ Pavia, IRCCS, Policlin S Matteo, Dipartimento Odontostomatol, I-27100 Pavia, Italy
[5] Osped S Bortolo, Div Chirurg Maxillofacciale, Vicenza, Italy
关键词
TMJ disc; disc derangement; cell adhesion molecule; CD44; immunohistochemistry;
D O I
10.1034/j.1399-0020.2000.290413.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
The expression pattern of the cell adhesion molecule CD44 standard form (CD44H) in dysfunctional human temporomandibular joint (TMJ) discs was studied immunohistochemically and compared with normal disc pattern in order to evaluate the expression of this adhesion molecule and correlate it to histopathological changes. Immunohistochemistry with anti-CD44H antibodies was performed on paraffin sections of pathological and normal discs. In normal TMJ discs, a moderate immunolabelling with anti-CD44H antibodies was detectable in fibroblastlike cells, in the few fibrochondrocytes and in chondrocytelike cells. In dysfunctional discs, the staining pattern and intensity varied according to the histopathological findings of the specimens. The TMJ discs showing abnormal collagen arrangement or fragmentation of collagen fibres presented overall the same immunolabelling pattern of normal discs. In the discs showing areas of fibrocartilaginous metaplasia, CD44H expression was upregulated in fibrochondrocytes and fibroblastlike cells. especially around the chondroid tissue. Overall. these results suggest that CD44H mediates the binding of some ECM proteins in TMJ disc cells. The up-regulation of CD44H observed in some dysfunctional TMJ discs seems to indicate a prevention of apoptosis in fibroblastlike cells and an important role in phenotypical change of fibrochondrocytes into chondroblastlike cells, enabling the aggregation of chondroid tissue pericellular matrix components.
引用
收藏
页码:296 / 300
页数:5
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