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DOI 10.1016/0278-2391(94)90051-5

Медицинская библиотека · Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons · 1994

An animal model for studying mechanisms in human temporomandibular joint disc derangement.

Mills D K, Daniel J C, Herzog S, Scapino R P

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Аннотация

PURPOSE: A method for producing disc displacement is presented in which remodeling events in the disc and posterior attachment (PA) are similar to those occurring in patients suffering from disc displacement (DD).

METHOD: Thirty-three adult New Zealand White rabbits were used in this study. A unilateral anterior DD was surgically induced in 18 animals. Six animals were sham operated and nine animals served as controls.

RESULTS

Macroscopically, DD was associated with gross thickening of the posterior band (PB), shortening of the disc anteroposteriorly, flexure of the intermediate zone (IZ), and loss of the biconcave shape. Microscopically, dramatic internal structural changes were observed in displaced discs, including extensive collagenous fiber reorganization and changes in cell morphology associated with a generalized loss of metachromatic staining. As in humans, the disc displacement caused abnormal loading of the PA and remodeling of this tissue into a disc-like structure characterized by the appearance of coarse collagenous fiber bundles and scattered chondrocytes surrounded by a matrix-containing cartilage-like glycosaminoglycans (GAGs).

CONCLUSION

These pathoanatomic changes bear a remarkable similarity to those described in human disc derangements and support the use of this method as an experimental model for the study of remodeling events in human DD arthropathies.

Для цитирования: Mills D K, Daniel J C, Herzog S, Scapino R P. An animal model for studying mechanisms in human temporomandibular joint disc derangement.. Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons. 1994. DOI: 10.1016/0278-2391(94)90051-5.

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