Age-related osteo-arthrotic degeneration of the temporomandibular joint in the mouse.

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Age-related osteo-arthrotic degeneration of the temporomandibular joint in the mouse. / Dreessen, D; Halata, Zdenek.

In: Acta Anat (Basel), Vol. 139, No. 1, 1, 1990, p. 91-96.

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Dreessen D, Halata Z. Age-related osteo-arthrotic degeneration of the temporomandibular joint in the mouse. Acta Anat (Basel). 1990;139(1):91-96. 1.

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@article{3aa8dbe2d1174c7a86a4cc7981e83863,
title = "Age-related osteo-arthrotic degeneration of the temporomandibular joint in the mouse.",
abstract = "The light-microscopic and ultrastructural characteristics of the temporomandibular joints (TMJs) of female STR/IN mice, aged from 3 to 12 months, were studied. Every TMJ of an adult mouse starts to degenerate in early adulthood and subsequently suffers from osteo-arthrosis. Ageing of the TMJ is characterized by thinning out of its cartilaginous components. The chondrocytes are no longer distributed regularly in the ground substance but form clusters. Cracks and fissures invade the condylar cartilage and lead to the formation of cartilage islands, which finally become loose as free bodies in the lower joint chamber and joint capsule. The lower joint chamber diminishes, but no ankylosis is observed. Ultrastructurally, the number of vesicles around the degenerated chondrocytes increases. Aged chondrocytes contain more lysosomes. The condylar surface becomes irregular and reveals microscars. Its surface is covered by an electron-dense fine granular material, considered to be built up by proteoglycans. Compared to the male ICR mouse, the osteo-arthrotic destruction of the cartilage, the subchondral sclerosis and the deformation of the underlying bone exhibit only minor states in the female STR/IN mouse. Concerning the aetiology and pathogenesis, the very early degeneration of the mostly unloaded TMJ seems to be based on a genetically altered composition of the articular cartilage, possibly due to failing articular chondrocyte responses to stimuli connected with degeneration and repair.",
author = "D Dreessen and Zdenek Halata",
year = "1990",
language = "Deutsch",
volume = "139",
pages = "91--96",
number = "1",

}

RIS

TY - JOUR

T1 - Age-related osteo-arthrotic degeneration of the temporomandibular joint in the mouse.

AU - Dreessen, D

AU - Halata, Zdenek

PY - 1990

Y1 - 1990

N2 - The light-microscopic and ultrastructural characteristics of the temporomandibular joints (TMJs) of female STR/IN mice, aged from 3 to 12 months, were studied. Every TMJ of an adult mouse starts to degenerate in early adulthood and subsequently suffers from osteo-arthrosis. Ageing of the TMJ is characterized by thinning out of its cartilaginous components. The chondrocytes are no longer distributed regularly in the ground substance but form clusters. Cracks and fissures invade the condylar cartilage and lead to the formation of cartilage islands, which finally become loose as free bodies in the lower joint chamber and joint capsule. The lower joint chamber diminishes, but no ankylosis is observed. Ultrastructurally, the number of vesicles around the degenerated chondrocytes increases. Aged chondrocytes contain more lysosomes. The condylar surface becomes irregular and reveals microscars. Its surface is covered by an electron-dense fine granular material, considered to be built up by proteoglycans. Compared to the male ICR mouse, the osteo-arthrotic destruction of the cartilage, the subchondral sclerosis and the deformation of the underlying bone exhibit only minor states in the female STR/IN mouse. Concerning the aetiology and pathogenesis, the very early degeneration of the mostly unloaded TMJ seems to be based on a genetically altered composition of the articular cartilage, possibly due to failing articular chondrocyte responses to stimuli connected with degeneration and repair.

AB - The light-microscopic and ultrastructural characteristics of the temporomandibular joints (TMJs) of female STR/IN mice, aged from 3 to 12 months, were studied. Every TMJ of an adult mouse starts to degenerate in early adulthood and subsequently suffers from osteo-arthrosis. Ageing of the TMJ is characterized by thinning out of its cartilaginous components. The chondrocytes are no longer distributed regularly in the ground substance but form clusters. Cracks and fissures invade the condylar cartilage and lead to the formation of cartilage islands, which finally become loose as free bodies in the lower joint chamber and joint capsule. The lower joint chamber diminishes, but no ankylosis is observed. Ultrastructurally, the number of vesicles around the degenerated chondrocytes increases. Aged chondrocytes contain more lysosomes. The condylar surface becomes irregular and reveals microscars. Its surface is covered by an electron-dense fine granular material, considered to be built up by proteoglycans. Compared to the male ICR mouse, the osteo-arthrotic destruction of the cartilage, the subchondral sclerosis and the deformation of the underlying bone exhibit only minor states in the female STR/IN mouse. Concerning the aetiology and pathogenesis, the very early degeneration of the mostly unloaded TMJ seems to be based on a genetically altered composition of the articular cartilage, possibly due to failing articular chondrocyte responses to stimuli connected with degeneration and repair.

M3 - SCORING: Zeitschriftenaufsatz

VL - 139

SP - 91

EP - 96

IS - 1

M1 - 1

ER -