Increasing thickness and fibrosis of the cartilage in acetabular dysplasia: a rabbit model research.
- Author:
Tian-You LI
1
;
Rui-Xue MA
Author Information
- Publication Type:Journal Article
- MeSH: Acetabulum; metabolism; pathology; ultrastructure; Animals; Cartilage, Articular; metabolism; pathology; ultrastructure; Female; Fibrosis; metabolism; pathology; Male; Microscopy, Electron, Scanning; Microscopy, Electron, Transmission; Polymerase Chain Reaction; Rabbits
- From: Chinese Medical Journal 2010;123(21):3061-3066
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDThe order and mechanism of pathological changes in acetabular dysplasia are still unclear. This study investigated cartilage changes in rabbit acetabular dysplasia models at different ages.
METHODSTwenty-seven 1-month-old New Zealand rabbits underwent cast immobilization of the left hind limb in knee extension. Serial acetabular dysplasia models were established by assessment of the acetabular index and Sharp's angle on radiographs. The thickness of the acetabular cartilage was measured under a microscope, and fibrosis was observed. Ultrastructural changes were investigated with scanning electron microscopy and transmission electron microscopy. The messenger RNA expression of collagen I and II, β1 integrin, and caspase-9 were measured by real-time fluorescence quantitative polymerase chain reaction.
RESULTSIn an immature group of rabbits, the acetabular index of the treated hip increased with animal growth. The cartilage on the brim of the left acetabulum was significantly thicker than that on the right side. The collagen fibrils on the surface of the cartilage became gross, and the chondrocytes in the enlargement layer underwent necrosis. In a mature group of rabbits, the left Sharp's angle increased in the rabbits with 6-week casting. The cartilage on the brim of the left acetabulum underwent fibrosis. The chondrocytes were weakly stained, and the number of lysosomes was much larger than normal. The messenger RNA expression of collagen I and II, β1 integrin, and caspase-9 in the cartilage differed significantly at different ages.
CONCLUSIONSIncreasing thickness followed by fibrosis may be the order of pathological cartilage changes in acetabular dysplasia, with changes in ultrastructure and collagen expression contributing to the process.