CELL-PROLIFERATION AND ENZYME-ACTIVITIES ASSOCIATED WITH THE DEVELOPMENT OF AVIAN TIBIAL DYSCHONDROPLASIA - AN INSITU BIOCHEMICAL-STUDY

被引:68
作者
FARQUHARSON, C
WHITEHEAD, C
RENNIE, S
THORP, B
LOVERIDGE, N
机构
[1] ROWETT RES INST,DIV BIOCHEM SCI,BONE GROWTH & METAB UNIT,BUCKSBURN AB2 9SB,ABERDEEN,SCOTLAND
[2] INST ANIM PHYSIOL & GENET RES,EDINBURGH RES STN,ROSLIN,MIDLOTHIAN,SCOTLAND
关键词
AVIAN TIBIAL DYSCHONDROPLASIA; BROMODEOXYURIDINE UPTAKE; INSITU BIOCHEMISTRY; ALKALINE PHOSPHATASE; GLUCOSE 6 PHOSPHATE DEHYDROGENASE; TARTRATE RESISTANT ACID PHOSPHATASE;
D O I
10.1016/8756-3282(92)90362-Z
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Avian tibial dyschondroplasia is a disorder of endochondral ossification which results in the accumulation of noncalcified, avascular cartilage. We have investigated the changes in cell proliferation and enzyme activities within specific cell types in the growth plate of chickens with differing severity of the disease using in situ biochemical techniques that allow the quantification of enzyme activity in unfixed undecalcified sections of tissue. Lactate dehydrogenase activity in the prehypertrophic zone and tartrate-resistant acid phosphatase activity in osteoclasts/chondroclasts were not affected by the severity of the disease. Glucose 6-phosphate dehydrogenase activity in both the proliferating and prehypertrophic zones of the growth plate was reduced in chicks with both moderate and severe lesions. Cell proliferation within the proliferating chondrocytes was slightly reduced in the severely affected birds. Alkaline phosphatase activity in the prehypertrophic chondrocytes was markedly elevated in chicks with moderate and severe lesions. These results rule out an increased rate of chondrocyte proliferation as a possible mechanism for the development of tibial dyschondroplasia. The aetiology of the disease therefore appears to be related to the control of chondrocyte differentiation, mineralization, and vascularization by local and/or systemic growth factors.
引用
收藏
页码:59 / 67
页数:9
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