1993 Fiscal Year Final Research Report Summary
Experimental Study on Fatigue Phenomenon of the Anterior Cruciate Ligament by Excessive Exercise
| Project/Area Number |
03670707
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
MIZUTA Hiroshi Kumamoto University School of Medicine Department of Orthopaedic Surgery Associate Professor, 医学部, 助教授 (60174025)
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| Co-Investigator(Kenkyū-buntansha) |
KUBOTA Kenji Kumamoto University School of Medicine Department of Orthopaedic Surgery Lecture, 医学部, 助手 (50205134)
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| Project Period (FY) |
1991 – 1993
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| Keywords | Anterior cruciate ligament / Enforced runnning / Biomechanical properties / Ultrastructural examination / Full-thickness articular cartilage defect / Cartilage repair / Basic Fibroblast Growth Factor |
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| Research Abstract |
1.The effect of enforced exercise on biomechanical properties and morphological characteristis of the anterior cruciate ligament(ACL) of bipedal rats was examined. The bipedal rats were forced to run on a motor-driven treadmill at 20 degrees decline and at a speed of 20 m/min for 30 min on each of six consecutive days during the four-week period. Strength results for bipedal rats with exercise (E(+)G) were significantly lower than those for bipedal rats without exercise(E(-)G)at the loading rates 8.3mm/sec and 1*10^3 mm/sec. A load relaxation test showed a larger load-relaxation phenomenon in E(-)G than in E(+)G.The viscosity of the ACL was higher in E(+)G than in E(-)G.In E(+)G,eighty-one percent of the fibroblasts in the ACL were spindle-shaped with indented nucleus. There was an increased number of rough surfaced endoplasmic reticula and lysosomal vesicles in the fibroblasts of E(+)G.The collagen fibril diameters of E(+)G varied in size from 20 to 120 nm. The mean collagen fibril diameter of E(+)G was significantly lower than that of E(-)G.
2.The effect of basic Fibroblast Growth Factor(bFGF) on the repair of full-thickness articular cartilage defects was studied. The smaller full-thickness defects(* 3 mm in diameter in adolescent rabbits) are repaired spontaneously, but the larger defects cannot be repaired with cartilage. The administration of bFGF (0.05ng/h) for two weeks elicited the differentiation from mesenchymal cells to chondrocytes in the 5 mm full-thickness defects in the femoral trochlea of adolescent rabbits. Within eight weeks, the defects showed almost complete recovery of epiphyseal morphology. On the other hand, the administration of neutralizing antibody to bFGF (50 ng/h) for two weeks inhibited chondrogenic differentiation in the center of the 3 mm full-thickness defects.
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