Extrinsic cell infiltration and revascularization accelerate mechanical deterioration of the patellar tendon after fibroblast necrosis.
This study was performed to determine the contribution of extrinsic cell infiltration and revascularization into the patellar tendon in alteration of the mechanical properties of the patellar tendon after intrinsic fibroblast necrosis using 77 rabbits. In Group I, after the patellar tendon underwent the in situ freeze-thaw treatment, a wrapping treatment was performed to inhibit any extrinsic cell infiltration into the tendon. In Group II, the patellar tendon underwent the freeze-thaw treatment without any of the wrapping treatment. In Group III, the patellar tendon underwent the same wrapping treatment but without any freeze-thaw treatment. The cell culture study demonstrated that the in situ freeze-thaw treatment killed from 97 to 100 percent of the cells in the patellar tendon. Histologically, no cells were found in the midsubstance of the patellar tendon in Group I at 1, 3, and 6 weeks. In Group II, a number of cells and some vessels were found scattered in the tendon at 3 and 6 weeks. Mechanically, the elastic modulus and the tensile strength of the patellar tendon of Group II were significantly lower than those of Groups I and III at 3 and 6 weeks. These facts suggest that extrinsic cell infiltration and revascularization from the surrounding tissues accelerate the deterioration of the mechanical properties of the patellar tendon matrix after intrinsic fibroblast necrosis.
Tohyama
H
H
Division of Medical Bioengineering and Sports Medicine, Department of Advanced Surgery, Hokkaido University School of Medicine, Kita-15 Nishi-7, Sapporo 060-8638, Japan.
Yasuda
K
K
D000818:Animals; D001696:Biomechanical Phenomena; D016923:Cell Death; D002478:Cells, Cultured; D004548:Elasticity; D005260:Female; D005347:Fibroblasts / Q000473:pathology*; D009336:Necrosis; D010329:Patella / Q000503:physiopathology*; D011817:Rabbits; D012016:Reference Values; D013314:Stress, Mechanical; D013710:Tendons / Q000098:blood supply* / Q000473:pathology*; D013718:Tensile Strength