title: Stress deprivation simultaneously induces over-expression of interleukin-1beta, tumor necrosis factor-alpha, and transforming growth factor-beta in fibroblasts and mechanical deterioration of the tissue in the patellar tendon.
abstract: To test the hypothesis that stress deprivation induces over-expression of cytokines in the patellar tendon, 40 rats were divided into the following two groups. In the stress-shielded group, we slackened the patellar tendon in the right knee by drawing the patella toward the tibial tubercle with flexible wires. In the control group, we performed a sham operation on the right knee. Animals were killed at 2 or 6 weeks for immunohistological evaluation and biomechanical examination. For IL-1beta, TNF-alpha and TGF-beta, the ratio of positively stained specimens to total specimens was significantly higher in the stress-shielded tendons than in the control tendons. The elastic modulus of the stress-shielded tendon was significantly lower than that of the control tendon, while the cross-sectional area of the stress-shielded tendon was significantly greater than that of the control tendon. Therefore, the present study indicated that stress shielding induced the over-expression of IL-1beta, TNF-alpha and TGF-beta in patellar tendon fibroblasts with mechanical deterioration of the tendon. Regarding clinical relevance, the present study suggests a possible application of an anti-IL-1beta or anti-TNF-alpha strategy for reducing the mechanical deterioration of tendons and ligaments in response to stress deprivation, although this study did not directly show that over-expression of IL-1beta or TNF-alpha in response to stress deprivation was the causation of mechanical deterioration of tendons.
authors.affiliation: Department of Sports Medicine and Joint Reconstruction Surgery, Hokkaido University School of Medicine, Kit-15 Nishi-7, Sapporo 060-838, Japan.
authors.forename: Hisaya
authors.initials: H
authors.lastname: Uchida
authors.forename: Harukazu
authors.initials: H
authors.lastname: Tohyama
authors.forename: Kazuo
authors.initials: K
authors.lastname: Nagashima
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Ohba
authors.forename: Hideo
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Toyama
authors.forename: Kazunori
authors.initials: K
authors.lastname: Yasuda
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D016207:Cytokines / Q000235:genetics*; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology*; D005786:Gene Expression Regulation / Q000502:physiology*; D007375:Interleukin-1 / Q000235:genetics; D008297:Male; D010329:Patella / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013314:Stress, Mechanical; D013710:Tendons / Q000473:pathology* / Q000503:physiopathology; D016212:Transforming Growth Factor beta / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha