We assessed proprioception in the knee using the angle reproduction test in 20 healthy volunteers, ten patients with acute anterior instability and 20 patients with chronic anterior instability after reconstruction of the anterior cruciate ligament (ACL). In addition, the Lysholm-knee score, ligament laxity and patient satisfaction were determined. Acute trauma causes extensive damage to proprioception which is not restored by rehabilitation alone. Three months after operation, there remained a slight decrease in proprioception compared with the preoperative recordings, but six months after reconstruction, restoration of proprioception was seen near full extension and full flexion. In the mid-range position, proprioception was not restored. At follow-up, 3.7 +/- 0.3 years after reconstruction, there was further improvement of proprioception in the mid-range position. There was no difference between open and arthroscopic techniques. The highest correlation was found between proprioception and patient satisfaction. After reconstruction of the ACL reduced proprioception may explain the poor functional outcome in some patients, despite restoration of mechanical stability.

The objective of the study was to investigate whether the response profile of the growth factor of human tendon fibroblasts could be beneficially influenced through the application of mechanical stretch. It was considered that this would elucidate structural and functional problems, often seen after tendon and ligament healing. The secretion pattern of transforming growth factor-beta (TGF-beta), platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) was determined in mechanically stretched fibroblasts and compared to non-stretched controls. Human tendon fibroblasts were experimentally stretched for 15 and 60 mm at a frequency of 1 Hz and an amplitude of 5%. The secretion of TGF-beta PDGF and bFGF was measured by enzyme-linked immuno-sorbent assay. All the growth factors investigated were indeed secreted by human tendon fibroblasts both in stretched cells and controls. Mechanical stretch increased the secretion pattern of the growth factors. The increased concentrations of TGF-beta bFGF and PDGF after cyclical mechanical stretching may have a positive influence on tendon and ligament healing through stimulation of cell proliferation, differentiation and matrix formation.

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Accelerated rehabilitation after tendon and ligament injuries is widely accepted to avoid adverse effects of immobilization. However, progressive rehabilitation may also lead to an excessive inflammatory soft tissue response. To investigate the amount of loading necessary to accelerate the healing process without causing damage to the healing tissue, we experimentally stretched human tendon fibroblasts of healthy tendons 15 and 60 min with 1 Hz and an elongation of 5% and measured the secretion of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta1 (TGF-beta1), platelet-derived growth factor (PDGF), and fibroblast growth factor basic (bFGF). Secretion of IL-6 was significantly induced by 15 min of cyclic biaxial mechanical stretching after 4 and 8 h observation time and by 60 min stretching and 2 h observation time. The growth factors TGF-beta1, bFGF, and PDGF were secreted by human tendon fibroblasts both in stretched cells and controls; however, no increases were related to mechanical stretching. There was no measurable secretion of TNF-alpha in human tendon fibroblasts. These findings suggest that the inflammatory reaction often seen during physiotherapy after tendon and ligament injuries is caused in part by secretion of IL-6 from the stretched human tendon fibroblasts. IL-6 may cause exaggerated proliferation of fibroblasts and synovial cells as seen in rheumatoid arthritis and arthrofibrosis. However, physiological proliferative reactions leading to repair of injured tissue are also possible. IL-6 measured in the synovial fluid may be an important predictor for monitoring and improving therapeutic strategies in terms of tendon/ligament healing.

Accelerated rehabilitation after tendon, ligament and bone injuries is widely accepted to avoid adverse effects of immobilization. However, progressive rehabilitation may also lead to an excessive inflammatory soft tissue response and often leads to structural and functional problems such as excessive scarring. The equivalent at the molecular/cellular level is in part the regulation of the sensitive homeostasis between proliferation and apoptosis. However, little attention has been paid to this aspect of tendon pathogenesis. This study investigated the response profile of human tendon fibroblasts in terms of apoptosis and anticipated alteration of Jun N-terminal kinase (JNK) activation to cyclic mechanical stretching. Human tendon fibroblasts of six patients were stretched for 15 or 60 min with 1 Hz and an elongation of 5%. Activation of stress-activated protein kinase (SAPK)/JNK was measured by western blot analysis. Apoptotic cells were determined in the stretched cells and in controls by annexin-V staining and detection by flow cytometry. Additionally DNA laddering was determined by ligation-mediated (LM) polymerase chain reaction (PCR). Application of 15 and 60 min stretch increased activation of SAPK/JNK at a maximum after 60 min. However, JNK activation after the longer stretch period 50% less than after the shorter stretch period (15 min). The apoptosis rate was correspondingly increased after short stretch application but not after longer stretch. This might be caused by an inactivation of the activated JNKs by cell protection mechanisms. The findings suggest that mechanical stretching directly activates intracellular signaling pathways, which in turn induce apoptosis. The longer stretch period resulted in a decreased apoptotic rate due to development of stress tolerance. This might be caused by heat-shock protein mediated suppression of JNK activation. This novel observation is an important issue, as defined mechanical stretching, depending on its duration, modulates apoptosis and thus affects tendon remodeling.