Abstract

Adhesion of the knee is a major concern after knee surgery, the treatment of which is difficult. Botulinum toxin A (BTX-A) injection is demonstrated as efficient in treating knee adhesion after surgery. However, the treatment outcomes and the mechanism of action are not yet determined. The aim of the present study was to examine the effects and molecular mechanism of a BTX-A treatment in preventing adhesion of the knee. Twenty-four Wistar rats were randomly divided into a BTX-A treatment group and a control group. BTX-A or saline was injected into the cavity of the knee in the BTX-A treatment or control group respectively. Gross and histopathological examinations of interleukin 1 (IL-1) and fibroblast growth factor (FGF) levels, as well as fibroblast cell numbers, were assessed in the knee intra-articular adhesions in each group 6 weeks after recovery from the surgery. Macroscopic observations showed a significant reduction in adhesion severity in the BTX-A treatment group compared with the control group. In addition, the levels of IL-1 and FGF were lower and the number of fibroblasts was smaller in the BTX-A treatment group compared with those in the control group. BTX-A prevented intra-articular adhesion of knee in the rats, which might be associated with reduced expressions of IL-1 and FGF.

Highlights

  • The formation of adhesion in the knee is a common complication after knee surgery [1]

  • The ELISA analysis revealed that the interleukin 1 (IL-1) and fibroblast growth factor (FGF) contents were remarkably lower in the Botulinum toxin A (BTX-A) treatment group than in the control group (Table 2)

  • Based on an anatomical dissection and a visual assessment under an unaided eye, the right knee joint showed mild and loose adhesions in the BTX-A treatment group, while pyknotic tubular fibrosis and arthrosclerosis were observed in the right knee joint of the rats in the control group

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Summary

Introduction

The formation of adhesion in the knee is a common complication after knee surgery [1]. The rate of arthrofibrosis following total knee arthroplasty (TKA) is estimated to be 8–12% [2] and the rate after ligament reconstruction is 0–4% [3], and it is up to 7% following a fracture of the tibial plateau high-energy fractures [4]. Arthrofibrosis of the knee leads to stiffness, a decreased range of motion and pain [5]. The loss of range of motion of the knee impairs the nutrition supply to the cartilage, resulting in cartilage degeneration and, eventually, loss of function in the knee [5]. A loss of extension of 5◦ in the knee joint significantly increases the energy consumption of the quadriceps muscle and produces a limp [7]

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