gms | German Medical Science

German Congress of Orthopedic and Trauma Surgery (DKOU 2018)

23.10. - 26.10.2018, Berlin

Effect of atorvastatin on joint contracture development in a rat model of posttraumatic joint contracture of the knee

Meeting Abstract

  • presenting/speaker Andreas Baranowski - Universitätsmedizin Mainz, Zentrum für Orthopädie und Unfallchirurgie, Mainz, Germany
  • Ekaterina Slotina - Universitätsmedizin Mainz, Zentrum für Orthopädie und Unfallchirurgie, Mainz, Germany
  • Tim Mickan - Universitätsmedizin Mainz, Zentrum für Orthopädie und Unfallchirurgie, Mainz, Germany
  • Ulrike Ritz - Universitätsmedizin Mainz, Zentrum für Orthopädie und Unfallchirurgie, Mainz, Germany
  • Irene Schmidtmann - Inst. of Med. Biostatistics, Epidemiology and Informatics, Mainz, Germany
  • Angelika Ackermann - Universitätsmedizin Mainz, Zentrum für Orthopädie und Unfallchirurgie, Mainz, Germany
  • Pol-Maria Rommens - Universitätsmedizin Mainz, Zentrum für Orthopädie und Unfallchirurgie, Mainz, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2018). Berlin, 23.-26.10.2018. Düsseldorf: German Medical Science GMS Publishing House; 2018. DocPT19-1146

doi: 10.3205/18dkou705, urn:nbn:de:0183-18dkou7057

Published: November 6, 2018

© 2018 Baranowski et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Objectives: Myofibroblasts have been associated with increased posttraumatic joint contracture, which has a devastating impact on articular function and activities of daily life. Atorvastatin has shown to reduce the rate of activation and proliferation of cardiac, hepatic and pulmonary myofibroblasts. However, there do not exist any in vivo models which analyze the effect on joint myofibroblasts so far. Therefore, the aim of this randomized and blinded study was to evaluate and compare the effect of orally administered Atorvastatin upon early (2 weeks) and complete (4 weeks) posttraumatic contracture (with and without remobilization) in a rat model of posttraumatic joint contracture of the knee.

Methods: Posterior capsular injury, extracartilaginous femoral condyle defect and Kirschner (K)-wire transfixation of the flexed knee joint were performed in 48 skeletally immature male Sprague-Dawley rats. Via randomization, the animals were distributed equally in either the Placebo or the Atorvastatin group of the study. Atorvastatin (15 mg/kg bw/day) or Placebo was administered daily orally till sacrifice. The rats were sacrificed at either 2 (n=16), 4 (n=16) or 8 (n=16) weeks after initial surgery. Rats euthanized at week 8 had their K-wire removed at week 4, followed by a remobilization period of another 4 weeks. The results were evaluated via X-ray and joint angle measurement.

Results: Development of a contracture was observable after 2 weeks and advanced up to the 4th week after operation. Remobilisation led to a reduction of contracture. Atorvastatin turned out to have no significant influence on the development of a contracture. At week 2, total joint contracture averaged 68.5° ± 15.7° for Atorvastatin and 60.9° ± 11.4° in the Placebo group (P >0.05). At week 4, we measured 76.1° ± 14.2° vs. 67.3 ± 8.9 and after 4 weeks of remobilization (week 8) 28.0° ± 9.4° vs. 35.3 ± 19.7 (P >0.05). The respective capsular contractures were similar between Atorvastatin and Placebo group (2 weeks: 31.0° ± 15.2° vs 31.2° ± 14.0°, 4 weeks: 59.2° ± 20.8° vs 43.8° ± 18.3°, 8 weeks: 15.3° ± 10.6° vs 14.9 ± 17.5°, P >0.05).

Conclusion: Atorvastatin in the applied concentration does not reduce the degree of contracture in our rat model of posttraumatic joint contracture of the knee.