Radiological features of experimental staphylococcal septic arthritis by micro computed tomography scan

PLoS One. 2017 Feb 2;12(2):e0171222. doi: 10.1371/journal.pone.0171222. eCollection 2017.

Abstract

Background: Permanent joint dysfunction due to bone destruction occurs in up to 50% of patients with septic arthritis. Recently, imaging technologies such as micro computed tomography (μCT) scan have been widely used for preclinical models of autoimmune joint disorders. However, the radiological features of septic arthritis in mice are still largely unknown.

Methods: NMRI mice were intravenously or intra-articularly inoculated with S. aureus Newman or LS-1 strain. The radiological and clinical signs of septic arthritis were followed for 10 days using μCT. We assessed the correlations between joint radiological changes and clinical signs, histological changes, and serum levels of cytokines.

Results: On days 5-7 after intravenous infection, bone destruction verified by μCT became evident in most of the infected joints. Radiological signs of bone destruction were dependent on the bacterial dose. The site most commonly affected by septic arthritis was the distal femur in knees. The bone destruction detected by μCT was positively correlated with histological changes in both local and hematogenous septic arthritis. The serum levels of IL-6 were significantly correlated with the severity of joint destruction.

Conclusion: μCT is a sensitive method for monitoring disease progression and determining the severity of bone destruction in a mouse model of septic arthritis. IL-6 may be used as a biomarker for bone destruction in septic arthritis.

MeSH terms

  • Animals
  • Arthritis, Infectious / diagnostic imaging*
  • Arthritis, Infectious / pathology
  • Disease Models, Animal
  • Disease Progression
  • Female
  • Joints / diagnostic imaging
  • Joints / microbiology
  • Joints / pathology
  • Mice
  • Staphylococcal Infections / diagnostic imaging*
  • Staphylococcal Infections / pathology
  • X-Ray Microtomography

Grants and funding

This work was supported by the Swedish Medical Research Council (grant 523-2013-2750 to T. Jin), the Swedish Medical Society (SLS-496741 and SLS-402871 to T. Jin), the Stiftelsen Clas Groschinskys Minnesfond (grant M1566, M14099, and M1626 to T. Jin), the Royal Society of Arts and Sciences in Gothenburg (grant to T. Jin and ML. Na), the Wilhelm and Martina Lundgren Foundation (grant to T. Jin, ML. Na, and A. Ali), the Scandinavian Society for Antimicrobial Chemotherapy Foundation (grant SLS-501701 to T. Jin), Rune och Ulla Amlövs Stiftelse för Neurologisk och Reumatologisk Forskning (grant 2015-00056 and 2016-075 to T. Jin), Professor Nanna Svartz Fond (grant 2015-00074 to T. Jin), and Adlerbertska Forskningsstiftelsen (grant to T. Jin and ML. Na), Coordination for the improvement of higher education personnel, CAPES (grant to F. Fatima and M. Nawaz), National Natural Science Foundation of China (grant 81460334 to Y. Fei), and the State Scholarship Fund of China Scholarship Council (grant 201508525101 to Y. Fei). The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.