A new model of implant‐related osteomyelitis in rats

Abstract

Infection related to osteosynthesis often has dramatic consequences for the patient. Prolonged hospitalization with systemic antibiotic therapy, several revision procedures, possible amputation, and even death may occur. To investigate the pathology of infection in orthopedic surgery, a new rat model of implant related osteomyelitis was developed. Three different concentrations (10(6), 10(3), and 10(2) colony-forming units (CFU)/10 microl) of Staphylococcus aureus were inoculated into the tibial medullary cavity with simultaneous insertion of a titanium Kirschner wire. Controls received phosphate-buffered saline (PBS). Each group consisted of 10 animals. Animals were followed for 4 weeks until sacrifice. X-rays of the tibiae were taken weekly, blood counts were analyzed, and body temperature and weight were determined. After sacrifice, infection was evaluated by histological and microbiological investigations. All animals inoculated with Staph. aureus in either concentration developed microbiological, histological, and radiological signs of osteomyelitis in correlation to the amount of inoculated bacteria. X-rays clearly revealed osseous destruction after 14 days with progression of osteomyelitis during the following weeks. CFU/g bone and bone weight after sacrifice showed dependence on the amount of inoculated CFU. The histological results confirmed the radiological findings. No significant changes in blood counts, body weight, and body temperature between the groups could be observed. The results demonstrate that it is possible to develop a model of implant-related osteomyelitis in rats with dependence on the amount of inoculated bacteria. No other promoters of infection besides intramedullary insertion of titanium Kirschner wires were used in this model.

Quantitative mouse model of implant‐associated osteomyelitis and the kinetics of microbial growth, osteolysis, and humoral immunity

“…First, the field has been overly concerned with intramedullary implant models, since this represents the more serious clinical condition. [8][9][10][11][12][13] Unfortunately, we found that this IMPLANT-ASSOCIATED OSTEOMYELITIS model gave rise to highly variable (temporal and spatial) lesions, making a reproducible, quantitative model very challenging, although others have recently succeeded. 24 In contrast, we have found that implantation of an infected transcortical pin always produces lesions adjacent to the pin, and never results in distal OM, hematogenous infection, or death (Fig.…”

“…As such, biofilm biology, which plays a critical role in resistance of chronic OM to antibiotic therapy by serving as a dominant protective barrier from the action of antibiotics, can only be studied with in vivo models. 4 To date, much of our knowledge of the pathogenesis of OM comes from animal models, 5 which have existed in chicken, 6 rat, 7,8 guinea pig, 9 rabbit, 10 dog, 11 sheep, 12 goat, 13 and most recently mouse. 14 While these models have been used to confirm the importance of bacterial adhesions identified from in vitro assays, [15][16][17] none of them contain quantitative endpoints that can determine bacterial load or growth in vivo.…”

Can Normal Fracture Healing Be Achieved When the Implant Is Retained on the Basis of Infection? An Experimental Animal Model

“…In histological evaluation, the results were consistent, although two specimens in each group were evaluated [15]. The callus tissues of both groups at the third week were similar, but at the sixth week, the callus formation remained immature in the infection group.…”

“…Torque to failure and stiffness both were lower in the infection group than in the control group at 6 weeks, but with the numbers available for testing, they were not different at 3 weeks (p = 0.615 and p = 1, respectively; Table 2 [3][4][5][6][7][8][9][10][11][12][13][14][15][16]; p = 0.004) both were greater in the control group than in the group with infection. Maximum torque to failure was lower in the infection group than in the control group at all time points.…”

“…Results Infection decreased callus strength at 6 weeks. Torque to failure (299.07 ± 65.53 Nmm versus 107.20 ± 88.81, mean difference with 95% confidence interval, 192 ; p = 0.007) and stiffness at 6 weeks (11.28 ± 2.67 Nmm versus 2.03 ± 1.68, mean difference with 95% confidence interval, 9 [3][4][5][6][7][8][9][10][11][12][13][14][15][16]; p = 0.004) both were greater in the control group than in the group with infection.…”