Orthopaedic implant use increases infection risk. Implant infection risk can be explained by the “race for the surface” concept, where there is competition between host-cell integration and bacterial colonisation. Although generally accepted, the temporal dynamics have not been elucidated in vivo. Using a bilateral intramedullary rat model, Staphylococcus aureus was injected into the tail vein either immediately after or 1, 3 and 7 d following implant placement. This allowed assessment of the temporal interplay between bacterial colonisation and host-cell adhesion by uncoupling implant placement and bacterial challenge. 2 weeks following inoculation, animals were anaesthetised, euthanised and implants and tissues harvested for bacterial enumeration. To assess host participation in implant... protection, additional animals were not inoculated but euthanised at 1, 3 or 7 d and the host cells adhered to the implant were evaluated by flow cytometry and microscopy. As time between implant placement and bacterial challenge increased, infection rate and bioburden decreased. All implants had measurable bioburden when challenged at day 1, but only two implants had recoverable bacteria when inoculated 7 d after implant placement. This protection against infection corresponded to a shift in host cell population surrounding the implant. Initially, cells present were primarily non-differentiated stem cells, such as bone marrow mesenchymal stem cells, or immature haematopoietic cells. At day 7, there was a mature monocyte/macrophage population. The present study illustrated a direct relationship between host immune cell attachment and decrease in bacterial colonisation, providing guidance for antimicrobial release devices to protect orthopaedic implants against bacterial colonisation.