Background Unstable implants in bone become surrounded by an osteolytic zone. This is seen around loose screws, for example, but may also contribute to prosthetic loosening. Previous animal studies have shown that such zones can be induced by fluctuations in fluid pressure or flow, caused by implant instability. Method To understand the roles of pressure and flow, we describe the 3-dimensional distribution of osteolytic lesions in response to fluid pressure and flow in a previously reported rat model of aseptic loosening. 50 rats had a piston inserted in the proximal tibia, designed to produce 20 local spikes in fluid pressure of a clinically relevant magnitude (700 mmHg) twice a day. The spikes lasted for about 0.3 seconds. After 2 weeks, the pressure was measured in vivo, and the osteolytic lesions induced were studied using micro-CT scans. Results Most bone resorption occurred at pre-existing cavities within the bone in the periphery around the pressurized region, and not under the piston. This region is likely to have a higher fluid flow and less pressure than the area just beneath the piston. The velocity of fluid flow was estimated to be very high (roughly 20 mm/s). Interpretation The localization of the resorptive lesions suggests that high-velocity fluid flow is important for bone resorption induced by instability.

Background: Periprosthetic joint infection (PJI) is a devastating complication following total joint arthroplasty. Current animal models of PJI are limited because of a lack of quantitative methods and failure to effectively recreate the periprosthetic space. We therefore developed a murine PJI model involving a 3-dimensionally printed Ti-6Al-4V implant capable of bearing weight and permitting quantitative analysis of periprosthetic bacterial load and evaluation of biofilm. Methods: Twenty-five 12-week-old C57BL/6 mice received a unilateral proximal tibial implant and intra-articular injection of either 3 × 10⁵ colony forming units (CFUs) of Staphylococcus aureus Xen 36 or saline solution. Postoperatively, mice underwent gait analysis, knee radiographs, and serum inflammatory marker measurements. Following euthanasia at 2 or 6 weeks, bone and soft tissues were homogenized to quantify bacteria within periprosthetic tissues. Implants were either sonicated to quantify adherent bacteria or examined under scanning electron microscopy (SEM) to characterize biofilm. Results: All mice survived surgery and were not systemically septic. The control mice immediately tolerated weight-bearing and had normal inflammatory markers and radiographic signs of osseointegration. Infected mice had difficulty walking over time, exhibited radiographic findings of septic implant loosening, and had significantly elevated inflammatory markers. Periprosthetic tissues of the infected animals displayed a mean of 4.46 × 10⁶ CFUs of S. aureus at 2 weeks and 2.53 × 10⁵ CFUs at 6 weeks. Viable S. aureus was quantified on retrieved implant surfaces. SEM demonstrated S. aureus cocci in clusters encased within biofilm. Conclusions: This animal model is, to our knowledge, the most clinically representative PJI replication to date. It is the first that we know of to produce infection through the same method hypothesized to occur clinically, utilize a weight-bearing implant that can osseointegrate, and provide quantitative data on 8 aspects of PJI, including radiographic features, inflammatory markers, and bacterial loads. Clinical Relevance: This novel animal model is, to our knowledge, the first to provide a load-bearing translational representation of clinical PJI that effectively recreates the periprosthetic space.