Pressure‐induced periprosthetic osteolysis: A rat model

Recent animal experiments have indicated that oscillating fluid pressure at the interface of bone and implant can lead to osteolysis. However, external nonphysiologic saline solutions were used to generate the pressure in these studies. In the present study on 15 Sprague‐Dawley rats, hydrostatic pressure fluctuations were applied to bone through body fluids, by compressing a soft‐tissue membrane adjacent to the proximal tibia. A titanium plate was fixed to the bone surface. After 28 days of osseointegration of the plate, a 1‐mm‐wide gap was created between it and the cortical bone and 5 days were given for fibrous tissue to form. Load was transmitted to this soft tissue by applying force on a piston mounted in the plate. In six rats, a cyclic pressure of 0.6 MPa was then applied to this tissue by 20 cycles twice a day with a frequency of 0.17 Hz for 5 days. The remaining rats served as controls, with the piston left untouched in its upper position. All of the rats were killed 10 days after creation of the gap. Histological sections were produced at a right angle to the loaded surface, In the pressurized specimens, osteoclastic bone resorption was dramatic. In all specimens, the original cortex was almost entirely resorbed but new woven bone had formed deeper in the marrow and walled off a cystic lesion. When necrotic remnants of the cortex were still in place, new woven bone was seen on the side away from the piston. This “lee effect” may indicate that bone formation was inhibited by fluid flow away from the pressurized tissue. The specimens with a nonloaded piston showed no signs of resorption. This new experimental model shows again that a moderate rise of hydrostatic pressure at the interface of bone and implant leads to considerable bone resorption. This could be a mechanism of prosthetic loosening.