Introduction: In a rat model, fluid pressure causes more bone resorption than particles. Does pressure also cause more inflammation?

Materials and Methods: Rats received a titanium plate at the proximal tibia. A central plug was inserted. After 5 weeks of osseointegration, the central plug was changed to either a piston or a hollow plug with titanium particles. Commercially pure titanium particles with 90% of particles lesser than 3,6 microns were used. The pressure piston was subjected to a transcutanous force of 8N. Each episode of pressure comprised 20 pressure cycles at 0.17 Hz, applied twice a day. 39 rats were randomized to 3 groups: Titanium particles (n=13), fluid pressure (n=13) and controls with neither particles nor fluid pressure (n=13). The rats were killed after 3 days. 6 rats in each group were used for histology and the others for gene expression. Extraction of total RNA was performed using the TRIspin method. Primers for cat K, RANK, RANKL, OPG IL-1, IL-b, TNF-a, iNOS and COX-2 were used. Each sample was normalized to 18S rRNA. Histology was evaluated qualitatively. Differences between the groups were analyzed by Kruskal Wallis and Mann-Whitney U-test.

Results: Both particles and fluid pressure increased the expression of osteoclastic genes. Particles induced an elevated expression of IL-6 and RANK compared to both controls and fluid pressure. There was a tendency that particles induced more expression of other inflammatory genes compared to fluid pressure.

Histology: The controls showed only few osteoclasts at the bone surface. The particle group showed osteoclasts at the surface towards the particles. In contrast, the pressure group showed resorption cavities spread out inside the bone.

Discussion: Although there was more resorption in the pressure group, there was a lesser inflammatory response. This suggests that pressure-induced resorption is mediated via different pathways.