This Ph.D thesis addresses the clinical problems regarding access and effect of wear debris to the bone-implant interface and the possible dissemination of PE particles to distant organs. Wear particles are believed to contribute to peri-implant osteolysis and to be a major cause of aseptic loosening of hip implants. The PhD is based on 3 studies investigating the influence of different surface textures on the accumulation of PE particles in the peri-implant tissue.
In all studies we used a modified Søballe implant device in dogs. Test implants were implanted in each distal femoral condyle. The test implants were surrounded by a gap, which was communicating with the joint space, allowing access of joint fluid to the bone-implant interface. Injections of polyethylene particles were performed in the right knee joint three weeks after surgery and repeated with weekly intervals. Left knee joint received sham injections. Specimens from the bone-implant interface were examined under plain and polarized light and the presence of PE-particles and bone ingrowth was analysed.
In study I we compared a grit blasted implant surface with a HA coated surface. After eight weeks, only few particles were found around HA-coated implants. In contrast peri-implant tissue around Ti implants contained large amounts of particles. HA-coated implants had approximately 35% bone ingrowth, whereas Ti implants had virtually no bone ingrowth and were surrounded by a fibrous membrane. PE particles did not cause inflammation or bone resorption in the periimplant fibrous membrane.
In study II, we wanted to test if the sealing effect of HA found in study I was durable. Furthermore, we wanted if a inflammatory response and bone resorption in the bone-implant interface occurred with time. We repeated therefore injections of PE particles for a period of 49 weeks. Around Ti implants huge amounts of PE particles were found mainly in the bone-implant interface. Infiltration of mononuclear inflammatory cells was present around 3 out of 7 Ti implants in relation to PE particles. HA implants had approximately 70 percent bone ongrowth. In contrast, no bone ongrowth was seen on any Ti implants, all being surrounded by a fibrous membrane. The number of PE particles was evaluated semi-quantitatively. We found significantly more PE particles around Ti implants as compared with HA implants (p<0.002). A significant difference in tissue-ingrowth was not found between PE-exposed and vehicle-exposed implants in the two groups. Specimens from iliac lymph nodes, liver, spleen and lung were examined and dissemination of PE particles was only detected in regional lymph nodes.
In study III plasma-sprayed porous implants with or without HA were investigated. Closed-pore porous coatings have been claimed to prevent the migration of wear debris due to reduced peri-implant fluid flow. The hypothesis of the present study was that HA could improve the sealing effect of a plasma-sprayed porous coating. PE particles were injected repeatedly until 16 weeks after surgery. The number of particles was reduced by the HA coating from a median value 2 (range 1-4) to 1 (0-1) (p=0.01). HA coated implants had approximately 60 percent bone ingrowth. Ti-implants had virtually no bone ingrowth, but were covered by a fibrous membrane.
Conclusion: The present studies demonstrates that hydroxyapatite applied on a grit-blasted or porous surface yields superior bony ingrowth, and provides an initial protection against the migration of polyethylene particles in the bone-implant interface as compared with non-HA-coated implants. After 52 weeks the sealing effect of HA remains and this long-term study indicates that chronic inflammation due to PE particles in the bone-implant interface may be inhibited by HA coating.