On biological failures of osseointegrated oral implants

Abstract

The purpose of this thesis was to gain a better understanding of biological failures of osseointegrated oral implants in order to optimize clinical success rates, material characteristics and clinical procedures.Systematic evidence-based reviews were used to acquire epidemiological data on implant failures and associated risk factors. Tissues surrounding 38 clinically failed BrÂnemark oral titanium implants were analyzed in relation to clinical and radiographic findings by means of LM, immunohistochemistry and TEM. Surface compositions and oxide thicknesses of additional 12 failed implants were determined using SEM and scanning Auger microprobe for surface composition.Radiographic examinations and implant mobility tests seemed reliable parameters in the assessment of the conditions and prognosis for osseointegrated oral implants. Losses of BrÂnemark implants were 7.7% over 5 years (bone grafts excluded). Implants placed in partially edentulous patients performed better than those placed in fully edentulous patients. Highest failure rates were observed in grafted bone. Maxillas displayed about 3 times more failures than mandibles. Losses were concentrated before prosthesis placement and decreased over a 5-year period. A very low prevalence of failures attributable to peri-implantitis affected machined threaded implants. Losses tended to cluster in few patients. Medical status, smoking, therapeutic irradiation, the characteristics of the bone recipient site, bone grafting, parafunctions, lack of preoperative antibiotics, operator experience, surgical trauma, bacterial contamination, immediate loading, non-submerged technique, number of supporting implants, implant design and surface characteristics were found to influence failure rates. Mobile ìasymptomaticî implants retrieved at abutment connection were surrounded by a soft tissue capsule displaying either epithelial downgrowth migration, often together with inflammatory cell infiltrates, or a dense connective tissue. Implants retrieved after abutment connection, but before prosthesis placement, had a heterogeneous interface such as bone detached from the implant surface, stratified connective tissue or cell infiltrates dominated by macrophages and multinucleated giant cells. Late failed implants, identified by peri-implant radiolucency on radiographs, were generally surrounded by stratified connective tissue with scarce inflammatory infiltrates. When present, inflammatory infiltrates were dominated by lymphocytes and macrophages. Plasma-cells were also observed, although in a lower proportion. PMNs and B cells were rare. Epithelial downgrowth was sometimes noticed.Surface analysis of failed implants did not show any significant changes in the titanium oxide layer composition or thickness as a result of implantation. No indication of surface or material related causes for implant failure could be found. The present findings indicate that the early failures analyzed may be attributed to impaired healing ability of the recipient site, disruption of a weak bone-to-implant interface and, in situations with extended/complicated surgery, infection. For late losses, excessive occlusal load in relation to host characteristics and deep infection might have been the major etiological factors.