Retrospective Analysis on Survival Rate of 1534 One-Piece Zirconia Ceramic Implants Placed in Healed Sites and Fresh Extraction Sockets: Results Between 1 and 13 Years of Follow-Up.
Introduction: The aim of this study was to evaluate the success rate of one-piece zirconia ceramic (Y-TZP) implants placed in fresh extraction sockets and healed sites between 1 and 13 years follow-up in private practice.
Method: One-piece zirconia dental implants with three different roughened surfaces were designed and manufactured for this study: coated, uncoated, and acid-etched. Seven different implant designs were manufactured. Standard or flapless surgical procedures were used for implant placement. Simultaneous bone augmentation or sinus elevation was performed when bone height or width was insufficient. Definitive all-ceramic restorations were placed 4 months after implant placement (8 months or more for implants when bone augmentation or sinus elevation was performed). The implants were followed up to 13 years (mean, 9.40 +/- 0.21).
Results: In all, 1534 implants were placed in 889 patients with a mean age of 51 years. The overall implant success rate after 13 years of follow-up was 97.60% for acid-etched implants. The success rate of the acid-etched surface group was significantly better than that of the other two.
Conclusion: From this long-term investigation, it can be concluded that one-piece zirconia dental implants with roughened surfaces might be a viable alternative for tooth replacement in selected patients. Further studies are needed to confirm these preliminary results.
The existence of a microgap in two-piece metal implant system has been well documented in the literature. This microgap is in microns size and several in-vitro studies tested the microleakage through the microgap and its effect on hard and soft tissues. It was proven that this gap acts as a reservoir for bacteria which induced peri-implant tissue inflammatory reactions.
Microgap is defined as the microscopic space that exists between the implant body and abutment. This gap is generally measured in microns meters and is located at the junction between the metal implant and implant abutment. The microgap may act as a reservoir for bacteria, which can lead to release of bacterial byproducts and induction of an inflammatory reaction at both soft and hard tissue level. The main mechanism proposed for microgap-related crestal bone loss is the role of this space as a trap for bacteria and thus, as a putative etiological factor for inflammatory reaction in the peri- implant soft tissues. The establishment of inflammatory cell infiltrates at the implant- abutment junction, even around implant with meticulous plaque control and clinically healthy soft tissue, has recently been shown histologically by Ericson et al. In another study, the implant-abutment interface at the alveolar bone crest was associated with persistent peri-implant inflammation. This second study was conducted to compare the distribution and amount of inflammatory cells adjacent to implant with a supra-crestal, crestal or sub-crestal implant-abutment interface. Polymorphonuclear leukocytes or neutrophils accumulated at the greatest levels near or immediately coronal to the interface. However, peri-implant neutrophils increased progressively as the implant-abutment interface depth increased. Thus, the inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. In a clinical study, Quirynen et al, suggested that the microorganisms detected from the inside of the implant three months after abutment connection may be the result of leakage at the implant-abutment interface or contamination during abutment connection.