An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 +/- 691 vs. 2398 +/- 1077 neutrophils/mm(2)). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.

The use of endosseous dental implants as transmucosal devices necessitates the successful integration of three different tissues: bone, connective tissue, and epithelium. So far, studies have predominantly focused on hard tissue integration. Much less is known about soft tissues. This study examined the dimensions of the implantogingival junction in relation to clinically healthy unloaded and loaded nonsubmerged implants. In total, 69 titanium plasma-sprayed (TPS) and sandblasted acid-etched (SLA) implants were placed in an alternating fashion in six foxhounds and allowed to heal for 3 months. Two dogs were sacrificed after the initial healing period. The remaining four dogs had crowns fabricated that were allowed to function for up to 12 months. These animals were sacrificed after 3 and 12 months of loading. Histometric analysis of undecalcified histologic sections included the evaluation of the sulcus depth (SD), the dimensions of the junctional epithelium (JE), and the connective tissue contact (CTC). Mean values in the 3 month unloaded group were 0.49 mm for SD, 1.16 mm for JE, and 1.36 mm for CTC. These dimensions were 0.50 mm for SD, 1.44 mm for JE, and 1.01 mm for CTC for the 3 month loaded group. After 12 months of loading, these values were 0.16 mm for SD, 1.88 mm for JE, and 1.05 mm for CTC. The sum of these measurements was similar for the different time points and similar to the same dimensions around teeth. TPS and SLA surfaces had no influence on the evaluated parameters (P > 0.05). The data suggest that a biologic width exists around unloaded and loaded nonsubmerged one-part titanium implants and that this is a physiologically formed and stable dimension as is found around teeth.

Current implant placement utilizes both nonsubmerged and submerged techniques. However, the implications of the location of a rough/smooth implant interface as well as the location of a microgap between implant and abutment on crestal bone changes are not well understood. The purpose of this study was to radiographically evaluate crestal bone changes around unloaded nonsubmerged and submerged titanium implants in a side-by-side comparison. Fifty-nine (59) implants were placed at different levels to the alveolar crest in 5 foxhounds. Standardized radiographs were taken at baseline and at monthly intervals until sacrifice at 6 months. Radiographic assessment was carried out by measuring the distance between the top of the implant/abutment and the most coronal bone-to-implant contact (DIB), and by evaluation of bone density changes using computer-assisted densitometric image analysis (CADIA). DIB measurements revealed that in 1-part, nonsubmerged implants, the most coronal bone-to-implant contact followed at all time points the rough/smooth implant interface. In all 2-part implants, nonsubmerged and submerged, the most coronal bone-to-implant contact was consistently located approximately 2 mm below the microgap. In addition, CADIA values for all 2-part implants were decreased in the most coronal area-of-interest (AOI). All bone changes were statistically significant and detectable 1 month after implant placement in nonsubmerged implants or 1 month after abutment connection in submerged implants. Neither implant position nor individual dog effects were statistically significant. These results demonstrate that the rough/smooth implant interface as well as the location of the microgap have a significant effect on marginal bone formation as evaluated by standardized longitudinal radiography. Bone remodeling occurs rapidly during the early healing phase after implant placement for non-submerged implants and after abutment connection for submerged implants.