Joachim S. Hermann

Persistent Acute Inflammation at the Implant-Abutment Interface:

The inflammatory response adjacent to implants has not been well-investigated and may influence peri-implant tissue levels. The purpose of this study was to assess, histomorphometrically, (1) the timing of abutment connection and (2) the influence of a microgap. Three implant designs were placed in the mandibles of dogs. Two-piece implants were placed at the alveolar crest and abutments connected either at initial surgery (non-submerged) or three months later (submerged). The third implant was one-piece. Adjacent interstitial tissues were analyzed. Both two-piece implants resulted in a peak of inflammatory cells approximately 0.50 mm coronal to the microgap and consisted primarily of neutrophilic polymorphonuclear leukocytes. For one-piece implants, no such peak was observed. Also, significantly greater bone loss was observed for both two-piece implants compared with one-piece implants. In summary, the absence of an implant-abutment interface (microgap) at the bone crest was associated with reduced peri-implant inflammatory cell accumulation and minimal bone loss.

Peri-implant Inflammation Defined by the Implant-Abutment Interface

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/mm2). 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.

Influence of a machined collar on crestal bone changes around titanium implants: a histometric study in the canine mandible

BACKGROUND It has been shown that peri-implant crestal bone reactions are influenced by both a rough-smooth implant border in one-piece, non-submerged, as well as an interface (microgap [MG] between implant/abutment) in two-piece butt-joint, submerged and non-submerged implants being placed at different levels in relation to the crest of the bone. According to standard surgical procedures, the rough-smooth implant border for implants with a smooth collar should be aligned with the crest of the bone exhibiting a smooth collar adjacent to peri-implant soft tissues. No data, however, are available for implants exhibiting a sandblasted, large-grit and acid-etched (SLA) surface all the way to the top of a non-submerged implant. Thus, the purpose of this study is to histometrically examine crestal bone changes around machined versus SLA-surfaced implant collars in a side-by-side comparison. METHODS A total of 60 titanium implants (30 machined collars and 30 SLA collars) were randomly placed in edentulous mandibular areas of five foxhounds forming six different subgroups (implant subgroups A to F). The implants in subgroups A to C had a machined collar (control), whereas the implants in subgroups D to F were SLA-treated all the way to the top (MG level; test). Furthermore, the MGs of the implants were placed at different levels in relation to the crest of the bone: the implants in subgroups A and E were 2 mm above the crest, in subgroups C and D 1 mm above, in subgroup B 3 mm above, and in subgroup F at the bone crest level. For all implants, abutment healing screws were connected the day of surgery. These caps were loosened and immediately retightened monthly. At 6 months, animals were sacrificed and non-decalcified histology was analyzed by evaluating peri-implant crestal bone levels. RESULTS For implants in subgroup A, the estimated mean crestal bone loss (± SD) was -0.52 ± 0.40 mm; in subgroup B, +0.16 ± 0.40 mm (bone gain); in subgroup C, -1.28 ± 0.21 mm; in subgroup D, -0.43 ± 0.43 mm; in subgroup E, -0.03 ± 0.48 mm; and in subgroup F, -1.11 ± 0.27 mm. Mean bone loss for subgroup A was significantly greater than for subgroup E (P = 0.034) and bone loss for subgroup C was significantly greater than for subgroup D (P <0.001). CONCLUSIONS Choosing a completely SLA-surfaced non-submerged implant can reduce the amount of peri-implant crestal bone loss and reduce the distance from the MG to the first bone-implant contact around unloaded implants compared to implants with a machined collar. Furthermore, a slightly exposed SLA surface during implant placement does not seem to compromise the overall hard and soft tissue integration and, in some cases, results in coronal bone formation in this canine model.