Peri-implantitis: An educator’s perspective
By Vincent J. Iacono, DMD
When educated by Professor Brånemark almost 40 years ago on the novel procedure of osseointegration of dental implants, it was essentially a technique that has evolved into a comprehensive discipline. Implants of machined Grade 1 pure titanium were routinely inserted into the anterior sextant of the edentulous mandible of patients under general anesthesia in an OR setting.
These osseointegrated implants often emerged through alveolar mucosa and supported hybrid prostheses. While peri-implant mucositis and peri-implantitis were not recognized at the time, complications of malposed implants (no CBCT scans), damage to vital structures, “spinners,” “sleepers,” and implant/restorative fractures were the concerns of the era. Yet times rapidly changed, as we began to place implants at virtually any edentulous site using concepts of guided bone regeneration, ridge expansion, sinus grafts and periodontal plastic surgical procedures.
The implant structures changed to Grade 4 titanium or its alloy for strength and some were plasma sprayed with either titanium or calcium phosphate salts. Peri-implant complications then became a major focus with the recognition that plasma spraying resulted in surfaces that when colonized by the plaque biofilm, tended to lead to significant circumferential alveolar bone resorption with loss of the implants. The plasma spraying days were over!
It was also noted that at times implants with cemented abutment crowns developed peri-implant bone loss. It was determined that this was due to excess cement extruding into the peri-implant area. However, when the protruding cement was removed during an access periodontal flap surgical procedure, there usually was a return to a normal osseointegrated state. It is likely that the adherent cement on the implant threads led to bone resorption and when removed the titanium surface was then able to osseointegrate.
The challenge to enhance the kinetics of osseointegration with a greater degree of bone contact led to the use of acid etching with or without sandblasting or expanding the oxide surface of machined/turned titanium implant surfaces to achieve moderate roughness. These implants have been superb for enhancing osseointegration. However, since their use, peri-implant mucositis and peri-implantitis have become significant complications that we have had to address. The incidence of peri-implantitis is increasing and its severity has similar risk factors to periodontitis including but not limited to a dysbiotic biofilm with aberrant host responses, uncontrolled type-2 diabetes, and an unexplained genetic predisposition.
Karoussis and colleagues compared the outcome of implant therapy in patients with or without a history of periodontitis in a 10-year longitudinal study. They demonstrated that the incidence of peri-implantitis at the implant level was 28.6% in patients with a history of periodontitis, while it was 5.8% in patients without a history of periodontitis. It is important that our patients have had appropriate periodontal therapy before implant placement and are compliant with biofilm control and maintenance visits. It is a challenge to treat lesions of peri-implantitis and to decide on whether to remove the failing implant. I leave it to clinical judgement for implant removal as to the extent of bone resorption and existing implant restoration.
For my periodontal residents, the incidence of peri-implantitis has been comparable to that reported in the literature. The osseous defects resulting from lack of care for may years have either been severe horizontal bone loss or varying degrees of “moat” like defects. We have found that for lesions with horizontal bone loss, virtually no techniques have led to significant regeneration of bone coronal to the alveolar crest regardless of the thickness of the surrounding peri-implant soft tissue. In these cases, clinical judgement prevails as to apically positioning the soft tissue to the alveolar crest and expose the non-integrated coronal portion of the implant, flap access procedures for implant surface decontamination, or implant removal depending on the extent of bone loss.
We have found successful results for “moat” like defects that are dependent on the distance of the walls of the “moat” to the implant surface. The techniques employed include significant implant decontamination with “standard” acceptable methods (e.g., hydrogen peroxide and saline rinses); followed with the use of a particulate osseous allograft/xenograft/biologic composite graft and covered with a tightly adapted resorbable barrier using a “lifesaver” or “poncho” method. Copious lavage with a biologic and post-operative antibiotic are routine. However successful outcomes have not been 100% due to the extent and configuration of alveolar bone loss.
We now frequently use hybrid implants that have highly anodized surfaces at their coronal portions; avoid subcrestal placement of implants that negatively impact on the dynamics of the implant abutment connection; place the smooth surface area coronal to the crest (bone level implants) and through the transmucosal layer (tissue level implants). So, a new era begins with the hope that the incidence of peri0implant inflammation will be reduced. Whether there will be a reduction in the effects of traumatic occlusal forces, release of titanium particles, and implant restorative designs (e.g., zirconia) will depend on the incorporation of evolving guidelines from basic/clinical research.
Unfortunately, I sense that some clinicians are resistant to accept the reasons for complications and follow a biased judgement with a false sense of security. It is critically important that we use our best judgement and follow the accepted guidelines for successful outcomes and not be “clouded” by podium science in decision making.