Implant loss was most frequently described (reported in about 100% of studies), while biological complications were considered in only 40-60% and technical complications in only 60-80% of the studies. This observation indicates that data on the incidence of biological and technical complications may be underestimated and should be interpreted with caution.

The aim of the present study was to analyze some features of the peri‐implant mucosa at sites in the dog model which had been exposed to plaque accumulation for periods up to 9 months. The experiment was carried out in 5 labrador dogs. The mandibular right and left 2nd, 3rd and 4th premolars (2P2, 3P3, 4P4) and the 1st molars (1M1) were extracted. Following a 3–month healing period, 3 titanium fixtures (Nobelpharma AB. Göteborg, Sweden) were installed in the edentulous premolar/molar regions. Abutment connection was performed 3 months later and a meticulous plaque control period of 3 months was initiated. A clinical examination was performed at the end of this preparatory period and a main study period of 9 months continued. During this period, the plaque control regimen was maintained in the mesial and central (left: L1, 2 and right: R1, 2) implant segments, whereas plaque was allowed to accumulate on the distal implants, i.e., L3 and R3. At the end of the main study period, i.e., 12 months after abutment connection, the clinical examination was repeated, the animals perfused and biopsies obtained. Semi‐thin sections were produced for histo‐metric and morphometric analyses. The peri‐implant mucosa at implant sites exposed to daily and comprehensive plaque control at biopsy was clinically non‐inflamed and the connective tissue lateral to a junctional epithelium was devoid of accumulations of inflammatory cells. On the other hand, termination of the plaque control program resulted in the accumulation of large amounts of plaque and calculus at the titanium abutments and the biopsies harvested from the implant sites after 9 months of plaque formation demonstrated an infiltrate which resided in the marginal portion of the peri‐implant mucosa. The histological analysis of the biopsy material also revealed that an inflammatory cell infiltrate was consistently present at the level of borderline between the abutment and the fixture part of the implant. This infiltrate, called abutment ICT, occurred both at sites which had been exposed to plaque control and at sites at which plaque had been allowed to form during a 9–month interval. The histometric determinations disclosed that (i) the bone crest consistently was located about 1–1.5 mm “apical” of the abutment/fixture level, (ii) there was a zone, about 1 mm wide, of a normal non‐infiltrated connective tissue that separated the apical portion of the abutment ICT and the bone crest. It is suggested that this infiltrate represents the efforts by the host to close off bacteria present within the implant system and that the establishment of an abutment ICT may explain the 1 mm bone loss observed during the course of the 1st year after bridge installation.

The process of bone modeling and remodeling at an implant placed in a fresh extraction socket differs from the resolution of marginal defects that may occur following implant installation in a healed ridge.

Spontaneous progression of experimentally induced peri-implantitis occurred at implants with different geometry and surface characteristics. Progression was most pronounced at implants of type D (TiUnite surface).

The aim of the present study was to examine the microbiota on the internal surface of the components of 28 Brånemark implants in 10 partially edentulous patients who had been treated with 1 fixed partial prostheses each. The prostheses had been in function for 1 to 8 years. The fixed prostheses were checked for mobility and removed. The abutment screws were loosened and classified as stable, easily removed or loose. Then, bacterial samples were obtained from the various internal surfaces of the implant system. Estimation and identification of the most predominant species was performed on the blood agar plates. Identification was based on Gram reaction, oxygen sensitivity and biochemical tests. Internal surfaces of different components of the Brånemark implants, after varying periods of function in the oral cavity, consistently harboured a heterogeneous and primarily anaerobic microbiota. The individual samples showed a great variation. No relation could be seen between type and length of abutment, abutment stability, bone loss and type and number of microorganisms found in the samples. The flora consisted mainly of facultative and anaerobic streptococci, Gram-positive anaerobic rods such as Propionibacterium, Eubacterium and Actinomyces species and Gram-negative anaerobic rods including Fusobacterium, Prevotella and Porphyromonas species. There are reasons to suggest that this presence of bacteria is the result of (i) a contamination of the fixture and abutment components during the 1st and/or 2nd stage of implant installation and/or (ii) a transmission of microorganisms from the oral environment during function subsequent to bridge installation.

Peri-implantitis is a condition that includes soft tissue inflammation and rapid loss of bone. Treatment of peri-implantitis includes both antimicrobial and bone augmenting methods. The question of whether true re-osseointegration may occur following treatment of peri-implantitis is controversial. The aim of this study was to investigate whether the character of the implant surface was of importance for the occurrence of re-osseointegration following treatment of peri-implantitis. Four beagle dogs were used. The mandibular premolars were extracted. After 12 months, 3 ITI(R) solid screw dental implants were placed in each side of the mandible. In the left side, implants with a turned surface (Turned sites) were used, while in the right side implants with a SLA surface (SLA sites) were placed. After 3 months of healing, peri-implantitis was induced by ligature placement and plaque accumulation. When about 50% of the initial bone support was lost, the ligatures were removed. Five weeks later, treatment was initiated. Each animal received tablets of Amoxicillin and Metronidazole for a period of 17 days. Three days after the start of the antibiotic regimen, one implant site (experimental site) in each quadrant was exposed to local therapy. Following flap elevation, the exposed titanium surface was cleaned with the use of cotton pellets soaked in saline. The implants were submerged. Six months later, biopsies were obtained. Treatment resulted in a 72% bone fill of the bone defects at Turned sites and 76% at SLA sites. The amount of re-osseointegration was 22% at Turned sites and 84% at SLA sites. A treatment regimen that included (i) systemic administration of antibiotics combined with (ii) granulation tissue removal and implant surface cleaning resulted in resolution of peri-implantitis and bone fill in adjacent bone defects. Further, while substantial "re-osseointegration" occurred to an implant with a rough surface (SLA), bone growth on a previously exposed smooth surface (Turned) was minimal.

Resolution of peri-implantitis following treatment without systemic or local antimicrobial therapy is possible but the outcome of treatment is influenced by implant surface characteristics.

The aim of the present experiment was i) to study the effect of anti-microbial therapy of experimentally induced peri-implantitis lesions and ii) to assess features of bone regrowth following treatment. Four beagle dogs were used. Three titanium fixtures (Brånemark System) were installed in each quadrant of the mandible (premolars previously extracted). Abutment connection was performed 5 months later and ligature induced breakdown was initiated. The ligatures were removed when approximately 50% of the initial bone support was lost. A 3-week antibiotic regimen (amoxicillin and metronidazole) was initiated 1 month later. Two days after the start of the antibiotic administration, the experimental implant sites were exposed to local therapy. The abutments were removed and the exposed fixture surfaces were treated with an abrasive (pumice) administered via a rotating brush (left side) or cleaned with cotton pellets soaked in saline (right side). Cover screws were attached to the fixtures and the implants were submerged. Fluorochromes were injected intravenously 2 weeks, 4 weeks and 12 weeks after surgery. The animals were killed 7 months after surgery and block biopsies of each implant site were dissected and prepared for histological analysis. The findings of the examinations disclosed that the inflammatory lesion was resolved and new bone formation had occurred in the previous defect following antimicrobial and local therapy. The amount of "re-osseointegration" that had taken place, however, was small. Indeed, at all experimental implant sites, a thin connective tissue capsule was found to separate the implant surface from the newly formed bone.