Different types of inflammatory reactions in peri‐implant soft tissues

Abstract

Abstract 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.