DIFFERENT TYPES OF INFLAMMATORY REACTIONS IN PERI-IMPLANT SOFT-TISSUES

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 pla que accumulation for periods up to 9 months. The experiment was carrie d out in 5 labrador dogs. The mandibular right and left 2nd, 3rd and 4 th premolars (2P2, 3P3, 4P4) and the 1st molars (1M1) were extracted. Following a 3-month healing period, 3 titanium fixtures (Nobelpharma A B, Goteborg, Sweden) were installed in the edentulous premolar/molar r egions. Abutment connection was performed 3 months later and a meticul ous plaque control period of 3 months was initiated. A clinical examin ation was performed at the end of this preparatory period and a main s tudy period of 9 months continued. During this period, the plaque cont rol regimen was maintained in the mesial and central (left: L1, 2 and right: R1, 2) implant segments, whereas plaque was allowed to accumula te on the distal implants, i.e., L3 and R3. At the end of the main stu dy period, i.e., 12 months after abutment connection, the clinical exa mination was repeated, the animals perfused and biopsies obtained. Sem i-thin sections were produced for histometric and morphometric analyse s. The peri-implant mucosa at implant sites exposed to daily and compr ehensive plaque control at biopsy was clinically noninflamed and the c onnective tissue lateral to a junctional epithelium was devoid of accu mulations 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 harv ested from the implant sites after 9 months of plaque formation demons trated 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 presen t at the level of borderline between the abutment and the fixture part of the implant. This infiltrate, called abutment ICT, occurred both a t 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 histom etric determinations disclosed that (i) the bone crest consistently wa s 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 conne ctive tissue that separated the apical portion of the abutment ICT and the bone crest. It is suggested that this infiltrate represents the e fforts by the host to close off bacteria present within the implant sy stem and that the establishment of an abutment ICT may explain the 1 m m bone loss observed during the course of the 1st year after bridge in stallation.