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 characterise microbiota and inflammatory host response around implants and teeth in patients with peri-implantitis. We included 17 partly edentulous patients with a total of 98 implants, of which 45 showed marginal bone loss of more than three fixture threads after the first year of loading. Nineteen subjects with stable marginal tissue conditions served as controls. Oral hygiene, gingival inflammation, and probing pocket depth were evaluated clinically at teeth and implants. Microbiological and crevicular fluid samples were collected from five categories of sites: 1) implants with peri-implantitis (PI), 2) stable implants (SI) in patients with both stable and peri-implantitis implants, 3) control implants (CI) in patients with stable implants alone, 4) teeth in patients (TP) and 5) controls (TC). Crevicular fluid from teeth and implants was analysed for elastase activity, lactoferrin and IL-1 beta concentrations. Elastase activity was higher at PI than at CI in controls. Lactoferrin concentration was higher at PI than at SI in patients with peri-implantitis. Higher levels of both lactoferrin and elastase activity were found at PI than at teeth in patients. The concentrations of IL-1 beta were about the same in the various sites. Microbiological DNA-probe analysis revealed a putative periodontal microflora at teeth and implants in patients and controls. Patients with peri-implantitis harboured high levels of periodontal pathogens, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus and Treponema denticola. These findings indicate a site-specific inflammation rather than a patient-associated specific host response.

Radiologic and clinical indicators of periodontal destruction were increased in individuals with poorly controlled T2D. Low SES aggravated the periodontal condition in individuals with T2D.

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.

Serological differences in subjects with periodontitis, some of which involve established risk factors for atherosclerosis, might provide insight into the reported epidemiological association between periodontitis and cardiovascular disease.