Inflammation associated with implants with different surface types

The aim of this study was to determine the nature of the inflammatory infiltrate associated with different transmucosal implant surfaces in dogs. Three experimental and one control single-stage implants were randomly placed on each side of the jaw in eight dogs. The transmucosal portion of the test implants consisted of an acid-etched surface (type A), a machined surface with a circumferential groove (type C) and a surface prepared by mild anodic oxidation (type D). The control was a standard machined surface (type B). In order to determine the response to the different surfaces, plaque control was carried out twice weekly following placement of the implants for the entire period of the experiment. At 6 months, gingival biopsies and plaque samples were obtained. The area of inflammatory infiltrate and the nature of the infiltrating cell types were determined using immunohistology. Real-time polymerase chain reaction was used to identify putative periodontal pathogens. Inflammatory infiltrates were associated with all implant surfaces and were commonly found subepithelially and perivascularly. T cells were the predominant infiltrating cell type in all lesions, associated with the different surfaces. In all lesions the CD4 : CD8 ratio was approximately 2 : 1. Statistical analysis showed that the type C surface (machined surface with a groove) had significantly larger inflammatory infiltrates than the type B surface (machined surface without a groove; P < 0.05). No statistically significant differences were found with respect to the size of the inflammatory infiltrates or in terms of the nature of infiltrating cells. However, despite the intensive plaque control regime, plaque was present on all implant surfaces at the time of biopsy 6 months after placement. All implants had similar numbers of Tannerella forsythia, Fusobacterium nucleatum and Porphyromonas gingivalis. Actinobacillus actinomycetemcomitans, was not detected in any sample. These results suggest that the development of inflammation associated with implants is independent of surface type, but is nevertheless associated with the presence of plaque. The different surfaces had no influence on the nature of the infiltrate, with T cells being the predominant cell type in all lesions. Finally, the different implant surface types seemed not to influence the peri-implant microbiota. However, the presence of the circumferential groove tended to be associated with larger infiltrates. Whether this is due to increased plaque accumulation remains to be determined