Bacterial adhesion on titanium implant surfaces has a strong influence on healing and long-term outcome of dental implants. Parameters like surface roughness and chemical composition of the implant surface were found to have a significant impact on plaque formation. The purpose of this study was to evaluate the influence of two physical hard coatings on bacterial adhesion in comparison with control surfaces of equivalent roughness. Two members of the oral microflora, Streptococcus mutans and Streptococcus sanguis were used. Commercially pure titanium discs were modified using four different surface treatments: physical vapour deposition (PVD) with either titanium nitride (TiN) or zirconium nitride (ZrN), thermal oxidation and structuring with laser radiation. Polished titanium surfaces were used as controls. Surface topography was examined by SEM and estimation of surface roughness was done using a contact stylus profilometer. Contact angle measurements were carried out to calculate surface energy. Titanium discs were incubated in the respective bacterial cell suspension for one hour and single colonies formed by adhering bacteria were counted by fluorescence microscopy. Contact angle measurements showed no significant differences between the surface modifications. The surface roughness (Ra) of all surfaces examined was between 0.14 and 1.00 microm. A significant reduction of the number of adherent bacteria was observed on inherently stable titanium hard materials such as TiN and ZrN and thermically oxidated titanium surfaces compared to polished titanium. In conclusion, physical modification of titanium implant surfaces such as coating with TiN or ZrN may reduce bacterial adherence and hence improve clinical results.

The results of this case-control study demonstrate a higher frequency of dentine caries in patients with IBD but the periodontal findings showed no distinct differences between cases and controls.

A major consideration in designing dental implants is to create a surface that provides strong attachment of the implant to bone, connective tissue and epithelium. The aim of the present study was to examine the influence of different treatments of titanium (Ti) implant surfaces on focal adhesion contact (FAC) formation in fibroblast cultures. Human gingival fibroblasts were cultured on glass sheets and polished Ti discs with different surface coatings (applied by physical vapor deposition (PVD): Ti, titanium nitride (TiN), zirconium nitride (ZrN)) or on Ti discs with different surface topographies. For characterization of all surfaces, modified estimation of surface roughness and spacing parameter was carried out using a contact stylus profilometer. Contact angle measurements were carried out to calculate surface energy. Fibroblasts were prepared for transmission electron microscopy at day 3 after seeding, and the number of FACs and the ratio FAC/cellular cross-sections was determined at a length of 300 microm in ultrathin sections. To visualize the extracellular fibronectin and vitronectin molecules and the intracellular actin and vinculin in FAC areas, immunogold labeling was performed. The results revealed a strong correlation between the number of FACs and the surface roughness. The highest number of FACs and the majority of the immunogold-labeled intra- and extracellular matrix molecules were counted on surfaces with the lowest surface roughness: glass sheets coated with either Ti, TiN or ZrN (roughness average=0.03-0.1 microm). These surfaces appear to favor cellular attachment of human gingival fibroblasts and moreover in previous studies the hard coatings have been shown to reduce bacterial adhesion.

A coating of glass surfaces with ZrN significantly reduced the species richness in early bacterial colonization but the diversity was not significantly changed. In consideration of the results obtained by this and former studies a ZrN coating appears to rather modify the quantity of early bacterial adherence than the quality of the microbial community structure.

Polymorphisms in the interleukin-1 (IL1) gene have been suggested to influence transcription of IL1A (interleukin-1alpha) and IL1B (interleukin-1beta) and thereby the pathophysiology of periodontitis. This case-control association study on 415 northern European Caucasian patients with aggressive periodontitis (AgP) and 874 healthy controls was conducted to examine 10 single-nucleotide polymorphisms (SNPs) in the genes of the IL1 cluster for association with IL1A, IL1B, CKAP2L (cytoskeleton-associated protein 2-like), and IL1RN (IL-1 receptor antagonist). The results do not support an association between variants in the IL1 gene cluster and AgP. This case-control study had at least 95% power to detect genuine associations with variants carrying relative risks of at least 1.5 for heterozygous carriers and 2.25 for homozygous carriers. Previous reports of an association between IL1 promoter SNPs and periodontitis might reflect subpopulation effects and have to be interpreted with care.