BackgroundThe objective of this study was to determine whether the addition of microsilver or nanosilver particles to an orthodontic primer affects shear bond strength (SBS) and bracket/adhesive failure.MethodsBovine incisors were randomly divided into six groups with 16 specimens in each: In group 1 (control), brackets were bonded with Transbond™ XT primer. In the experimental groups, microsilver (groups 2 and 3) and nanosilver (groups 4–6) particles of different sizes were added to Transbond XT primer and light cured for 15 seconds [group 2: 0.1% (w/w) microsilver particle size 3.5–18 μm; group 3: 0.3% (w/w) microsilver particle size 3.5–18 μm; group 4: 0.11% (w/w) nanosilver particle size 12.6–18.5 nm; group 5: 0.18% (w/w) nanosilver particle size 12.6–18.5 nm; group 6: 0.33% (w/w) nanosilver particle size 12.6–18.5 nm]. Thereafter, brackets were bonded by light curing the adhesive for 20 seconds. After 24 hours of storage in distilled water at 37°C, SBS was measured with a Zwicki 1120 testing machine. The adhesive remnant index and the prevalence of silver spots on the specimen surface were determined under 10× magnification. Statistical two-way analysis of variance was performed to compare SBS, and a chi-square test was used to compare ARI scores and the prevalence of silver spots.ResultsNo significant differences in SBS (control: 16.59 ± 6.82 MPa; group 2: 20.6 ± 4.19 MPa; group 3: 16.98 ± 4.84 MPa; group 4: 17.15 ± 5.92 MPa; group 5: 20.09 ± 3.35 MPa; group 6: 16.44 ± 4.51 MPa; p > 0.665) and ARI scores (p = 0.901) were found between the control group and any experimental group. Only experimental groups with nanosilver particles revealed statistically more silver spots on the remaining adhesive.ConclusionsAddition of small concentrations of microsilver or nanosilver particles affects neither SBS nor ARI scores. Addition of nanosilver particles results in silver spots in the remaining primer visible under 10× magnification. Further studies are needed to investigate the anti-caries potential and clinical performance of conventional orthodontic primer with incorporated nanosilver or microsilver particles.

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To investigate the possible role of the local tissue kallikrein-kinin system in spermatogenesis, we analyzed gene expression and cellular distribution of the bradykinin subtype-2 receptor (B(2) receptor) in the rat testis. Reverse transcription-polymerase chain reaction revealed B(2) receptor expression in testis and primary cultures of Sertoli cells and peritubular cells isolated from immature and mature rats. In situ hybridization of the B(2)-receptor mRNA showed intense labeling of cells on the base of the seminiferous tubule, whereas the autoradiographic signals gradually decreased toward the lumen. Immune histochemistry using testicular sections of pubertal and adult rats showed specific staining for the B(2)-receptor protein in cells of the adluminal compartment of the seminiferous tubules, especially on pachytene spermatocytes and spermatids. This immunostaining varied with the stages of the seminiferous cycle. The receptor protein was also observed on peritubular cells of pubertal rats. In conclusion, we demonstrated a stage-specific expression of the bradykinin B(2) receptor in different cells of the seminiferous tubules of the rat testis. The results point to a possible function of the tissue kallikrein-kinin system in the local regulation of spermatogenesis.