Surface topography modulates initial platelet adhesion to titanium substrata.

The clinical success of implanted biomaterials such as dental implants is largely determined by the molecular signaling that occurs at the tissue-implant interface. The modification of surface topography is a widely-employed strategy for optimizing tissue integration with dental implants. However, little is known regarding the direct, cellular-level effects of substratum topography on platelet signaling and adhesion, despite these cells being the first to encounter the implant surface during surgical placement. Here we compared platelet adhesion and secretion on four (4) different titanium surfaces, notably, the modifications applied to commercially available dental implants: smooth (S) titanium; acid-etched (AE), sandblasted (SB) and a combined acid-etching/sandblasting procedure (SLA). Platelets were isolated from human blood, washed, and seeded on to the 4 test surfaces; platelet adhesion was quantified by microscopy. In addition, the secretion of critical molecules stored in platelet granules (platelet factor 4, PF4; soluble P-selectin, sCD62P; transforming growth factor-beta1, TGF-ß1; platelet-derived growth factor-AB, PDGF-AB) was measured by enzyme-linked immunosorbent assay (ELISA) analysis of the supernatants. There was greater platelet adhesion to the rougher AE and SB surfaces, however, the concentration of the secreted growth factors was comparable on all surfaces. We conclude that while surface topography can be engineered to modulate initial platelet adhesion, granule secretion is likely regulated as a separate and independent process.

The effects of surface treatments on tensile bond strength of polyether-ketone-ketone (PEKK) to veneering resin.

OBJECTIVES: To test the different PEKK surface treatment methods on the tensile bond strength (TBS) of a resin composite to PEKK. METHODS: Two hundred and fifty polished PEKK specimens were fabricated, divided into 5 groups (n = 50) and underwent the following treatments: no pre-treatment (control group C), 110 µm Al2O3 gritblasting at 2 bar for 10 s (Group Al), 98 wt% sulfuric acid etching for 60 s (Group SA), tribochemical silica-coating through air-abrasion with Rocatec Plus 110 µm at 2 bar for 10 s (Group Trib), and sulfuric acid etching and subsequent tribochemical silica-coating (Group SATrib). Ten specimens in each group were taken out for surface characterization. On the samples of Groups Trib and SATrib, a silane coupling agent was applied. Then, for all groups, veneering resin stubs (diameter: 3 mm) were bonded on the treated surfaces. Half of the specimens (n = 20) in each group were submitted to thermo-cycling for 7000 cycles between 5 °C and 55 °C. The TBS of all groups was examined using a universal testing machine. Fracture analysis was performed. For statistical analyses, one-way ANOVA (post-hoc: Bonferroni) and t-test were used at α = 0.05. RESULTS: Although the surface treatment methods used in this study were able to increase PEKK surface roughness, none of them showed impact on TBS between PEKK and the resin composite before thermal cycling (p > 0.05). However, after thermo-cycling, significantly higher TBS was measured for Groups Trib and SATrib (p < 0.05). Furthermore, the TBS for the SATrib group was not significantly affected by thermal cycling. Groups SA, Trib and SATrib illustrated an increase of Weibull moduli after thermocycling, but decrease was observed in Groups C and Al. CONCLUSION: Despite low tensile bond strengths were found in all groups in this study, Tribochemical silica-coating through air-abrasion with Rocatec Plus on polished or sulfuric-etched PEKK surface can significantly increase the tensile bonding stability as well as durability of resin composite to PEKK.

Polyphosphate/platelet factor 4 complexes can mediate heparin-independent platelet activation in heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is a thrombotic disorder initiated by antibodies to complexes between platelet factor 4 (PF4) and heparin. The risk of recurrent thromboembolism persists after heparin is cleared and platelet activation leading to release of PF4 has dissipated. We asked whether antigenic complexes between polyphosphates and PF4 released from activated platelets might intensify or sustain the prothrombotic phenotype of HIT. PF4 forms stable, ultralarge complexes with polyphosphates of various sizes, including those released from platelets, which are recognized by the HIT-like monoclonal KKO, an immunoglobulin G2bκ monoclonal heparin/PF4 binding antibody, and by human HIT antibodies. KKO helps to protect PF4/polyphosphate complexes from degradation by phosphatases. Complement is activated when HIT antibodies bind to PF4/polyphosphate complexes and PF4 reverses the inhibition of complement by polyphosphates. Polyphosphates and PF4 are stored primarily in separate granules in resting platelets, but they colocalize when the cells are activated. Platelets activated by subaggregating doses of thrombin receptor activating peptide release polyphosphates and PF4, which form antigenic complexes that allow KKO to further activate platelets in the absence of heparin and exogenous PF4. These studies suggest that thrombin- or immune complex-mediated release of endogenous antigenic PF4/polyphosphate complexes from platelets may augment the prothrombotic risk of HIT and perpetuate the risk of thrombosis after heparin has been discontinued.

Effects of different blasting materials on charge generation and decay on titanium surface after sandblasting.

It has been reported that sandblasting titanium with alumina (Al2O3) powder could generate a negative electric charge on titanium surface. This has been proven to promote osteoblast activities and possibly osseointegration. The purpose of this pilot study was to investigate the effects of different blasting materials, in terms of the grit sizes and electro-negativity, on the generation of a negative charge on the titanium surface. The aim was also to make use of these results to deduct the underlying mechanism of charge generation by sandblasting. Together 60 c.p. 2 titanium plates were machine-cut and polished for sandblasting, and divided into 6 groups with 10 plates in each. Every plate in the study groups was sandblasted with one of the following 6 powder materials: 110µm Al2O3 grits, 50µm Al2O3 grits, 150-300µm glass beads, 45-75µm glass beads, 250µm Al powder and 44µm Al powder. The static voltage on the surface of every titanium plate was measured immediately after sandblasting. The static voltages of the titanium plates were recorded and processed using statistical analysis. The results suggested that only sandblasting with 45-75µm glass beads generated a positive charge on titanium, while using all other blasting materials lead to a negative charge. Furthermore, blasting grits of the same powder material but of different sizes might lead to different amount and polarity of the charges. This triboelectric effect is likely to be the main mechanism for charge generation through sandblasting.

Effects of surface charges on dental implants: past, present, and future.

Osseointegration is a major factor influencing the success of dental implantation. To achieve rapid and strong, durable osseointegration, biomaterial researchers have investigated various surface treatment methods for dental subgingival titanium (Ti) implants. This paper focuses on surface-charge modification on the surface of titanium dental implants, which is a relatively new and very promising methodology for improving the implants' osseointegration properties. We give an overview on both theoretical explanations on how surface-charge affects the implants' osseointegration, as well as a potential surface charge modification method using sandblasting. Additionally, we discuss insights on the important factors affecting effectiveness of surface-charge modification methods and point out several interesting directions for future investigations on this topic.