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Air particle abrasion (APA) using bioactive glass (BG) effectively decontaminates titanium (Ti) surface biofilms and the retained glass particles on the abraded surfaces impart potent antibacterial properties against various clinically significant pathogens. The objective of this study was to investigate the effect of BG APA and simulated body fluid (SBF) immersion of sandblasted and acid-etched (SA) Ti surfaces on osteoblast cell viability. Another goal was to study the antibacterial effect against Streptococcus mutans. Square-shaped 10 mm diameter Ti substrates (n = 136) were SA by grit blasting with aluminum oxide particles, then acid-etching in an HCl-H2SO4 mixture. The SA substrates (n = 68) were used as non-coated controls (NC-SA). The test group (n = 68) was further subjected to APA using experimental zinc-containing BG (Zn4) and then mineralized in SBF for 14 d (Zn4-CaP). Surface roughness, contact angle, and surface free energy (SFE) were calculated on test and control surfaces. In addition, the topography and chemistry of substrate surfaces were also characterized. Osteoblastic cell viability and focal adhesion were also evaluated and compared to glass slides as an additional control. The antibacterial effect of Zn4-CaP was also assessed against S. mutans. After immersion in SBF, a mineralized zinc-containing Ca-P coating was formed on the SA substrates. The Zn4-CaP coating resulted in a significantly lower Ra surface roughness value (2.565 μm; p < 0.001), higher wettability (13.35°; p < 0.001), and higher total SFE (71.13; p < 0.001) compared to 3.695 μm, 77.19° and 40.43 for the NC-SA, respectively. APA using Zn4 can produce a zinc-containing calcium phosphate coating that demonstrates osteoblast cell viability and focal adhesion comparable to that on NC-SA or glass slides. Nevertheless, the coating had no antibacterial effect against S. mutans. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the surface characteristics of a nanocrystalline hydroxyapatite coating made through atomic layer deposition (ALD-HA) on titanium surfaces and to investigate its effect on blood coagulation and platelet adhesion. Grade 2 square titanium discs (0.7 cm, 1 mm thick) were used (n = 108). Half of the substrates (n = 54) were coated with ALD-HA, and the other half were used as the non-coated control. Surface free energy (SFE), contact angle (CA), surface roughness (Ra), and chemical composition were evaluated. Blood thrombogenic properties were assessed on ALD-HA and non-coated surfaces using the kinetic clotting time method. The platelets' adhesion and morphology were also evaluated. The ALD-HA-coated surfaces demonstrated significantly higher polar SFE (p < 0.001) and lower CA (p < 0.001) values compared to the non-coated surfaces. In addition, the surface roughness was significantly lower for the ALD-HA (p < 0.001) than for the non-coated surfaces. Platelets adhered to both surfaces; however, there was variability in platelet morphologies in different areas with higher platelet density on the ALD-HA surfaces. There was no significant difference in the overall absorbance values of the hemolyzed hemoglobin for both substrates, and the total clotting time was achieved at 60 min. It can be concluded that the ALD-HA coating of titanium can enhance surface wettability, increase surface free energy, and support blood coagulation and platelet adhesion. [ABSTRACT FROM AUTHOR]

Insulin-like growth factor-I (IGF-I) levels, which are reduced by age, and cortical bone dimensions are major determinants of fracture risk in elderly subjects. Inactivation of liver-derived circulating IGF-I results in reduced periosteal bone expansion in young and older mice. In mice with lifelong depletion of IGF-I in osteoblast lineage cells, the long bones display reduced cortical bone width. However, it has not previously been investigated whether inducible inactivation of IGF-I locally in bone in adult/old mice affects the bone phenotype. Adult tamoxifen-inducible inactivation of IGF-I using a CAGG-CreER mouse model (inducible IGF-IKO mice) substantially reduced IGF-I expression in bone (−55%) but not in liver. Serum IGF-I and body weight were unchanged. We used this inducible mouse model to assess the effect of local IGF-I on the skeleton in adult male mice, avoiding confounding developmental effects. After tamoxifen-induced inactivation of the IGF-I gene at 9 months of age, the skeletal phenotype was determined at 14 months of age. Computed tomography analyses of tibia revealed that the mid-diaphyseal cortical periosteal and endosteal circumferences and calculated bone strength parameters were decreased in inducible IGF-IKO mice compared with controls. Furthermore, 3-point bending showed reduced tibia cortical bone stiffness in inducible IGF-IKO mice. In contrast, the tibia and vertebral trabecular bone volume fraction was unchanged. In conclusion, inactivation of IGF-I in cortical bone with unchanged liver-derived IGF-I in older male mice resulted in reduced radial growth of cortical bone. This suggests that not only circulating IGF-I but also locally derived IGF-I regulates the cortical bone phenotype in older mice. [ABSTRACT FROM AUTHOR]

Hydroxyapatite (HA; Ca10(PO4)6(OH)2) coating of bone implants has many beneficial properties as it improves osseointegration and eventually becomes degraded and replaced with new bone. We prepared HA coating on a titanium substrate with atomic layer deposition (ALD) and compared monocyte differentiation and material resorption between ALD-HA and bone. After stimulation with macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL), human peripheral blood monocytes differentiated into resorbing osteoclasts on bovine bone, but non-resorbing foreign body cells were observed on ALD-HA. The analysis of the topography of ALD-HA and bone showed no differences in wettability (water contact angle on ALD-HA 86.2° vs. 86.7° on the bone), but the surface roughness of ALD-HA (Ra 0.713 µm) was significantly lower compared to bone (Ra 2.30 µm). The cellular reaction observed on ALD-HA might be a consequence of the topographical properties of the coating. The absence of resorptive osteoclasts on ALD-HA might indicate inhibition of their differentiation or the need to modify the coating to induce osteoclast differentiation. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.02.019 Byline: Petri Itaranta (a), Lijun Chi (a), Tiina Seppanen (a), Mikael Niku (a), Juha Tuukkanen (b), Hellevi Peltoketo (a), Seppo Vainio (a) Keywords: Wnt-4 signaling; Kidney development; Smooth muscle cells; Pericytes; Vascularization Abstract: Wnt-4, a member of the Wnt family of secreted signaling molecules, is essential for nephrogenesis, but its expression in the presumptive medulla suggests additional developmental roles in kidney organogenesis. We demonstrate here that Wnt-4 signaling plays also a role in the determination of the fate of smooth muscle cells in the medullary stroma of the developing kidney, as a differentiation marker, smooth muscle [alpha]-actin ([alpha]-SMA), is markedly reduced in the absence of its signaling. Wnt-4 probably performs this function by activating the Bmp-4 gene encoding a known differentiation factor for smooth muscle cells, since Bmp-4 gene expression was lost in the absence of Wnt-4 while Wnt-4 signaling led to a rescue of Bmp-4 expression and induction of [alpha]-SMA-positive cells in vitro. Recombinant Bmp-4 similarly rescued the differentiation of [alpha]-SMA-expressing cells in cultured Wnt-4-deficient embryonic kidney. The lack of smooth muscle cell differentiation leads to an associated deficiency in the pericytes around the developing vessels of the Wnt-4-deficient kidney and apparently leads to a secondary defect in the maturation of the kidney vessels. Thus, besides being critical for regulating mesenchymal to epithelial transformation in the cortical region in nephrogenesis, Wnt-4 signaling regulates the fate of smooth muscle cells in the developing medullary region. Author Affiliation: (a) Biocenter Oulu, Department of Medical Biochemistry and Molecular Biology, Laboratory of Developmental Biology, University of Oulu, Aapistie 5A, P.O. Box 5000, University of Oulu, FIN-90220, Finland (b) Biocenter Oulu, Department of Anatomy and Cell Biology, University of Oulu, Oulu, Finland Article History: Received 12 May 2005; Revised 13 February 2006; Accepted 15 February 2006

Background. Rheumatoid arthritis (RA) and osteoarthritis (OA) are common joint diseases associated with changes in local, as well as systemic bone structure and osteoclast function. We investigated how the different soluble inflammatory stimuli in these diseases can affect osteoclastogenesis and bone resorption in vitro. Methods. Human peripheral blood mononuclear cell-derived osteoclasts were cultured on bone slices with serum from treatment-naïve RA patients and healthy controls and with synovial fluid samples acquired from RA and OA patients. The concentrations of 29 different cytokines and related proteins, including RANKL and OPG, were analyzed in the fluids tested. Results. RA serum and synovial fluid increased both osteoclastogenesis and bone resorption. Osteoclastogenesis and activity increased more in the cultures containing OA than RA synovial fluid. The osteoclasts cultured in different culture media exhibited different phenotypes, especially the cells cultured with OA synovial fluid were generally larger and had more nuclei. A general increase in proinflammatory cytokines in RA synovial fluid and serum was found. Surprisingly, OA synovial fluid showed lower levels of osteoclastogenesis inhibiting cytokines, such as IL-4 and IL-10, than RA synovial fluid, which at least partly explains more pronounced osteoclastogenesis. No significant difference was found in RANKL or OPG levels. Conclusion. The proinflammatory stimulus in OA and RA drives the monocyte differentiation towards inflammatory osteoclastogenesis and altered osteoclast phenotype. [ABSTRACT FROM AUTHOR]

Background: The increasing demand for bone implants with improved osseointegration properties has prompted researchers to develop various coating types for metal implants. Atomic layer deposition (ALD) is a method for producing nanoscale coatings conformally on complex three-dimensional surfaces. We have prepared hydroxyapatite (HA) coating on titanium (Ti) substrate with the ALD method and analyzed the biocompatibility of this coating in terms of cell adhesion and viability. Methods: HA coatings were prepared on Ti substrates by depositing CaCO3 films by ALD and converting them to HA by wet treatment in dilute phosphate solution. MC3T3-E1 preosteoblasts were cultured on ALD-HA, glass slides and bovine bone slices. ALD-HA and glass slides were either coated or non-coated with fibronectin. After 48h culture, cells were imaged with scanning electron microscopy (SEM) and analyzed by vinculin antibody staining for focal adhesion localization. An 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) test was performed to study cell viability. Results: Vinculin staining revealed similar focal adhesion-like structures on ALD-HA as on glass slides and bone, albeit on ALD-HA and bone the structures were thinner compared to glass slides. This might be due to thin and broad focal adhesions on complex three-dimensional surfaces of ALD-HA and bone. The MTT test showed comparable cell viability on ALD-HA, glass slides and bone. Conclusion: ALD-HA coating was shown to be biocompatible in regard to cell adhesion and viability. This leads to new opportunities in developing improved implant coatings for better osseointegration and implant survival. [ABSTRACT FROM AUTHOR]