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PubMedDate not supplied

Osteoblast viability and detachment following exposure to ultrasound in vitro.

Ultrasound has been used in dentistry for over 40 years and has recently been proposed for cutting bone. The purpose of this study was to establish the effects of ultrasonic instruments on osteoblasts. A 25 kHz magnetostrictive ultrasound generator and a TFI-1 tip (Dentsply, UK) were used as the ultrasound generating instruments. Primary osteoblast cultures were established from the parietal bones of two-day-old Albino Wistar rats grown on tissue culture (TC) petri dishes (Corning, UK) in alphaMEM (Sigma, UK). Once confluent, the osteoblasts were harvested using 0.05% trypsin in 0.02% EDTA then 1.7 x 10(5) cells in 2.5 ml of alphaMEM were either re-seeded immediately onto TC dishes and allowed to adhere for 24 h or kept in suspension before application of ultrasound with different tip displacements prior to re-seeding the cells. Osteoblast viability was assessed using 0.4% Trypan Blue following the initial dose of ultrasound then periodically over a 20 h period for both adherent and suspension osteoblasts. This study demonstrated that ultrasound caused osteoblast detachment and loss of viability in vitro, both when adherent to a substrate or in suspension. Loss of osteoblast viability was related to the maximum displacement of the ultrasonic tip and continued throughout the 20 h period observed for osteoblasts adherent to TC dishes.

Journal Article↗

PubMed2002

Modulation of gene expression in human osteoblasts by targeting a distal promoter region of human estrogen receptor-alpha gene.

Estrogen receptor (ER) alpha is expressed during osteoblast differentiation; however, both its functional role in bone metabolism and its involvement in osteoporotic pathogenesis caused by estrogen deficiency are not well understood. Loss of ER alpha gene expression could be one of the mechanisms leading to osteoporosis. Therefore, we investigated a possible modulation of ER alpha gene expression in a human osteoblastic cell line and in four primary osteoblast cultures by using a decoy strategy. Double stranded DNA molecules, mimicking a regulatory region of the ER alpha gene promoter (DNA-102) and acting as a 'silencer' in breast cancer cells, were introduced into osteoblasts as 'decoy' cis-elements to bind and functionally inactivate a putative negative transcription factor, and thus to induce ER alpha gene expression. We found that the DNA-102 molecule was able to specifically bind osteoblast nuclear proteins. Before decoy treatment, absence or variable low levels of ER alpha RNAs in the different cultures were detected. When the cells were transfected with the DNA-102 decoy, an increase in expression of ER alpha and osteoblastic markers, such as osteopontin, was observed, indicating a more differentiated osteoblastic phenotype both in the cell line and in primary cultures. These results showed that the DNA-102 sequence competes with endogenous specific negative transcription factors that may be critical for a decrease in or lack of ER alpha gene transcription. Therefore, osteoblastic transfection with the DNA-102 decoy molecule may be considered a tempting model in a putative therapeutic approach for those pathologies, such as osteoporosis, in which the decrease or loss of ER alpha expression plays a critical role in bone function.

Biomarkers↗

PubMed1999

Osteoblastic differentiation and mRNA analysis of STRO-1-positive human bone marrow stromal cells using primary in vitro culture and poly (A) PCR.

Investigation of osteoblast dysfunction in osteoporosis has been hampered by a poor understanding of normal early osteoblast differentiation, due to a relative lack of markers for the earliest cells in the lineage. Attempts to identify such markers have used cultures of animal or immortalized human cells, of uncertain relevance to human biology, or heterogeneous cultures in which genetic variability precludes the isolation of stage-specific genotypic markers. Primary in vitro generation of clonal populations of human bone marrow stromal cells was used in order to overcome these problems. Fibroblast-like stromal cells were isolated from human sternal bone marrow. They showed differentiation to an osteoblastic phenotype when stimulated with dexamethasone (10(-7) M) and fluorescence activated cell analysis demonstrated immunopositivity for STRO-1 (an antibody that recognizes osteoprogenitor stem cells of the colony-forming unit-fibroblastic) in from 8 to 40 per cent of the cells, dependent on time post-harvest. Cells positive for STRO-1 were immunoselected using magnetic activated cell sorting and seeded at low density (10 cells/cm2) to produce clones. Each clone was subpassaged, osteoblastic differentiation stimulated with dexamethasone, and mRMA-extracted at time points post-stimulation (0 h and 1-14 days). A novel poly (A) reverse transcriptase-polymerase chain reaction (RT-PCR) was used to amplify cDNA representative of all transcripts expressed at each time point. Differential gene expression within the amplified cDNA was assessed using 3' end cDNA probes to osteocalcin, osteopontin, and collagen type I (positive), demonstrating the acquisition of an osteoblastic phenotype. Time-specific gene products for early osteoblast differentiation have been generated from primary human cultures, utilizing very low density seeding and poly (A) RT-PCR. These products overcome the problems associated with animal, immortalized or heterogeneous culture and can be used to study normal and altered early osteoblast differentiation, indicating the possibility of using the same system to study other disease states.

Adult↗

PubMed1998

Temporal and spatial patterns of osteoblast activation following implantation of beta-TCP particles into bone.

Temporal and spatial patterns of osteoblast activation around beta-TCP particles implanted into bone were analyzed by in situ hybridization with digoxygenin-labeled procollagen alpha 1(I) RNA probes. beta-TCP particles (150-300 microns in diameter) were implanted into rat tibiae, and specimens were collected 3, 5, 7, 14, and 28 days after operation. Activated osteoblasts displayed intense procollagen alpha 1(I) RNA specific labeling. At day 3, osteoblasts lining pre-existing trabeculae in places showed a specific signal. Additionally, scattered activated cells compatible with preosteoblasts also were observed in the vicinity of the trabeculae among red blood cells that filled the space between beta-TCP particles. Osteoblast activation on the surface of beta-TCP rarely was observed. At days 5 and 7, osteoblast activation and bone formation advanced centripetally. At the forefront of bone formation positive cells were scattered in the blood cell clots, and some of the positive cells colonized forming new bone matrix. Formation of new bone did not always begin at the surface of beta-TCP. At day 14, most of the beta-TCP particles were tightly associated with newly formed bone, and the number of positive osteoblasts was reduced. At day 28, absorption of the newly formed bone and the beta-TCP by multinuclear cells was sporadically demonstrated. Such cells often were accompanied by active osteoblasts, suggesting early bone remodeling. In conclusion, in situ hybridization with procollagen alpha 1(I) was employed to demonstrate precisely the mode of recruitment of bone cell precursors. beta-TCP does not positively guide collagen I expressing bone cells along its surface. It has no apparent effects on bone regeneration.

Animals↗

PubMed1998

Degradable and highly porous polyesterurethane foam as biomaterial: effects and phagocytosis of degradation products in osteoblasts.

Recently, a new class of biodegradable PHB-based polyesterurethane (DegraPol/btc) has been prepared and found to exhibit favorable cell and tissue compatibility. The present study has been designed to evaluate the response of primary isolated rat tibia osteoblasts to small crystalline particles of short-chain poly[(R)-3-hydroxybutyric acid] (PHB-P diameter: 2-20 microm), of fluorescent-labeled analogs (DPHP-P), and of lysine methyl ester as possible degradation products of DegraPol/btc. Observations made using confocal microscopy clearly indicate that osteoblasts have the capability of taking up PHB-P particles. Although in single-cell analysis the number of DPHB-P-positive osteoblasts gradually increased up to 16 days, the fluorescence intensity per osteoblast increased only during the first 4 h after DPHB-P incubation, and then it retained the 4 h level up to 16 days. No significant change in the production levels of collagen type I and osteocalcin was detectable after treatment with low concentrations of PHB-P for up to 32 days. In contrast, a time- and dose-dependent alteration of the alkaline phosphatase (ALP) activity was found. Maximal activity was measured after 4 days of treatment with 2 microg of PHB-P/mL (170% of control cells). Rat peritoneal macrophages co-cultured with osteoblasts in a transwell culture system mimicked the observed PHB-P induced ALP elevation. Therefore, the PHB-P-induced ALP increase could be the result of direct or indirect stimulation of osteoblasts, possibly via soluble factors produced by contaminating osteoclasts. Taken collectively, the data demonstrate that osteoblasts are capable of phagocytosing PHB-P and that this process is accompanied at low PHB-P concentrations by dose- and time-dependent alteration of alkaline phosphatase activity but not of collagen type I or osteocalcin.

Alkaline Phosphatase↗

PubMed1999

The cytotoxic effect of titanium particles phagocytosed by osteoblasts.

The cytotoxic effect of different concentrations of titanium particles on osteoblasts was studied in vitro. It was found that the viability of the osteoblasts was inversely proportional to the particle concentration. Phagocytosis of particles by the osteoblasts was evident and was demonstrated to be responsible for cell necrosis. Moreover, during and after phagocytosis, the osteoblasts released products that were cytotoxic for other osteoblasts, as established with a conditioned medium assay. The titanium particles thus had both a direct and an indirect effect on osteoblast viability. It also was observed that the titanium particles induced a process of programmed cell death (apoptosis) when co-cultured with osteoblasts. The results of this study suggest that not only is the amount of wear debris generated important, but the local accumulation of the debris also may have a significant impact on bone cell function.

Analysis of Variance↗

PubMed1997

Runt homology domain proteins in osteoblast differentiation: AML3/CBFA1 is a major component of a bone-specific complex.

The AML/CBFA family of runt homology domain (rhd) transcription factors regulates expression of mammalian genes of the hematopoietic lineage. AML1, AML2 and AML3 are the three AML genes identified to date which influence myeloid cell growth and differentiation. Recently AML-related proteins were identified in an osteoblast-specific promoter binding complex that functionally modulates bone-restricted transcription of the osteocalcin gene. In the present study we demonstrate that in primary rat osteoblasts AML-3 is the AML family member present in the osteoblast-specific complex. Antibody specific for AML-3 completely supershifts this complex, in contrast to antibodies with specificity for AML-1 or AML-2, AML-3 is present as a single 5.4 kb transcript in bone tissues. To establish the functional involvement of AML factors in osteoblast differentiation, we pursued antisense strategies to alter expression of rhd genes. Treatment of osteoblast cultures with rhd antisense oligonucleotides significantly decreased three parameters which are linked to differentiation of normal diploid osteoblasts: the representation of alkaline phosphatase-positive cells, osteocalcin production, and the formation of mineralized nodules. Our findings indicate that AML-3 is a key transcription factor in bone cells and that the activity of rhd proteins is required for completion of osteoblast differentiation.

Animals↗

PubMed1996

Modulation of PDGF mediated osteoblast chemotaxis by leukemia inhibitory factor (LIF).

Cell migration is a key event in tissue repair and remodeling. PDGF, a growth factor for multiple target cells, has been shown to be a potent chemoattractant for a variety of mesenchymal cells. However, it is likely that PDGF-mediated cell migration will be influenced by other cytokines that can be produced during physiological and pathological conditions. Leukemia inhibitory factor (LIF), a cytokine that is produced by a variety of cells including osteoblasts, may promote bone formation, but the mechanism is not known. Since osteoblasts are responsible for laying down new matrix during skeletal remodeling, in this report we have examined whether PDGF or LIF influences the migration of osteoblasts. Among several cytokines and growth factors tested, only PDGF was able to elicit a major chemotactic (directed migration) and a minor chemokinetic (random-migration) response in osteoblasts. LIF alone was not active in either chemotaxis or chemokinesis but when included with PDGF it caused a reduction in chemokinesis. Further, pretreatment of osteoblasts with LIF caused an increase in PDGF-driven chemotaxis. Finally, osteoblasts exposed briefly to LIF synthesized a higher level of non-collagenous proteins upon further treatment with PDGF. These observations are consistent with a role for LIF in promoting bone formation, both by influencing directional migration of osteoblasts and in laying down new matrix.

Alkaline Phosphatase↗

PubMed2001

Neuropilin-1 expression in osteogenic cells: down-regulation during differentiation of osteoblasts into osteocytes.

The expression of neuropilin-1 (NRP1), a recently described VEGF and semaphorin receptor expressed by endothelial cells (EC) but some non-EC types as well, was analyzed in osteoblasts in vitro and in vivo. Cultured MC3T3-E1 osteoblasts expressed NRP1 mRNA and bound VEGF(165) but not VEGF(121), characteristic of the VEGF isoform-specific binding of NRP1. These cells did not express VEGFR-1 or VEGFR-2 so that VEGF binding to osteoblasts was strictly NRP1-dependent. In a chick osteocyte differentiation system, NRP1 was expressed by osteoblasts but its expression was absent as the cells matured into osteocytes. Immunohistochemical localization of NRP1 within the developing bones of 36-day-old mice and embryonic Day 17 chicks demonstrated that NRP1 was expressed by osteoblasts migrating alongside invading blood vessels within the metaphysis of the growth plate, as well as by osteoblasts at the developing edge of trabeculae within the marrow cavity. On the other hand, NRP1 was not expressed by osteocytes in either species, consistent with the in vitro results. In addition to osteogenic cells, NRP1 expression by EC was observed throughout the bone. Together these results suggest that NRP1 might have a dual function in bone by mediating osteoblast function directly as well as angiogenesis.

3T3 Cells↗

PubMed1978

Immuno-histochemical localization of cyclic nucleotides in mineralized tissues: mechanically-stressed osteoblasts in vivo.

Previous experiments indicate that bone cells respond to external stimuli with fluctuations of cyclic nucleotide levels. The objective of this experiment was to study the response of alveolar bone to the application of tensile forces through an examination of the osteoblastic staining pattern for cAMP and cGMP. Cat canines were tipped by 80-g force for 0 to 48 hours. Fresh frozen, unfixed, undecalcified jaws were sectioned sagittally and stained immuno-histochemically for cAMP and cGMP. In tension sites, osteoblastic staining intensity for cAMP decreased gradually from one to three hours, and then increased by 24 hours. Intense staining for cGMP, visible in osteoblasts of all treated cats, peaked after three hours of treatment and then again at 24 hours. Generally, groups of cGMP-stained osteoblasts were found adjacent to unstained osteoblasts. The observed fluctuations in the osteoblasts staining pattern for cAMP and cGMP indicates involvement of these substances in the early response of osteoblasts to mechanical stimuli in vivo.

Animals↗

PubMed1986

Osteoblast and osteoclast precursors in primary cultures of calvarial bone cells.

Bone cells obtained by digestion of fetal mouse or chicken calvaria were tested for their ability to form or resorb bone in vitro. The isolated cells were precultured for 6 days and subsequently cocultured for 11 days with periosteum-free noninvaded fetal mouse long bone rudiments. Bone formation and resorption during coculture were evaluated by histology and 45Ca release from prelabeled bones. The calvarial origin of cells in cocultures was traced by labeling the cells with 3H-thymidine before coculture, followed by autoradiography. Many osteoblasts and osteoclasts as well as fibroblasts developed from mouse periosteal cells released late in the sequential digestion procedure and previously denoted as "osteoblastlike" (BL). No or few osteoblasts and osteoclasts but many fibroblasts developed from early released cell fractions that have previously been denoted as "osteoclastlike" (CL). Only osteoblasts and fibroblasts but not osteoclasts developed from chicken calvarial cell fractions. The osteoblasts developed primarily from cell fractions from the inner layer of the periosteum, previously denoted as "osteoblastlike" (OB). Cells obtained from the outer layer of the periosteum (PF) gave rise mainly to fibroblasts. These studies show that osteoblast and osteoclast precursor cells are maintained in monolayer cultures of periosteal cell fractions. However, sequential digestion of mouse calvaria does not lead to separation of the two types of bone cells. Rather, osteoclast and osteoblast precursors are released jointly, from the periosteal cell layers closest to the bone surface. In the chicken cell fractions osteoclast precursors are absent after preculture, resulting in a more homogeneous population of osteoblast and fibroblast but not osteoclast precursors.

Animals↗

PubMed2004

A new bone to pick: osteoblasts and the haematopoietic stem-cell niche.

Two recent publications highlight the role of bone-forming cells, the osteoblasts, in controlling the development of neighboring haematopoietic stem cells (HSCs).1,2 Using two distinct transgenic mouse models, one using the conditional deletion of the Bone Morphogenetic Protein Receptor 1A (BMPR1A) gene, the other using over-expression of an active PTH/PTHrP receptor (PPR) mutant within osteoblasts, the authors show parallel, concordant increases in the generation of trabecular osteoblasts and the number of HSCs. In situ staining showed that rarely cycling HSCs sporadically attach to endosteal osteoblasts, while in vitro assays indicated that ligation of Jag1 on osteoblasts by Notch1 on HSCs promotes HSC proliferation. These two independent works have revived and revitalized the notion that osteoblasts are a major, defining component of the HSC niche within the bone marrow (BM). This minireview discusses these results in the context of other recent studies of mesenchymal cells within the BM microenvironment, presents one potential unified model of the functional anatomy of the BM HSC niche, and highlights new questions raised by these and other studies of osteoblasts and HSCs.

Animals↗

PubMed2006

Differentiation of mesenchymal stem cells into osteoblasts on honeycomb collagen scaffolds.

Tissue engineering using living cells is emerging as an alternative to tissue or organ transplantation. The adult mesenchymal stem cells can be differentiated into multilineage cells, such as adipocytes, chondrocytes, or osteoblasts when cultured with specific growth factors. In the present investigation, we have studied the effect of honeycomb collagen scaffolds for the adhesion, differentiation and proliferation of bone marrow-derived mesenchymal stem cells into osteoblasts. Mesenchymal stem cells were isolated from 6-week old albino rat femur bone marrow, and cultured in alpha-MEM medium without beta-glycerophosphate and dexamethasone. Honeycomb collagen discs were prepared from bovine dermal atelocollagen, cross-linked by UV-irradiation and sterilized by heat. The honeycomb discs were placed on the culture dishes before seeding the stem cells. The cells attached quickly to the honeycomb collagen scaffold, differentiated and proliferated into osteoblasts. The differentiated osteoblasts were characterized by morphological examination and alkaline phosphatase activity. The osteoblasts also synthesized calcium-deficient hydroxyapatite (pseudo-hydroxyapatite) crystals in the culture. The mineralization was confirmed by Von Kossa staining and the crystals were analyzed by X-ray diffraction. Light microscopy and DNA measurements showed that the differentiated osteoblasts multiplied into several layers on the honeycomb collagen scaffold. The results demonstrated that the honeycomb collagen sponge is an excellent scaffold for the differentiation and proliferation of mesenchymal stem cells into osteoblasts. The data further proved that honeycomb collagen is an effective substrate for tissue engineering applications, and is very useful in the advancing field of stem cell technology and cell-based therapy.

Alkaline Phosphatase↗

PubMed2006

Buried alive: how osteoblasts become osteocytes.

During osteogenesis, osteoblasts lay down osteoid and transform into osteocytes embedded in mineralized bone matrix. Despite the fact that osteocytes are the most abundant cellular component of bone, little is known about the process of osteoblast-to-osteocyte transformation. What is known is that osteoblasts undergo a number of changes during this transformation, yet retain their connections to preosteoblasts and osteocytes. This review explores the osteoblast-to-osteocyte transformation during intramembranous ossification from both morphological and molecular perspectives. We investigate how these data support five schemes that describe how an osteoblast could become entrapped in the bone matrix (in mammals) and suggest one of the five scenarios that best fits as a model. Those osteoblasts on the bone surface that are destined for burial and destined to become osteocytes slow down matrix production compared to neighbouring osteoblasts, which continue to produce bone matrix. That is, cells that continue to produce matrix actively bury cells producing less or no new bone matrix (passive burial). We summarize which morphological and molecular changes could be used as characters (or markers) to follow the transformation process.

Animals↗

PubMed1993

Histological and biochemical evaluation of osteoblasts cultured on bioactive glass, hydroxylapatite, titanium alloy, and stainless steel.

We investigated the behavior of fetal rat osteoblasts cultured on four bone replacing materials: bioactive glass, hydroxylapatite, a titanium alloy, and stainless steel. The cultures were histologically examined for individual cell morphology and osteoblast expression after several periods of time using scanning electron, fluorescence, and normal light microscopy. Other cultures were used for biochemical determinations of alkaline phosphatase activity (APA) and DNA content. Osteoblasts cultured on bioactive glass showed a better osteoblast-like morphology and a higher proliferation rate, leading to confluent cultures with higher cell density and a generally better expression of the osteoblast phenotype in comparison with the other substrates. The confluent bioactive glass cultures also showed significantly higher DNA content and APA as well as the calculated APA/DNA ratio. Based on the evaluation of histological and biochemical parameters we conclude that osteoblasts cultured on bioactive glass show a generally better osteoblast character than on the other materials.

Actins↗

PubMed2003

Type I collagen production by osteoblast-like cells cultured in contact with different bioactive glasses.

Bioactive glasses are silica-based, surface-active bone substitutes that have shown good biocompatibility both in bone and in soft tissue and are used in oral and maxillofacial bone augmentation. Previous in vitro studies showing that bioactive glasses support the growth and maturation of rat osteoblast-like cells and promote the expression and maintenance of the osteoblastic phenotype have suggested that there is both a solution-mediated and a surface-controlled effect on cell activity. In this study, we investigated the behavior of human primary osteoblast-like cells cultured in contact with three different bioactive glasses and compared them with amorphous silica (SiO2) used in the form of granules. The specific activity of alkaline phosphatase determined biochemically was significantly higher at 2 and 4 days on the bioactive glass with 46.1 mol % silica content (45S5 Bioglass) cultures than in the control cultures and in the bioactive gel-glass cultures, which had 60 mol % (58S) and 80 mol % (77S) silica content. Osteoblasts synthesize collagen type I, which is subsequently mineralized. Immunoblot and biochemical studies showed increased collagen release from osteoblast-like cells cultured in contact with bioactive glasses over that of controls. Among the three bioactive glasses, 45S5 is the highest inducer of osteoblast-like cell collagen release; moreover, mRNA for type I collagen was stimulated approximately three- to fivefold after 45S5 treatment. 77S bioactive glass similarly increased type I collagen synthesis even though alkaline phosphatase was not higher. These results suggest that 45S5 Bioglass not only induces osteogenic differentiation of human primary osteoblast-like cells, but can also increase collagen synthesis and release. The newly formulated bioactive gel-glass 77S seems to have potential applications for tissue engineering, inducing increased collagen synthesis.

Adult↗

PubMed2005

Adsorption of serum fetuin to hydroxylapatite does not contribute to osteoblast phenotype modifications.

Osteoblasts exhibit enhanced differentiation and altered gene profiles when cultured on hydroxyapatite (HA) compared to plastic surfaces. To begin determining mechanisms for this response, we used proteomics to identify proteins predominantly found in osteoblasts on HA but not plastic surfaces. Two-dimensional gel electrophoresis and Western analyses indicate that fetuin is abundant in extracts from HA, but not plastic surfaces. Incubation of HA and plastic surfaces with cell culture medium (containing 10% serum) under cell-free conditions shows that fetuin is predominantly derived from the culture medium serum and readily adsorbs to the HA surface. However, we did detect low levels of fetuin B mRNA in osteoblasts. Serum albumin, actin-beta, apolipoprotein-AI, and vimentin also adsorbed to HA. To determine the role of fetuin in the HA-induced osteoblast phenotype changes, osteoblasts were seeded onto fetuin-coated or uncoated HA under serum-free conditions. Osteoblast morphology was similar on both HA surfaces, suggesting that HA alone (without adsorbed serum proteins) is sufficient for cell attachment and spreading. Similarly, genes previously reported to be modulated by HA (glvr-1, DMP-1, osteoglycin, and proliferin 3) were modulated even in the absence of fetuin or other serum proteins. These data show that HA surface can be enriched selectively with fetuin from serum; however, neither fetuin or other serum proteins are required to mediate HA-induced osteoblast attachment, spreading, or changes in expression of genes examined. This finding suggests that factors intrinsic to HA are required for the response.

Adsorption↗

PubMed2006

Concentration-dependent effects of titanium and aluminium ions released from thermally oxidized Ti6Al4V alloy on human osteoblasts.

Thermal oxidation treatments of Ti6Al4V, at 500 and 700 degrees C, for 1 h result in the formation of an outer "ceramic" layer of rutile, which enhances osteoblast response. In the present study, we have measured in vitro Ti and Al ion release from Ti64 alloy in the as-received state and after thermal oxidation treatments at 500 or 700 degrees C, to culture medium under standard cell-culture conditions. Concentrations of both Ti and Al released from both thermal oxidation treatments were lower than from polished alloy. Al was released from the treated or untreated surfaces in substantially lower extent than Ti. Titanium and aluminium ions affected primary human osteoblast proliferation, metabolic activity, and differentiation in a dose-dependent manner. Treatments with individual Ti or Al metal ions in similar concentration ranges than released from the surfaces did not alter osteoblast response, which also remained unaffected after treatments with combinations of Ti plus Al applied in the proportional relations than detected in ion-release experiments. We then selected higher concentrations of Ti that impaired osteoblast proliferation and differentiation, while the proportional lower concentrations of Al did not alter osteoblast behavior. In spite of its inert character, it was found that Al significantly enhanced the deleterious effect of Ti on osteoblast differentiation. Therefore, thermal oxidation treatments of Ti6Al4V alloy may improve the biocompatibility of the alloy by reducing both Ti and Al release, and thus attenuating ion-mediated interference with osteoblast differentiation.

Aged↗