TiO2 bioactive implant surfaces doped with specific amount of Sr modulate mineralization.

One of the main problems that remain in the implant industry is poor osseointegration due to bioinertness of implants. In order to promote bioactivity, calcium (Ca), phosphorus (P) and strontium (Sr) were incorporated into a TiO2 porous layer produced by micro-arc oxidation. Ca and P as bioactive elements are already well reported in the literature, however, the knowledge of the effect of Sr is still limited. In the present work, the effect of various amounts of Sr was evaluated and the morphology, chemical composition and crystal structure of the oxide layer were investigated. Furthermore, in vitro studies were carried out using human osteoblast-like cells. The oxide layer formed showed a triplex structure, where higher incorporation of Sr increased Ca/P ratio, amount of rutile and promoted the formation of SrTiO3 compound. Biological tests revealed that lower concentrations of Sr did not compromise initial cell adhesion neither viability and interestingly improved mineralization. However, higher concentration of Sr (and consequent higher amount of rutile) showed to induce collagen secretion but with compromised mineralization, possibly due to a delayed mineralization process or induced precipitation of deficient hydroxyapatite. Ca-P-TiO2 porous layer with less concentration of Sr seems to be an ideal candidate for bone implants.

Influence of macroporosity on NIH/3T3 adhesion, proliferation, and osteogenic differentiation of MC3T3-E1 over bio-functionalized highly porous titanium implant material.

Highly porous Ti implant materials are being used in order to overcome the stress shielding effect on orthopedic implants. However, the lack of bioactivity on Ti surfaces is still a major concern regarding the osseointegration process. It is known that the rapid recruitment of osteoblasts in bone defects is an essential prerequisite for efficient bone repair. Conventionally, osteoblast recruitment to bone defects and subsequent bone repair has been achieved using growth factors. Thus, in this study highly porous Ti samples were processed by powder metallurgy using space holder technique followed by the bio-functionalization through microarc oxidation using a Ca- and P-rich electrolyte. The biological response in terms of early cell response, namely, adhesion, spreading, viability, and proliferation of the novel biofunctionalized highly porous Ti was carried out with NIH/3T3 fibroblasts and MC3T3-E1 preosteoblasts in terms of viability, adhesion, proliferation, and alkaline phosphatase activity. Results showed that bio-functionalization did not affect the cell viability. However, bio-functionalized highly porous Ti (22% porosity) enhanced the cell proliferation and activity. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 107B: 73-85, 2019.

Tribocorrosion behavior of bio-functionalized highly porous titanium.

Titanium and its alloys are widely used in orthopedic and dental implants, however, some major clinical concerns such as poor wear resistance, lack of bioactivity, and bone resorption due to stress shielding are yet to be overcome. In order to improve these drawbacks, highly porous Ti samples having functionalized surfaces were developed by powder metallurgy with space holder technique followed by anodic treatment. Tribocorrosion tests were performed in 9g/L NaCl solution using a unidirectional pin-on-disc tribometer under 3N normal load, 1Hz frequency and 4mm track diameter. Open circuit potential (OCP) was measured before, during and after sliding. Worn surfaces investigated by field emission gun scanning electron microscope (FEG-SEM) equipped with energy dispersive X-ray spectroscopy (EDS). Results suggested bio-functionalized highly porous samples presented lower tendency to corrosion under sliding against zirconia pin, mainly due to the load carrying effect given by the hard protruded oxide surfaces formed by the anodic treatment.

Intrinsic denervation of the colon is associated with a decrease of some colonic preneoplastic markers in rats treated with a chemical carcinogen

Denervation of the colon is protective against the colon cancer; however, the mechanisms involved are unknown. We tested the hypothesis that the denervated colonic mucosa could be less responsive to the action of the chemical carcinogen dimethylhydrazine (DMH). Three groups of 32 male Wistar rats were treated as follows: group 1 (G1) had the colon denervated with 0.3 mL 1.5 mM benzyldimethyltetradecylammonium (benzalkonium chloride, BAC); G2 received a single ip injection of 125 mg/kg DMH; G3 was treated with BAC + the same dose and route of DMH. A control group (Sham, N = 32) did not receive any treatment. Each group was subdivided into four groups according to the sacrifice time (1, 2, 6, and 12 weeks after DMH). Crypt fission index, ß-catenin accumulated crypts, aberrant crypt foci, and cell proliferation were evaluated and analyzed by ANOVA and the Student t-test. G3 animals presented a small number of aberrant crypt foci and low crypt fission index compared to G2 animals after 2 and 12 weeks, respectively. From the second week on, the index of ß-catenin crypt in G3 animals increased slower than in G2 animals. From the 12th week on, G2 animals presented a significant increase in cell proliferation when compared to the other groups. Colonic denervation plays an anticarcinogenic role from early stages of colon cancer development. This finding can be of importance for the study of the role of the enteric nervous system in the carcinogenic process.

Intrinsic denervation of the colon is associated with a decrease of some colonic preneoplastic markers in rats treated with a chemical carcinogen.

Denervation of the colon is protective against the colon cancer; however, the mechanisms involved are unknown. We tested the hypothesis that the denervated colonic mucosa could be less responsive to the action of the chemical carcinogen dimethylhydrazine (DMH). Three groups of 32 male Wistar rats were treated as follows: group 1 (G1) had the colon denervated with 0.3 mL 1.5 mM benzyldimethyltetradecylammonium (benzalkonium chloride, BAC); G2 received a single ip injection of 125 mg/kg DMH; G3 was treated with BAC + the same dose and route of DMH. A control group (Sham, N = 32) did not receive any treatment. Each group was subdivided into four groups according to the sacrifice time (1, 2, 6, and 12 weeks after DMH). Crypt fission index, ss-catenin accumulated crypts, aberrant crypt foci, and cell proliferation were evaluated and analyzed by ANOVA and the Student t-test. G3 animals presented a small number of aberrant crypt foci and low crypt fission index compared to G2 animals after 2 and 12 weeks, respectively. From the second week on, the index of ss-catenin crypt in G3 animals increased slower than in G2 animals. From the 12th week on, G2 animals presented a significant increase in cell proliferation when compared to the other groups. Colonic denervation plays an anticarcinogenic role from early stages of colon cancer development. This finding can be of importance for the study of the role of the enteric nervous system in the carcinogenic process.