Nanostructured Cu-doped TiO2 with photothermal effect for prevention of implant-associated infection.

Bacterial infection of titanium (Ti) dental implants is still a major clinical complication. In this study, a combination of copper (Cu) ions and photothermal therapy is used to combat implant-associated infection. Cu doped TiO2 (TiO2-Cu) films were prepared on Ti by magnetron sputtering and subsequently annealing. TiO2-Cu films had efficient photothermal conversion ability due to the generated nanostructure during the annealing process. Under the irradiation of 808 near infrared light, the combined actions of hyperthermia and Cu ions gave rise to excellent antibacterial activity against Streptococcus mutans on Ti as demonstrated by the experiments conducted in vitro and in vivo. The TiO2-Cu films also exhibited excellent biocompatibility. In addition, the surface hardness and corrosion resistance of TiO2-Cu films were greatly improved.

Construction of a TiO2/MoSe2/CHI coating on dental implants for combating Streptococcus mutans infection.

Infection and inflammation are the main causes resulting in the failure of dental implants. In this work, molybdenum diselenide (MoSe2) was synthesized hydrothermally on the surface of porous TiO2 coating prepared by micro-arc oxidation on titanium (Ti) implants to render the coating excellent in situ antibacterial activity under the irradiation of near-infrared (NIR) light. Chitosan (CHI) was adsorbed on the surface of MoSe2 nanosheets by electrostatic bonding to improve the biocompatibility. The introduction of MoSe2 significantly improved the photothermal and photodynamic ability of TiO2 coating and made the implants possess excellent in vitro and in vivo antibacterial property against Streptococcus mutans (S. mutans) under the irradiation of 808 nm NIR light for 15 min because of the synergistic of hyperthermia and reactive oxygen species (ROS). The immobilization of CHI improved the hydrophilicity and biocompatibility of MoSe2, and the hybrid coating (TiO2/MoSe2/CHI) promoted osseointegration even in the presence of infection in vivo under 808 nm light irradiation. The light - assisted antibacterial coating described here has large clinical potential in dental implants applications.

Light-assisted therapy for biofilm infected micro-arc oxidation TiO2 coating on bone implants.

Implant-associated infections is a main factor leading to the failure of titanium (Ti) implants. Micro-arc oxidation is a convenient and effective technique to form a biocompatible metal (Ag+, Cu2+ and Zn2+) ions-doped TiO2 coatings to combat bacterial infections. However, compared with the sterilization by metal ions, light-triggered antibacterial therapies have accepted more attention due to its higher antibacterial efficiency and security. Although TiO2 is an excellent photocatalyst, it can be triggered by ultraviolet light due to the wide band gap. Herein, molybdenum disulfide (MoS2) modified TiO2 coating was fabricated on Ti by a hybrid process of micro-arc oxidation and hydrothermal treatment. The hybrid coating exhibits excellent antibacterial activity under the irradiation of 808 nm near-infrared light because of the synergistic antibacterial effects of reactive oxygen species and hyperthermia, and Staphylococcus aureus (S. aureus) biofilm can be eradicated within 15 min both in vivo and in vitro. Furthermore, collagen decorated on the surface of the hybrid coating can improve the proliferation, adhesion and spreading of MC3T3-E1 osteoblasts.

Synergistic antibacterial activity of physical-chemical multi-mechanism by TiO2 nanorod arrays for safe biofilm eradication on implant.

Treatment of implant-associated infection is becoming more challenging, especially when bacterial biofilms form on the surface of the implants. Developing multi-mechanism antibacterial methods to combat bacterial biofilm infections by the synergistic effects are superior to those based on single modality due to avoiding the adverse effects arising from the latter. In this work, TiO2 nanorod arrays in combination with irradiation with 808 near-infrared (NIR) light are proven to eradicate single specie biofilms by combining photothermal therapy, photodynamic therapy, and physical killing of bacteria. The TiO2 nanorod arrays possess efficient photothermal conversion ability and produce a small amount of reactive oxygen species (ROS). Physiologically, the combined actions of hyperthermia, ROS, and puncturing by nanorods give rise to excellent antibacterial properties on titanium requiring irradiation for only 15 min as demonstrated by our experiments conducted in vitro and in vivo. More importantly, bone biofilm infection is successfully treated efficiently by the synergistic antibacterial effects and at the same time, the TiO2 nanorod arrays improve the new bone formation around implants. In this protocol, besides the biocompatible TiO2 nanorod arrays, an extra photosensitizer is not needed and no other ions would be released. Our findings reveal a rapid bacteria-killing method based on the multiple synergetic antibacterial modalities with high biosafety that can be implemented in vivo and obviate the need for a second operation. The concept and antibacterial system described here have large clinical potential in orthopedic and dental applications.

[Dental caries conditions of 3,439 disabled Yi and Han individuals in Liangshan Yi Autonomous Prefecture in Sichuan province, China].

OBJECTIVE: This study aims to conduct a survey of the oral health status of disabled individuals in Liangshan Autonomous Prefecture in Sichuan province. This study was also conducted to prepare caries prevention planning in the region. METHODS: On the basis of the Oral Health Surveys: Basic Methods of WHO and the Third National Oral Health Epidemiological Sample Survey Scheme, we investigated caries infecting disabled individuals who live in one big city (Xichang city), three counties (Bhutto county, Muli Tibetan autonomous county, and Huili county), and 46 towns and villages of Liangshan Autonomous Prefecture in Sichuan province, by multi-stage stratified and cluster sampling. RESULTS: Among 3,439 disabled individuals, 2,085 were males and 1,354 were females; among these individuals, 815 live in the city and 2,624 live in rural areas. Furthermore, 2,177 were Han natives and 1,262 were Yi natives (ethnic). The caries prevalence rate and mean DMFT of disabled individuals in Liangshan Autonomous Prefecture in Sichuan province were 87.1% and 9.53, respectively. In Yi, the caries prevalence rate and mean DMFT of disabled individuals in Liangshan Autonomous Prefecture in Sichuan province were 85.8% and 9.93, respectively; in Han, the caries prevalence rate and mean DMFT of disabled individuals in Liangshan Autonomous Prefecture in Sichuan province were 87.9% and 9.29, respectively. No significant difference was found in the two groups of native (P > 0.05). A very low filling rate of 0.2% was also recorded. CONCLUSION: Disabled individuals from Liangshan Autonomous Prefecture in Sichuan province exhibited a high prevalence of caries in permanent teeth. The oral health status of this special group of disabled individuals should be provided intensive care.

Effect of vitamin B12 on cleft palate induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin and dexamethasone in mice.

The purpose of this study was to investigate the effect of vitamin B12 on palatal development by co-administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dexamethasone (DEX). We examined the morphological and histological features of the palatal shelf and expression levels of key signaling molecules (transforming growth factor-ß3 (TGF-ß3) and TGF-ß type I receptor (activin receptor-like kinase 5, ALK5)) during palatogenesis among a control group (Group A), TCDD+DEX exposed group (Group B), and TCDD+DEX+vitamin B12 exposed group (Group C). While we failed to find that vitamin B12 decreased the incidence of cleft palate induced by TCDD+DEX treatment, the expression levels of key signaling molecules (TGF-ß3 and ALK5) during palatogenesis were significantly modulated. In TCDD+DEX exposed and TCDD+DEX+vitamin B12 exposed groups, palatal shelves could not contact in the midline due to their small sizes. Our results suggest that vitamin B12 may inhibit the expression of some cleft palate inducers such as TGF-ß3 and ALK5 in DEX+TCDD exposed mice, which may be beneficial against palatogenesis to some degree, even though we were unable to observe a protective role of vitamin B12 in morphological and histological alterations of palatal shelves induced by DEX and TCDD.

[The preliminary study on transforming growth factor-beta 3, activin receptor-like kinase 5 expression in 2, 3, 7, 8-tetrachloro-p-dibenzodioxin and dexamethasone induced palatal cleft in mice].

OBJECTIVE: To establish a good animal model of cleft palate and confirm whether 2, 3, 7, 8-tetrachloro-p-dibenzodioxin (TCDD) and Dexamethasone (DEX) induced palatal cleft in mice is related to the fold change of transforming growth factor-beta 3 (TGF-beta3) and activin receptor-like kinase 5 (Alk5). METHODS: Pregnant mice were treated with oral medication of TCDD and intraperitoneal injection with DEX on GD10-12 in experimental group while the control group without any treatment. Then embryos were examined on GD17.5 under stereomicroscope for calculating the incidence of cleft palate and palatal shelves were dissected from the staged embryos respectively for RNA extraction on GD13.5, GD14.5 and GD15.5. At last the real-time PCR and SYBR Green I detection were used for RNA relative quantification. RESULTS: Cleft palate could be induced 100% in C57BL/6J fetal mice with TCDD and DEX, thus established a stable animal model for further molecular studies of cleft palate. There were no significant difference in expression level of TGF-beta3 and Alk5 on GD13.5 among the groups, but the differences were statistically significant on GD14.5 and GD15.5 (P < 0.05). On the contrary, the expression level of Alk5 were significantly higher in experimental group (P < 0.05). CONCLUSION: Combined effects of TCDD and DEX could induce a stable formation of cleft palate and down-regulated mRNA of TGF-beta3 and up-regulated Alk5 may contribute to the occurrence of cleft palate.