Chronic exposure to TiO2 micro- and nano particles: A biochemical and histopathological experimental study.

The aim of this work was to analyze the effects of long-term exposure to titanium dioxide (TiO2) micro- (MPs) and nanoparticles (NPs) (six and 12 months) on the biochemical and histopathological response of target organs using a murine model. Male Wistar rats were intraperitoneally injected with a suspension of TiO2 NPs (5 nm; TiO2-NP5 group) or MPs (45 µm; TiO2-NP5 group); the control group was injected with saline solution. Six and 12 months post-injection, titanium (Ti) concentration in plasma and target organs was determined spectrometrically (ICP-MS). Blood smears and organ tissue samples were evaluated by light microscopy. Liver and kidney function was evaluated using serum biochemical parameters. Oxidative metabolism was assessed 6 months post-injection (determination of superoxide anion by nitroblue tetrazolium (NBT) test, superoxide dismutase (SOD) and catalase (CAT), lipid peroxidation, and paraoxonase 1). Titanium (Ti) concentration in target organs and plasma was significantly higher in the TiO2-exposed groups than in the control group. Histological evaluation showed the presence of titanium-based particles in the target organs, which displayed no structural alterations, and in blood monocytes. Oxidative metabolism analysis showed that TiO2 NPs were more reactive over time than MPs (p < .05) and mobilization of antioxidant enzymes and membrane damage varied among the studied organs. Clearance of TiO2 micro and nanoparticles differed among the target organs, and lung clearance was more rapid than clearance from the lungs and kidneys (p < .05). Conversely, Ti concentration in plasma increased with time (p < .05). In conclusion, neither serum biochemical parameters nor oxidative metabolism markers appear to be useful as biomarkers of tissue damage in response to TiO2 micro- and nanoparticle deposits at chronic time points.

Systemic effect of TiO2 micro- and nanoparticles after acute exposure in a murine model.

The surface of a biomedical implant can be a potential endogenous source of release of microparticles (MPs) and nanoparticles (NPs) into the biological environment. In addition, titanium particles from exogenous sources can enter the body through inhalation, ingestion, or dermal contact. The aim of this work was to evaluate the biological response of the lung, liver, and kidneys to acute exposure to titanium dioxide (TiO2 ). Male Wistar rats were intraperitoneally injected with a suspension of 45 µm or 5 nm TiO2 particles. One month post-exposure, titanium concentration was determined spectrometrically (ICP-MS) in plasma and target organs. Blood smears and organ tissue samples were examined histopathologically, and oxidative metabolism was analyzed (superoxide anion by nitro blue tetrazolium (NBT) test; superoxide dismutase (SOD) and catalase (CAT); lipid peroxidation; paraoxonase 1). Liver (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase) and kidney (urea, creatinine) function was evaluated using serum biochemical markers. Microchemical and histological analysis revealed the presence of particles, though no structural alterations, in TiO2 -exposed groups. NBT test showed an increase in the percentage of reactive cells and antioxidant enzyme consumption in lung samples in the 45 µm and 5 nm TiO2 -exposed groups. Only the 5 nm particles caused a decrease in SOD and CAT activity in the liver. No changes in renal oxidative metabolism were observed in either of the TiO2 -exposed groups. Determination of serum biochemical markers and analysis of oxidative metabolism are not early bioindicators of tissue damage caused by TiO2 MPs and NPs.

Titanium dental implant-related pathologies: A retrospective histopathological study.

OBJECTIVES: To perform a retrospective, descriptive, histopathological study of peri-implant tissue pathologies associated with titanium dental implants (TDI), and to evaluate the presence of metallic particles in samples from a single diagnostic center. METHODS: Sixty-eight cases of TDI-associated lesions were retrieved from the Surgical Pathology Laboratory archives, School of Dentistry, University of Buenos Aires (UBA) (1990-2018). The study included re-examining the histopathological features of the biopsy samples, analyzing the inflammatory infiltrate, and examining the samples to detect metallic particles whose chemical composition was determined spectrophotometrically (EDS). Available clinical and radiographic data were also reviewed. RESULTS: The retrieved cases ranged from lesions of inflammatory origin to neoplastic lesions. Metallic particles were observed in 36 cases (52.9%), all of which showed inflammation. Particle length ranged from 2 to 85µm. EDS analysis of the particles/deposits observed in the tissues showed the presence of aluminum, titanium, iron, and nickel, among other elements. CONCLUSIONS: A significant number of TDI-associated lesions, including cases not reported to date and diagnosed at a single diagnostic center, are shown here. Cases showing particles exhibited an inflammatory response, irrespective of the histopathological diagnosis. The role of metallic particles in the development of TDI-associated lesion is yet to be established.

Oral exfoliative cytology and corrosion of metal piercings. Tissue implications.

OBJECTIVES: A group of adolescents with oral piercings was studied to determine the presence of metallic particles in cells exfoliated from the mucosa surrounding their metal oral piercings and the association between such particles and the metal jewelry, and to evaluate subsequent tissue implications. MATERIALS AND METHODS: Sixteen teenage patients who had tongue and/or lip piercings were included. The clinical features of the oral mucosa and lip skin were evaluated. Exfoliative cytology was performed in the area surrounding the piercing. The surface of used and unused jewelry was studied by scanning electron microscopy and energy dispersive X-ray analysis. RESULTS: Hyperplastic, leukoedematous, and lichenoid lesions were observed in the mucosa, as well as lesions associated with metallosis of the lip skin. Cytological smears showed the presence of particles inside the epithelial cells; the particles were found to contain aluminum, tungsten, and molybdenum. In one case requiring surgical removal of the piercing, histological examination of the tissue associated with the piece of jewelry showed the presence particles containing aluminum, iron, and tin inside multinucleated giant cells. Although surface finish defects were observed on both unused and used piercing jewelry, they were more evident on the used pieces. CONCLUSIONS: Ion particles are released from the metal piercings and could have been adjuvant factors in the development of the observed lesions. Cells exfoliated from the oral mucosa surrounding metal piercings may serve as bioindicators of corrosion processes. CLINICAL RELEVANCE: We propose the use of exfoliative cytology to monitor corrosion processes and for routine clinical follow up.