Objective To investigate the toxic effects of combined yttrium and lead exposure on liver and kidney functions in male Sprague-Dawley (SD) rats. Methods Adult male specific pathogen-free SD rats were randomly divided into four groups. Rats in the low-, medium-, and high-dose groups were co-administered with yttrium acetate (10.0, 50.0, and 100.0 mg/kg body weight, respectively) and lead acetate (4.0, 20.0, and 40.0 mg/kg body weight, respectively) by intragastric gavage, once per day for 28 consecutive days. Rats in the control group received an equal volume of deionized water. Yttrium and lead levels in whole blood, liver, and kidney tissues of the rats were measured using inductively coupled plasma mass spectrometry. Serum index of liver and kidney function were measured by a double reagent method, and histopathological changes in the liver and kidney were observed. Results The body weights of rats in all the three exposure groups were lower than those in the control group from day 14 of exposure until the end of exposure (all P<0.05). Body weight gain of rats was observed only in the low-dose group at day 28, whereas no body weight gain was observed throughout the exposure period in the medium- and high-dose groups. Histopathological examination showed dose-dependent liver and kidney injuries in rats of the three exposure groups compared with the control group. Specifically, the liver exhibited widening of intercellular spaces and increased inflammatory cell infiltration, while the kidney showed increased tissue hemorrhage and increased damage to glomeruli and renal tubules. Lead levels in whole blood, liver, and kidney tissues of the rats were higher than yttrium levels in all the three exposure groups (all P<0.05). Blood yttrium levels in rats of the high-dose group were higher than those in the other three groups (all P<0.05), and yttrium levels in the liver and kidney tissues of the three exposure groups were higher than those in the control group (all P<0.05). Lead levels in whole blood, liver, and kidney tissues of the rats increased with increasing exposure dose (all P<0.05). At the end of exposure, the kidney organ coefficient of rats in the high-dose group was higher than those in the other three groups (all P<0.05). The serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) ratio of rats in the high‑dose group was lower than that in the control group (P<0.05). The serum urea and uric acid levels in the medium‑ and high‑dose groups were lower than those in the control group (both P<0.05). The serum cystatin C level in the high‑dose group was higher than that in the control group (P<0.05). Blood yttrium and blood lead levels were each negatively correlated with serum ALT/AST ratio, serum urea nitrogen, and uric acid levels (both P<0.05). Both yttrium and lead levels in liver tissue were each negatively correlated with serum ALT/AST ratio (all P<0.05). Both yttrium and lead levels in kidney tissue were each negatively correlated with both serum urea nitrogen and uric acid levels (all P<0.05), and each positively correlated with serum cystatin C levels (both P<0.05). Conclusion Co-exposure to yttrium and lead induces dose‑dependent hepatotoxicity and nephrotoxicity in male SD rats. Lead exhibits a more pronounced accumulation effect and contributes more substantially to the observed toxicity.

Objective:To evaluate and compare the outcomes of maxillary protraction treatment assisted by temporary anchorage devices (TADs) and removable biteplate in cleft lip and palate patients using cephalometric analysis.Methods:Fifty-four cleft lip and palate patients were divided into 3 groups based on different maxillary protraction treatments: bitepalate removable appliance group (group A), maxillary protraction treatment assisted by TADs group (group B) and control group (group C). Lateral cephalograms were taken at the start and the end of maxillary protraction. Skeletal, dental and soft tissue changes were measured using Dolphin software and compared between groups.Results:The average protraction time of groups A and B were (8.51±1.33) and (9.20±1.45) months ( P=0.146), respectively. A point moved forward by 4.08 mm in group A and 4.83 mm in group B were noted, without significant differences between the two groups. Compared to group C, ANB and wits was highly improved after protraction in groups A and B. U6-VRmx increased by 0.46 mm and U1-pp increased by 0.63 mm in group B, both of which were significantly smaller than those of group A (both P<0.05), suggesting that maxillary protraction treatment assisted by TADs could reduce molar advancement and upper incisor protrusion. Conclusions:Both maxillary protraction treatment assisted by TADs and removable biteplate could significantly improve skeletal class Ⅲ malocclusion in unilateral cleft and palate patients. Maxillary protraction treatment assisted by TADs could reduce molar advancement and upper incisor protrusion.

Objective To study the clinical effect of bone-anchored pendulum in treatment for class Ⅱ malocclusion .Methods Twelve patients treated by bone-anchored pendulum were chosen .In each patient ,two microscrews were inserted in the anterior paramedian region of the median palatal suture ,6-9 mm posterior to the incisive foramen and 3 – 6 mm lateral to the median line .Pendulum that based on the microscrews was used to distalize maxillary first molar ,and the force applied was 250 g .Skeletal and dental changes were measured on cephalograms before (T1 ) and after (T2 ) distal-ization .Results Class Ⅰ molar relationship had been obtained 7 month after distalization .The aver-age distal movement of the maxillary first molars was 7 .07 mm ,and the inclination was 9 .93° .The second premolars were distalized an average of 5 .44 mm with inclinations of 5 .22° .The first premolars were distalized an average of 4 .09 mm with inclinations of 3 .95° .The maxillary anterior teeth were re-truded 0 .93 mm and palatally inclined 1 .66° .There was statistical difference in that change .Conclusions By the use of microscrew ,pendulum can distalize maxillary molar effectively without mesial move-ment of premolar and labial movement of incisor ,and no loss of dental anchorage is observed during the distal movement .

Objective To investigate the effects of the different concentration of mineral trioxide aggregate (MTA) on the proliferation and differentiation of dental pulp stem cells (DPSCs) from the young permanent teeth.Methods DPSCs were isolated from the young permanent teeth and cultured by tissue explant method.The expression of STRO-1 was detected by using immunofluorescence technology.DPSCs were cultured with different concentrations of MTA (0.02,0.20,2.00,20.00 g/L).Cell proliferation was detected by MTT array.Cells were cultured in the appropriate concentration of MTA for 4 weeks,and then stained by Alizarin red to detect their mineralized nodule formation capacity.The cells were cultured with the appropriate concentration of MTA and collected after 12,24,36,48 h.The mRNA expression of ALP,BSP,OC and DSP after the treatment of MTA were detected by quantitative PCR.Results DPSCs were positive for STRO-1.The capacity of 0.20 g/L MTA promoting the proliferation of DPSCs was stronger than other concentrations.After 4 weeks,the mineralized nodules of DPSCs were observed after alizarin red staining.The PCR showed that with increasing induction time,the expression levels of DSP and OC were up-regulated.But that of ALP and BSP was increased first and then decreased.Conclusions In this study,MTA can promote the proliferation of DPSCs at 0.02,0.20,2.00 g/L concentration.It can induce odontoblast differentiation effectively by 0.20 g/L MTA.

OBJECTIVETo evaluate the effects of casein osphopeptide-amorphous calcium phosphate (CPP-ACP) in preventing enamel demineralization.

METHODSEnamel blocks were prepared from premolars extracted from orthodontic patients. The specimens were treated for 30 min daily for 7 days with one of the following agents: deionized water (negative control), CPP-ACP paste, and NaF solutions (positive controls) (0.2% and 2%). After the treatments, the specimens were immersed in a demineralizing solution (pH 4.5) for 7 days. The morphology and depth of the lesion were observed using scanning electron microscopy, and the content of Ca, P, Mg in the demineralized enamel was measured by electron probe micro-analyzer.

RESULTSThe demineralization rates in all the treatment groups were significantly smaller than those in the control group after 7 days of demineralization.

CONCLUSIONThe application of CPP-ACP to the enamel surfaces can inhibit enamel demineralization with an equivalent effect to 0.2% NaF.

Adolescent ; Caseins ; therapeutic use ; Dental Enamel ; Humans ; Sodium Fluoride ; Tooth Demineralization ; prevention & control ; Tooth Remineralization

Objective To evaluate the effects of casein osphopeptide-amorphous calcium phosphate (CPP-ACP) in preventing enamel demineralization. Methods Enamel blocks were prepared from premolars extracted from orthodontic patients. The specimens were treated for 30 min daily for 7 days with one of the following agents:deionized water (negative control), CPP-ACP paste, and NaF solutions (positive controls) (0.2% and 2%). After the treatments, the specimens were immersed in a demineralizing solution (pH 4.5) for 7 days. The morphology and depth of the lesion were observed using scanning electron microscopy, and the content of Ca, P, Mg in the demineralized enamel was measured by electron probe micro-analyzer. Results The demineralization rates in all the treatment groups were significantly smaller than those in the control group after 7 days of demineralization. Conclusion The application of CPP-ACP to the enamel surfaces can inhibit enamel demineralization with an equivalent effect to 0.2%NaF.

Objective To evaluate the effects of casein osphopeptide-amorphous calcium phosphate (CPP-ACP) in preventing enamel demineralization. Methods Enamel blocks were prepared from premolars extracted from orthodontic patients. The specimens were treated for 30 min daily for 7 days with one of the following agents:deionized water (negative control), CPP-ACP paste, and NaF solutions (positive controls) (0.2% and 2%). After the treatments, the specimens were immersed in a demineralizing solution (pH 4.5) for 7 days. The morphology and depth of the lesion were observed using scanning electron microscopy, and the content of Ca, P, Mg in the demineralized enamel was measured by electron probe micro-analyzer. Results The demineralization rates in all the treatment groups were significantly smaller than those in the control group after 7 days of demineralization. Conclusion The application of CPP-ACP to the enamel surfaces can inhibit enamel demineralization with an equivalent effect to 0.2%NaF.