2014-2021年陕西省饮水型地方性氟中毒监测结果分析

目的了解陕西省饮水型地方性氟中毒病区降氟改水工程运转情况、水氟含量现状以及氟中毒病情变化趋势,评价防治措施效果。方法2014年3月至2021年12月,以陕西省饮水型地方性氟中毒病区大荔、定边、靖边、泾阳和礼泉5个县的15个病区村为监测村,调查改水工程运转情况;并采集水样,依据《生活饮用水标准检验方法无机非金属指标》(GB/T 5750.5-2006)检测水氟含量。采用《氟斑牙诊断》(WS/T 208-2011),对监测村出生并居住的全部8~12岁儿童进行氟斑牙检查。采用《地方性氟骨症诊断标准》(WS/T 192-2008)和《尿中氟化物测定离子选择电极法》(WS/T 89-2015),分别对监测村25岁以上且在当地居住5年以上成人进行氟骨症X线检查和尿氟含量测定。结果2014-2021年共调查改水工程122个,均正常运转;水氟合格率从2014年的81.25%(13/16)上升至2021年的100.00%(11/11)。共检查8~12岁儿童5595例,检出氟斑牙儿童1790例,检出率为31.99%;儿童氟斑牙检出率从2014年的52.05%(304/584)下降至2021年的9.68%(93/961),整体呈现下降趋势(χ^(2)_(趋势)=533.76,P<0.001)。2014年检查成人791例,检出氟骨症患者256例,检出率为32.36%;2019年检查成人770例,检出氟骨症患者88例,检出率为11.43%;2019年成人氟骨症检出率低于2014年,差异有统计学意义(χ^(2)=99.54,P<0.001)。2014年采集成人尿样754份,尿氟几何均值为2.571 mg/L;2019年采集成人尿样770份,尿氟几何均值为1.292 mg/L;2019年成人尿氟几何均值低于2014年,差异有统计学意义(Z=-12.74,P<0.001)。结论2014-2021年,陕西省饮水型地方性氟中毒病区改水工程均正常运转,水氟合格率升高。儿童氟斑牙和成人氟骨症患病情况均减轻。后期应持续加强改水工程监测管理工作,防止水氟回升引起居民病情反弹。

渗透树脂联合美白技术修复微裂氟斑牙

背景:微研磨、家庭美白联合渗透树脂治疗氟斑牙具有良好的效果,但该方法对氟斑牙微裂纹的影响尚不清楚。目的:探究微研磨、家庭美白联合渗透树脂修复微裂氟斑牙的效果。方法:①临床研究:选择2020年7月至2021年3月就诊于天津医科大学口腔医院修复科的23例微裂氟斑牙患者,包括255颗微裂氟斑牙,均接受牙齿微研磨术、家庭美白与渗透树脂联合治疗,对比治疗前及治疗结束后1周、1个月的牙齿颜色、牙齿敏感程度和牙齿疼痛阈值。②体外实验:收集牙齿表面至少存在一条裂纹的氟斑牙60颗,随机分3组处理:对照组不进行任何处理,美白组进行微研磨与家庭美白处理,联合组进行微研磨、家庭美白和渗透树脂联合处理,每组20颗,测量处理后3组牙齿样本的显微硬度。结果与结论:①临床研究:治疗结束后6个月,255颗微裂氟斑牙中牙齿美白治疗显效207颗、有效48颗,总体治疗有效率为100%。随着治疗时间的延长,中、重度牙齿度敏感程度占比呈下降趋势,治疗结束后6个月,255颗氟斑牙中无重度敏感、15颗为中度敏感、125颗为轻度敏感、115颗无敏感,与治疗前的氟斑牙敏感程度相比差异有显著性意义(P<0.05)。治疗前与治疗结束后1周、6个月的牙齿疼痛阈值比较差异无显著性意义(P>0.05)。②体外实验:美白组牙齿显微硬度值低于对照组、联合组(P<0.05),对照组与联合组牙齿显微硬度值比较差异无显著性意义(P>0.05)。③结果表明,微研磨、家庭美白联合渗透树脂治疗微裂氟斑牙具有较好的疗效。

山东省淄博市饮水型地方性氟中毒流行现状调查与分析

目的采用横断面调查的方法,对山东省淄博市饮水型地方性氟中毒流行现状进行调查与分析。方法于2021年6月至12月对淄博市辖区内7个区县(张店区、临淄区、周村区、博山区、桓台县、高青县、沂源县)原有的氟中毒病区村及疑似病区村进行逐一调查登记,对8~12岁1200名在校儿童进行氟斑牙患病率的调查分析,并对淄博市采取的114个改水降氟工程运行情况及运行后的水质状况进行监测与分析。结果地方性氟中毒在淄博市分布广泛,7个区县共3102个行政村中地方性氟中毒病区村459个,高氟危及人群达28万人。高青县是淄博市地方性氟中毒最为严重的地区,病区村占总数的75.2%;高青县中病区村数量占中病区村总数的92.2%,12个重病区均位于高青县。高青县也是8~12岁儿童氟斑牙的患病率最高的地区,20个村的88名儿童的氟斑牙检出率为100%,因受地理环境、气候及经济状况的影响,高青县345个病区村中仅有224个实施了改水降氟工程,占64.9%,是淄博市病区改水率最低的地区。结论淄博市地方性氟中毒总体处于低度流行趋势,但高青县地方性氟中毒防治形势仍然十分严峻,应加大防治经费的投入及改水降氟措施的落实力度,为早日控制地方性氟中毒的流行,保障人民群众免受地方性氟病的威胁做出努力。

氟中毒大鼠脑组织中NMDA受体及内质网应激相关通路蛋白的表达

背景:前期研究发现N-甲基-D-天冬氨酸(N-methyl-D-aspartic acid receptor,NMDA)受体与氟相关,但其在氟诱导的内质网应激中的作用尚不明确。目的:观察实验性氟中毒大鼠脑组织中兴奋性神经递质NMDA受体及内质网应激IRE1α-ASK1-JNK通路蛋白表达变化,并应用NMDA受体抑制剂干预SH-SY5Y细胞,探讨氟中毒神经系统损伤的发病机制。方法:(1)动物模型:18只1月龄SD大鼠随机分为对照组(饮水含氟量<0.5 mg/L)、低氟组(饮水含氟量为10.0 mg/L)、高氟组(饮水含氟量为100.0 mg/L),每组6只,雌雄各半。饮水摄氟饲养6个月后,观察大鼠氟斑牙发生情况,测定24 h尿氟含量;大鼠麻醉处死后取脑组织观察组织病理变化,蛋白印迹法检测脑组织中NMDA受体及IRE1α、ASK1、JNK蛋白表达。(2)细胞模型:体外培养SH-SY5Y细胞,选择终浓度为0.3 mmol/L和3 mmol/L的氟化钠染氟处理,并用10μmol/L的NMDA受体拮抗剂Ifenprodil、MK-801对染氟细胞进行干预,观察相关蛋白改变。结果与结论:(1)高氟组大鼠氟斑牙发生率、尿氟水平显著高于对照组和低氟组(P<0.05);(2)与对照组相比,低氟组大鼠海马CA3区神经细胞胞质嗜碱性略增加,高氟组CA3区神经细胞排列紊乱,嗜碱性增加,部分细胞核固缩;(3)大鼠脑组织内,高氟组NR2A与低氟组NR2B的蛋白表达明显高于对照组(P<0.05),且高氟组NR2B、IRE1、ASK1、p-JNK蛋白表达明显高于对照组和低氟组(P<0.05);(4)SH-SY5Y细胞内,高氟组NR1、NR2A、NR2B蛋白表达明显高于对照组(P<0.05),且高氟+Ifenprodil组、高氟+MK-801组NR1、NR2A蛋白表达均明显低于高氟组(P<0.05),高氟+Ifenprodil组NR2B蛋白表达也明显低于高氟组(P<0.05);(5)SH-SY5Y细胞内,高氟组IRE1、ASK1、p-JNK蛋白表达明显高于对照组(P<0.05),且高氟+Ifenprodil组、高氟+MK-801组ASK1、p-JNK蛋白表达均明显低于高氟组(P<0.05),高氟+Ifenprodil组IRE1蛋白水平也明显低于高氟组(P<0.05);(6)提示:过量氟摄入可激活中枢神经系统NMDA受体,引起内质网应激IRE1α、ASK1、p-JNK蛋白表达增加,使用NMDA受体抑制剂对氟中毒所致内质网应激具有一定缓解作用。

氟中毒对神经细胞损伤及自噬的影响

目的探讨氟中毒对小鼠小胶质细胞株BV2和小鼠来源神经母细胞瘤细胞株N2a及小鼠大脑皮质神经细胞损伤及自噬的影响。方法8周龄清洁级雄性C57BL/6J野生型小鼠,随机分为对照组(饮水含氟量<0.5 mg/L)、低氟组(饮水含氟量10.0 mg/L)和高氟组(饮水含氟量50.0 mg/L),每组10只喂养12周;BV2及N2a正常培养后分对照组、低氟组(培养基含氟量1.0 mmol/L)和高氟组(培养基含氟量1.5 mmol/L);采用CCK8检测不同浓度氟处理下BV2和N2a细胞增殖活力变化,氟离子选择电极法检测造模小鼠尿、血、骨氟含量变化;蛋白免疫印迹法(Western blot)检测BV2、小鼠大脑皮质中小胶质细胞活化标志物离子钙结合衔接分子1(Iba-1)的表达变化及N2a细胞、BV2细胞和小鼠大脑皮质中自噬相关微管相关蛋白1轻链3(LC3)及自噬受体蛋白P62蛋白(SQSTM1/P62)的表达水平;线粒体动力学及自噬融合分裂相关蛋白线粒体融合蛋白1(Mfn1)、线粒体融合蛋白2(Mfn2)、动力相关蛋白1(Drp1)、张力蛋白同源物诱导的假定激酶1(Pink1)及E3泛素连接酶(Parkin)的表达水平。结果CCK8结果显示,1.5 mmol/LNaF处理的BV2、N2a细胞增殖活力明显下降(P<0.001,);低氟组小鼠氟斑牙发生率为60%,高氟组小鼠氟斑牙发生率为80%;与对照组比较,染氟组小鼠尿、血、骨氟含量明显上升(P<0.001);蛋白免疫印迹结果显示,与对照组比较,高氟组的小鼠大脑皮质和BV2的小胶质细胞活化标志物Iba-1表达水平显著升高(P<0.001,P<0.01),高氟组的小鼠大脑皮质和BV2及N2a细胞自噬相关蛋白LC3、Parkin、Pink1表达量显著增加(P<0.05)、P62水平显著下降(P<0.01);线粒体融合蛋白Mfn1、Mfn2水平显著增加(P<0.001),分裂蛋白Drp1无明显变化。结论氟中毒可导致线粒体损伤、破坏线粒体融合分裂平衡并引起细胞自噬,为阐明氟中毒神经系统损伤与细胞自噬之间相互关系提供新思路。

蛋白质组学技术及其在氟中毒研究中的应用

氟在自然界中广泛存在,是机体必需微量元素之一。摄入少量氟对机体骨骼及牙齿有保护作用,但长期过量摄入氟会造成机体慢性氟中毒,对机体造成骨相及非骨相损伤,严重威胁着动物的健康。随着蛋白质组学技术的发展及其在氟中毒研究中的应用,人们对氟的骨相及非骨相毒性的分子机制研究越来越深入。笔者主要介绍了包括质谱分析、双向电泳、高效液相色谱分析、免疫共沉淀、同位素标记相对和绝对定量及蛋白质芯片等蛋白质组学技术的原理及特点,并概述了这些蛋白质组学技术在氟的骨相和非骨相毒性研究中的应用,旨在为进一步探究氟中毒的致病机制提供思路和见解。

过量氟对小鼠髁突软骨损伤及自噬相关因子LC3、p62表达的影响

目的:研究过量氟对小鼠髁突软骨损伤及髁突软骨中自噬相关因子的表达。方法:将30只4周龄雄性C57BL/6小鼠随机分为对照组和实验组,每组15只,对照组自由饮用去离子水,实验组自由饮用含氟离子浓度为75 mg/L的去离子水,持续喂养8周。通过改良番红O-固绿软骨染色观察髁突纤维软骨层结构变化;免疫组织化学染色检测软骨细胞外基质降解标志物基质金属蛋白酶13(Matrix metalloproteinase 13,MMP-13)、Ⅱ型胶原蛋白的表达水平及自噬相关因子微管相关蛋白轻链3(microtubule-associated protein light chain 3,LC3)、自噬底物蛋白p62的表达水平。采用SPSS 22.0软件包对免疫组织化学染色半定量结果进行双因素方差分析。结果:与对照组相比,实验组纤维软骨层变薄,软骨细胞体积变小,核变小,染色加深。免疫组织化学染色结果显示,实验组MMP-13表达量增加,Ⅱ型胶原蛋白表达量降低;LC3表达量增加,p62表达量下降。结论:用含氟离子浓度为75 mg/L的去离子水喂养小鼠8周,可导致髁突软骨退变,髁突软骨发生自噬。

慢性氟中毒环境对大鼠正畸牙移动过程中牙周组织VEGF和eNOS表达的影响

目的:通过观察慢性氟中毒大鼠牙移动过程中牙周组织内血管内皮生长因子(vascular endothelial growthfactor,VEGF)、内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)的表达变化,初步探究机体慢性氟中毒状态对大鼠正畸牙移动过程中牙周组织血管生成的影响。方法:选取3周龄SPF级SD大鼠120只,体重(60±5)g,随机分为空白组(C)、染氟组(F)、正畸组(O)、染氟正畸组(FO),每组雌雄各15只,根据正畸加力时间分为0、3、7、14、28 d组,共5个时间亚组。分别相应时间点处死各组大鼠,苏木精-伊红染色观察牙周组织血管情况,免疫组织化学染色观察大鼠牙周组织VEGF及eNOS蛋白表达情况。结果:(1)慢性氟中毒大鼠及正畸牙移动大鼠模型复制成功;(2)O组牙周纤维排列较C组紊乱,牙周血管数量增多,管腔不规则。FO组血管新生分布不及O组突出。(3)各组雌雄大鼠间VEGF、eNOS表达无明显性别差异,O组、FO组张力侧VEGF、eNOS表达与压力侧相比无明显统计学差异。(4)FO组VEGF、eNOS的蛋白平均表达水平高于F组,但低于O组,且差异有统计学意义。(5)O组、FO组VEGF、eNOS蛋白表达随时间延长呈先升高后降低趋势,第3天表现为峰值。结论:慢性氟中毒会抑制大鼠牙移动过程中牙周组织VEGF、eNOS的表达。

强直性脊柱炎误诊文献分析

目的分析误诊为强直性脊柱炎(AS)的病例文献及鉴别诊断方法。方法以“AS”“误诊”为关键词,采用万方数据库、中国知网数据库、中华医学期刊全文数据库,检索其他疾病误诊为AS文献报道,对患者基本资料、症状、炎性指标、人类白细胞抗原B27(HLA-B27)、影像学资料、诊断疾病进行总结及分析。结果共检索到其他疾病误诊为AS文献报道63篇,共计纳入误诊为AS病例193例,年龄11~78岁,平均(36.14±16.72)岁。临床表现主要以腰背痛84例次(43.52%)、晨僵71例次(36.79%)、腰骶部疼痛48例次(24.87%)、发热38例次(19.69%)、膝关节痛37例次(19.17%)为主。血沉升高74例(38.34%),CRP升高65例(33.68%)。HLA-B27阳性43例(22.28%),阴性123例(63.73%)。关节面正常20例(10.36%),异常158例(81.87%)。脊柱呈竹节样改变46例(23.83%)。误诊疾病以骶髂关节感染57例(29.53%),布鲁氏菌病22例(11.40%),细菌感染20例(10.36%),结核15例(7.77%),氟骨症42例(21.76%),血液系统疾病15例(7.77%)为主。结论AS临床症状与多种疾病相似,须注意鉴别,防止误诊。

YAG激光联合渗透树脂辅助诊室漂白治疗氟斑牙的临床疗效和舒适度分析

目的 探讨在诊疗室应用YAG激光配合渗透性树脂漂白对氟斑牙的疗效。方法 选取2020-2022年石家庄市第二医院口腔科诊治的氟斑牙患者90例,按照随机数字表法分为A、B组,每组45例。A组采用低能量(YAG)激光处理,同时加以诊室漂白,B组采用低能量(YAG)激光处理,并与渗透树脂辅助诊室漂白相联合,用VITA比色板作脱色前后对比,以分光比色仪记录美白后釉质表面的色阶和色度。使用分光光度计和Vita指南记录每个时间节点的牙齿颜色变化,2年的随访中,评估牙齿美白前后的颜色反色效应。比较2组患者治疗后的牙齿敏感发生率。结果 治疗后2组患者牙齿颜色均变白,但B组患者牙齿颜色等级显著低于A组,差异有统计学意义(P<0.001)。1周美白治疗后,A、B组患者的漂白总有效率分别为75.56%、73.33%,差异无统计学意义(P>0.05);6个月后,B组和A组的漂白总有效率分别为80.00%和75.56%,差异无统计学意义(P>0.05);1年后,B组和A组的漂白总有效率分别为100%和80.00%,差异有统计学意义(P<0.05);2年后,B组总有效率为100%,A组为82.22%,差异有统计学意义(P<0.05)。治疗后立即牙敏感率B组为40.00%明显小于A组的93.33%(P<0.05);2组在用药24 h内均未出现过敏反应。结论 YAG激光联合渗透树脂辅助诊室漂白治疗中度氟斑牙在临床上具有相对更好的疗效和舒适度。

2022年内蒙古自治区饮茶型地方性氟中毒流行现状调查

目的了解内蒙古自治区(简称内蒙古)饮茶型地方性氟中毒(简称地氟病)流行现状,为制定和评价防控措施提供理论依据和基础数据。方法2022年5-10月,采用横断面调查方法,在2019年全区普查中确定的有饮茶习惯、日人均茶氟摄入量>3.5 mg且存在氟骨症患者的重点地区(6个盟市的168个行政村)开展调查。每个行政村入户调查10户家庭的砖茶饮用情况,采集砖茶样品测定氟含量。调查所有8~12岁儿童氟斑牙和16岁及以上成人氟骨症患病情况,并采集氟骨症患者尿样检测尿氟含量。结果调查地区98.40%(1657/1684)的家庭有饮用砖茶习惯,年人均砖茶消耗量和日人均茶氟摄入量分别为5.07 kg和5.38 mg。砖茶样品氟含量合格率为55.64%(922/1657);除黑砖茶(291.08 mg/kg)外,其余砖茶品种氟含量均值均超过国家标准限值(300 mg/kg)。共检查8~12岁儿童2747人,氟斑牙检出率为13.91%(382/2747),病情以极轻度为主;各年龄组氟斑牙检出率比较,差异无统计学意义(χ^(2)=5.53,P=0.238)。共检查16岁及以上成人71708人,氟骨症检出率为1.02%(734/71708),患者年龄集中在>50~70岁,各年龄组病情均以轻度为主。采集并检测715份患者尿样,55.24%(395/715)的尿样氟含量>1.6 mg/L。结论内蒙古饮茶型地氟病流行地区高氟砖茶占比大,儿童氟斑牙和成人氟骨症检出率较高,饮茶型地氟病防控形势依然严峻。

高氟干预成釉细胞钙稳态差异表达基因的筛选及分析

背景:氟牙症是长期摄入大量氟所导致的牙釉质发育障碍,病因复杂,其发病机制有待深入研究。目的:通过转录组测序技术筛选高氟干预成釉细胞与钙稳态相关的差异表达基因,并进一步探索氟斑牙形成的分子机制。方法:分别用浓度为0,0.4,0.8,1.6,3.2,6.4 mmol/L的NaF处理成釉细胞LS824,48,72 h,检测细胞形态、细胞活性与细胞内钙离子浓度。分别用浓度为0,1.6,3.2 mmol/L的NaF处理成釉细胞LS824 h,通过转录组测序筛选差异表达基因,并对差异表达基因进行验证。结果与结论:①处理24 h后,NaF浓度0,0.4,0.8 mmol/L组细胞生长状态良好,细胞的数量增多,细胞轮廓清晰;当NaF浓度≥1.6 mmol/L,随着NaF浓度的增加,细胞体积逐渐皱缩变小、细胞数量减少。处理48,72 h后,NaF浓度0,0.4 mmol/L组细胞数量增加,0.8,1.6,3.2 mmol/L组细胞数量逐渐减少,细胞形态变圆、变小,6.4 mmol/L组细胞皱缩变圆悬浮于培养基中,几乎无细胞贴壁。当NaF浓度相同时,处理24 h后LS8细胞的生长状态最佳。CCK-8检测结果显示,当NaF浓度相同时,随着处理时间的延长,细胞活性减弱;当处理时间相同时,随着NaF浓度的增加,细胞活性减弱。处理24 h后,随着NaF浓度的增加,细胞内钙离子浓度增加。②转录组测序分析发现参与调控细胞钙稳态的基因:Hsp90b1、Canx、Calr、Hspa5的表达显著上调(P<0.05),Cacna1a的表达显著下调(P<0.05),该结果得到了RT-qPCR检测的验证。③结果显示,NaF对LS8细胞增殖的抑制作用可能与细胞内Ca2+浓度异常增加有关,其机制可能由蛋白质加工合成通路Hsp90b1、Canx、Calr、Hspa5表达上调和钙信号通路Cacna1a表达下调所导致。

组蛋白乙酰化/甲基化在口腔疾病中的研究进展

组蛋白乙酰化和甲基化能影响染色质构象,进而调控多种生物学活动。异常的组蛋白乙酰化和甲基化修饰与多种口腔疾病的发生发展有关。在牙的发育过程中,组蛋白乙酰化和甲基化修饰有序地升高或降低,调控牙的发育,氟离子能够破坏组蛋白乙酰化和甲基化修饰的平衡,这可能与氟牙症的发生有关。此外,组蛋白乙酰化和甲基化修饰也参与调控了口腔的炎症性疾病,炎症微环境下,组蛋白乙酰转移酶GCN5表达下降,使Dickkopf 1(DKK1)表达下降,从而激活Wnt/β⁃catenin通路,最终抑制牙周膜干细胞的成骨分化。Zeste增强子同源物2(enhancer of zeste homolog 2,EZH2)与H3K27me3在炎症牙髓组织和牙髓细胞中下降,抑制EZH2可抑制炎症刺激导致的人牙髓细胞中白细胞介素⁃1b、白细胞介素⁃6和白细胞介素⁃8的表达。组蛋白乙酰化/甲基化修饰能够与多条信号通路相互作用,促进口腔肿瘤的发生发展,并与唾液腺肿瘤的高侵袭性有关。靶向组蛋白乙酰化和甲基化相关酶的小分子药物能调控组蛋白甲基化/乙酰化修饰水平,在口腔颌面部疾病治疗中展现出应用潜能,例如组蛋白去乙酰化酶抑制剂——伏立诺他,其既能够抑制炎症的相关细胞因子的分泌,还能促进成牙本质细胞分化并形成牙本质相关基质,展现出了在保髓治疗中的潜力。了解组蛋白乙酰化/甲基化修饰在口腔疾病发生发展中的作用,有助于推进表观遗传修饰在口腔疾病的研究深入,提供新的疾病诊疗视角。

Role of Inhibition of Osteogenesis Function by Sema4D/Plexin-B1 Signaling Pathway in Skeletal Fluorosis In Vitro

Summary： Skeletal fluorosis is a chronically metabolic bone disease with extensive hyperostosis osteosclerosis caused by long time exposure to fluoride. Skeletal fluorosis brings about a series of abnormal changes of the extremity, such as joint pain, joint stiffness, bone deformity, etc. Differentiation and maturation of osteoblasts were regulated by osteoclasts via Sema4D/Plexin-B 1 signaling pathway. Furthermore, the differentiation and maturation of osteoclasts are conducted by osteoblasts via RANKL/RANK/OPG pathway. Both of these processes form a feedback circuit which is a key link in skeletal fluorosis. In this study, an osteoblast-osteoclast co-culture model in vitro was developed to illustrate the mechanism of skeletal fluorosis. With the increase of fluoride concentration, the expression level of Sema4D was decreased and TGF-β1 was increased continuously. OPG/RANKL mRNA level, however, increased gradually. On the basis of that, the inhibition of Sema4D/Plexin-B1/RhoA/ROCK signaling pathway caused by fluoride promoted the level of TGF-β1 and activated the proliferation of osteoblasts. In addition, osteroprotegerin （OPG） secreted by osteoblasts was up-regulated by fluoride. The competitive combination of OPG and RANKL was strengthened and the combination of RANKL and RANK was hindered. And then the differentiation and maturation of osteoclasts were inhibited, and bone absorption was weakened, leading to skeletal fluorosis.

Association of Dietary Carotenoids Intake with Skeletal Fluorosis in the Coal-burning Fluorosis Area of Guizhou Province

Objective To explore whether the intake of dietary carotenoids could protect against skeletal fluorosis in Guizhou province in which coal-burning fluorosis is endemic. Methods A case-control study of 196 patients with skeletal fluorosis and 196 age and gender-matched controls was conducted in Zhijin, Guizhou Province. Face-to-face interviews were conducted to assess habitual dietary intake using a 75-item food frequency questionnaire and various covariates with structured questionnaires. Urinary fluoride was measured using an ion-selective electrode method. The genotype of superoxide dismutase 2（SOD2） rs11968525 was detected by Taq Man method. Results We observed significant dose-dependent inverse associations of skeletal fluorosis with intake of β-carotene, lutein/zeaxanthin, lycopene, and total carotenoids（P-trend = 0.002 to 0.018）, whereas α-carotene and β-cryptoxanthin intakes were not found to be related to skeletal fluorosis, after adjustment for potential confounders. The adjusted ORs and 95% CI of skeletal fluorosis for the highest versus lowest quartile were 0.30（0.10, 0.86） for β-carotene, 0.23（0.08, 0.66） for lycopene, 0.26（0.10, 0.75） for lutein/zeaxanthin and 0.34（0.14, 0.74） for total carotenoids（all P-trend ＆lt; 0.05）. Stratified analyses showed that the protective effects of lutein/zeaxanthin and total carotenoids on skeletal fluorosis were more evident for individuals with the AG＋AA genotypes of SOD2（rs11968525）. Conclusion Increased intakes of β-carotene, lutein/zeaxanthin, lycopene, and total carotenoids are independently associated with a lower risk of coal-burning skeletal fluorosis. SOD2（rs11968525） polymorphisms might modify the inverse associations between dietary carotenoids and skeletal fluorosis.

Relationships between daily total fluoride intake and dental fluorosis and dental caries

Objective： To explore the relationships between the daily total intake of fluoride, dental fluorosis and dental caries. Methods： An epidemiological method was used to investigate the daily total intake of fluoride, dental fluorosis, and dental caries among 236 and 290 children aged 8-13 years in a severe endemic area and in a non-fluorosis control area, respectively. The children were divided into eight subgroups according to each child＇ s estimated daily total intake of fluoride. The prevalence of dental fluorosis and dental caries in each group was calculated. Results： As expected, elevated levels of fluoride intake were significantly associated with a higher prevalence of dental fluorosis and an increasing amount of more severe defect dental fluorosis. When the daily total F intake was 2.78 mg/child/day, the prevalence of dental fluorosis was nearly 100%, with the prevalence of defect dental fluorosis increasing with increasing fluoride intake. There was also a significant negative（inverse） dose-response relationship between the daily total intake of fluoride and the overall prevalence of dental caries, the prevalence of which decreased when the daily total intake of fluoride increased up to 3.32 mg/child/day. However, at higher levels of daily total intake of fluoride the prevalence of dental caries increased, giving rise to a U-shaped dose-response relationship curve. Conclusion： It is important to monitor total fluoride exposure and protect children from excessive fluoride intake, especially during the years of tooth development.

Investigation and Analysis on Current Situation of Coal-Burning Fluorosis Prevalence

Objective: The purpose of the paper is to provide the result from investigation on the current situation of coal-burning fluorosis prevalence in Chongqing City and make an assessment on the prevention and curing measures. Method: The Dean’s Method is applied to investigate on the fluorotic teeth of locally-born children aged between 8 to 12;investigate how modified cooking stoves are utilized by households and how food maize and hot pepper are being dried;and test the urinary fluorine content and pepper fluorine content. Result: The investigations show that, in the 661 villages with illness history from the 100 townships of 13 districts in Chongqing City, 11.28% (7464/ 66,162) of the children aged between 8 and 12 suffer from dental fluorosis;the stoves modified rate, qualified rate of modified stoves, and correct utilization rate of qualified modified stoves are respectively 100%, 98.82%, and 99.45%;and food maize and hot pepper’s drying rates are respectively 99.88% and 99.75%. Conclusion: The result shows that the coal-burning type fluorosis prevalence in the endemic area of Chongqing City has decreased dramatically, the preventive measure is effectively implemented, and a long-term preventive mechanism has preliminarily been established.

Prevalence of Brick Tea-type Fluorosis in Children Aged 8–12 Years in Qinghai Province,China

Fluorosis is a serious health problem,and an endemic disease in certain areas in China,India,and some countries in Africa[1].There are three types of fluorosis which includes drinking-water type fluorosis,coal-burning pollution type fluorosis,and brick tea-type fluorosis.Coal-burning pollution type fluorosis and brick tea-type fluorosis are found only in China's Mainland mainland.

Relationship between the Contents of MDA, the Activity of SOD in Serum of the Milk Goat with Fluorosis and the Erythrocytic Membrane Liquidity

To research the relation among the erythrocytic membrane.liquidity and the contents of MDA, the activity of SOD in serum of the milk goat with fluorosis. An animal model with fluorosis was constructed, and the fluorescent probe technique of DPH was used to measue the erythrocytic membrane liquidity. At the same time, the contents of MDA and the activity of SOD in serum were measured. The results showed that the erythrocytic membrane liquidity in the control group and flurosis group were 5.6742 ± 0.4417 and 3.7248 ± 0.4521 （P 〈0.01） respectively, the contents of MDA in serum were 2.0408 ± 0.198 and 4.494± 0.438 （P 〈0.01） respectively, the activities of SOD were 175.638 ± 22.201 and 113.714 ± 34.258 （P 〈0.01） respectively. The correlation analysis indicated that the relation between the activity of SOD and the liquidity of erythrocytic membrane was positive correlation （ r= 0.7321, P 〈0.05）, whereas the relation between the contents of MDA and the liquidity of erythrocytic membrane was negative correlation （r = -0.6438, P 〈0.01）. The erythrocytic membrane liquidity decreased in milk goat with fluorosis, which played a role in the occurrence and development of the fluorosis. There was correlation among the erythrocytic membrane liquidity and the contents of MDA, the activity of SOD.

Pathological evaluation of pancreatic exocrine glands in experimental fluorosis

Objective:To monitor the pathological alterations in pancreas of rat during experimental fluorosis. Methods:Sixty Sprague Dawley albino rats of both sexes were divided into 12 experimental groups and one control group.The rats of control group were administered subcutaneously double distilled water 1 mL/kg bw daily.The experimental groups were injected with 30,45,and 75 mg NaF/kg bw/day.The experimental period was divided into 4 phases at interval of 15,22,30,and 36 days.Animals were sacrificed from each group at the end of 16,23,31,and 37 days.Results: The following changes were observed in this study:(1) Pathological examination of pancreas after 15 days of fluoride treatment revealed:hypertrophy of acini,leucocytes infilteration and pycnouc nuclei due to necrosis of acini in group 1;uremic alterations,invulsion and infoldings of reticular layer of islets of Langerhans in group 2;and a decrease in number of acini and interlobular connective tissues resulted in an increase in intercellular spaces in pancreas of rats in group 3.(2)Hyalinization and hypertrophy in the lobules of acini and hyperplasia and hypertrophy in intercalated duct with mucinous secretion in pancreas of rat of group 4;squamous metaplasia of pancreatic duct,adenoma of pancreas,hemorrhagic necrosis in group 5;and hyperplasia of acini and reduction in number of pancreatic islets in group 6.(3) Disorganization and atrophy of pancreatic lobules and presence of vacuoles in a group of six were visible in pancreas of rats in group 7;acute pancreatic and lamellated inflammatory cells in test rats of group 8;and islet adenoma and decrease in number of islets cells,and exudation in acini were noticed in experimental rats of group 9.(4) In the last phase of experimentation,atrophic alterations in pancreatic acini,invulsions,and necrosis was prominent in group 10,deep inflammation and proliferation of connective tissue of pancreas in experimental group 11,and periodical fibrosis, hyperplasia of acini,degenerative changes in pancreas of rats in group 12.Conclusion:The histopathological examination of pancreas of fluoridated rats exhibited structural alterations in the exocrine glands.The acini revealed hypertrophy,pyknotic nucleus,necrosis and uremic alterations.Acini became lobulated and reveal increased pigmentation.