2012～2015年北京市海淀区13所幼儿园2～6岁儿童患龋趋势研究

目的了解北京市海淀区2~6岁儿童2012~2015年间乳牙龋病的患病趋势,为海淀区儿童龋病防治工作提供依据。方法 2012~2015年间对北京市海淀区13所幼儿园2~6岁儿童,连续4年进行口腔健康状况调查,采用WHO推荐的检查方法和龋病诊断标准,调查4年间海淀区2~6岁儿童乳牙龋病的患病趋势。口腔检查由2年以上工作经验的儿童口腔医生进行,所有的检查者都经过培训和校准。结果 4年来13所幼儿园2~6岁儿童乳牙患龋率、龋均(dft)和龋面均(dfts)逐年升高,5岁组儿童乳牙患龋率为69.06%~72.08%,dft为4.04~4.30,dfts为5.15~5.80。3~5岁儿童重度低龄儿童龋的患病率分别为22.09%~29.54%,26.92%~31.18%和32.18%~35.84%,随年龄增加而上升。2~6岁患龋儿童接受治疗率和龋补充填比呈下降趋势,分别为82.60%~61.46%和55.61%~42.96%。结论 海淀区2~6岁儿童乳牙患龋率、龋均和SECC患病率处于较高水平,在幼儿园采取龋病综合防治措施非常有效,但应同时加强龋病的预防工作,特别是对龋高危儿童的监控和防治。     

北京市西城区幼儿园口腔保健对龋病的影响

1995年全国第二次口腔健康流行病学调查显示:北京地区5岁儿童乳牙患龋率71.97%,龋均3.84[1],而在美国5岁儿童乳牙患龋率在1988年就已下降至2.7%[2].因此,如何降低儿童的患龋率和提高龋齿充填比(矫治率)是目前幼儿园口腔保健的重要工作.为了解北京市西城区儿童近年乳牙龋病发病趋势,评价预防效果,对该区1999年～2004年5岁儿童乳牙患龋情况进行了调查分析.     

2015年北京市学龄前儿童乳牙龋现况及10年变化(2005～2015)

目的 了解2015年北京市3～5岁儿童乳牙龋现况,并纵向分析2005～2015年10年间5岁儿童乳牙患龋状况的变化.方法 参照第四次全国口腔健康流行病学调查方案,北京地区扩大样本量,随机抽取3、4、5岁儿童各972人,检查乳牙患龋状况.纵向分析北京市2005～2015年10年间7次口腔流行病学调查5岁组儿童乳牙患龋状况.结果 北京市2015年3、4、5岁儿童乳牙患龋率分别为38.4％、52.3％、61.0％,龋均分别为1.41、2.24、2.92,龋补充填比分别为14.7％、21.3％、30.1％.10年内5岁儿童乳牙龋呈现先上升后下降的趋势.5岁儿童乳牙患龋率,2005～2011年上升18.8％(P<0.001),2011～2015年下降12.4％(P<0.001).5岁儿童龋补充填比从2011年的19.3％上升到2015年的30.1％,上升55.6％(P<0.001).结论 2015年北京市儿童乳牙龋患龋率保持在较高水平,且近10年来乳牙患龋状况呈现先上升后下降的趋势,乳牙龋治疗率有显著上升,乳牙龋的防控形势依然严峻.     

402名南宁民办幼儿园学龄前儿童龋病状况调查

目的 了解南宁市民办幼儿园3～7岁学龄前儿童乳牙龋患病及治疗情况。方法 随机抽取南宁市3所民办幼儿园402名3～7岁儿童为对象,其中男214名,女188名,按照第3次全国口腔健康流行病学调查诊断标准进行口腔检查后,提取龋病情况资料,包括患龋率、龋均、龋面均、龋坏充填率等进行统计学分析。结果 受检儿童中,261例发现明确龋坏,总患龋率为64.93%,龋均3.56,龋面均6.11,龋坏充填率0.84%。其中3～、4～、5～、6～7岁年龄段人数分别为111、133、108、50例,患龋人数(率)分别为53(47.75%)、89(66.92%)、80(74.07%)和39(78.00%);龋均分别为2.23、3.17、4.86和4.7。统计分析表明患龋率随年龄增大而增高,差别具有统计学意义(χ2=22.34,P<0.001)。结论 南宁市民办幼儿园3～7岁儿童乳牙患龋状况严峻,患龋率高,龋坏充填率低。?     

低龄儿童乳牙龋病流行病学及龋活跃性分析

目的:调查3～6岁儿童乳牙龋病的流行情况,研究龋活跃性与患龋严重程度的关系。方法:纳入南京市6所幼儿园1 375名3～6岁儿童进行口腔检查和龋活跃性试验。结果:3～6岁儿童平均患龋率和龋均分别为50.48%和2.13,龋齿充填率6.93%,其中5岁年龄组患龋率和龋均分别为61.42%和2.92。龋活跃性各分值之间的患龋率及龋均差异显著(P<0.01)。龋活跃性与患龋率及龋均呈高度正相关(P<0.01)。结论:3～6岁年龄段儿童的患龋情况严重,且治疗率十分低,应加强口腔健康教育,开展多种防龋措施。龋活跃性检测结果能够真实反映患龋现状,有助于筛选龋易感者。     

北京市海淀区3岁儿童龋病患病状况及龋病活跃性检测的研究

目的 通过了解北京市2所大学附属幼教机构学龄前儿童的口腔健康状况、龋病活跃性,了解儿童患龋情况与龋病活跃性之间的关系,探讨龋病活跃性检测筛查龋易感儿童及反映龋活跃性检测试剂的灵敏性和特异性,评价其对患龋预测的有效性和可行性.方法 对3岁年龄组儿童进行连续1年的口腔检查和龋活跃性检测,分析儿童患龋情况的变化与龋病活跃性之间的关系.结果 3岁儿童的患龋率为44.80%,龋均dft为2.04,龋面均dfs为2.79,儿童龋活跃性检测结果的各个分值与儿童患龋程度呈高度正相关关系(P<0.001).1年后随访,龋高危组儿童的新龋发生率显著高于龋低危组,经统计学检验其差异具有显著性意义(P<0.001).Cariostat法进行龋活跃性检测的敏感度可达95.1%,特异度达50.2%.结论 龋活跃性检测能够准确的反映儿童龋患现状,预测儿童患龋的趋势,为儿童制定个性化的预防保健计划.     

兰州市学龄前儿童龋病调查分析与防治对策

目的　了解兰州市幼儿园儿童龋患情况 ,为制定适合的幼儿园儿童口腔保健规划提供依据。方法　对西北师范大学幼儿园 357名 4～ 6岁儿童进行口腔健康检查 ,并作统计分析。结果　 4岁、5岁、6岁儿童患龋率分别为 52 .54%、69.44%、84.2 1 % ,其龋均分别为 1 .73、3.43、5.1 1 ,不同年龄组之间患龋率、龋均都有显著性差异 (P <0 .0 1 )。 4岁组乳上前牙患龋率最高 ,6岁组下颌乳磨牙患龋率最高。结论　乳牙龋齿患病随年龄而递增 ;幼儿园口腔预防保健工作的重点是低龄儿童 ,宜采取局部用氟及窝沟封闭为主的方法 ,同时加强口腔健康教育。     

沈阳市幼儿园5岁儿童乳牙龋病流行病学抽样调查报告

目的 调查沈阳市幼儿园5岁儿童乳牙龋患病情况.方法 采用分层等容量随机抽样的方法,抽取沈阳市内5区5岁常住人口440人及其家长,男女各半.检查儿童全口乳牙牙冠龋病情况,统计患龋率、龋均等,将所得数据与本地区1995年的调查数据进行比较;并对家长进行儿童饮食习惯、刷牙情况等的问卷调查.结果 乳牙患龋率为67.05％,龋均为3.10,龋齿充填完好率5.51％,曾接受过龋齿治疗的占8.41％.与1995年沈阳市幼儿园5岁儿童乳牙龋病情况比较,患龋率有所下降(P＜0.001),龋均亦有下降(P＜0.001).问卷调查中有睡前进甜食行为者占41.28％,定期进行口腔健康检查者只占2.04％,在家长监督下有效刷牙率为10.17％,家长对儿童口腔健康状况满意率为82.91％.结论 沈阳市幼儿园5岁儿童乳牙患龋率与1995年相比虽然有所下降,但仍占较高比例.家长对儿童口腔健康认识程度低与高患龋率有关,对家长的口腔健康教育有待加强.     

贵阳市南明区3～5岁儿童龋病流行病学调查

目的了解贵阳市南明区学龄前儿童乳牙龋患病状况,为乳牙龋防治工作提供依据。方法按照第三次全国口腔健康流行病学调查的要求,参照世界卫生组织《口腔健康调查基本方法》,随机抽取贵阳市3~5岁儿童432名,进行龋病检查。结果 432名受检儿童中,乳牙患龋率为46.3%,龋均为1.71。各年龄组间比较显示:随年龄增长各年龄组患龋率和龋均均显著上升,各组间患龋率与龋均比较均有显著性差异(P<0.05);乳牙龋充填率为5.83%,随年龄增长龋充填率逐渐上升。。结论贵阳市3~5岁儿童乳牙患龋率较高,充填率较低,应加强乳牙龋的早期防治。     

上海市长宁区3岁沪籍与非沪籍儿童乳牙龋病1259例调查

目的了解上海市长宁区3岁沪籍与非沪籍儿童的乳牙患龋情况。方法按全国口腔流行病学调查标准,对645名沪籍、614名非沪籍3岁儿童的乳牙龋病进行调查。结果本区3岁沪籍儿童乳牙患龋率26.98%,龋均0.87,龋面均1.51;非沪籍儿童乳牙患龋率47.07%,龋均1.76,龋面均3.08。两组均存在显著性差异(P<0.01)。结论上海市长宁区3岁儿童中,非沪籍儿童乳牙龋病患病率明显高于本区沪籍儿童,因此更需加强非沪籍儿童龋病的防治。     

Localization of SOST/sclerostin in cementocytes in vivo and in mineralizing periodontal ligament cells in vitro

Jäger A, Götz W, Lossdörfer S, Rath‐Deschner B. Localization of SOST/sclerostin in cementocytes in vivo and in mineralizing periodontal ligament cells in vitro. J Periodont Res 2009; doi: 10.1111/j.1600‐0765.2009.01227.x. © 2009 John Wiley & Sons A/S Background and Objective: Cementum and bone are rather similar hard tissues, and osteocytes and cementocytes, together with their canalicular network, share many morphological and cell biological characteristics. However, there is no clear evidence that cementocytes have a function in tissue homeostasis of cementum comparable to that of osteocytes in bone. Recent studies have established an important role for the secreted glycoprotein sclerostin, the product of the SOST gene, as an osteocyte‐derived signal to control bone remodelling. In this study, we investigated the expression of sclerostin in cementocytes in vivo as well as the expression of SOST and sclerostin in periodontal ligament cell cultures following induction of mineralization. Material and Method: Immunolocalization of sclerostin was performed in decalcified histological sections of mouse and human teeth and alveolar bone. Additionally, periodontal ligament cells from human donors were cultured in osteogenic conditions, namely in the presence of dexamethasone, ascorbic acid and β‐glycerophosphate, for up to 3 wk. The induction of calcified nodules was visualized by von Kossa stain. SOST mRNA was detected by real‐time PCR, and the presence of sclerostin was verified using immunohistochemistry and western blots. Results: Expression of sclerostin was demonstrated in osteocytes of mouse and human alveolar bone. Distinct immunolocalization in the cementocytes was shown. In periodontal ligament cultures, following mineralization treatment, increasing levels of SOST mRNA as well as of sclerostin protein could be verified. Conclusion: The identification of SOST/sclerostin in cementocytes and mineralizing periodontal ligament cells adds to our understanding of the biology of the periodontium, but the functional meaning of these findings can only be unravelled after additional in vitro and in vivo studies.     

Local variations in turnover of periodontal collagen fibers in rats

Henneman S, Reijers RR, Maltha JC, Von den Hoff JW. Local variations in turnover of periodontal collagen fibers in rats. J Periodont Res 2012; 47: 383–388. © 2011 John Wiley & Sons A/S Background and Objective: The exact cause of orthodontic relapse is still unclear, although it is often suggested to be caused by periodontal collagen fibers. We hypothesize that long‐lived collagen fibers in the periodontium cause relapse. The aim was to determine the half‐life of periodontal collagen fibers around rat molars. Material and Methods: Thirty weanling rats were repeatedly injected with ³H‐proline, and autoradiography of histological sections was performed at 1, 4, 8, 15, 22, 29, 36, 57, 78 and 113 d after labeling. Grain densities determined in specific areas of the periodontium were used to calculate collagen half‐life. Results: The half‐life (t_½) was found to decrease from the supra‐alveolar region to the apical periodontal ligament region. It was longer in the supra‐alveolar region (1.39 ± 0.14 wk) compared with the deeper regions (p < 0.05). The t_½ of the upper periodontal ligament region (0.78 ± 0.20 wk) was longer than that of the inter‐radicular periodontal ligament region (0.42 ± 0.07 wk, p < 0.05). The t_½ of the apical periodontal ligament region was 0.61 ± 0.15 wk. Conclusion: The data indicate that long‐lived collagen fibers do not exist in the soft tissues of the periodontium, and are probably not responsible for relapse. The differences in collagen half‐life might be caused by local variations in compressive strain induced by normal function.     

Analysis of age-related changes in the functional morphologies of salivary glands in mice

Background and Objectives

Salivary glands in the elderly commonly exhibit salivary dysfunction resulting dry mouth, poor oral hygiene, and dental caries. However, in vivo changes of salivary glands during aging have not been well documented in the literature. This study was undertaken to determine age-related morphometric and functional changes of salivary glands using an aging mouse model.

Methods

Male C57BL/6 mice were divided into three groups, group A (10 weeks old; n = 10), group B (30 weeks old; n = 10), and group C (90 weeks old; n = 10). Body weights, salivary gland weights, salivary flow rates, and salivary lag times were measured and compared. Histomorphometric examinations and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays were performed. In addition, changes in salivary uptake and excretion were observed by single-photon emission computed tomography (SPECT).

Results

Body and gland weights increased with age. Gland weight was significantly higher in group B than in groups A and C. Salivary lag time was significantly greater in group C than in groups A and B, and salivary flow rate was significantly greater in group B than in groups A and C. Histologic evaluations exhibited acinar cell atrophy, cytoplasmic vacuolization, lymphocyte infiltration, small mucin component and more periductal fibrosis in salivary glands of group C. TUNEL assays revealed that apoptotic salivary epithelial cells were significantly more numerous in group C than in groups A and B. ^99mTc-pertechnetate excretion rate was significantly lower in group C than in groups A and B in SPECT.

Conclusion

Various morphometric and histopathological changes were observed in the salivary glands of aging mouse as well as relevant functional alterations, such as, decreased saliva production and excretion. Increased number of apoptotic salivary epithelial cells may contribute to the observed functional deterioration.     

The role of USP34 in the fixation of titanium implants in murine models

Ubiquitin-specific protease 34 (USP34), a member of the ubiquitin-specific protease family, regulates osteogenic differentiation of bone marrow mesenchymal stem cells via bone morphogenetic protein signaling. This study aimed to investigate the role of USP34 in fixation of titanium implants in mouse models. Eight-week-old Usp34-knockout (Prx1-Cre;Usp34^f/f) mice and their Usp34 wild-type (Usp34^f/f) control littermates were used. Experimental titanium implants were inserted into the distal ends of femurs and the edentulous area of maxillae. Two and four weeks after surgery, samples of femur and maxilla were obtained, and micro-computed tomography scanning, histomorphometric analyses, and push-in tests were performed on the samples. Compared with controls, Prx1-Cre;Usp34^f/f mice showed reduced bone volume for both femurs and maxillae; a decreased femoral bone–implant contact ratio (BIC) at 2 wk [mean (standard error of the mean): 62.17% (2.15%) vs. 44.06% (3.45%)] and 4 wk [72.46% (1.61%) vs. 64.53% (1.93%)]; decreases in femoral bone volume fraction (BV/TV) and push-in resistance; and lower BIC and BV/TV of the maxillae. Taken together, our data demonstrate that specific deletion of Usp34 in mesenchymal stem cells impairs fixation of titanium implants in mice.     

Validity of MicroCT for in vitro detection of proximal carious lesions in primary molars

Objective

This study aimed to validate the MicroCT for detection of proximal carious lesions in primary molars, using histology as the gold standard.

Methods

Forty-eight proximal surfaces of primary molars were examined. Two calibrated examiners conducted the examinations independently. Proximal surfaces were visually scored, using ICDAS. Bitewing radiographs, Micro-CT and histological analyses used caries scores: 0 = sound; 1 = outer enamel; 2 = inner enamel; 3 = not spread dentine; 4 = outer dentine; 5 = inner dentine. Axial and sagital images were used for Micro-CT analysis, whilst for histology, tooth sections (400 μm) were analyzed stereomicroscopically (×15).

Results

Inter-examiner agreement ranged from 0.87 to 0.93 kappa coefficient (k). Histological analysis revealed a frequency of sound tooth surfaces (18.8%) enamel carious lesions (E1) (48%) and dentine carious lesions (D1) (33.3%). MicroCT showed high correlation with histology (r_s0.88). At both diagnostic thresholds (E1 and D1), sensitivity and accuracy were higher for MicroCT. Inter-device agreement between MicroCT and histology was k = 0.81. No difference was found between MicroCT and histology as gold standards for detecting carious lesions using ICDAS.

Conclusion

MicroCT can be used as a gold standard for detecting carious lesions in proximal surfaces in primary molars.     

EIS study of solid-state transformations in the passivation process of bismuth in sulfide solution

Anodic oxidation of polycrystalline bismuth in alkaline medium, containing sulfide ions was investigated in situ. Cyclic voltammetry was used to define the potential regions of formation and stability of anodic Bi₂S₃ and Bi₂O₃ semiconductor films that translate bismuth to the passive state. The mechanism of elementary steps of the passivation process has been investigated using electrochemical impedance spectroscopy (EIS). The electric and dielectric properties of anodic films and structural parameters of the interfaces Bi–growing film–electrolyte in a wide region of potentials and frequencies of six decades, were determined. The EIS data have been analyzed and discussed in the frame of the point defect model (PDM) of anodic film formation and growth. The growth of passive surface films on bismuth takes place via transport of anionic vacancies generated at the metal–film interface. The slow step of the process is the layer-limited diffusion of anionic vacancies (D≈ 10^?16 cm² s^?1).Solid-state transformation of sulfide to the oxide film is a consequence of OH^? ion capture into the anionic vacancies of the sulfide film, the generation and transport of cation vacancies from the film–solution interface, their annihilation and formation of a vacancy condensate of a critical size at the metal–film interface.     

Effect of chronic stress on capsaicin-induced dental nociception in a model of pulpitis in rats

ObjectiveChronic stress can alter nociceptive sensitivity. However, the effect of stress exposure on dental nociception has been less addressed. Therefore, the present study investigated the effects of chronic exposures to some social and psychological stresses on pulpal nociceptive responses.DesignThe stress groups were constructed as follows: forced swimming (n = 6), restraint (n = 6), and mild (n = 10) and severe (n = 15) crowding stresses. Rats were subjected to stress for 1 h per day for a week. At the end of the stress session, pulp irritation was induced by intradental application of capsaicin (100 μg). There were another capsaicin or capsaicin plus stress training groups that received articaine 5 min before the administration of capsaicin. Nociceptive responses were recorded for 40 min. The time (in s) of continuous shaking of the lower jaw and excessive grooming and rubbing of the mouth near the procedure site was measured as nociceptive behaviors. Data was analyzed using one-way analysis of variance (ANOVA) followed by post hoc Tukey’s test.ResultsSignificant nociceptive responses were evoked by the administration of capsaicin. Exposures to forced swimming (p < 0.01), restraint (p < 0.001), and both mild and severe crowding stresses (p < 0.05) exaggerated capsaicin-induced nociceptive reaction. There was, however, no significant difference in nociceptive reaction time between the different stress groups. Articaine buccal infiltration attenuated nociceptive time in capsaicin and capsaicin plus stress training groups (p < 0.001).ConclusionsThe current data support the association between chronic stress exposures and nociceptive behavior following intradental capsaicin administration.