北京市海淀区13所幼儿园3岁儿童龋病患病趋势调查

目的了解北京市海淀区3岁儿童2012～2015年间乳牙龋病的患病趋势,为海淀区低龄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3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,调查海淀区3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3岁儿童的患龋率为46.26%～51.62%,逐年上升(P<0.05),平均48.78%。龋均(dft)2.06～2.57,龋面均(dfs)2.63～3.37,重度低龄儿童龋(SECC)患病率为22.09%～29.54%,龋均、龋面均和SECC患病率从2012年到2014年呈上升的趋势,2015年略有下降,差异有统计学意义(P<0.01)。患龋儿童接受治疗的百分比为79.14%～41.46%,龋补充填比(ft/dft)为65.09%～31.45%,二者从2012年到2014年呈下降的趋势,2015年明显有回升,差异有统计学意义(P<0.01)。结论近年来3岁儿童患龋率逐年上升,低龄化趋势明显,患龋严重程度呈上升趋势。     

西安市2829名学龄前儿童乳牙龋患率调查

目的:了解西安市学龄前儿童乳牙龋病患病情况,便于更好地指导并开展龋病防治工作。方法:对西安市6所幼儿园2 829名学龄前儿童进行口腔检查。结果:2 829名受检儿童中,乳牙患龋儿童2 329名,患龋率82.33%,龋均4.4,乳磨牙窝沟封闭率为1.28%,性别间患龋率无差异,患龋率和龋均随年龄增高而上升,6岁患儿最高。结论:西安市学龄前儿童乳牙患龋率高于全国平均水平,应当引起足够重视,提高家长和社会的口腔健康意识,加大防治力度,保护儿童健康成长。     

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。     

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.     

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。     

泰州市3～6岁儿童龋病流行现状调查

目的了解泰州市3~6岁儿童龋病流行状况,为龋病防治提供科学依据。方法采用随机整群抽样的方法,参考《第三次全国口腔健康流行病学调查方案》,对泰州市7154名3~6岁儿童进行调查,对患龋率和龋齿充填率进行描述性分析。结果泰州市3~6岁儿童患龋率为57.80%,男性为57.60%、女性为58.26%,患龋率均随着年龄的增加而呈升高趋势;3~6岁儿童龋齿充填率为1.11%,男性为1.14%,女性为0.99%;公办幼儿园3~6岁儿童患龋率为49.76%,低于民办幼儿园的65.00%,而龋齿填充率为1.82%,则高于民办幼儿园的0.44%,差异均有统计学意义(P<0.05)。结论泰州市3~6岁儿童患龋率高,龋齿充填率低,尤其是民办幼儿园儿童口腔健康状况显著差于公办幼儿园,提示需要进一步强化口腔卫生保健宣传工作。     

重庆市学龄前儿童龋病状况调查

目的 了解重庆市学龄前儿童乳牙龋患病情况,同时比较公办幼儿园和民办幼儿园学龄前儿童的乳牙龋患病情况。方法 以重庆市渝中区40所民办幼儿园和16所公办幼儿园的5 030名3~6岁儿童为调查对象,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,提取龋病情况资料,包括患龋率、龋均、龋齿充填率等。采用SPSS 21.0软件进行统计学分析。结果 5 030名受检儿童中,最容易患龋的牙位为上颌乳中切牙和下颌乳磨牙。患龋率为54.08％（2 720/5 030）,龋均为2.58,龋齿充填率为0.98%（127/12 993）。随着年龄增长,儿童患龋率和龋均增加（P<0.05）。6岁年龄儿童的龋齿充填率最高（P<0.05）,不同性别的龋齿充填率无统计学差异（P>0.05）。民办幼儿园的患龋率、龋均和龋齿充填率分别为61.04%（1 656/2 713）、3.12和0.35%（30/8 465）,公办幼儿园的患龋率、龋均和龋齿充填率分别为45.92%（1 064/2 317）、1.95和2.14%（97/4 528）,民办幼儿园与公办幼儿园之间有统计学差异（P<0.05）。结论 重庆市学龄前儿童乳牙患龋率较高,龋齿充填率较低,其中民办幼儿园学龄前儿童的口腔健康状况明显差于公办幼儿园。     

上海市闵行区2010-2014学年3～15岁儿童口腔健康状况调查

目的调查闵行区2010—2014学年不同年龄儿童的患龋率及龋均情况,分析5年来儿童易患龋年龄段及易患龋牙位情况。方法闵行区2010年9月—2015年8月公立中小幼机构3~15岁儿童进行口腔检查,获得其基线资料,建立个人口腔健康档案。应用SPSS 20.0软件包进行结果分析。结果从10至14学年,幼儿园学生、小学生5年来患龋率和龋均并无趋势可言(P>0.05),已趋于平稳,闵行区幼儿园学生患龋率在50%左右,小学生患龋率在60%左右;而中学生患龋率及龋均逐年下降,2014学年中学生患龋率下降至28.57%,龋均1.14,均明显低于幼儿园学生和小学生(P<0.01);就每个年级而言,3~8岁儿童随年龄增加患龋率和龋均升高,9~12岁儿童患龋率和龋均随年龄增加下降,13~15岁儿童随年龄增加患龋率下降,而龋均逐渐缓慢升高。结论幼儿园和小学学生的龋病预防和干预是关键,8岁前儿童主要预防乳牙龋,8岁以后第一磨牙的预防及早期干预尤为重要。     

1052例上海市普陀区外来儿童龋病调查

目的 了解上海市普陀区外来儿童的龋病发病情况。方法 按全国口腔流行学调查标准，对1052名外来儿童的龋病进行调查。结果 乳牙患龋率85．8％，龋均4．61；恒牙患龋率6．45％，龋均1．4。结论 上海市普陀区外来儿童乳牙龋病患病率仍处较高水平，防治是关键。     

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.