ライフサイエンスコーパス: caries

1 tes), and a prospective cohort study (dental caries).

2 es of GICs in order to prevent the secondary caries.

3 ll as new insights in the etiology of dental caries.

4 and commensals in the pathogenesis of dental caries.

5 riogenicity in vivo in a rat model of dental caries.

6 ted with Candida albicans in early childhood caries.

7 e and metabolism of sugar alcohols in dental caries.

8 ention programs and with a low prevalence of caries.

9 dhesive reduces the progression of secondary caries.

10 s lacking known or plausible roles in dental caries.

11 n between amount of sugars intake and dental caries.

12 h loss resulting from periodontal disease or caries.

13 prospects to inhibit biofilms and secondary caries.

14 this same SNP who showed a reduced level of caries.

15 from children affected with early childhood caries.

16 and the progressive lifelong development of caries.

17 had proximal bone loss but minimal proximal caries.

18 tension, obesity-related cancers, and dental caries.

19 plaque biofilms are the causative agents of caries.

20 he principal cariogenic bacterium for dental caries.

21 us mutans, a causative agent of human dental caries.

22 hair disorders and susceptibility to dental caries.

23 to the levy on obesity, diabetes, and dental caries.

24 composite restorations is the recurrence of caries.

25 r dentin-pulp complex regeneration in dental caries.

26 ral pathogen commonly associated with dental caries.

27 rginine in dentifrices helps protect against caries.

28 e tooth organ is damaged by either trauma or caries.

29 ainst demineralization of teeth (i.e. dental caries), a highly prevalent infectious disease associate

30 from children affected with early-childhood caries, a prevalent and costly oral disease.

31 mutans is a major etiologic agent of dental caries, a prevalent worldwide infectious disease and a s

32 (34%) in the intervention group converted to caries active compared to 213 (39%) in the control group

33 aries free, to prevent the children becoming caries active over the subsequent 36 mo.

34 caries active with enamel lesions (CAE), and caries active with dentin carious lesions (CA).

35 t 12 months and grouped as caries free (CF), caries active with enamel lesions (CAE), and caries acti

36 Swedish caries-active adolescents were typically colonized by Ac

37 nce of caries and no dental care and Swedish caries-active and caries-free adolescents in caries prev

38 0.81) or in the number of teeth extracted in caries-active children ( P = 0.95).

39 In light of these results, caries-free and caries-active children should be considered as 2 separat

40 decayed, missing, or filled teeth (dmfs) in caries-active children, number of episodes of pain, and

41 e measure was conversion from caries-free to caries-active states assessed by calibrated and blinded

42 e measure was conversion from caries-free to caries-active states.

43 OT070 were prevalent in Romanian and Swedish caries-active subjects but not caries-free subjects.

44 ong tooth surfaces and children of different caries activities.

45 haracterized by sweet snacks, and those with caries activity were also characterized by Prevotella, A

46 rage, and associate it to an unreported anti-caries activity.

47 ffered substantially from those found during caries activity.

48 served decreases in mechanical properties of caries-affected dentin and reduce the ability of caries-

49 es-affected dentin and reduce the ability of caries-affected dentin to remineralize.

50 udies, to exhibit an increased prevalence of caries, although the underlying cause for this increase

51 oral inflammatory burden (periodontitis and caries) among adolescents with early pathologic findings

52 h loss resulting from periodontal disease or caries and 1.07 (95% CI = 0.62 to 1.85), P-trend = 0.11

53 to 12 mo but a positive association between caries and breastfeeding of longer duration, at times th

54 included in oral products to protect against caries and erosion.

55 nd palate have a higher prevalence of dental caries and gingivitis.

56 This review will describe MMP functions in caries and hybrid layer degradation and explore the pote

57 ll lots of challenges due to their secondary caries and low mechanical properties.

58 Indigenous persons had more untreated dental caries and missing teeth, fewer teeth that had been rest

59 manian adolescents with a high prevalence of caries and no dental care and Swedish caries-active and

60 us mutans is the etiological agent of dental caries and one of the many bacterial species implicated

61 hygiene-therapists when screening for dental caries and periodontal disease in regularly attending as

62 dental care professionals when screening for caries and periodontal disease was 0.81 (95% CI, 0.74 to

63 dental care professionals when screening for caries and periodontal disease was 0.87 (0.78 to 0.92) a

64 herapists could be used to screen for dental caries and periodontal disease.

65 s of clinicians made an assessment of dental caries and periodontal disease.

66 ensitivity and specificity values for dental caries and periodontal disease.

67 crobes contribute to the formation of dental caries and periodontitis; however, there is little under

68 ssion in the teeth of patients affected with caries and pulpitis.

69 onfounders assessed were governorate, dental caries and restorations, and obesity by waist circumfere

70 idate all epidemiologic data about untreated caries and subsequently generate internally consistent p

71 h hyposalivation are at high risk for dental caries and thus require aggressive oral hygiene regimens

72 revalence of obesity and incidence of dental caries and type 2 diabetes.

73 us correlated with Romanian adolescents with caries and with limited access to dental care, whereas S

74 tion, limiting a drop in pH that can lead to caries, and denitrification, which could inhibit several

75 nsumption or reduced saliva flow can lead to caries, and excessive plaque accumulation increases the

76 rns, including nutrient displacement, dental caries, and weight gain.

77 include the misconception of defining dental caries as a tooth or surface-level condition versus a pe

78 rease in presentation and severity of dental caries as compared with wild-type control mice.

79 ilm removal strategies is important to limit caries, as well as halt progression to gingivitis and pe

80 Caries assessment was repeated annually from ages 1 to 4

81 log link function on 3-time repeated dental caries assessments.

82 bial region of lactoferrin that acts against caries associated bacteria.

83 We investigated the caries-associated microbiome among Canadian First Nation

84 ugar-related feeding practices affect dental caries between the ages of 6 and 18 y.

85 centage point increase in the probability of caries between the wealthiest and every other quintile,

86 expected to encourage the discovery of novel caries biomarkers and the development of next-generation

87 NP kills mutans streptococci associated with caries by >1 log.

88 and Capnocytophaga species and those free of caries by Actinomyces, Prevotella, Selenomonas, Streptoc

89 the differential effects of MA use on dental caries by comparing the patterns of decayed, missing, an

90 3F1 treatment effectively prevented dental caries by controlling S. mutans in a rat caries model wi

91 Dental caries can be described as a dysbiosis of the oral micro

92 Dental caries is prevalent, and secondary caries causes restoration failures.

93 strates activity against the dominant dental caries-causing pathogen as well as the first lysin that

94 ext-generation diagnostics and therapies for caries control.

95 etic background of initial periodontitis and caries could be detected using an active matrix metallop

96 ass correlation coefficient (ICC) for dental caries data at tooth and surface level, 2) to provide an

97 The ICC for dental caries data was 0.21 (95% confidence interval [CI], 0.20

98 During caries, dental pulp expresses a range of pro-inflammator

99 l of sugar consumption was related to dental caries, despite the use of fluoride.

100 In conclusion, visual caries detection method has good overall performance.

101 of the study was to establish the pattern of caries development from childhood into adolescence and t

102 ans in dental plaque biofilms play a role in caries development.

103 n of oral biofilms, and (IV) the severity of caries due to a native Cnm(+) isolate.

104 a predictable increasing burden of untreated caries due to population growth and longevity and a sign

105 Early childhood caries (ECC) is the most common infection in children.

106 rediction, as they relate to early childhood caries (ECC)-a common complex disease with significant n

107 between breastfeeding duration and childhood caries, either at baseline or over time.

108 Dental caries, endodontic infections and periodontal diseases a

109 ce of its unique role in causing a worldwide caries epidemic.

110 In support of the ecological nature of caries etiology, a steady transition in community specie

111 ansitioned into cariogenesis, or experienced caries exacerbation.

112 .55 to 2.78) and 4 times more likely to have caries experience (OR = 4.06; 95% CI: 2.24 to 7.34) than

113 behaviors; those would lead to lower dental caries experience and better self-reported oral health b

114 sed to generate two common indices of dental caries experience which were tested for association with

115 y carbohydrates caused an increase in dental caries following the development of agriculture, mediate

116 actobacilli have been associated with dental caries for over a century.

117 th dental appliances-have been used to study caries formation around dental composites.

118 iterature shows that many factors may affect caries formation, including marginal gap formation, gap

119 dhesin contributes to tooth colonization and caries formation.

120 at baseline and at 12 months and grouped as caries free (CF), caries active with enamel lesions (CAE

121 onstrate that the intervention kept children caries free, but there was evidence that once children g

122 Compared with those who were caries free, children with S-ECC came from households wi

123 of children initially aged 2 to 3 y who were caries free, to prevent the children becoming caries act

124 no dental care and Swedish caries-active and caries-free adolescents in caries prevention programs an

125 In light of these results, caries-free and caries-active children should be conside

126 e cost-effectiveness of caries prevention in caries-free children aged 2 to 3 y attending general pra

127 ons children <72 mo of age with S-ECC and 20 caries-free children were recruited in Winnipeg, Canada.

128 ries lesions, but they are largely absent in caries-free children.

129 their permanent dentition compared to their caries-free contemporaries.

130 antly different plaque microbiome than their caries-free counterparts, with the S-ECC group containin

131 Resin-based FS was applied to caries-free FPMs and maintained at 6-mo intervals.

132 e 5- and 2-fold higher, respectively, in the caries-free group.

133 The microbial communities of the S-ECC and caries-free groups did not differ in terms of species ri

134 n and Swedish caries-active subjects but not caries-free subjects.

135 primary outcome measure was conversion from caries-free to caries-active states assessed by calibrat

136 primary outcome measure was conversion from caries-free to caries-active states.

137 Plaque samples from caries-free tooth surfaces (PF) and from enamel carious

138 studies to report the development of dental caries from childhood into adolescence.

139 lated feeding practices on changes in dental caries from early childhood to young adulthood.

140 could not deny the role of sucrose in dental caries given the scientific evidence.

141 ral infections, but its relevance for dental caries has only been theorized to date.

142 ith the initiation and progression of dental caries has yet to be fully characterized.

143 An increased risk of caries (i.e. high prevalence of aciduric/non-aciduric sp

144 me-wide association scans (GWASs) for dental caries in a population-based cohort of 12 000 Hispanic/L

145 sponse association between sugars intake and caries in adults, 2) the relative contribution of freque

146 ed in separate metaregressions for untreated caries in deciduous and permanent teeth, respectively, u

147 affecting 2.4 billion people, and untreated caries in deciduous teeth was the 10th-most prevalent co

148 ectiveness of FS and FV in preventing dental caries in first permanent molars (FPMs) in 6- to 7-y-old

149 how the distribution and severity of dental caries in MA users differ from the general population.

150 In 2010, untreated caries in permanent teeth was the most prevalent conditi

151 The high prevalence of dental caries in recent humans is attributed to more frequent c

152 The development of secondary caries in the bonding interface was then examined by con

153 Mean dmfs of those with caries in the intervention group was 7.2 compared to 9.6

154 erest was the disease trajectory of dentinal caries in the permanent teeth in groups defined by the p

155 fined by the presence or absence of dentinal caries in the primary teeth.

156 Children who developed caries in their primary dentition had a very different c

157 ce interval, 3.90-5.16) in those pupils with caries in their primary dentition than in those without.

158 by 3F1 was able to effectively reduce dental caries in vivo without affecting the overall oral microb

159 We calculated the relative child caries incidence, adjusted for confounding, following hi

160 reduced bacterial load and suggested reduced caries increment in adults with 1 to 7 baseline cavitate

161 omotion (OHP) intervention (INT) at reducing caries increment in Navajo children attending Head Start

162 of these 3 putative early life factors with caries increment over a 4-y period among young children.

163 Adjusted analysis showed that dental caries increment ratio between ages 6 and 18 y was 20% a

164 understand whether the intervention reduced caries increment through its action on potential mediato

165 along the life course, the higher the dental caries increment.

166 birth weight and smoking mothers had greater caries increments than those with normal weight and non-

167 t assessed results in terms of reductions in caries increments.

168 lacement; p < 0.001), as well as "artificial caries induction time" (p < 0.001).

169 quired from 15, 20 and 25 days of artificial caries induction were analyzed with three-way ANOVA at a

170 s were the proportion of children developing caries into dentine (D4-6MFT) on any 1 of up to 4 treate

171 17.5%) versus FS ( n = 82, 19.6%) developed caries into dentine on at least 1 FPM (odds ratio [OR] =

172 Dental caries is a costly and prevalent disease characterized b

173 Dental caries is a microbially mediated disease that can result

174 stimated that 10% of the variance in surface caries is attributable to the individual level and 30% o

175 al level and 30% of the variance in surfaces caries is attributable to variation between teeth within

176 Dental caries is closely associated with the virulence of Strep

177 Dental caries is considered a diet-mediated disease, as sugars

178 s is to misunderstand that the only cause of caries is dietary sugars.

179 is evidence of moderate quality showing that caries is lower when free-sugars intake is < 10% E.

180 astfeeding and maternal smoking on childhood caries is mainly cross-sectional.

181 ent longitudinal studies have suggested that caries is most strongly correlated with total sugar inta

182 Remineralization of dentin during dental caries is of considerable clinical interest.

183 Dental caries is prevalent, and secondary caries causes restora

184 ere is evidence that the burden of untreated caries is shifting from children to adults, with 3 peaks

185 Dental caries is the most common chronic disease worldwide, and

186 anization (WHO) stated that globally, dental caries is the most important oral condition.

187 Dental caries is the most prevalent infection globally and a su

188 The importance of sugars as a cause of caries is underemphasized and not prominent in preventiv

189 inflammatory disease mainly caused by dental caries, is one of the most prevalent infectious diseases

190 e primary aetiological agent of human dental caries, is unknown.

191 ut there was evidence that once children get caries, it slowed down its progression.

192 h the aMMP-8 chairside test and at least one caries lesion positivity.

193 An extreme caries lesion scenario was created by collagenase digest

194 Caries lesions could also be detected, but less efficien

195 The restoration of dentine lost in deep caries lesions in teeth is a routine and common treatmen

196 Lactobacilli present in caries lesions represent both a major contributor to car

197 uld be one of the main factors for arrest of caries lesions treated with SDF.

198 The sensitivity of the immunoassay for >/=1 caries lesions was 76.5%, and the specificity was 96.7%

199 handful of Lactobacillus species is found in caries lesions, but they are largely absent in caries-fr

200 on the human body meet these specifications: caries lesions, the stomach, and the vagina.

201 isual method had good accuracy for detecting caries lesions.

202 t lactobacilli in the oral cavity arise from caries lesions.

203 assessed accuracy of the method in detecting caries lesions; 2) were performed on occlusal, proximal,

204 of frequency and amount of sugars intake to caries levels, and 3) whether the association between su

205 The Caries Management By Risk Assessment (CAMBRA) randomized

206 tal caries by controlling S. mutans in a rat caries model without perturbing the oral microbiota.

207 a result of periodontal disease (n = 70) or caries (n = 558) (total n = 780).

208 igh rates and distinctive patterns of dental caries observed could be used 1) to alert dentists to co

209 Caries occurred at a relatively constant rate over the p

210 users were twice as likely to have untreated caries (odds ratio [OR] = 2.08; 95% confidence interval

211 de-mineralization states in humans, such as caries of teeth and osteoporosis of bones.

212 e, but there are few longitudinal studies of caries onset and progression in children.

213 Caries onset delayed microbiota development, which is ot

214 Thus, caries onset in apparently healthy teeth can be predicte

215 al microbiome homeostasis can lead to either caries or periodontitis, two of the most common human di

216 associated with oral diseases such as dental caries or periodontitis.

217 c (cyt c) is electron transfer, the protein caries out an additional secondary function involving it

218 the importance of risk factors in predicting caries outcome.

219 the role of mutans streptococci as a primary caries pathogen appears less pronounced in populations w

220 protein-encoding mRNA (irvA) from the dental caries pathogen Streptococcus mutans directly modulates

221 tin, mainly focusing on their role in dentin caries pathogenesis and loss of collagen in the adhesive

222 characteristics, smoking, tooth loss, dental caries, periodontal status, and OHRQoL in adults with sy

223 sive medication; smoking; tooth loss; dental caries; periodontal status (bleeding on probing, calculu

224 Hyposalivation contributes to dental caries, periodontitis, and microbial infections.

225 vironment on oral microbiome composition and caries phenotypes, we profiled the supragingival plaque

226 Mean caries prevalence (% D3MFT > 0) was 16.7% at the first c

227 (+12.9 INT vs. +10.8 UC; P = 0.216), as did caries prevalence (86.5% to 96.6% INT vs. 90.1% to 98.2%

228 Other outcomes included caries prevalence and caregiver oral health-related know

229 and upward sugar consumers had higher dental caries prevalence and mean DMFT in all cohort waves when

230 Baseline mean dmfs/caries prevalence equaled 19.9/86.5% for the INT group a

231 here were significant income inequalities in caries prevalence in the youngest age group, marginal ef

232 ures representing very different outcomes (2 caries prevalence measures, decayed/missing/filled teeth

233 on the efficacy of behavioral approaches to caries prevention for children up to 18 y of age.

234 led trial measured the cost-effectiveness of caries prevention in caries-free children aged 2 to 3 y

235 caries-active and caries-free adolescents in caries prevention programs and with a low prevalence of

236 am, semiannual application of FV resulted in caries prevention that was not significantly different f

237 and/or dentinal fluid may affect the dentin caries process at the early phases of demineralization.

238 e combined action on multiple aspects of the caries process rather than through any single factor.

239 ated disease, as sugars are essential in the caries process.

240 In 1971, the NIDR launched the National Caries Program (NCP).

241 esions represent both a major contributor to caries progression and a major reservoir to the gastroin

242 s/need for replacement, reversible pulpitis, caries progression, etc.) and major failure (irreversibl

243 estimate caries risk and derive person-level caries propensities.

244 dependent and protective by directly killing caries-provoking bacteria (reducing proximal decay).

245 The etiology of dental caries reflects a complex interplay of biochemical, micr

246 dental care more frequently had a subsequent caries-related treatment (20.6% vs 11.3%, P < .001), hig

247 come and Measures: Two-part models estimated caries-related treatment and expenditures.

248 There was no association with subsequent caries-related treatment and preventive dental care from

249 4 per child per year (95% CI, 0.11-0.16) and caries-related treatment expenditures by $40.77 per chil

250 ive dental care did not significantly affect caries-related treatment use or expenditures.

251 veness of preventive dental care in reducing caries-related treatment visits among Medicaid enrollees

252 d with an increase in the expected number of caries-related treatment visits by 0.14 per child per ye

253 ly to have subsequent dental care, including caries-related treatment, and greater expenditures than

254 ver, some gaps in knowledge about the sugars-caries relationship still need addressing.

255 he specific genes influencing risk of dental caries remain largely unknown.

256 rdized prevalence and incidence of untreated caries remained static between 1990 and 2010.

257 directly onto vital pulp tissues after deep caries removal to stimulate the regeneration of reparati

258 The present study examined the mechanism for caries resistance and the pulp responses in vital teeth

259 esent in vitro study evaluated the secondary caries resistance potential of acid-etched human coronal

260 -pressure adhesive displacement improves the caries resistance property of bonded dentin and does not

261 nd advances in methods available to estimate caries risk and derive person-level caries propensities.

262 mportant developmental milestone influencing caries risk and the timing of sealant placement.

263 icle concludes with the notion that accurate caries risk assessment at the population level and "prec

264 bacterial load, fluoride levels, and overall caries risk based on the composite of bacterial challeng

265 For dental practice, the potential caries risk of long-duration breastfeeding should be par

266 ibility for dental anomalies do not increase caries risk or that the seemingly higher risk for dental

267 risk ratio, 1.98; 95% CI, 1.68-2.33) in high caries risk patients.

268 We used data from a 4-y longitudinal caries-risk assessment study carried out among Scottish

269 om a higher degree of severe early childhood caries (S-ECC) than the general population, leading to s

270 Regarding a link to caries, standard terminology for exposures (e.g., noctur

271 table oral bacteria were not associated with caries state, did not tend to co-occur with other taxa,

272 sed with shared host genotype, regardless of caries state.

273 sed including periodontal, oral mucosal, and caries status in Eastern Finland from 2014 to 2015.

274 dental plaques from children with different caries status.

275 ed, including periodontal, oral mucosal, and caries status.

276 significantly clustered into groups based on caries status.

277 However, the appearance of dental caries suggest a diet high in fermentable-carbohydrates.

278 irst mechanistic insight into the heightened caries susceptibility associated with CLP and indicate a

279 Understanding the factors influencing dental caries susceptibility may lead to improvements in predic

280 During the treatment of dental caries that has not penetrated the tooth pulp, maintenan

281 coccus mutans, the causative agent of dental caries, the most prevalent childhood disease.

282 We propose that, for caries, this SNP is ethnicity independent and protective

283 is approach is based on modulating the pH of caries to a physiological state to enable spontaneous to

284 ason is that researchers mistakenly consider caries to be a multifactorial disease; they also concent

285 clusion, this was the largest GWAS of dental caries, to date and was the first to target Hispanic/Lat

286 e developed a model, Microbial Indicators of Caries, to diagnose ECC from healthy samples with 70% ac

287 Dental caries (tooth decay) is a polymicrobial biofilm disease

288 r widespread application to eradicate dental caries (tooth decay) within a decade.

289 their primary dentition had a very different caries trajectory in their permanent dentition compared

290 ion programs compared to populations lacking caries treatment and prevention strategies.

291 er the association between sugars intake and caries varies by exposure to fluoride toothpaste.

292 MPPED2 was significantly associated with caries via meta-analysis across the 5 childhood samples,

293 of the history of tooth loss attributable to caries was observed with increasing concentrations of 25

294 consumption groups, the increment of dental caries was slightly higher between ages 6 and 12 y than

295 or breastfeeding in preventing malocclusion, caries was the only included disease condition unfavorab

296 us mutans, a causative agent of human dental caries, was detected for the aqueous leaf extract and it

297 Regarding caries, well-conducted studies report a benefit with bre

298 nish (FV) are effective in preventing dental caries when compared with a no-treatment control.

299 ose-response relationship between sugars and caries, with amount of intake being more important than

300 Tooth loss, dental caries, worse periodontal status, and smoking were direc