ライフサイエンスコーパス: caries

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

2 1.07, 1.23) compared to those without dental caries.

3 tribute to the initiation and progression of caries.

4 enamel defects that can increase the risk of caries.

5 effect to reduce the occurrence of secondary caries.

6 ewing with a forward focus to prevent future caries.

7 opment of many microbial diseases, including caries.

8 80), respectively, for moderate to extensive caries.

9 o fluoride for a better prevention of dental caries.

10 cause of the eventual incidence of recurrent caries.

11 and severity of dental fluorosis and dental caries.

12 on between breastfeeding duration and dental caries.

13 daptation, postoperative pain, and secondary caries.

14 nge of infectious diseases, including dental caries.

15 strategy to combat the prevalence of dental caries.

16 nditionally-independent risk loci for dental caries.

17 ciated with a decreased prevalence of dental caries.

18 the oral community, and the pathogenesis of caries.

19 e risk factors with periodontitis and dental caries.

20 jor contributor to the development of dental caries.

21 sociation between breastfeeding duration and caries.

22 on the relationship between sugar intake and caries.

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

24 ted with Candida albicans in early childhood caries.

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

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

27 d, reducing the local pH, and causing dental caries.

28 [EBV]) were more prevalent in children with caries.

29 ct biofilms formed on teeth of toddlers with caries.

30 ren in a trajectory of high levels of dental caries.

31 on reduces the local pH, resulting in dental caries.

32 tudy period, 28,623 (23.7%) women had dental caries.

33 lationship between SDS and/or RDS and dental caries; 16 (12 studies) considered oral cancer; and 2 st

34 Fracture (39.5%), caries (26.3%), and periodontal disease (23.7%) were the

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

36 (34%) in the intervention group converted to caries active compared to 213 (39%) in the control group

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

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

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

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

41 ffered substantially from those found during caries activity.

42 lly in liquid form, increases risk of dental caries, adiposity, and type 2 diabetes.

43 sed by developmental defects or tooth decay (caries), affect health and quality of life, with associa

44 4,741 (16.6%) women were treated for dental caries after diagnosis.

45 Therefore, it is extensively used as an anti-caries agent in clinical practice and daily life.

46 ully uncover the precise locations of dental caries, allowing convenient screening of hidden dental l

47 Dental caries, although preventable, remains one of the most pr

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

49 strategy for reducing disparities in dental caries among young children.

50 comes, including periodontitis and untreated caries, among US adults.

51 cation of genetic factors in the etiology of caries and 2) new data about the role of genetics in ter

52 okines were analyzed across 23 children with caries and 24 children with healthy dentition.

53 s to evaluate the association between dental caries and adverse pregnancy outcomes and the effect of

54 Cases were defined as individuals with deep caries and AP (n = 188); controls had deep caries and no

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

56 Dental caries and dental visiting patterns have been recorded i

57 stic curve (AUC) for the diagnosis of enamel caries and dentin caries were calculated to quantify the

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

59 s used topically to prevent or arrest dental caries and has been tested clinically in toddlers to eld

60 uts: diet and behavior in the case of dental caries and immune system interactions in the case of per

61 rinking water and dental products to prevent caries and improve dental health.

62 Dental caries and its treatment were not associated with preter

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

64 p caries and AP (n = 188); controls had deep caries and no AP (n = 230).

65 Better understanding of dental caries and other oral conditions has guided new strategi

66 time has widened our view of the etiology of caries and periodontal and peri-implant diseases and has

67 lic health that oral diseases such as dental caries and periodontal disease and general health condit

68 Both dental caries and periodontal disease are mediated by synergist

69 Dental caries and periodontal disease are together the most pre

70 ent advanced oral disease endpoints, such as caries and periodontal disease.

71 Dental caries and periodontitis account for a vast burden of mo

72 ly diagnosis of oral diseases such as dental caries and periodontitis, can be potentially achieved by

73 e was no increased risk in women with dental caries and treatment compared with those without.

74 included: 22 assessed the effects on dental caries, and 1 considered oral cancer.

75 rproximal probing depth (iPD), 3) numbers of caries, and 4) missing teeth.

76 ociation between periodontal disease, dental caries, and cocaine use, select co-usage elevated the ri

77 howed less periodontal disease, fewer dental caries, and loss of fewer teeth over a 5-y period.

78 of gingivitis, periodontal disease, smoking, caries, and other clinical variables.

79 -related quality of life, outcomes of dental caries, and outcomes of tooth loss.

80 haracteristics of mothers who develop dental caries are not treated.

81 t and antibiofilm dentin-resisting recurrent caries around bonded restorations.

82 is study systematically reviewed the dentine caries arrest capabilities of silver diamine fluoride (S

83 When comparing the caries arrest lesions of SDF and NaF, SDF was found to b

84 o be statistically more effective in dentine caries arrest of primary teeth during the 18 and 30 mont

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

86 usceptible oral bacterial species, including caries-associated Streptococcus mutans as well as severa

87 robiota and specifically the acidophilic and caries-associated Streptococcus mutans in 17-year old Sw

88 essible to medical practitioners to forecast caries at 2 and 3 y of age.

89 sociation between breastfeeding duration and caries attenuated after adjustment for other factors.

90 log(10) colony forming units (CFU) data from caries biopsies following colour and hardness clinical e

91 cted detrimental effect of sucrose on dental caries but no effect on CHD.

92 reatment of dental caries, women with dental caries but no treatment had an increased risk of deliver

93 d, for some NAFLD measures, untreated dental caries but not overall caries experience after controlli

94 3F1 treatment effectively prevented dental caries by controlling S. mutans in a rat caries model wi

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

96 Dental caries can compromise quality of life and is associated

97 erate-severe periodontitis, untreated dental caries, caries experience, and tooth loss (<20 teeth) on

98 Secondary caries caused by dental plaque is one of the major reaso

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

100 Seven caries clusters were identified, which had estimates of

101 rchical clustering of tooth surfaces (termed caries clusters).

102 Flossers showed less coronal caries compared to nonflossers (P = 0.02).

103 Despite development of new technologies for caries control, tooth decay in primary teeth remains a m

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

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

106 s was diagnosed using modified International Caries Detection and Assessment System criteria.

107 s lesions were diagnosed using International Caries Detection and Assessment System II, and plaque sa

108 Caries-free (ICDAS [International Caries Detection and Assessment System] score 0) childre

109 Dynamic mechanisms in caries development are hypothesized to be responsible fo

110 uoride-based interventions) is to manage the caries disease process at a lesion level and minimize th

111 from ages 6 to 12 months and early childhood caries (ECC) at age 2 to 3-years.

112 ildren in the United States, early childhood caries (ECC) has a profound impact on a child's quality

113 Early childhood caries (ECC) is a chronic disease affecting the oral hea

114 Early childhood caries (ECC) is a largely preventable condition that occ

115 nic dental records to assess early childhood caries (ECC) status using highest decayed, missing, fill

116 prolonged breastfeeding and early childhood caries (ECC), but the evidence to date is inconsistent,

117 d that TA@RAs could prevent secondary dental caries effectively.

118 Dental caries, endodontic infections and periodontal diseases a

119 These findings advance our understanding of caries etiology from an ecological perspective.

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

121 rious lesions may play a fundamental role in caries etiology.

122 s known to be associated with disparities in caries experience (e.g., race/ethnicity and insurance st

123 valence ratio, 1.29; 95% CI, 1.18-1.41), any caries experience (odds ratio, 1.40; 95% CI, 1.19-1.65),

124 res, untreated dental caries but not overall caries experience after controlling for several key soci

125 There were U-shape distributions of caries experience among breastfeeding groups, being more

126 g duration and usage of fluoridated water on caries experience has not been investigated.

127 s a 29% decrease in the relative risk of new caries experience in the DR-BNI group as compared with c

128 The odds of new caries experience occurring were reduced by 51% in the D

129 Reductions in caries experience were recorded in many countries, attri

130 st all models use dental factors (e.g., past caries experience) to predict future caries risk, with l

131 outcome measures were 1) summary indices of caries experience, 2) parameters representing trajectory

132 vere periodontitis, untreated dental caries, caries experience, and tooth loss (<20 teeth) on NAFLD w

133 ental fracture, dental fluorosis, and dental caries experience.

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

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

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

137 d; 36 children developed ECC and 20 remained caries free.

138 Caries-free (ICDAS [International Caries Detection and A

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

140 m II, and plaque samples were collected from caries-free and carious tooth surfaces.

141 vals for 24 mo from a subset of 56 initially caries-free children from an ongoing cohort of 189 child

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

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

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

145 62% developed new caries in teeth that were caries-free or unerupted at baseline, as compared with 4

146 findings indicate that the oral ecosystem of caries-free toddlers is highly heterogeneous and dynamic

147 oreover, the data are biased by mislabeling "caries-free" populations.

148 l markers were significantly elevated in the caries group, and co-occurrence analysis provided an atl

149 a multivariable analysis, women with dental caries had an increased risk of delivering large-for-ges

150 nraveling the exact biological mechanisms in caries has the potential to reveal novel host-microbial

151 To reduce the prevalence of early childhood caries, improved efforts are needed to limit foods high

152 etween dietary practices and early childhood caries in a birth cohort of Australian preschoolers.

153 The prevalence and severity of caries in children aged 5 to 6 y were primary outcomes.

154 ogical study of oral microbiology and dental caries in children from a localized Alabama population.

155 demonstrated a greater prevalence of dental caries in children residing in radiation-contaminated ar

156 DR-BNI)-in reducing the recurrence of dental caries in children who have a primary tooth extracted.

157 ly reducing the risk of recurrence of dental caries in children.

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

159 The increased risk of dental caries in HI children suggest immune-mediated changes in

160 rs and explained 16% of variation in fissure caries in molar teeth but little variation in other clus

161 ng and prevalence of periodontal disease and caries in older adults.

162 a safer option for the diagnosis of proximal caries in posterior teeth that can be applied to the pat

163 c accuracy of 3D imaging of OCT for proximal caries in posterior teeth.

164 ment strategies over 3 y for managing dental caries in primary teeth in UK primary dental care.

165 lm microbiota composition and risk of dental caries in Swedish adolescents.

166 In the control group, 62% developed new caries in teeth that were caries-free or unerupted at ba

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

168 condition that occurs when children develop caries in their primary teeth before the age of six.

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

170 Dental caries is a cariogenic bacteria-mediated, fermentable ca

171 Dental caries is a costly and prevalent disease characterized b

172 Considering that caries is a polymicrobial infection resulting from dysbi

173 We show that the heritability of dental caries is enriched for conserved genomic regions and par

174 most common chronic disease globally, dental caries is induced by host-microbial dysbiosis in childre

175 Previous studies report that dental caries is partially heritable, but there is uncertainty

176 Dental caries is prevalent, and secondary caries causes restora

177 Dental caries is the most common human infectious disease and i

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

179 Preventing the onset of caries is the ultimate goal of a caries management plan.

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

181 tes to the enamel-destructive disease dental caries, lacks the capabilities to generate WTA.

182 Dental caries left untreated threaten exposure of the dental pu

183 0 test subjects with a suspected active root caries lesion by monitoring thermal emission from the to

184 Resin infiltration's capacity to arrest caries lesion progression in noncavitated proximal lesio

185 Caries lesions develop when acid production from bacteri

186 film model was established, and by comparing caries lesions on enamel blocks cocultured with biofilms

187 Caries lesions were diagnosed using International Caries

188 ained to "lift the lip" to identify anterior caries lesions.

189 he onset of caries is the ultimate goal of a caries management plan.

190 Therefore, SDF is a more effective caries management reagent than NaF.

191 ng that the processes contributing to dental caries may have undesirable downstream effects on health

192 demineralization model and in vivo secondary caries model were applied and demonstrated that TA@RAs c

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

194 In the in vivo caries model, enamel and dentin carious lesions were sig

195 associated with the control outcome, dental caries (odds ratio [OR] 1.04 per log(10) transformed eff

196 comes and the effect of treatment for dental caries on adverse pregnancy outcomes.

197 However the influence of dental caries on pregnancy is unknown.

198 cation (key virulence traits associated with caries onset) when interacting with S. mutans, and a new

199 focused on the microflora in disease-either caries or periodontitis-and only recently have they cons

200 S. mutans (OR (95% CI): 0.5 (0.3, 0.8)), and caries (OR 0.6 (0.3, 0.9)), whereas haploblock 4 TTG ass

201 alence of S. mutans (OR: 2.7 (1.2, 5.9)) and caries (OR: 2.3 (1.2, 4.4)).

202 nmental factors in the etiology of different caries outcomes using a twin-based design.

203 care decision making, to ultimately improve caries outcomes.

204 tudy that will increase the understanding of caries pathogenesis and guide therapeutic development.

205 s in permanent posterior teeth demonstrating caries penetrating into inner enamel or outer dentin wer

206 l and systemic human diseases such as dental caries, periodontal disease, obesity, and cardiovascular

207 a on oral health outcomes relating to dental caries, periodontal disease, or oral cancer.

208 f health and disease, with specific focus on caries, periodontal diseases, and cancer.

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

210 nd that innate liability to some patterns of caries presentation may partially explain why groups of

211 th but little variation in other clusters of caries presentation.

212 confidence interval [CI], 1.59-3.65), dental caries prevalence (prevalence ratio, 1.29; 95% CI, 1.18-

213 rth to evaluate if differences regarding the caries prevalence can be observed compared to non-contam

214 esent study analyzed the data concerning the caries prevalence in children born and permanently resid

215 Methods used to assess the caries prevalence were limited to DMFT/dmft (decayed, mi

216 asing intervention access reduced population caries prevalence, but increased disparities between dif

217 measures such as sealant programs to control caries prevalence, disparities are seen among ethnic gro

218 on are that it provides substantial lifelong caries prevention, is economic, and reduces health inequ

219 This technique opens opportunities in caries prevention, remineralization, tooth whitening, an

220 ducing dental fluorosis without compromising caries prevention.

221 rovided the basis for the use of fluoride in caries prevention.

222 ntions targeting early feeding practices for caries prevention.

223 ce, 2) parameters representing trajectory in caries progression derived from longitudinal modeling, a

224 nfiltration was 100% successful in arresting caries progression in inner enamel lesions (E2) and 64%

225 nding of how genetic factors might influence caries progression or caries subtypes.

226 tine is susceptible to damage as a result of caries, pulp infection and inflammation all of which are

227 Caries rates at ages 2 y (n = 535) and 3 y (n = 721) wer

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

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

230 be a good option for chemomechanical dentin caries removal due to its reduced removal time and lower

231 ication to teeth to prevent or arrest dental caries results in plasma and tissue silver concentration

232 mproving the oral health of children at high caries risk (ISRCTN 24958829).

233 experienced by these participants with high caries risk and established disease (trial registration:

234 tial source for accurate and reliable dental caries risk and onset.

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

236 Caries risk assessment (CRA) is a critical component of

237 Caries risk assessment (CRA) models for toddlers and pre

238 In fact, although numerous caries risk assessment tools are available, most are not

239 Risk prediction models predicting overall caries risk at 2 and 3 y demonstrated area under the cur

240 association between total starch intake and caries risk but that RDS intake may significantly increa

241 duals, or even tooth surfaces based on their caries risk has become a reality to address the skewed d

242 However, no validated caries risk instrument exists for use in primary health

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

244 ent's prognosis relies on the development of caries risk prediction models (CRPMs).

245 ased disparities between different groups of caries risk profiles.

246 To help resolve this gap, a 52-item caries risk questionnaire was developed and targeted to

247 as to identify BGCs in S. mutans from a high-caries risk study population using whole-genome sequenci

248 Predictive models have been used with caries risk tools, periodontitis occurrence, and permane

249 at years 2 and 3, respectively, for overall caries risk, while AUC was 0.84 (0.76-0.92) and 0.75 (0.

250 ., past caries experience) to predict future caries risk, with limited clinical/community applicabili

251 hanisms among those considered to be at high caries risk.

252 ions) appropriate for the management of high caries risk.

253 t that RDS intake may significantly increase caries risk.

254 advised to treat the child as being at high caries risk.

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

256 est reported rates of severe early childhood caries (S-ECC).

257 ined between 49.1% and 62.7% of variation in caries scores and between 50.0% and 60.5% of variation i

258 n derived from longitudinal modeling, and 3) caries scores in groups of biologically similar tooth su

259 Addition of anterior caries significantly increased AUC in all year 3 models

260 Dental caries (similar to periodontitis) was considered to be a

261 Associations with caries status and secreted CA6 protein were also evaluat

262 genetics in terms of longitudinal changes in caries status and specific patterns of disease presentat

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

264 Eighty-three adults of different caries status were recruited and assigned to treatment w

265 In early childhood caries, Streptococcus mutans and Candida albicans are of

266 ta, and were found to be highly expressed in caries subjects.

267 actors might influence caries progression or caries subtypes.

268 The new ecological hypothesis for dentin caries suggests that an alteration in the microbial comm

269 ences between SDF and NaF regarding arrested caries surfaces was calculated and showed nearly double

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

271 cal CRA models may be promising in screening caries-susceptible infants/toddlers, especially when med

272 However, why sucrose causes severer dental caries than other sugars is largely unknown.

273 mutans is an etiologic agent of human dental caries that forms dental plaque biofilms containing func

274 Dental caries, the most common chronic infectious disease world

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

276 an introduce a microbiota imbalance favoring caries to a greater degree than other sugars.

277 ers are linked to oral diseases, from dental caries to gum disease.

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

279 al biofilms associated with severe childhood caries (tooth decay), a prevalent pediatric oral disease

280 sequential oral diseases globally are dental caries (tooth decay), periodontal disease, tooth loss, a

281 raits, including periodontal disease, dental caries, tooth agenesis, cancers of the head and neck, or

282 of sugar-sweetened beverages (SSBs) with 4-y caries trajectories among Scottish young children.

283 take were positively associated with steeper caries trajectories.

284 and between 50.0% and 60.5% of variation in caries trajectories.

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

286 of nonrestorative or non- and microinvasive caries treatment (fluoride- and nonfluoride-based interv

287 and steroid use in these subjects, smoking, caries, utilizing a removable prosthesis, and plaque ind

288 Dental caries was a positive control outcome.

289 Childhood dental caries was clinically determined (including noncavitated

290 Caries was diagnosed using modified International Caries

291 Untreated dental caries was not associated with preterm birth or preeclam

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

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

294 or the diagnosis of enamel caries and dentin caries were calculated to quantify the diagnostic abilit

295 When women with dental caries were divided on the basis of the treatment of den

296 substance co-used, odds of having untreated caries were greater among those reporting cigarettes (ad

297 People with any untreated caries were more likely to have NAFLD (USON: OR = 1.51,

298 s regarding a hereditary component of dental caries were reported as early as the 1920s.

299 presence of lower oral pH and is enriched in caries, with mechanistic studies in animal models sugges

300 ided on the basis of the treatment of dental caries, women with dental caries but no treatment had an