ライフサイエンスコーパス: periodontal disease

1 dontia, early onset of severe and aggressive periodontal disease).

2 c inflammatory diseases (e.g., arthritis and periodontal diseases).

3 effect of therapeutic intervention for RA on periodontal disease.

4 enetic neighbor, is strongly associated with periodontal disease.

5 emoval among patients with various states of periodontal disease.

6 dered as a potential inflammatory marker for periodontal disease.

7 hils found in the oral cavity during chronic periodontal disease.

8 region often reveals early clinical signs of periodontal disease.

9 ring the development of localized aggressive periodontal disease.

10 7 pathway is involved in the pathogenesis of periodontal disease.

11 nflammatory neutrophil population in chronic periodontal disease.

12 on of the bone loss associated with advanced periodontal disease.

13 are impeded, resulting in different forms of periodontal disease.

14 been considered as susceptibility factors in periodontal disease.

15 ight be a potential diagnostic parameter for periodontal disease.

16 esents a high prevalence of mild to moderate periodontal disease.

17 history or incidence of tooth loss caused by periodontal disease.

18 role in B cell-mediated immune responses in periodontal disease.

19 a private practice and a personal history of periodontal disease.

20 ssociated with the LPS model of experimental periodontal disease.

21 gical and non-surgical therapies in treating periodontal disease.

22 - 5.2) years, and 16.3% (n = 114) had severe periodontal disease.

23 therapeutic strategies for the treatment of periodontal disease.

24 ould be used to screen for dental caries and periodontal disease.

25 observed to be increasingly associated with periodontal disease.

26 cal attachment level (CAL) to treat advanced periodontal disease.

27 ion were assessed for clinical parameters of periodontal disease.

28 eumatoid arthritis patients with concomitant periodontal disease.

29 f the sampled population had moderate/severe periodontal disease.

30 ining the presence, risk, and progression of periodontal disease.

31 ians made an assessment of dental caries and periodontal disease.

32 and specificity values for dental caries and periodontal disease.

33 okers as increased incidence and severity of periodontal disease.

34 osteolytic role of IL-12 in pathogenesis of periodontal disease.

35 val [95% CI]: 1.82 to 5.15) as those without periodontal disease.

36 be a potential novel inflammatory marker of periodontal disease.

37 immune responses to periodontal pathogens in periodontal disease.

38 bidirectional relationship between OSAS and periodontal disease.

39 SCFAs in the saliva of patients with severe periodontal disease.

40 al microbe implicated in the pathogenesis of periodontal disease.

41 These conditions are risk factors for periodontal disease.

42 of the most studied inflammatory markers in periodontal disease.

43 an be considered a marker of inflammation in periodontal disease.

44 athogenic oral bacteria, a putative cause of periodontal disease.

45 NA-SD might increase the risk of periodontal disease.

46 indicating a relationship between YKL-40 and periodontal disease.

47 uld be included as a diagnostic indicator of periodontal disease.

48 revicular fluid (GCF) and extent/severity of periodontal disease.

49 ed as a protective and therapeutic agent for periodontal disease.

50 Smoking is a major risk factor for periodontal disease.

51 ining the presence, risk, and progression of periodontal disease.

52 pproach to modulate host response in chronic periodontal disease.

53 ic and alternative pathways in health and in periodontal disease.

54 ne model of lipopolysaccharide (LPS)-induced periodontal disease.

55 nism for sex dimorphism for the incidence of periodontal disease.

56 sts an association between preterm birth and periodontal disease.

57 ntrol mice did not show the same severity of periodontal disease.

58 e implicated a role for Filifactor alocis in periodontal disease.

59 racy, and conceptual knowledge) and signs of periodontal disease.

60 periodontal tissue integrity as a result of periodontal disease.

61 oncomitant decrease in those associated with periodontal disease.

62 ne model of lipopolysaccharide (LPS)-induced periodontal disease.

63 F-1 and IL-34 in whole saliva in relation to periodontal disease.

64 (GCF) among patients with untreated chronic periodontal disease.

65 have an increased incidence and severity of periodontal disease.

66 aps contributing to the OC pool in states of periodontal disease.

67 s and MRGPRX2-expressing mast cells promotes periodontal disease.

68 pecies biofilm, and is a direct precursor of periodontal disease.

69 ntify how providers can help patients manage periodontal disease.

70 ype at 24 wk, consistent with HPP-associated periodontal disease.

71 e been explored to modulate host response to periodontal disease.

72 ls are higher in individuals who have severe periodontal disease.

73 isting the early diagnosis and prevention of periodontal disease.

74 l among individuals with type 2 diabetes and periodontal disease.

75 uld be a biomarker for cardiovascular and/or periodontal disease.

76 maturation in regulating immune responses in periodontal disease.

77 possible involvement in the pathobiology of periodontal disease.

78 -mediated inflammation is also implicated in periodontal diseases.

79 alcitonin (ProCT) in patients with different periodontal diseases.

80 ion of regenerative therapy for treatment of periodontal diseases.

81 el is suggested as a potential biomarker for periodontal diseases.

82 obstetricians and/or gynecologists regarding periodontal diseases.

83 of the inflammatory and infectious nature of periodontal diseases.

84 studies are required to evaluate its role in periodontal diseases.

85 used as adjunctive treatment modalities for periodontal diseases.

86 s such, is a good candidate for treatment of periodontal diseases.

87 ve plaque accumulation increases the risk of periodontal diseases.

88 ion and tissue destruction that characterize periodontal diseases.

89 at 7, 15, and 30 days after the induction of periodontal disease: 1) group C: no treatment control gr

90 Periodontal disease, a chronic bacterial infection of th

91 ss index (OSI), a novel value as a marker of periodontal disease activity, are investigated in serum

92 seful and practical parameter for evaluating periodontal disease activity.

93 he inflammatory burden as a result of severe periodontal disease acts as an insult to the endothelium

94 fy the most relevant gaps of knowledge about periodontal diseases among the general public and to dis

95 (microorganisms that are not associated with periodontal disease) among youth with t1DM.

96 ed when combining a measure of self-assessed periodontal disease and a measure of dentist-diagnosed d

97 de of studies suggest an association between periodontal disease and adverse birth outcomes, but the

98 nas gingivalis is an established pathogen in periodontal disease and an emerging pathogen in serious

99 uctive sleep apnea syndrome (OSAS) risk with periodontal disease and anthropometric measures in Class

100 clinical cohort study, 215 participants with periodontal disease and at least one molar treated with

101 teria may contribute to associations between periodontal disease and cancer.

102 ressed prostatic secretions of patients with periodontal disease and CPr or BPH.

103 Furthermore, history of periodontal disease and disease severity, as well as its

104 ival oral spirochete closely associated with periodontal disease and has been detected in atheroscler

105 ng is the largest modifiable risk factor for periodontal disease and has many deleterious health effe

106 (GCF), saliva, and plasma levels of IL-35 in periodontal disease and health.

107 cular fluid (GCF) and serum of patients with periodontal disease and healthy individuals.

108 Because of the potential association between periodontal disease and inflammation, the purpose of the

109 While research concerning the effects of periodontal disease and its surgical and non-surgical tr

110 al diseases, such as butanoate production in periodontal disease and metabolism of sugar alcohols in

111 s little evidence on the association between periodontal disease and oral health-related quality of l

112 There was no association between periodontal disease and OSAS risk in Class III obese pat

113 igenetic modifications in the development of periodontal disease and present emerging therapeutic str

114 uence of synthetic parstatin on experimental periodontal disease and repair in rats.

115 clinical evidence for an association between periodontal disease and rheumatoid arthritis, it is impo

116 These data support the relationships among periodontal disease and some biochemical parameters such

117 elation between the onset and progression of periodontal disease and the onset of ileitis in SAMP mic

118 T. denticola is closely associated with periodontal disease and the rapid progression of atherom

119 a Porphyromonas gingivalis-induced model of periodontal disease and to analyze underlying cellular m

120 tio as a diagnostic and prognostic marker of periodontal disease and treatment outcome.

121 roviding a possible mechanistic link between periodontal disease and tumor development.

122 onadaceae comprising species associated with periodontal disease and Veillonellaceae predominated in

123 f periodontal therapy in pregnant women with periodontal disease and, further, whether any of these s

124 s its determination useless for detection of periodontal disease and/or its severity, salivary levels

125 Association supports an association between periodontal diseases and atherosclerosis but not a causa

126 hibits anti-inflammatory effects and reduces periodontal diseases and atherosclerosis; however, its r

127 ontributes to the development of destructive periodontal diseases and delays its healing process.

128 are reported to be elevated in patients with periodontal diseases and may have a modulating role in c

129 s may have implications for the treatment of periodontal diseases and may partly explain the persiste

130 nism promoting the pathogenic progression of periodontal diseases and may potentially suggest the inv

131 Periodontal diseases and peri-implant diseases share man

132 Poor awareness of periodontal diseases and their consequences has been rep

133 ess and poor knowledge about the etiology of periodontal diseases and their relation with systemic di

134 The search strategy was "periodontitis OR periodontal disease" and "knowledge OR awareness" as key

135 questions aimed to assess "dentist-diagnosed periodontal disease" and two inquired about "self-assess

136 he association of systemic oxidative stress, periodontal disease, and levels of CRP.

137 n chewing and swallowing foods, tooth decay, periodontal disease, and microbial infections.

138 Number of natural teeth, periodontal disease, and root canal treatment were not a

139 tential proinflammatory marker for diabetes, periodontal disease, and treatment outcomes.

140 Types I to IV defined increasing severity of periodontal disease, and Type V defined referrals for ne

141 miR-138 was significantly upregulated in our periodontal disease animal model.

142 Smoking and periodontal disease are emerging risk factors for the de

143 Dental caries, endodontic infections and periodontal diseases are bacterially driven diseases tha

144 Many studies have shown that periodontal diseases are risk factors for adverse pregna

145 pdated prediction model was demonstrated for periodontal disease as measured by the calibrated CPI de

146 PRP) and related plasma preparations against periodontal disease-associated bacteria were evaluated.

147 significant differences in the prevalence of periodontal disease between the apnea-hypopnea index (AH

148 affecting bone health, baseline measures of periodontal disease, body mass index, and recreational p

149 is use for up to 20 years is associated with periodontal disease but is not associated with other phy

150 r cardiovascular disease, is associated with periodontal disease, but few studies have been prospecti

151 woman who had suffered from severe juvenile periodontal disease, but was otherwise healthy, and iden

152 cteria may contribute to the pathogenesis of periodontal diseases by mechanisms such as bacterial avo

153 pecific IgG levels, which in the presence of periodontal disease can result in an enhanced systemic C

154 During the inflammatory process in periodontal disease, chemokines are upregulated to promo

155 ts association with microbial, biologic, and periodontal disease clinical parameters is examined.

156 icroorganisms and an increased percentage of periodontal disease clinical parameters, suggesting the

157 Management of periodontal disease, dental interventions, pulmonary hyp

158 limited field of view CBCT may be useful for periodontal disease diagnoses due to less radiation dosa

159 ype V defined referrals for needs other than periodontal disease (e.g., crown lengthening and implant

160 The effect of periodontal disease experience on quality of life was co

161 ded to prevent and control the occurrence of periodontal disease following APT.

162 nant women (6 to 20 weeks of gestation) with periodontal disease (>/= 3 sites with attachment loss >/

163 evere periodontal disease, those with severe periodontal disease had a four-fold greater rate of inci

164 Infection-induced periodontal disease has been primarily focused on a smal

165 er, the role of sugar intake in the cause of periodontal disease has not been adequately studied.

166 Yet, a possible role of IL-12 in periodontal disease has not been clarified.

167 on between chronic inflammatory prostate and periodontal diseases has been demonstrated by the presen

168 Low-cost models for treatment of periodontal disease have not been tested in controlled s

169 e, calculated from registered attendance; 3) periodontal disease history; 4) peri-implant radiographi

170 ion of leukotrienes has been associated with periodontal diseases; however their relative contributio

171 is a newly appreciated taxon associated with periodontal diseases; however, little is known about the

172 diovascular risk factors, has been linked to periodontal diseases; however, the contribution of perio

173 ion of leukotrienes has been associated with periodontal diseases; however, their relative contributi

174 th the transitional phase between health and periodontal disease (i.e., gingivitis).

175 liva and seem to have complementary roles in periodontal disease: IL-34 in steady-state and CSF-1 in

176 le of added sugar intake was associated with periodontal disease in >/=2 teeth (PR: 1.73; 95% CI: 1.1

177 yndrome predicts tooth loss and worsening of periodontal disease in a cohort of 760 men in the Depart

178 study examines the accuracy of self-reported periodontal disease in a cohort of older females.

179 resent results demonstrate the occurrence of periodontal disease in a mouse model of progressive CD-l

180 se, whether coffee intake is associated with periodontal disease in adult males was explored.

181 ty of data on the validity of self-report of periodontal disease in African Americans.

182 is needed to understand the possible role of periodontal disease in carcinogenesis.

183 ed Pg models were the most representative of periodontal disease in humans, whereas the oral gavage m

184 was associated with a greater prevalence of periodontal disease in middle [prevalence ratio (PR): 1.

185 (PR: 1.73; 95% CI: 1.19, 2.52) but not with periodontal disease in only one tooth (PR: 0.85; 95% CI:

186 Recent evidence suggests a high incidence of periodontal disease in patients with Crohn disease (CD).

187 th the initiation and progression of induced periodontal disease in rat molars.

188 rapists when screening for dental caries and periodontal disease in regularly attending asymptomatic

189 any deleterious health effects, treatment of periodontal disease in smokers remains a challenge of pe

190 sess the prevalence, extent, and severity of periodontal diseases in an adult group from Oman.

191 nificant decrease in 10 taxa associated with periodontal disease including Treponema spp.

192 For periodontal disease, income inequalities were mediated b

193 p C: no treatment control group; 2) group L: periodontal disease induced by ligature; 3) group G-Pg:

194 rely on how effectively they can ameliorate periodontal disease-induced oxidative stress during oral

195 Periodontal disease is a major complication of type 1 di

196 Evidence that periodontal disease is a possible risk factor for cognit

197 The aim of this study is to assess whether periodontal disease is a risk indicator for poor physica

198 Increased periodontal disease is associated with aging.

199 The authors seek to examine to what extent periodontal disease is associated with kidney function d

200 Tooth loss or periodontal disease is associated with systemic endothel

201 n of host-microbe homeostasis at the site of periodontal disease is considered a key factor for disea

202 search targeting prevention and treatment of periodontal disease is decreasing (P <0.001) in favor of

203 Periodontal disease is one of the most common inflammato

204 Various studies have shown periodontal disease is one of the risk factors for coron

205 Severe periodontal disease is prevalent among a population at h

206 Their potential involvement in periodontal disease is yet unknown.

207 of the more severe and irreversible forms of periodontal disease, is a microbial-induced chronic infl

208 Periodontal disease knowledge and consideration levels i

209 Periodontal disease may be considered a risk indicator f

210 ydroxyvitamin D [25(OH)D] concentrations and periodontal disease may be partially explained by the an

211 It has been suggested that periodontal disease may increase in severity with increa

212 level, and initial level of the appropriate periodontal disease measure.

213 25(OH)D and the subsequent 5-year change in periodontal disease measures was observed.

214 erved between baseline 25(OH)D and change in periodontal disease measures, overall or in a subset (n

215 Patients with a history of periodontal disease multiplied their probability of bein

216 rting a history of tooth loss as a result of periodontal disease (n = 70) or caries (n = 558) (total

217 Inflammatory conditions as they occur during periodontal disease often result in decreased alveolar b

218 valuate the impact of long-term treatment of periodontal disease on glycemic control among individual

219 Findings support an effect of periodontal disease on OHRQoL in people with systemic ar

220 However, there was no influence of periodontal disease on OSAS risk.

221 The causal effect of periodontal disease on prostatic inflammation has not be

222 investigated differences in the severity of periodontal disease on referral for specialist care betw

223 ry (prevalence) of tooth loss resulting from periodontal disease or caries and 1.07 (95% CI = 0.62 to

224 r the incidence of tooth loss resulting from periodontal disease or caries.

225 on probing (P = 0.03) and higher severity of periodontal disease (P = 0.02).

226 imes with respect to not having a history of periodontal disease (P = 0.02).

227 s to be a promising host modulatory agent in periodontal disease pathogenesis regarding IL-17/IL-23 a

228 e implicating TLR9-triggered inflammation in periodontal disease pathogenesis, thereby identifying a

229 al aspect of an effective immune response to periodontal disease pathogens, as new blood vessel forma

230 ne loss is a result of an aggressive form of periodontal disease (PD) associated with Aggregatibacter

231 nto control, stress (STR), probiotic (PROB), periodontal disease (PD), STR-PROB, STR-PD, STR-PROB-PD,

232 P-9 immunoexpression in gingiva with induced periodontal disease (PD).

233 tionship between metabolic syndrome (MS) and periodontal disease (PD).

234 mune dysregulation that is characteristic of periodontal disease (PD).

235 Periodontal disease (PdD) has been shown to be related t

236 itive for both the Bq and ESS, and 97.2% had periodontal disease (periodontitis = 85.2% and gingiviti

237 During inflammatory periodontal disease, peripheral blood mononuclear cells

238 Although many factors can affect periodontal disease, presence of inflammatory arthritis

239 equate information regarding the severity of periodontal disease, presenting a need to investigate al

240 s using half-mouth designs for assessment of periodontal disease prevalence have reported that enviro

241 Higher periodontal disease prevalence is found among pregnant w

242 s essential to increase our knowledge of the periodontal disease process.

243 We conclude that TLR9 modulates periodontal disease progression at both the cellular and

244 hol consumption may be beneficial to prevent periodontal disease progression in males.

245 be tied to the underlying pathophysiology of periodontal disease progression in smokers and suggest t

246 trengthening the evidence that mechanisms of periodontal disease progression in smokers may differ fr

247 morphisms with level of tissue breakdown and periodontal disease progression is not clear.

248 ere used to estimate hazards of experiencing periodontal disease progression with or without adjustme

249 expression of hTERT might be associated with periodontal disease progression, suggesting that hTERT c

250 -chain fatty acids, from bacteria that cause periodontal disease promote lytic replication of KSHV, t

251 thin gingival biotype (<1 mm) and history of periodontal disease received one maxillary implant each.

252 uating 126,805 individuals with diabetes and periodontal disease receiving care at all Veterans Admin

253 However, their relationship with periodontal disease remains unclear.

254 = 259; 26.6%) had worse oral hygiene habits, periodontal disease risk factors, and clinical periodont

255 ion, the authors examined the association of periodontal disease (severe versus non-severe) with inci

256 cular fluid (GCF) and their association with periodontal disease severity and activity.

257 oefficient of 0.246 between AHI severity and periodontal disease severity categories.

258 ptake inhibitor, has been reported to reduce periodontal disease severity in a rat ligature-induced p

259 Non-surgical periodontal therapy and periodontal disease severity were not associated with si

260 questionnaire items with respect to clinical periodontal disease severity.

261 Patients with periodontal disease showed high risk for OSAS (82.9%) an

262 ed inflammatory cell infiltrate into chronic periodontal disease sites treated surgically and dramati

263 reduction was observed in the percentage of periodontal diseased sites, gingival index, plaque index

264 reduction in probing depth and percentage of periodontal diseases sites, as well as lower total bacte

265 in analyses that were stratified by baseline periodontal disease status.

266 (TPCs A to G) ranging from health to severe periodontal disease status.

267 usal females in the Buffalo Osteoporosis and Periodontal Disease Study (1997 to 2000), an ancillary s

268 usal women aged 50 to 79 years enrolled in a periodontal disease study ancillary to the Women's Healt

269 les enrolled in the Buffalo Osteoporosis and Periodontal Disease Study were followed prospectively.

270 (GCF) endocan levels in the pathogenesis of periodontal diseases, supported with vascular endothelia

271 nization following inoculation and increased periodontal disease susceptibility, reflected by higher

272 ssociated with current clinically determined periodontal disease taxonomies, upon replication and mec

273 patients with RA have a higher incidence of periodontal disease than individuals without RA.

274 nts referred in 2000 had greater severity of periodontal disease than those referred 20 years ago.

275 al role in periodontal biofilm dysbiosis and periodontal disease that warrants further investigation.

276 Based on a murine model of periodontal disease, the function of IL-33 was determine

277 Compared with participants with non-severe periodontal disease, those with severe periodontal disea

278 nts with dental terminology and knowledge of periodontal disease to provide education on oral hygiene

279 Further research is needed to determine if periodontal disease treatment alters the trajectory of r

280 tissues, thus displaying a potential use for periodontal disease treatment or to functionalize dental

281 (Leptospira interrogans), and contribute to periodontal diseases (Treponema denticola)(1).

282 The accuracy of a prediction model for periodontal disease using the community periodontal inde

283 professionals when screening for caries and periodontal disease was 0.81 (95% CI, 0.74 to 0.87) and

284 professionals when screening for caries and periodontal disease was 0.87 (0.78 to 0.92) and 0.75 (0.

285 ng teeth and having a prevalent diagnosis of periodontal disease was associated with a 1.85-fold incr

286 Periodontal disease was induced in Balb/c mice by direct

287 Periodontal disease was induced in Balb/c mice by direct

288 At week 12, periodontal disease was induced in groups PERIO and CAF+

289 The overall incidence rate ratio of severe periodontal diseases was 39% higher in the NA-SD cohort

290 f the most prevalent strains in the onset of periodontal diseases, was used as a model of oral bacter

291 IL)-1beta levels, and clinical parameters of periodontal disease were examined.

292 Similarly, significant effects of history of periodontal disease were obtained for peri-implantitis f

293 Given the beneficial role of such factors in periodontal disease, whether coffee intake is associated

294 ycetemcomitans is associated with aggressive periodontal disease, which is characterized by inflammat

295 Patients with periodontal disease who undergo procedures for subgingiv

296 m the insurance claims data of patients with periodontal disease who were free of ESRD from 1997 to 2

297 A has been epidemiologically associated with periodontal disease, whose main infective agent is Porph

298 atus on number of natural teeth, teeth lost, periodontal disease with bone loss, and root canal treat

299 rsy exists regarding possible correlation of periodontal disease with rheumatoid arthritis (RA) and a

300 e presence of gingival apoptosis at sites of periodontal disease, with females having the highest inc