ライフサイエンスコーパス: chronic periodontitis

1 abits periodontal pockets and contributes to chronic periodontitis.

2 mically healthy individuals with generalized chronic periodontitis.

3 ting active periodontitis, and 2) predicting chronic periodontitis.

4 c anaerobe, is a major causative organism of chronic periodontitis.

5 diagnostic abilities, together or alone, in chronic periodontitis.

6 s (metanephrine and total metanephrines) and chronic periodontitis.

7 their numbers are elevated in patients with chronic periodontitis.

8 individuals without obesity with generalized chronic periodontitis.

9 s between 7% and less than 9%, and untreated chronic periodontitis.

10 of intrabony defects (IBDs) in patients with chronic periodontitis.

11 he oral microorganisms associated with human chronic periodontitis.

12 l osteopenic females with moderate-to-severe chronic periodontitis.

13 re related to the occurrence and severity of chronic periodontitis.

14 ith type 2 diabetes and moderate to advanced chronic periodontitis.

15 atment of intrabony defects in patients with chronic periodontitis.

16 ms of periodontal disease, most closely with chronic periodontitis.

17 sal osteopenic women with moderate to severe chronic periodontitis.

18 e characteristic of many diseases, including chronic periodontitis.

19 has never been investigated in patients with chronic periodontitis.

20 lay an important role in the pathogenesis of chronic periodontitis.

21 atment of intrabony defects in patients with chronic periodontitis.

22 ng status were recorded for 56 patients with chronic periodontitis.

23 RP) of individuals with moderate-to-advanced chronic periodontitis.

24 ss index >30 kg/m(2)) patients affected with chronic periodontitis.

25 ere, seven with moderate, and four with mild chronic periodontitis.

26 cted, with a diagnosis of generalized slight chronic periodontitis.

27 tent with a dampening of COX-2 expression in chronic periodontitis.

28 nd Porphyromonas gingivalis in patients with chronic periodontitis.

29 as a local contributing factor in localized chronic periodontitis.

30 was referred to our clinic for treatment of chronic periodontitis.

31 gingivalis is etiologically associated with chronic periodontitis.

32 as a local contributing factor in localized chronic periodontitis.

33 was referred to our clinic for treatment of chronic periodontitis.

34 in individual subgingival sites affected by chronic periodontitis.

35 gingivalis is implicated in the etiology of chronic periodontitis.

36 resented for treatment of generalized severe chronic periodontitis.

37 6 mm was sampled in each of 20 subjects with chronic periodontitis.

38 in the treatment of intraosseous defects of chronic periodontitis.

39 ing data have been gathered from adults with chronic periodontitis.

40 pplied to subjects with severe, generalized, chronic periodontitis.

41 ia of 127 subjects with moderate to advanced chronic periodontitis.

42 ngivalis (Pg) is a major etiologic agent for chronic periodontitis.

43 lating properties that may positively affect chronic periodontitis.

44 ) is a keystone pathogen in the aetiology of chronic periodontitis.

45 inical parameters and OHRQL of patients with chronic periodontitis.

46 nate in the inflammatory infiltrate of human chronic periodontitis.

47 es, and influencing factors in patients with chronic periodontitis.

48 o predict treatment outcome of patients with chronic periodontitis.

49 F + HA in treatment of IBDs in patients with chronic periodontitis.

50 hanges, but these changes are not evident in chronic periodontitis.

51 NLRP3 transcription were modulated in human chronic periodontitis.

52 as one of the major periodontal pathogens in chronic periodontitis, a common infectious disease chara

53 Chronic periodontitis, a destructive inflammatory disord

54 nth cranial nerves was diagnosed with severe chronic periodontitis affecting only the right maxillary

55 erella forsythia is strongly associated with chronic periodontitis, an inflammatory disease of the to

56 mblages from 25 individuals with generalized chronic periodontitis and 25 periodontally healthy indiv

57 moderate to advanced periodontitis (63 with chronic periodontitis and 27 with aggressive periodontit

58 y healthy patients >45 years of age (30 with chronic periodontitis and 30 without periodontitis) were

59 Forty-five patients with chronic periodontitis and a total of 164 screw-typed imp

60 romonas gingivalis, a pathogen implicated in chronic periodontitis and atherosclerosis.

61 A sample of 236 patients with chronic periodontitis and clinical depression were asses

62 Twenty-two patients with advanced chronic periodontitis and displaying one deep intrabony

63 IL-21 levels were compared between chronic periodontitis and healthy gingival tissues and c

64 190 subjects with generalized aggressive or chronic periodontitis and in 90 periodontally healthy su

65 Patients with chronic periodontitis and intraoral Porphyromonas gingiv

66 robiota of smokers versus never-smokers with chronic periodontitis and matched probing depths (PDs) u

67 Four patients with severe chronic periodontitis and scheduled to receive complete

68 me individual were obtained from adults with chronic periodontitis and screened for their ability to

69 Five patients with chronic periodontitis and treatment planned for a maxill

70 ntal diagnosis ranged from healthy to severe chronic periodontitis, and for whom "checkerboard" DNA-D

71 er mean serum IL-6 levels than those without chronic periodontitis, and there was a positive correlat

72 vated in gingival tissues from patients with chronic periodontitis as compared with healthy tissues (

73 Infection by the chronic periodontitis-associated pathogen Porphyromonas

74 ntraoral sites in 35 patients with untreated chronic periodontitis before and 1.5, 3, and 6 months af

75 surgery needs is evaluated in patients with chronic periodontitis before and after completion of non

76 D, and clinical and microbial parameters of chronic periodontitis before and after treatment.

77 xist as a consortium that is associated with chronic periodontitis but also exhibit synergistic virul

78 s is associated with IL-6 genetic factors in chronic periodontitis cases.

79 utcomes prior to root surface debridement in chronic periodontitis cases.

80 Thirteen patients with generalized severe chronic periodontitis completed the study.

81 45 patients with chronic periodontitis comprising 164 screw-typed implant

82 ival crevicular fluid (GCF) of patients with chronic periodontitis contains galactose (Gal)-deficient

83 Inflammatory conditions, such as chronic periodontitis, could disrupt this homeostasis, a

84 rs (DAI), and absent in melanoma 2 (AIM2) in chronic periodontitis (CP versus healthy) (H) tissues.

85 severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls).

86 ingivitis (n = 15), and patients with severe chronic periodontitis (CP) (n = 15) without any systemic

87 king individuals with gingivitis (n = 20) or chronic periodontitis (CP) (n = 20) and periodontally he

88 Patients with aggressive (AgP) (n = 24) and chronic periodontitis (CP) (n = 34) as well as healthy c

89 um were obtained from 47 adult patients with chronic periodontitis (CP) and 10 healthy controls.

90 samples were collected from 19 patients with chronic periodontitis (CP) and 16 control individuals wi

91 biopsies were obtained from 17 patients with chronic periodontitis (CP) and 18 periodontally healthy

92 viduals were included in this study, 20 with chronic periodontitis (CP) and 22 classified as periodon

93 Twenty-six patients with T2DM and chronic periodontitis (CP) and 26 without T2DM with CP w

94 One hundred ten patients with chronic periodontitis (CP) and 50 healthy controls were

95 rance Database 2000 for 71,182 patients with chronic periodontitis (CP) and 71,182 controls without p

96 ntal treatment in 40 patients with COPD with chronic periodontitis (CP) and a history of >/=1 infecti

97 ss MDA levels in the saliva of patients with chronic periodontitis (CP) and acute coronary syndrome (

98 is difficult to differentiate some cases of chronic periodontitis (CP) and aggressive periodontitis

99 rase reverse transcription (hTERT) enzyme in chronic periodontitis (CP) and aggressive periodontitis

100 hy patients and patients with gingivitis and chronic periodontitis (CP) and correlates these levels w

101 odontal clinical parameters of patients with chronic periodontitis (CP) and diabetes mellitus (DM).

102 among non-smoking and smoking patients with chronic periodontitis (CP) and generalized aggressive pe

103 ta from individuals with aggressive (AgP) or chronic periodontitis (CP) and healthy controls (HC), as

104 xidative DNA damage marker, in patients with chronic periodontitis (CP) and hyperlipidemia.

105 generalized aggressive periodontitis (GAgP), chronic periodontitis (CP) and in patients with no histo

106 e existence of an association between severe chronic periodontitis (CP) and nailfold microvascular, g

107 Chronic periodontitis (CP) and rheumatoid arthritis (RA)

108 -8) patterns in smokers and non-smokers with chronic periodontitis (CP) and test the utility of basel

109 al papilla are investigated in patients with chronic periodontitis (CP) and TGF-beta1 29C/T gene poly

110 Patients with chronic periodontitis (CP) and those with healthy period

111 cemic and metabolic control in patients with chronic periodontitis (CP) and type 2 diabetes mellitus

112 propolis supplementation in individuals with chronic periodontitis (CP) and type 2 diabetes mellitus

113 loss (MBL) when compared with patients with chronic periodontitis (CP) and/or healthy patients (HPs)

114 DM and chronic periodontitis (CP) are associated with each othe

115 Rheumatoid arthritis (RA) and chronic periodontitis (CP) are the most common chronic i

116 oriasis (PS), psoriatic arthritis (PsA), and chronic periodontitis (CP) are the most common chronic i

117 althy individuals and patients with moderate chronic periodontitis (CP) before and 6 weeks after peri

118 e macrophage activation pathways involved in chronic periodontitis (CP) by the detection of the indir

119 Genome-wide association studies (GWAS) of chronic periodontitis (CP) defined by clinical criteria

120 s also wanted to check whether patients with chronic periodontitis (CP) exhibit different modulations

121 eralized aggressive periodontitis (GAgP), or chronic periodontitis (CP) groups.

122 Chronic periodontitis (CP) has a genetic component, part

123 The low-grade oral infection chronic periodontitis (CP) has been implicated in corona

124 oncentrations in the saliva of patients with chronic periodontitis (CP) has not been explored despite

125 y, genome-wide association studies (GWAS) of chronic periodontitis (CP) have been unsuccessful in dis

126 study investigates whether susceptibility to chronic periodontitis (CP) in a Thai population is assoc

127 RP) in the treatment of intrabony defects in chronic periodontitis (CP) in patients with type 2 diabe

128 ve periodontitis (AgP) not only differs from chronic periodontitis (CP) in terms of clinical manifest

129 and IL1B (+3954), have been associated with chronic periodontitis (CP) in whites.

130 Chronic periodontitis (CP) is a common oral disease that

131 Chronic periodontitis (CP) is a continuous, reversible s

132 Chronic periodontitis (CP) is an inflammatory condition

133 Chronic periodontitis (CP) is an inflammatory disease in

134 subgingival debridement in the treatment of chronic periodontitis (CP) is controversial.

135 Patients with chronic periodontitis (CP) may yield multiple species of

136 nt genome-wide association studies (GWAS) of chronic periodontitis (CP) offer rich data sources for t

137 , thus providing evidence that the impact of chronic periodontitis (CP) on the activity of circulatin

138 ukin (IL)-1beta in patients with generalized chronic periodontitis (CP) or aggressive periodontitis (

139 terleukin (IL)-6, and IL-10 in patients with chronic periodontitis (CP) or aggressive periodontitis (

140 f individuals without periodontitis and with chronic periodontitis (CP) or generalized aggressive per

141 o be significantly elevated in patients with chronic periodontitis (CP) or oral lichen planus (OLP).

142 ) and serum of rheumatoid arthritis (RA) and chronic periodontitis (CP) patients to assess whether cy

143 ral polymorphonuclear neutrophils (oPMNs) in chronic periodontitis (CP) refractory to conventional th

144 aliva (UWS) of patients with prediabetes and chronic periodontitis (CP) remains uninvestigated.

145 ion of FcGR and TNFA gene polymorphisms with chronic periodontitis (CP) susceptibility has been found

146 A significant proportion of patients with chronic periodontitis (CP) test positive for antiCl, lik

147 s of peripheral neutrophils in patients with chronic periodontitis (CP) that generate different level

148 65 patients with DM with moderate-to-severe chronic periodontitis (CP) was recruited, and 15 individ

149 itis (GAgP) and 71 patients with generalized chronic periodontitis (CP) were compared to 88 periodont

150 oxidant/antioxidant status in patients with chronic periodontitis (CP) who experienced familial Medi

151 ar fluid of patients with moderate-to-severe chronic periodontitis (CP) who have been treated using S

152 a novel predictive marker for patients with chronic periodontitis (CP) with and without type 2 diabe

153 atment of intrabony defects in patients with chronic periodontitis (CP) with type 2 diabetes (DM) com

154 included in this study: 21 individuals with chronic periodontitis (CP), 14 individuals with generali

155 viduals were included in this study; 20 with chronic periodontitis (CP), 20 with generalized aggressi

156 agnosed with aggressive periodontitis (AgP), chronic periodontitis (CP), and clinically healthy perio

157 m localized aggressive periodontitis (LAgP), chronic periodontitis (CP), and periodontally healthy su

158 e gingival crevicular fluid (GCF) in health, chronic periodontitis (CP), and T2DM.

159 sfatin in gingival tissue from patients with chronic periodontitis (CP), patients with CP and type 2

160 sion in gingival biopsies from patients with chronic periodontitis (CP), patients with gingivitis (GV

161 In chronic periodontitis (CP), the gene polymorphism of int

162 MDA) in blood and saliva of individuals with chronic periodontitis (CP).

163 matory processes in the oral cavity, such as chronic periodontitis (CP).

164 stase (NE) in patients with hypertension and chronic periodontitis (CP).

165 ctivity in serum and saliva of patients with chronic periodontitis (CP).

166 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

167 lood cultures from patients with and without chronic periodontitis (CP).

168 of smokers and non-smokers with generalized chronic periodontitis (CP).

169 concentrations of visfatin in patients with chronic periodontitis (CP).

170 hemokines and dendritic cells (DCs) in human chronic periodontitis (CP).

171 oup 2 (n = 20), individuals with generalized chronic periodontitis (CP).

172 uals with aggressive periodontitis (AgP) and chronic periodontitis (CP).

173 vertical defects in smokers with generalized chronic periodontitis (CP).

174 ne irrigation and SRP alone in patients with chronic periodontitis (CP).

175 some additional benefit in the treatment of chronic periodontitis (CP).

176 individuals who are normal weight (NW) with chronic periodontitis (CP).

177 study its clinical effects on patients with chronic periodontitis (CP).

178 eatment of patients with type 2 diabetes and chronic periodontitis (CP).

179 ht to have a faster rate of progression than chronic periodontitis (CP).

180 types of periodontitis, aggressive (AgP) and chronic periodontitis (CP).

181 bonucleic acid (DNA) damage in patients with chronic periodontitis (CP).

182 6 months in patients with severe generalized chronic periodontitis (CP).

183 SRP) in the treatment of moderate and severe chronic periodontitis (CP).

184 group of untreated patients with generalized chronic periodontitis (CP).

185 opsies of patients with type 2 diabetes with chronic periodontitis (CP).

186 riodontitis individuals and 25 patients with chronic periodontitis (CP).

187 ling and root planing (SRP) in subjects with chronic periodontitis (CP).

188 en with polycystic ovary syndrome (PCOS) and chronic periodontitis (CP).

189 ealthy unrelated children and to adults with chronic periodontitis (CP).

190 g and root planing (SRP) in the treatment of chronic periodontitis (CP).

191 bony defect (IBD) treatment in patients with chronic periodontitis (CP).

192 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

193 intrabony defects (IBDs) in individuals with chronic periodontitis (CP).

194 nts with type 2 diabetes mellitus (T2DM) and chronic periodontitis (CP).

195 urgical periodontal therapy for smokers with chronic periodontitis (CP).

196 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

197 s biomarkers in smokers and non-smokers with chronic periodontitis (CP).

198 nd adiponectin in patients with obesity with chronic periodontitis (CP).

199 of intrabony defects (IBDs) in patients with chronic periodontitis (CP).

200 d IL-6, are evaluated in human patients with chronic periodontitis (CP).

201 initial periodontal therapy in patients with chronic periodontitis (CP).

202 n average values for patients diagnosed with chronic periodontitis (CP).

203 tes in the peripheral blood of patients with chronic periodontitis (CP).

204 ided into two groups: 1) 24 individuals with chronic periodontitis (CP); and 2) 23 individuals withou

205 into three groups: 1) healthy (control); 2) chronic periodontitis (CP); and 3) myocardial infarction

206 with aggressive periodontitis (AgP, n = 25), chronic periodontitis (CP, n = 14), and gingivitis (G, n

207 ivary cotinine) smokers and non-smokers with chronic periodontitis (CP: n = 13) or aggressive periodo

208 sive periodontitis [AgP], and the group with chronic periodontitis [CP]) and 15 volunteers who exhibi

209 ls (27 healthy controls and 27 patients with chronic periodontitis [CP]) were enrolled in the study.

210 ive for poor oral hygiene, 95% sensitive for chronic periodontitis (defined as at least two sites wit

211 yromonas gingivalis, a principal pathogen in chronic periodontitis, did not induce NKT cell activatio

212 3 (IL-33) can differentiate individuals with chronic periodontitis from individuals with healthy peri

213 f these species in subjects with generalized chronic periodontitis (GChP; n = 30), generalized aggres

214 donic acid (AA) in patients with generalized chronic periodontitis (GCP) and compare these results wi

215 Finnish dentate adults: 84 with generalized chronic periodontitis (GCP), 65 with localized chronic p

216 al signs: 1) control; 2) AMI; 3) generalized chronic periodontitis (GCP); and 4) GCP + AMI.

217 IL-21 was overexpressed in chronic periodontitis gingival tissues and correlated wi

218 response of patients with generalized severe chronic periodontitis (GSCP) treated with one-stage, ful

219 Transplant subjects with chronic periodontitis had higher mean serum IL-6 levels

220 Forty patients diagnosed with severe chronic periodontitis had subgingival samples harvested

221 (SRP) has been proposed for the treatment of chronic periodontitis; however, its effectiveness and cl

222 strongly associated with generalized severe chronic periodontitis in North American whites.

223 scaling and root planing (SRP) for treating chronic periodontitis in patients with type 2 diabetes.

224 nct to scaling and root planing for treating chronic periodontitis in smokers.

225 pocket reduction surgery in the treatment of chronic periodontitis in smokers.

226 nces (P <0.05) were recorded by diagnosis of chronic periodontitis in the a* coordinate when comparin

227 a higher prevalence of oral diseases (e.g., chronic periodontitis) in aged populations have received

228 tained from 32 otherwise healthy, non-smoker chronic periodontitis individuals and 25 systemically an

229 asma levels of IL-33 could not differentiate chronic periodontitis individuals and periodontally heal

230 rations of IL-33 were significantly lower in chronic periodontitis individuals than in healthy indivi

231 Chronic periodontitis is a chronic disease of the period

232 Chronic periodontitis is a local inflammatory disease in

233 Chronic periodontitis is associated with incidence of CH

234 Chronic periodontitis is controlled without antibiotics

235 Chronic periodontitis is induced by a dysbiotic microbio

236 Chronic periodontitis is linked to systemic inflammation

237 urther examined in localized and generalized chronic periodontitis (LCP and GCP).

238 ronic periodontitis (GCP), 65 with localized chronic periodontitis (LCP), and 81 controls without per

239 eripheral neutrophil hyper-responsiveness in chronic periodontitis leads to excessive reactive oxygen

240 n of type I NKT cells in aggressive, but not chronic, periodontitis lesions in vivo.

241 d:YAG or Er:YAG wavelengths for treatment of chronic periodontitis may be equivalent to scaling and r

242 healthy controls (n = 10) and patients with chronic periodontitis (n = 17) was investigated.

243 thy individuals (n = 2) and individuals with chronic periodontitis (n = 2) was done via immunohistoch

244 trolled trial was conducted in patients with chronic periodontitis (N = 22) presenting at least three

245 recovered from separate patients with severe chronic periodontitis (n = 50) before treatment, were su

246 Sixty patients with chronic periodontitis on 6-month PMT intervals to be fol

247 iodontopathogenic bacteria in aggressive and chronic periodontitis on a patient basis (pooled samples

248 f typical medication use among patients with chronic periodontitis or destructive periodontal disease

249 fold; caspase-3, 6.8-fold; Xiap: 2.5-fold in chronic periodontitis) (P < 0.05), highlighting their po

250 les of gingival biopsies were collected from chronic periodontitis patients (n = 10) and controls (n

251 e expression of IL-21 in gingival tissues of chronic periodontitis patients and correlate/associate t

252 Sixty-one chronic periodontitis patients, each contributing a 2- o

253 Forty-two chronic periodontitis patients, each contributing a 2-wa

254 ated in human gingival tissue specimens from chronic periodontitis patients, further confirming the b

255 ily in ASC-deficient THP1 cells with that in chronic periodontitis patients.

256 ion of statin use with reduced tooth loss in chronic periodontitis patients.

257 virus may be associated with inflammation in chronic periodontitis patients.

258 yperreactivity in terms of ROS production in chronic periodontitis patients.

259 ealth, gingivitis/peri-implant mucositis, or chronic periodontitis/peri-implantitis.

260 ecession, aggressive or acute periodontitis, chronic periodontitis, periodontosis, accretions, other

261 hogens, including a key etiological agent of chronic periodontitis, Porphyromonas gingivalis, infect

262 Sixteen smokers with chronic periodontitis presenting a minimum of four pocke

263 eptible to periodontitis were diagnosed with chronic periodontitis prior to implant therapy.

264 128 post-menopausal osteopenic women with chronic periodontitis randomly received SDD or placebo t

265 Forty individuals with severe chronic periodontitis received periodontal surgery, dail

266 Persons with chronic periodontitis receiving immunosuppressive treatm

267 width in subjects with severe, generalized, chronic periodontitis seemed to be significantly greater

268 Use of statins on adult patients with chronic periodontitis shows a positive effect on their p

269 oup with 5 periodontally healthy sites and 5 chronic periodontitis sites.

270 h ex vivo-isolated blood mDCs and serum from chronic periodontitis subjects and healthy controls.

271 milar migratory profile; moreover, sera from chronic periodontitis subjects expressed elevated levels

272 Thirty-nine chronic periodontitis subjects were randomly assigned to

273 Ex vivo-isolated mDCs from the blood of chronic periodontitis subjects, but not healthy controls

274 lood neutrophils isolated from patients with chronic periodontitis, suggesting that oral neutrophils

275 Given the known association between IL-6 and chronic periodontitis, the aim of our study was to asses

276 A major etiological agent of chronic periodontitis, the Gram-negative bacterium Porph

277 hogen Porphyromonas gingivalis, which causes chronic periodontitis, the most prevalent dysbiosis-driv

278 val samples harvested from human healthy and chronic periodontitis tissues (Apaf-1, 19.2-fold; caspas

279 controlled trial, 85 patients diagnosed with chronic periodontitis underwent different treatment prot

280 A total of 40 patients with severe, chronic periodontitis underwent periodontal surgery and

281 Thirty non-smoking patients suffering severe chronic periodontitis were allocated to this randomized,

282 Individuals with chronic periodontitis were classified as RP (n = 17) bas

283 Twenty-four patients with chronic periodontitis were divided randomly into three g

284 s and six females, aged 25 to 45 years) with chronic periodontitis were enrolled in the study.

285 linical study, data from 34 individuals with chronic periodontitis were evaluated after full-mouth SR

286 d three disease sites of 65 patients who had chronic periodontitis were evaluated for the presence an

287 Twenty non-smoking patients with severe chronic periodontitis were included in the study.

288 ed 29 to 45 years, with severe, generalized, chronic periodontitis were included in the study.

289 Seventy-seven patients with chronic periodontitis were measured for plaque, relative

290 ing habit and generalized moderate to severe chronic periodontitis were randomized to the test (surge

291 Patients with chronic periodontitis were randomly assigned to receive

292 defects in healthy non-smoking patients with chronic periodontitis were randomly divided in control (

293 y-eight systemically healthy volunteers with chronic periodontitis were recruited and monitored clini

294 A total of 34 subjects with chronic periodontitis were selected and divided into two

295 Thirty-five patients with chronic periodontitis were selected for the split-mouth

296 Fifty-one adult volunteers with generalized chronic periodontitis were treated by full-mouth SRP usi

297 Twenty-six patients (52 sites) with chronic periodontitis were treated either with autologou

298 nts with type 2 diabetes mellitus (t2DM) and chronic periodontitis who participated in the Diabetes a

299 al therapy in >/= 10 patients diagnosed with chronic periodontitis with a follow-up period of >/= 2 y

300 been studied predominantly in patients with chronic periodontitis with limited data available regard