ライフサイエンスコーパス: periodontal

1 treatment PSR scores of 4 and a pretreatment periodontal access surgery need continued to have surgic

2 Periodontal access surgery needs for all sextants were d

3 ent PSR evaluations for estimating potential periodontal access surgery needs in patients to be initi

4 index scores of 4 were a strong indicator of periodontal access surgery needs in untreated dentition

5 rding (PSR) index sextant scores to estimate periodontal access surgery needs is evaluated in patient

6 ores of 4 identified untreated sextants with periodontal access surgery needs significantly better th

7 sextants with PSR scores of 4 or 3 revealed periodontal access surgical needs when Class II or III f

8 onsidering the suggested association between periodontal and cardiovascular diseases, this study soug

9 re identification and definition of distinct periodontal and tooth profile classes (PPCs/TPCs) among

10 rms used included: 1) refer; 2) referral; 3) periodontal; and 4) periodontist.

11 nd develop preventative or plan interceptive periodontal augmentation (soft tissue and/or bone augmen

12 NETs were found to entrap, but not kill, all periodontal bacteria tested.

13 reactive oxygen species (ROS) in response to periodontal bacteria, as well as the underlying pathways

14 pact of DHA with low-dose aspirin therapy on periodontal bacterial profile in patients with periodont

15 Presence of 40 periodontal bacterial species at baseline and 3 months w

16 hydrogel sites showed significantly reduced periodontal bone loss (P <0.05) and inflammatory infiltr

17 CD5(+) B cell transfer demonstrated reduced periodontal bone loss compared to the no-transfer group

18 ne the effects of TLR-activated B10 cells on periodontal bone loss in experimental periodontitis.

19 ligand (RANKL), which, in turn, promotes the periodontal bone loss via upregulation of osteoclastogen

20 Periodontal bone loss was significantly decreased and th

21 ic regimen targeting DC-STAMP could suppress periodontal bone loss.

22 dependent indicators of amount and extent of periodontal breakdown in both CP and AgP and could poten

23 festations that are hidden under the current periodontal classification schemas.

24 aim of the present study is to evaluate the periodontal clinical and microbiologic responses and pos

25 est PPC and TPC using LCA can provide robust periodontal clinical definitions that reflect disease pa

26 All periodontal clinical parameters and GCF IL-lbeta concent

27 ion between periodontitis and ED by means of periodontal clinical parameters and salivary markers int

28 ), as well as elucidate its association with periodontal clinical status.

29 Treponema denticola (P <0.03) are related to periodontal condition in patients with RA.

30 Periodontal condition was classified as healthy/mild, mo

31 there appears to be a trend for more severe periodontal conditions being referred to periodontists.

32 This is concerning given that more severe periodontal conditions tend to be more difficult to mana

33 Patients with RA had worse periodontal conditions than HC participants.

34 ositive patients with RA suffered from worse periodontal conditions than RF-negative patients (P = 0.

35 Periodontal conditions were assessed for 1,911 dentate a

36 Periodontal data were presented from 1,066 participants.

37 Prx1-cKO mice exhibited the same array of periodontal defects but featured less affected molar den

38 Here, we show progressive periodontal defects in mice in which both BMP1 and TLL1

39 ential for use as regenerative treatment for periodontal defects.

40 mary, despite their reciprocal relationship, periodontal destruction and diabetes may be independent

41 ngs did not indicate additive interaction of periodontal destruction and diabetes regarding all-cause

42 urpose of this study was to evaluate whether periodontal destruction interacts with diabetes on all-c

43 Periodontal destruction was assessed via clinical attach

44 nabolic phase of periodontal homeostasis and periodontal development, miRNAs direct periodontal fibro

45 ations are essential in establishing correct periodontal diagnoses as well as providing appropriate t

46 CBCT imaging can improve the periodontal diagnostic acumen regarding alveolar bone al

47 esses the long-term "biologic remodeling" of periodontal dimensions of teeth treated with free gingiv

48 edures may modify the biologic remodeling of periodontal dimensions over time associated with aging.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Their potential involvement in periodontal disease is yet unknown.

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

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

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

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

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

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

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

72 questionnaire items with respect to clinical periodontal disease severity.

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

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

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

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

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

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

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

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

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

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

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

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

85 al microbe implicated in the pathogenesis of periodontal disease.

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

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

88 oncomitant decrease in those associated with periodontal disease.

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

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

91 periodontal tissue integrity as a result of periodontal disease.

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

93 have an increased incidence and severity of periodontal disease.

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

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

96 ntify how providers can help patients manage periodontal disease.

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

98 isting the early diagnosis and prevention of periodontal disease.

99 effect of therapeutic intervention for RA on periodontal disease.

100 dered as a potential inflammatory marker for periodontal disease.

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

102 ssociated with the LPS model of experimental periodontal disease.

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

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

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

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

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

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

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

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

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

112 ion and tissue destruction that characterize periodontal diseases.

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

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

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

116 A full-mouth clinical periodontal evaluation was performed for each patient.

117 It is not clear how using partial-mouth periodontal examination (PMPE) protocols affects estimat

118 e general health examination of DANHES had a periodontal examination consisting of half-mouth registr

119 A complete periodontal examination consisting of probing depth, ble

120 tis, the Centers for Disease Control updated periodontal examination procedures in 2009 for the Natio

121 d for 1,911 dentate adults with a full-mouth periodontal examination.

122 Periodontal examinations of bleeding on probing (BOP), p

123 Full-mouth periodontal examinations were performed, and serum and s

124 Full-mouth periodontal examinations with six sites per tooth were c

125 al attachment level determined by full-mouth periodontal examinations) among 10,935 adult participant

126 iodontal probe is the gold standard tool for periodontal examinations, including probing depth measur

127 s and periodontal development, miRNAs direct periodontal fibroblasts toward alveolar bone lineage dif

128 nes, such as IL-6 and IL-8, in primary human periodontal fibroblasts.

129 BMP1 and TLL1 in maintaining homeostasis of periodontal formation, partly via biosynthetic processin

130 rs for approximately 2 to 4 weeks and better periodontal healing in terms of conventional flap sites.

131 evels in gingival crevicular fluid (GCF) and periodontal healing.

132 r, only a fraction of the miRNAs involved in periodontal health and disease are known today.

133 onship between sFRP5 and Wnt5a expression in periodontal health and disease, paving the way to clinic

134 a flow-mediated dilation (FMD) assessment in periodontal health and disease.

135 tical associations with clinical measures of periodontal health at a level that could be considered o

136 n in some countries, poses emergent oral and periodontal health concerns.

137 f keratinized tissue (KT) for maintenance of periodontal health has been debated for many years.

138 elationship between health literacy (HL) and periodontal health is insufficient to identify how provi

139 e impact of alcohol cessation initiatives on periodontal health should be evaluated.

140 imicrobials into periodontal pockets improve periodontal health.

141 further investigation of factors influencing periodontal health.

142 lthy counterparts with different statuses of periodontal health.

143 s of the extracellular matrix environment to periodontal homeostasis and contributes toward understan

144 um, miRNAs play key roles in development and periodontal homeostasis and during the loss of periodont

145 As part of the anabolic phase of periodontal homeostasis and periodontal development, miR

146 ontribute equally to the catabolic aspect of periodontal homeostasis as they affect osteoclastogenesi

147 eview is to introduce key miRNAs involved in periodontal homeostasis, summarize the mechanisms by whi

148 using these drugs in treating patients with periodontal IBDs.

149 / MB-B-DL/MB-DB-ML-DL); and 4) the community periodontal index.

150 mplified oral hygiene and modified Community Periodontal Indices, respectively, on sixth-grade school

151 available regarding the effects of long-term periodontal infection on diabetes mellitus (DM) control.

152 control of patients with DMt2 by eliminating periodontal infection.

153 Periodontal inflamed surface area (PISA) and FMD were as

154 he adoptive transfer of B10 cells alleviated periodontal inflammation and bone loss in experimental p

155 ne the effect of local B10 cell induction on periodontal inflammation and bone loss in ligature-induc

156 er, we showed that sFRP5 blocks experimental periodontal inflammation and bone loss, suggesting a pro

157 induction of B10 cell activity could inhibit periodontal inflammation and bone loss.

158 Periodontal inflammation and self-perceived OSs were poo

159 biological pathways by which TLR9 instigates periodontal inflammation are yet to be identified.

160 yromonas gingivalis, as the biofilm ages and periodontal inflammation increases.

161 is environment are associated with localized periodontal inflammation, and they are also part of an a

162 and their role has not been characterized in periodontal inflammation.

163 young adults might be increased by combining periodontal information, sociodemographic information, a

164 bone grafting material has been used to fill periodontal intrabony defects (IBDs), resulting in clini

165 te efficacy of statins on treating localized periodontal intrabony defects (IBDs).

166 ivalis, contributing to the deterioration of periodontal lesion through an increased persistence of t

167 le and programed cell death, contributing to periodontal lesion worsening.

168 uct methylglyoxal (MGO) has been detected in periodontal lesions, the precise effect of collagen glyc

169 tent osteoclast-stimulating factor, by human periodontal ligament (hPDL) cells.

170 n conditionally ablated, including malformed periodontal ligament (PDL) (recently shown to play key r

171 tract (STE) on cell survival and motility of periodontal ligament (PDL) and gingival fibroblasts in v

172 The periodontal ligament (PDL), which connects the teeth to

173 human gingival fibroblasts (HGFs) and human periodontal ligament fibroblasts (HPLFs) stimulated with

174 steogenic differentiation of stem cells from periodontal ligament in vitro, and suggest a therapeutic

175 Periodontal ligament mesenchymal stem cells (PDLMSCs) ar

176 Human periodontal ligament stem cells were seeded on an OPN-co

177 Full-mouth clinical periodontal measurements (seven clinical parameters) fro

178 measures at the tooth level, including both periodontal measurements and tooth loss.

179 Clinical periodontal measurements were recorded, and GCF samples

180 ffects of clarithromycin (CLM) combined with periodontal mechanical therapy in the treatment of patie

181 t decade of the 20th century, the concept of periodontal medicine was introduced to explain the corre

182 of elevating the virulence potential of the periodontal microbial community.

183 is investigation aims to identify changes in periodontal microbiome after treatment with EMD using a

184 d AIM2 SNPs associated with higher levels of periodontal microorganisms and an increased percentage o

185 ants with peri-implantitis were colonized by periodontal microorganisms.

186 to a more comprehensive understanding of the periodontal miRNA world, and a systematic effort toward

187 troduction into the therapeutic potential of periodontal miRNAs.

188 eters of oral health were assessed including periodontal, oral mucosal, and caries status in Eastern

189 MMP-8 levels were determined and related to periodontal outcome.

190 period presented higher risk of unfavorable periodontal outcomes (rate ratio [RR]: 1.45 for AL and B

191 l obesity has a direct effect on unfavorable periodontal outcomes in MSMs.

192 Periodontal outcomes were percentage of teeth with bleed

193 e the controlled direct effect of obesity on periodontal outcomes.

194 dge, there are no studies that have compared periodontal parameters and self-perceived oral symptoms

195 The aim of this study is to assess periodontal parameters and self-perceived OSs among vapi

196 Correlation was negative among clinical periodontal parameters and serum MMP-9 levels and MMP-9/

197 ibited a positive correlation among clinical periodontal parameters and serum MMP-9 levels or salivar

198 Clinical periodontal parameters correlated positively with CSF-1,

199 ween local levels of biomarkers and clinical periodontal parameters in only GDM group.

200 plex with the presence of CP (P = 0.008) and periodontal parameters PD, CAL, and BOP was identified.

201 Anthropometric, metabolic, and periodontal parameters were assessed at baseline and re-

202 Odds ratios were calculated for OSs, and periodontal parameters were assessed using analysis of v

203 Periodontal parameters were significantly improved in th

204 therapy resulted in improvement in clinical periodontal parameters.

205 (TG) levels and gemfibrozil consumption with periodontal parameters.

206 ients) and related to the following clinical periodontal parameters: bleeding on probing, probing dep

207 Finally, the abundance of the periodontal pathogen Porphyromonas gingivalis trended wi

208 We found the periodontal pathogen Tannerella forsythia to be associat

209 Porphyromonas gingivalis (Pg) is a major periodontal pathogen that contains immunostimulatory com

210 s is a keystone pathogen that contributes to periodontal pathogenesis by disrupting host-microbe home

211 nflammatory cytokines that are important for periodontal pathogenesis using primary human gingival fi

212 ve patients with RA was found, importance of periodontal pathogenic bacteria and rheumatoid parameter

213 It is known that periodontal pathogens elicit host-derived immune respons

214 However, some periodontal pathogens have developed strategies to evade

215 The periodontal pathogens Pg, Pi, Tf, and Fn are associated

216 that growth of the PFOR-containing anaerobic periodontal pathogens, grown in both monospecies as well

217 ilable polymerase chain reaction test for 11 periodontal pathogens.

218 ely as a result of increased colonization of periodontal pathogens.

219 molecules will greatly benefit the future of periodontal patient care.

220 evaluated use of this therapy adjunctive to periodontal plastic surgery procedures.

221 rochete that inhabits the gingival sulcus or periodontal pocket.

222 r of the human oral microbiome that inhabits periodontal pockets and contributes to chronic periodont

223 t that local delivery of antimicrobials into periodontal pockets improve periodontal health.

224 o the age profile of patients in the typical periodontal practice.

225 lysis of 384 charts was completed from three periodontal practices across the east coast of Australia

226 Intermetropolitan comparisons of periodontal practices showed no statistically significan

227 sted on online sites appears problematic for periodontal practices, the author urges periodontists to

228 The periodontal probe is the gold standard tool for periodon

229 h novel photoacoustic imaging and a Williams periodontal probe.

230 ) + aspirin therapy has been shown to reduce periodontal probing depth (PD) and local inflammatory me

231 an levels, VEGF-A, and TNF-alpha levels with periodontal probing depth (PD).

232 vey (NHANES), including full-mouth, six-site periodontal probing, and attachment loss assessment.

233 The LCA method identified seven distinct periodontal profile classes (PPCs A to G) and seven dist

234 form a diverse microbiome regardless of the periodontal profile of patients.

235 Assigning a periodontal prognosis and determining the severity of pe

236 h to classify the periodontitis and assign a periodontal/prosthetic prognosis.

237 Periodontal regeneration can be defined as complete rest

238 ix derivative (EMD) has been used to promote periodontal regeneration, little is known of its effect

239 compared with previously reported results of periodontal regenerative surgery.

240 result in inadvertently biased filtering of periodontal reviews and subsequently poor performance in

241 The validity of using pretreatment Periodontal Screening and Recording (PSR) index sextant

242 Additionally, degree of periodontal severity was determined and recorded.

243 of teeth, bleeding score, plaque score, and periodontal severity with linear and ordinal logistic re

244 to conventional non-surgical treatment of a periodontal site would be advantageous.

245 d bacterial species between peri-implant and periodontal sites in the same individuals, suggesting si

246 ailable on NCFs associated with referrals to periodontal specialists.

247 CFs found to be associated with referrals to periodontal specialists.

248 ion (papillary bleeding index [PBI]); and 3) periodontal status (probing depth [PD], attachment loss

249 ive cohort study is to evaluate influence of periodontal status on changes of glycated hemoglobin (Hb

250 Patients with hypertriglyceridemia had worse periodontal status than healthy controls.

251 Periodontal status was assessed by measurement of probin

252 Periodontal status was examined in patients with severe

253 riodontitis shows a positive effect on their periodontal status.

254 luding bone loss that may weaken skeletal or periodontal strength.

255 investigated for renewal of lost supporting periodontal structures and tested for furcation defect t

256 tudy aims to assess compliance to supportive periodontal therapy (SPT) among patients treated with de

257 iologic effects of a two-phase antimicrobial periodontal therapy and tested microbiologic, clinical,

258 d better compliance than those without prior periodontal therapy experiences.

259 eatment and after completion of non-surgical periodontal therapy for 213 sextants in 38 patients by t

260 systemic antibiotic usage, with non-surgical periodontal therapy resulted in improvement in clinical

261 Periodontal therapy was successful in reducing clinical

262 Long-term microbiologic outcomes of periodontal therapy with adjunctive antibiotics either i

263 ilure or success 5 years after completion of periodontal therapy, none of the four strategies produce

264 ts to be initially treated with non-surgical periodontal therapy.

265 before and after completion of non-surgical periodontal therapy.

266 ccess needs after completion of non-surgical periodontal therapy.

267 al disease in smokers remains a challenge of periodontal therapy.

268 s remaining after completion of non-surgical periodontal therapy.

269 growing interest in the use of probiotics in periodontal therapy; however, until now, most research h

270 Prostaglandin (PG)E2 accumulates in inflamed periodontal tissue and induces receptor activator of nuc

271 nical attachment level-a measure of lifetime periodontal tissue destruction-was conducted in a large,

272 teeth to the alveolar bone, is essential for periodontal tissue homeostasis.

273 riodontal homeostasis and during the loss of periodontal tissue integrity as a result of periodontal

274 hodontic/dentofacial orthopedic treatment on periodontal tissues (i.e., alveolar bone) were included.

275 usion with associated risk on the supporting periodontal tissues (namely, dentoalveolar bone); and 3)

276 he underlying effects of tobacco products on periodontal tissues may be due to direct inhibition of n

277 These differences in the response of periodontal tissues to orthodontic force in the presence

278 n be defined as complete restoration of lost periodontal tissues to their original architecture and f

279 age caused by periodontitis not only affects periodontal tissues, but also increases the severity of

280 >4,000 chemical components that could affect periodontal tissues, less is understood about the effect

281 th factors that promotes restoration of lost periodontal tissues.

282 (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histopathologic examination of ging

283 ed studies dealing with mechanically induced periodontal trauma, has been available and potentially u

284 and tobacco use, diabetes mellitus, and past periodontal treatment (model 1: adjusted OR [aOR]: 1.4,

285 lymorphism and counting number of supportive periodontal treatment (SPT) visits.

286 Patients received standard non-surgical periodontal treatment at each time point as appropriate.

287 Patients who had received periodontal treatment demonstrated better compliance tha

288 ever, effect of locally delivered statins on periodontal treatment has not yet been systematically an

289 fication of these risk factors suggests that periodontal treatment may improve glycemic control of pa

290 a way to predict the outcome of non-surgical periodontal treatment on a site-specific basis.

291 ased guidelines on its necessity and use for periodontal treatment planning.

292 chronic or aggressive periodontitis received periodontal treatment supplemented with 375 mg amoxicill

293 (26 males and 27 females) undergoing initial periodontal treatment were used for this analysis.

294 itis (n = 11) were subjected to non-surgical periodontal treatment, whereupon changes in salivary CSF

295 esence of JP2 in individuals with LAgP after periodontal treatment.

296 creased remission after otherwise successful periodontal treatment.

297 thy controls (n = 39), and patients received periodontal treatment.

298 ted with impaired remission of disease after periodontal treatment.

299 eriodontitis and decreased with non-surgical periodontal treatment.

300 Periodontal wound healing has been accelerated by differ