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 i-infective therapeutics to prevent or treat periodontal disease.

4 notion has to be tested in animal models of periodontal disease.

5 CCL2 MPs provides a novel approach to treat periodontal disease.

6 is study evaluated caspase-8, -9, and AIF in periodontal disease.

7 ich included other anaerobes associated with periodontal disease.

8 genera decreased in co-existing diabetes and periodontal disease.

9 nd immune system interactions in the case of periodontal disease.

10 udies) considered oral cancer; and 2 studied periodontal disease.

11 cal manipulation of these receptors to treat periodontal disease.

12 in the development and progression of human periodontal disease.

13 onsequence of exposure to tobacco and not to periodontal disease.

14 aring to differ between none/mild and severe periodontal disease.

15 ial diseases such as bacterial vaginosis and periodontal disease.

16 reening illness perceptions in patients with periodontal disease.

17 uggested that SEMA4D and PAD2 are related to periodontal disease.

18 for Oral Health (IPQ-R-OH) in patients with periodontal disease.

19 h metabolic disorders, may also be linked to periodontal disease.

20 est that these cells may be of importance in periodontal disease.

21 y event in the initiation and development of periodontal disease.

22 periodontal tissue integrity as a result of periodontal disease.

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

24 isting the early diagnosis and prevention of periodontal disease.

25 effect of therapeutic intervention for RA on periodontal disease.

26 dered as a potential inflammatory marker for periodontal disease.

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

28 ssociated with the LPS model of experimental periodontal disease.

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

30 al microbe implicated in the pathogenesis of periodontal disease.

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

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

33 oncomitant decrease in those associated with periodontal disease.

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

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

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

37 have an increased incidence and severity of periodontal disease.

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

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

40 ntify how providers can help patients manage periodontal disease.

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

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

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

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

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

46 maturation in regulating immune responses in periodontal disease.

47 possible involvement in the pathobiology of periodontal disease.

48 crease the activity of NLRP3 and IL-1beta in periodontal disease.

49 enetic neighbor, is strongly associated with periodontal disease.

50 ors represents a potential strategy to treat periodontal disease.

51 -1 has a pro-resorptive role in experimental periodontal disease.

52 t were associated with increased severity of periodontal disease.

53 al and systemic inflammation associated with periodontal disease.

54 verages could potentially impact the risk of periodontal disease.

55 m, is now a proposed diagnostic indicator of periodontal disease.

56 ied the association between sleep and severe periodontal disease.

57 ly beneficial in suppressing inflammation in periodontal disease.

58 o-be-realized potential for the treatment of periodontal disease.

59 lammatory tissue destruction associated with periodontal disease.

60 d oral disease endpoints, such as caries and periodontal disease.

61 sts a mechanism for systemic consequences of periodontal disease.

62 urs/night were less likely to exhibit severe periodontal disease.

63 (SLE) increase susceptibility to destructive periodontal diseases.

64 yielding new possibilities for treatment of periodontal diseases.

65 l studies would better clarify their role in periodontal diseases.

66 as tooth eruption and movement and also for periodontal diseases.

67 status is not significantly associated with periodontal diseases.

68 F-1alpha/VEGF pathway in the pathogenesis of periodontal diseases.

69 ion and tissue destruction that characterize periodontal diseases.

70 ts microbiota and increase susceptibility to periodontal diseases.

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

72 P; group-3: Non-diabetic individuals without periodontal diseases.

73 ve plaque accumulation increases the risk of periodontal diseases.

74 partite motif-containing (TRIM) proteins, in periodontal diseases.

75 (APE) are assumed to be more susceptible to periodontal diseases.

76 mically healthy individuals with and without periodontal diseases.

77 Fracture (39.5%), caries (26.3%), and periodontal disease (23.7%) were the most common causes

78 orders were haircoat disorders (411, 12.7%), periodontal disease (365, 11.3%), overgrown nails (234,

79 The most investigated outcomes were periodontal diseases (42%) and oral cancers (30%).

80 , medico-legal reasons, patient awareness of periodontal disease (47.3%), and lack of training (43.2%

81 ing the heterogeneity of case definitions of periodontal disease across studies, accounting for featu

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

83 A new classification of periodontal diseases aimed to identify periodontal disea

84 iversity differed between no/mild and severe periodontal disease, although considerable overlap was n

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

86 tween home use of flossing and prevalence of periodontal disease and caries in older adults.

87 studies have shown the relationship between periodontal disease and chronic kidney disease, but ther

88 cal conditions may worsen the course of both periodontal disease and CKD.

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

90 ndings show the importance of evaluating the periodontal disease and detecting herpesviruses in patie

91 with diagnosis and risk assessment for both periodontal disease and diabetes.

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

93 that oral diseases such as dental caries and periodontal disease and general health conditions such a

94 A possible association between periodontal disease and gestational diabetes has also be

95 uncontrolled BP, as well as with more active periodontal disease and greater changes in clinical para

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

97 Bacteria oligotypes associated with periodontal disease and health were determined by minimu

98 This study investigates the link between periodontal disease and incident CHD.

99 y, studies have shown an association between periodontal disease and multiple causes of ischemic stro

100 ntal bacteria may serve to functionally link periodontal disease and oral cancer.

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

102 ival crevicular fluid (GCF) in patients with periodontal disease and patients with healthy periodonti

103 itatively that low income is associated with periodontal disease and poor oral health-related quality

104 Periodontal disease and pregnancy outcomes have been cla

105 elated identically with clinical measures of periodontal disease and recorded similar post-treatment

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

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

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

109 icular fluid (GCF) in patients with advanced periodontal diseases and identify their association with

110 a striking association has been made between periodontal diseases and primary cancers in the absence

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

112 The index is referred to as the burden of periodontal diseases and tooth loss (BPT).

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

114 Redondovirus sequences were associated with periodontal disease, and abundances decreased with treat

115 that increased in abundance with increasing periodontal disease, and in diabetics relative to non-di

116 association has been reported between RA and periodontal disease, and Porphyromonas gingivalis, a kno

117 Currently, there is no therapy for reversing periodontal disease, and treatment is generally restrict

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

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

120 and disease, with specific focus on caries, periodontal diseases, and cancer.

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

122 Both dental caries and periodontal disease are mediated by synergistic interact

123 Dental caries and periodontal disease are together the most prevalent micr

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

125 Periodontal diseases are initiated by bacteria that accu

126 Periodontal diseases are of high prevalence globally and

127 studies of pregnant women have demonstrated periodontal disease as a risk factor for preterm birth,

128 was one of the first researchers to identify periodontal disease as a risk factor for various adverse

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

130 ollow-Up Study, who were healthy and free of periodontal disease at baseline (1986).

131 cally significantly associated with clinical periodontal disease at baseline, were examined with dise

132 a larger number of bacteria associated with periodontal disease at the end of the experiment compare

133 arried out using data from 517 patients with periodontal disease attending the dental clinic at the U

134 on of periodontal diseases aimed to identify periodontal disease based on a multidimensional staging

135 Smoking is a risk factor for periodontal disease because of its complex impact on the

136 Seven days after induction of periodontal disease, both groups were mated with healthy

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

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

139 is is supported by the fact that severity of periodontal disease (CAL) is associated with the presenc

140 Periodontal diseases can lead to chronic inflammation af

141 crobiome differed significantly across the 3 periodontal disease categories.

142 Maternal periodontal disease causes LBW, IR, activation of inflam

143 Disease risk and most thoughts about periodontal disease changed across time (P < 0.05).

144 ficantly associated with a specific stage of periodontal disease characterized by severe tooth loss,

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

146 erate/severe) (n = 55) according to the 2017 Periodontal Diseases Classification.

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

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

149 ) and their function were also identified in periodontal disease compared with health.

150 diabetics and increased with progression of periodontal disease compared with periodontally healthy

151 ecting subgingival calculus in patients with periodontal disease compared with photographic assessmen

152 accepted index that summarizes the burden of periodontal diseases, considering the number of teeth re

153 n addition to a positive association between periodontal disease, dental caries, and cocaine use, sel

154 d for several diseases and traits, including periodontal disease, dental caries, tooth agenesis, canc

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

156 ignificantly associated with the presence of periodontal disease during pregnancy.

157 d several key genera previously described in periodontal disease (e.g. Treponema and Filifactor) and

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

159 Flossers showed less periodontal disease, fewer dental caries, and loss of fe

160 re distributed into control and experimental periodontal disease groups.

161 Maternal periodontal disease has been linked to adverse pregnancy

162 Periodontal disease has been linked to coronary heart di

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

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

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

166 dontal behaviors, with low recurrence of the periodontal disease; however, obesity was related to inc

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

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

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

170 ntion targets to prevent systemic effects of periodontal disease if further studies establish a causa

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

172 Moreover, we induced periodontal disease in 2 animal models through inoculati

173 e the association between sleep duration and periodontal disease in a national US population study in

174 steoporosis or osteopenia is associated with periodontal disease in a population of adult women.

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

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

177 g that it may be a useful tool for screening periodontal disease in different populations; yet they h

178 resorption associated with ligature-induced periodontal disease in female rats.

179 inal study was to evaluate the recurrence of periodontal disease in obese and normal weight patients

180 anding of the oral microbiome in relation to periodontal disease in older adults is limited.

181 The aim was to assess the effects of periodontal disease in promoting liver fibrosis in a rat

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

183 tentially rejuvenate oral health and reverse periodontal disease in the elderly.

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

185 her chronic comorbidities, the prevalence of periodontal disease increases with aging.

186 In periodontal disease, inflammation, and microbial dysbios

187 atment strategies for CVD and may inform how periodontal disease influences CVD.

188 Periodontal disease involves an inflammatory destructive

189 evaluate in the adult offspring of rats with periodontal disease: IR, inflammatory pathways, DNA meth

190 This concept suggests that periodontal disease is a group of distinct conditions.

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

192 Periodontal disease is a significant health burden, caus

193 Periodontal disease is an age-associated disorder clinic

194 ne of the main infectious agents that causes periodontal disease is an anaerobic bacterium-Porphyromo

195 Periodontal disease is associated with metabolic syndrom

196 Tooth loss or periodontal disease is associated with systemic endothel

197 Biologically informed stratification of periodontal disease is both feasible and desirable.

198 us risk factors for oral cancer, among which periodontal disease is gaining increasing recognition.

199 A second shift in periodontal disease is taking place.

200 Periodontal disease is the chronic infectious disease of

201 Their potential involvement in periodontal disease is yet unknown.

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

203 Maternal periodontal disease leads to low birth weight (LBW), ins

204 lora within the oral cavity leads to chronic periodontal disease, local tissue destruction, and vario

205 Active periodontal disease may result in downregulation of infl

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

207 ersity were observed in relation to clinical periodontal disease measures.

208 emic inflammatory burden, which is common to periodontal disease, metabolic syndrome, and adverse pre

209 ion, using an in vivo P. gingivalis-mediated periodontal disease model, we show that JAK3 inhibition

210 ncrease in bacterial species associated with periodontal disease, more clinical attachment loss, and

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

212 rance of bacterial infection, wound healing, periodontal disease, neurogenic inflammation, and inflam

213 stemic human diseases such as dental caries, periodontal disease, obesity, and cardiovascular disease

214 l shift in our understanding of the basis of periodontal disease occurred early in the 2000s.

215 sleeping are 40% less likely to have severe periodontal disease (odds ratio [OR] = 0.6, P < 0.05), a

216 istributed into control offspring (CN-o) and periodontal disease offspring (PED-o) groups.

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

218 0 y, with particular focus on the effects of periodontal disease on 3 pathological conditions: cardio

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

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

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

222 of the relationship between sleep and severe periodontal disease (OR = 4.8, P < 0.05).

223 l health outcomes relating to dental caries, periodontal disease, or oral cancer.

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

225 ADAMTS-1 may play a role in advanced periodontal disease pathogenesis in correlation with tis

226 how variants of IFI16 and AIM2 contribute to periodontal disease pathogenesis may lead to treatment o

227 ey proinflammatory cytokines associated with periodontal disease pathogenesis.

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

229 ng and Self-Monitoring (GPS) intervention on periodontal disease patients' clinical and psychological

230 Periodontal disease (PD) has been suggested to be a risk

231 Periodontal disease (PD) is known to be associated with

232 ctive associations among Hp sero-positivity, periodontal disease (Pd), and infections with incident A

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

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

235 Recent epidemiological studies link Periodontal disease(PD) to age-related macular degenerat

236 Given the association between periodontal disease (PdD) and Alzheimer's disease (AD),

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

238 n the plaque biofilm of patients with severe periodontal disease, perturbs neutrophil function by mod

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

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

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

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

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

244 sociation between subgingival microbiota and periodontal disease progression in older women, for whic

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

246 med microbial relative abundances and 5-year periodontal disease progression was measured with genera

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

248 ct microbiota increased in both diabetes and periodontal disease progression, these genera decreased

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

250 The new classification of periodontal diseases recognizes the key role of the inte

251 However, their relationship with periodontal disease remains unclear.

252 administration preserves bone volume during periodontal disease, repairs bone defects surrounding de

253 Inflammatory conditions as they occur during periodontal disease result in unique histone methylation

254 Microbial dysbiosis that occurs in periodontal disease results from a hyperinflammatory sta

255 using human-associated 16S rRNA samples for periodontal disease, rheumatoid arthritis and inflammato

256 behavioral intervention using individualized periodontal disease risk communication, with or without

257 ospectively, with adjustment for established periodontal disease risk factors.

258 eived an individualized calculation of their periodontal disease risk using only the Previser Risk Ca

259 questionnaire items with respect to clinical periodontal disease severity.

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

261 Here, we highlight studies indicating that periodontal disease significantly increases the risk of

262 , but smaller than the effect of gingivitis, periodontal disease, smoking, caries, and other clinical

263 Periodontal disease status and salivary cytokine levels

264 Differences according to periodontal disease status were determined by analysis o

265 the taxa differing in abundance according to periodontal disease status, 53% had multiple oligotypes

266 ered significantly in abundance according to periodontal disease status.

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

268 with oxidative stress; however, its role in periodontal disease still remains elusive.

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

270 tions seeking to unveil the genomic basis of periodontal disease susceptibility.

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

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

273 This is particularly true of periodontal diseases that relate to many systemic diseas

274 sideration of the extent and severity of the periodontal diseases, the distribution of affected teeth

275 Because apoptosis is involved in periodontal disease, this study evaluated caspase-8, -9,

276 tion and infection is critical for combating periodontal disease to improve overall health outcomes.

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

278 es globally are dental caries (tooth decay), periodontal disease, tooth loss, and cancers of the lips

279 ngoing clinical trial testing the benefit of periodontal disease treatment as a strategy to reduce ri

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

281 he biogenesis and function of these critical periodontal disease virulence factors.

282 revalence of none/mild, moderate, and severe periodontal disease was 25.1%, 58.3%, and 16.6%, respect

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

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

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

286 The extent/severity or absence of periodontal disease was noted using two different case d

287 One of the hallmark features of destructive periodontal disease, well documented over the last 50 y,

288 st of the genera known to be associated with periodontal disease were also identified in healthy cats

289 Presence and severity of periodontal disease were defined by Centers for Disease

290 The parameters of periodontal disease were evaluated.

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

292 and their oligotypes in health and levels of periodontal disease were investigated in this study on o

293 healthy, male, young BR-1 minipigs, with no periodontal disease were treated.

294 resorption associated with the experimental periodontal disease; whereas in vitro macrophage inflamm

295 and a "keystone pathogen" that causes severe periodontal disease, which is among the most prevalent i

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

297 These parameters are related to periodontal diseases, which are directly and indirectly

298 ani as adjuvant therapy in the management of periodontal diseases, whose efficacy will need to be tes

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

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