ライフサイエンスコーパス: periodontal tissue

1 ithin their biological niche (inflamed human periodontal tissues).

2 of FOXP3(+) T regulatory (Treg) cells in the periodontal tissue.

3 ns in the destruction of the highly vascular periodontal tissue.

4 stem cells that could be used to regenerate periodontal tissue.

5 plications for repairing and/or regenerating periodontal tissue.

6 involve a local renin-angiotensin system in periodontal tissue.

7 periodontal surgery for the regeneration of periodontal tissue.

8 on the tooth surface and affect the adjacent periodontal tissue.

9 asts (HGF) derived from healthy and diseased periodontal tissue.

10 s unclear how angiogenin is regulated in the periodontal tissue.

11 etween bacteria and the host in healthy mice periodontal tissue.

12 to structural and physiological functions in periodontal tissue.

13 such as IL1B, IL6, and TNFa in the diseased periodontal tissue.

14 s IL1beta, IL6, and TNFalpha in the diseased periodontal tissue.

15 es, with only DTrp protecting both joint and periodontal tissue.

16 KL and increased BMP-2 and OPG levels in the periodontal tissue.

17 x immunoassay and ELISA in serum samples and periodontal tissues.

18 ost common esthetic concerns associated with periodontal tissues.

19 morbidities, possibly synergically affecting periodontal tissues.

20 n by >85% and decreased the T-cell number in periodontal tissues.

21 hment and cell motility of cells relevant to periodontal tissues.

22 sal forces may have a damaging effect on the periodontal tissues.

23 important participants in the destruction of periodontal tissues.

24 tory condition leading to the destruction of periodontal tissues.

25 rized by the inflammation and destruction of periodontal tissues.

26 acterized by inflammation and destruction of periodontal tissues.

27 f Periostin was also immunostained in murine periodontal tissues.

28 cell proliferation and revascularization in periodontal tissues.

29 ng development as well as in regeneration of periodontal tissues.

30 th factors in the repair and regeneration of periodontal tissues.

31 ibers, and new bone tissue similar to native periodontal tissues.

32 native treatment strategy to deliver BMPs to periodontal tissues.

33 design successful therapies for regenerating periodontal tissues.

34 so determine the levels of sIL-6r within the periodontal tissues.

35 mote significant anaplasis of the supporting periodontal tissues.

36 ion is significantly upregulated in inflamed periodontal tissues.

37 tions may be important during development of periodontal tissues.

38 f gene therapy for sustained PDGF release in periodontal tissues.

39 e periodontal microvasculature or within the periodontal tissues.

40 gulating inflammatory responses in the human periodontal tissues.

41 gulating inflammatory responses in the human periodontal tissues.

42 hat these proteins can be used to regenerate periodontal tissues.

43 evelopment, maintenance, and regeneration of periodontal tissues.

44 nd potentially important source of PGE(2) in periodontal tissues.

45 s play important roles in the homeostasis of periodontal tissues.

46 de trigger factors required for regenerating periodontal tissues.

47 o have significantly (P< or =0.05) healthier periodontal tissues.

48 ases between clinically healthy and inflamed periodontal tissues.

49 scalers which may cause injury to pulpal and periodontal tissues.

50 level reported as deleterious to pulpal and periodontal tissues.

51 l-ECM interactions, and thus in regenerating periodontal tissues.

52 propagation of T. denticola within inflamed periodontal tissues.

53 dult periodontitis and patients with healthy periodontal tissues.

54 ses necessary for repair and regeneration of periodontal tissues.

55 tabolic and immunoinflammatory parameters in periodontal tissues.

56 s are prevalent inflammatory diseases of the periodontal tissues.

57 However, excessive MMP may rapidly destroy periodontal tissues.

58 rier and locally delivered into the inflamed periodontal tissues.

59 th factors that promotes restoration of lost periodontal tissues.

60 AM20C is required for maintenance of healthy periodontal tissues.

61 nimize the potential effects of bone loss on periodontal tissues.

62 nomodulatory effects of PT in intestinal and periodontal tissues.

63 ately useful for the regenerative therapy of periodontal tissues.

64 may play a role in repair and homeostasis of periodontal tissues.

65 exacerbation of the inflammatory response in periodontal tissues.

66 to restore the structure and function of the periodontal tissues.

67 eated mice because of reduced osteoclasts in periodontal tissues.

68 a role in detrimental effects of smoking on periodontal tissues.

69 oc2-GFP reporter was reactivated in adjacent periodontal tissues 4 days after tooth avulsion injury.

70 ent at relatively high concentrations in the periodontal tissues after surgery.

71 Height of periodontal tissues also increased with the addition of

72 illus actinomycetemcomitans, also invade the periodontal tissue and are virulent organisms.

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

74 erived EVs in the immune microenvironment of periodontal tissue and their underlying regulatory mecha

75 ze for maximal inflammatory responses in the periodontal tissue and uncover a novel pharmacological t

76 y significant degree of bone fill within the periodontal tissues and also better results in terms of

77 f protective and destructive immunity in the periodontal tissues and facilitate the pathogenicity of

78 we detected GAL and GAL receptors in healthy periodontal tissues and in the proximity of blood vessel

79 successfully inhibit iPGE2 production in the periodontal tissues and in this way may help reduce post

80 modulating immunoinflammatory parameters in periodontal tissues and reducing periodontopathogens exp

81 an be detected in lipid extracts of diseased periodontal tissues and teeth of humans.

82 ay not trigger the regenerative potential of periodontal tissues and that it requires a combined inte

83 leptin receptor (LepR) regulates changes in periodontal tissues and that the overexpression of the r

84 The gingival epithelium protects periodontal tissues and the alveolar bone by maintaining

85 Heart blood, gingival and periodontal tissue, and hemimaxillae were collected.

86 l fibroblasts are the most abundant cells in periodontal tissue, and they play a role in maintaining

87 trumental for the successful regeneration of periodontal tissues, and thus events and modifiers of ce

88 to quantify the IL-6 levels in the serum and periodontal tissues, and to explore their association.

89 lationship with periodontopathic bacteria in periodontal tissue are examined.

90 that not all neutrophils trafficking through periodontal tissues are fully activated.

91 extracellular matrix molecules expressed in periodontal tissues are indeed substrates of FAM20C.

92 ent, the immune response of peri-implant and periodontal tissues, as assessed by cytokine levels in P

93 t EDNRA may function in the breakdown of the periodontal tissues associated with periodontitis by pro

94 ieve a selective chemoattraction of Tregs to periodontal tissues, attenuating experimental periodonti

95 port describes a case of rapidly progressive periodontal tissue breakdown and bone loss in an HIV-inf

96 ative stress has been linked to the onset of periodontal tissue breakdown and systemic inflammation,

97 It can be concluded that EA reduced periodontal tissue breakdown and the expression of some

98 Doxycycline helps to prevent periodontal tissue breakdown by inhibiting local and sys

99 adequate inflammatory response and exhibits periodontal tissue breakdown compatible with other model

100 Parstatin suppresses the periodontal tissue breakdown followed by experimental pe

101 ent matrix metalloproteinase (MMP)-dependent periodontal tissue breakdown in an animal model of perio

102 n apoptosis as part of a unique mechanism of periodontal tissue breakdown, in which novel proteinases

103 Furthermore, Bsp(-/-) mice have marked periodontal tissue breakdown, with a lack of acellular c

104 rders may confer increased susceptibility to periodontal tissue breakdown.

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

106 ated the root resorption volume and examined periodontal tissue cathepsin K, Runx2, TNF-alpha, and IL

107 itis is a chronic inflammation that destroys periodontal tissues caused by the accumulation of bacter

108 ence the progression/worsening of dental and periodontal tissue conditions of untreated GR defects.

109 Hence, we developed a model where periodontal tissue constructs (PTCs) are made by casting

110 approach offers a fundament for engineering periodontal tissue constructs with characteristic 3D mic

111 e defects in hyperglycemia may contribute to periodontal tissue damage by impairing the innate immune

112 e of reactive oxygen and nitrogen species in periodontal tissue damage, as well as in microbial killi

113 arriving in gingival exudates from inflamed periodontal tissues, degrades the acidic proline-rich sa

114 in significantly limits the ligature-induced periodontal tissue destruction (P <0.01).

115 Periodontal tissue destruction and local IL-6 synthesis

116 Periodontal tissue destruction and osteoclast numbers we

117 mineral density (BMD) and clinical signs of periodontal tissue destruction and tooth loss over a 2-y

118 Thus, much of the damage that occurs during periodontal tissue destruction can be attributed to IL-1

119 re + P. gingivalis) group, where significant periodontal tissue destruction characterized by attachme

120 ne mineral density and the clinical signs of periodontal tissue destruction in a large population of

121 response to the microorganism as factors in periodontal tissue destruction in children.

122 These findings suggest that severe periodontal tissue destruction in Papillon-Lefevre syndr

123 odontal microorganisms in the development of periodontal tissue destruction is still unclear.

124 ese data indicate that Pg infection worsened periodontal tissue destruction through specific pathogen

125 patterns of immune response operating toward periodontal tissue destruction), we are only beginning t

126 that diabetes is associated with accelerated periodontal tissue destruction, it remains unknown wheth

127 Periodontal tissue destruction, osteoclast number, and i

128 It is characterized by periodontal tissue destruction, progressively driven by

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

130 n inhibition of alveolar bone resorption and periodontal tissue destruction.

131 lar gingival enlargement with ulceration and periodontal tissue destruction.

132 ge into an overlapping clinical phenotype of periodontal tissue destruction.

133 to an excessive host response, resulting in periodontal tissue destruction.

134 CF), and elevated levels are associated with periodontal tissue destruction.

135 sorptive cytokine, have been associated with periodontal tissue destruction.

136 osteopenia may be a predisposing factor for periodontal tissue destruction.

137 easures of systemic bone mineral density and periodontal tissue destruction.

138 ify several molecules associated with active periodontal tissue destruction.

139 mmatory host response significantly provokes periodontal tissue destruction.

140 abis is emerging as a likely risk factor for periodontal tissue destruction.

141 Periodontal tissue dimensions were obtained by computed

142 We studied the effects of insulin in periodontal tissues during the state of obesity-induced

143 Periodontal tissues during tooth movement (OTM) in T1D a

144 demonstrate the first successful evidence of periodontal tissue engineering using ex vivo gene transf

145 h factor delivery offers a novel approach to periodontal tissue engineering.

146 hSG-MSCs could be a potential MSC source for periodontal tissue engineering.

147 hich, in turn, shapes the current concept of periodontal tissue engineering.

148 A goal for periodontal tissue engineering/regenerative medicine is

149 ogenitor cells, and matrices used in current periodontal tissue-engineering approaches.

150 RNA was extracted from periodontal tissue, examined by mRNA profiling, and furt

151 We found that P. gingivalis-infected mouse periodontal tissues expressed significantly more SFRP1 c

152 dase (MPO) activity of gingival tissues, and periodontal tissue expression of collagen type I, RUNX2,

153 aluated as an adjunct in the regeneration of periodontal tissues following periodontal disease.

154 /muOCT can characterize healthy and inflamed periodontal tissues for diagnosis and disease activity m

155 is a key transcription factor of dental and periodontal tissue formation and is involved in many mol

156 Human periodontal tissue from five healthy subjects, including

157 ntial importance of VSC in the transition of periodontal tissues from clinical health to gingivitis a

158 Periodontal tissues from Ifi204(-/-) mice were evaluated

159 The goals of this study were 1) to compare periodontal tissue gene expression in different clinical

160 Histologic evaluation of periodontal tissues generally has included only areas ad

161 ell as the influence of diabetes mellitus on periodontal tissues has been well documented.

162 lyses of inflammatory cells in PD with human periodontal tissue have generally focused on mRNA quanti

163 Periodontal tissues have been recently evaluated, but th

164 gh the detrimental effects of tobacco on the periodontal tissues have been reported extensively, litt

165 ise, procedures aimed at regeneration of the periodontal tissues have shown limited success.

166 gest that the mononuclear cells derived from periodontal tissues have the capacity to respond to comp

167 e indicates that wounds in alveolar bone and periodontal tissue heal faster and more efficiently in t

168 s jeopardized clinically and molecularly the periodontal tissue healing at least up to 1 year of foll

169 /subgingival direct composite restoration on periodontal tissue healing.

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

171 es no doubt that neutrophils are integral to periodontal tissue homeostasis and health.

172 vitamin D(3) and play a fundamental role in periodontal tissue homeostasis and inflammatory response

173 rimentation to dissect the role of miRNAs in periodontal tissue homeostasis and pathology.

174 ns in PDL and clarifies the role of PDLCs in periodontal tissue homeostasis and repair.

175 hension of the role of platelet signaling in periodontal tissue homeostasis.

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

177 r bone loss is a normal component of healthy periodontal tissue homeostasis.

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

179 ic (intestine and adipose tissue) and local (periodontal tissues) impact of probiotic therapy in rats

180 both the mRNA and protein levels in healthy periodontal tissue in mice.

181 dipokines may contribute to the breakdown of periodontal tissue in periodontitis by stimulating the e

182 930 and 1,325 nm, for structural analysis of periodontal tissue in porcine jaws.

183 PRF promotes regenerative ability within the periodontal tissues in Grade II furcation defects to a g

184 ate the molecular characteristics of healthy periodontal tissues in men and women as they age, using

185 findings suggest that PDL DPCs can organize periodontal tissues in the jaw, at the site of previousl

186 injection of AAV-shRNA-Atp6i/TIRC7 into the periodontal tissues in vivo protected mice from P. gingi

187 To date, attempts to regenerate functional periodontal tissues (including cementum) are largely uns

188 d a criterion for successful regeneration of periodontal tissues, including formation of periodontal

189 tal diseases that lead to the destruction of periodontal tissues--including periodontal ligament (PDL

190 onchial inflammation than those without such periodontal tissue infection.

191 correlation was found between the amount of periodontal tissue inflamed in the oral cavity and marke

192 are positively associated with the degree of periodontal tissue inflammation and destruction.

193 f cytokines that are known to be involved in periodontal tissue inflammation and osteoclastogenesis-s

194 inhibited LPS-induced alveolar bone loss and periodontal tissue inflammation in rats with MS.

195 ed the hypothesis that PA is associated with periodontal tissue inflammation promoting a greater syst

196 t may be suggested that PTX3 is related with periodontal tissue inflammation.

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

198 ls in inflamed periodontal tissues, restored periodontal tissue integrity, and enhanced osteogenesis

199 lts suggest that neuronal TRPV1 signaling in periodontal tissue is crucial for the regulation of oste

200 Periodontal tissue is innervated by abundant pain-sensin

201 ch smoking contributes to the destruction of periodontal tissue is not clear and cannot be attributed

202 by which smoking augments the destruction of periodontal tissue is not clear.

203 Homeostasis of healthy periodontal tissues is affected by innate and adaptive i

204 reased release of prostaglandins (PG) within periodontal tissues is considered to play a pathogenetic

205 Regeneration of periodontal tissues is one of the most important goals f

206 d in other organs, its physiological role in periodontal tissues is unclear.

207 nduced inflammatory disease mainly affecting periodontal tissues, leading to periodontal inflammation

208 >4,000 chemical components that could affect periodontal tissues, less is understood about the effect

209 se of this study is to assess alterations in periodontal tissue levels 6 months after CL surgery and

210 association was found between the extent of periodontal tissue loss and these thyroid-related marker

211 ore severe periodontal disease and increased periodontal tissue loss.

212 ant criterion for predictable restoration of periodontal tissues lost as a consequence of disease.

213 l surface; and 4. cytokines originating from periodontal tissues may alter respiratory epithelium to

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

215 Citrullination of proteins within inflamed periodontal tissues may provide an important link betwee

216 ic periodontitis (CP) and those with healthy periodontal tissues/mild gingivitis were included.

217 This periodontal tissue-mimicking microenvironment is a poten

218 In addition, histological analysis of periodontal tissues, myeloperoxidase (MPO) activity of g

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

220 sed by the comparable presence of dye in the periodontal tissues of both types of mice.

221 f the receptor and ligand is elevated in the periodontal tissues of patients with periodontitis.

222 Similarly, Il33 expression was higher in periodontal tissues of Porphyromonas gingivalis-infected

223 effects of orthodontic movement (OM) on the periodontal tissues of rats with ligature-induced period

224 assess the impact of the amount of inflamed periodontal tissue on the levels of systemic inflammator

225 al progenitor cells (DPCs) to form organized periodontal tissues on titanium implants would be a sign

226 ex vivo testing, eight subjects with healthy periodontal tissues or with Stage II to IV periodontitis

227 ased the number of inflammatory cells in the periodontal tissue (P <0.05).

228 actinomycetemcomitans increased LF levels in periodontal tissue (P = 0.01) and saliva (P = 0.0004) of

229 as to evaluate the positional changes of the periodontal tissues, particularly the biological width,

230 rons that innervate the dental pulp (DP) and periodontal tissues (PDL).

231 Therefore, in periodontal tissues pre-exposed to bisphosphonate, bacte

232 Previous results have suggested that periodontal tissue progenitors reside in perivascular ar

233 ts that use cell and gene therapy to enhance periodontal tissue reconstruction and its biomechanical

234 s been developed to promote tooth-supporting periodontal tissue regeneration and functional restorati

235 er proteins have also been used to encourage periodontal tissue regeneration and histological evaluat

236 no-bisphosphonate group, is known to enhance periodontal tissue regeneration by inhibiting osteoclast

237 ap-1+ PDLCs during periodontal injury showed periodontal tissue regeneration by PDLCs.

238 eta-tricalcium phosphate (bTCP) granules for periodontal tissue regeneration in a baboon model.

239 ding periosteum used as a barrier for guided periodontal tissue regeneration in interproximal bony de

240 c protein family, has been used to encourage periodontal tissue regeneration.

241 (PDLF) are responsible for wound healing and periodontal tissue regeneration.

242 tal periodontitis in rats and did not impair periodontal tissue repair, despite its antiangiogenic ef

243 ementum/PDL-like structure and contribute to periodontal tissue repair.

244 data indicated that Msx2 pathway influenced periodontal tissue response to experimental periodontiti

245 n therapy resulted in glycemic control and a periodontal tissue response to orthodontic forces that w

246 Periodontal tissue response was assessed by histomorphom

247 e number of SETD1-positive cells in inflamed periodontal tissues, restored periodontal tissue integri

248 abolic changes that can negatively influence periodontal tissues, resulting in impaired periodontal r

249 abolic changes that can negatively influence periodontal tissues, resulting in more prevalent and sev

250 Analysis of gene expression in periodontal tissue revealed that HFD and LPS injection c

251 plete periodontal examination, and blood and periodontal tissue samples were collected for quantifica

252 Intravenous blood and biopsy of periodontal tissue samples were taken on the third day.

253 In periodontal tissue sections, a significantly reduced apo

254 Periodontal tissue specimens were harvested at baseline,

255 tal regenerative therapies is to reconstruct periodontal tissues such as bone, cementum, and periodon

256 reported to be absent or reduced in diseased periodontal tissues, suggesting an imbalance between the

257 Periodontal tissue supports teeth in the alveolar bone s

258 unresolved chronic inflammation destroys the periodontal tissues that surround and support the teeth,

259 o-localized and express MMPs in the diseased periodontal tissue, the effect of interaction between th

260 ice may attenuate the damage caused by PE to periodontal tissues, the placenta, intestines, and anthr

261 These results indicate that in periodontal tissues there are unusual host-parasite inte

262 ired by the hierarchical structure of native periodontal tissues, tissue engineering technology provi

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

264 ular matrix and the local immune response of periodontal tissues to plaque antigens.

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

266 nflammatory process mediating destruction of periodontal tissues triggered by bacterial insult.

267 At periodontal tissues under repair, parstatin increased th

268 Then, periodontal tissue was collected and analyzed.

269 ession of HIF-1alpha, MMP-9, and NFkappaB in periodontal tissues was also evaluated through immunoflu

270 polymorphonuclear leukocyte infiltration in periodontal tissues was found in group HcP.

271 IF-1alpha, MMP-9, and NFkappaB expression in periodontal tissues was reduced in M101 gels treated mic

272 Revascularization of the periodontal tissues was studied following guided tissue

273 n clarithromycin concentrations in serum and periodontal tissue were 0.465 mug/mL and 2.61 mug/g, res

274 s 0, 3, 7 and 14, the pattern of OTM and the periodontal tissues were analyzed by micro-CT, histomorp

275 clinical human T-cell isolates from diseased periodontal tissues, where the presence of increasing IF