ライフサイエンスコーパス: periodontal tissue

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

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

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

4 plications for repairing and/or regenerating periodontal tissue.

5 periodontal surgery for the regeneration of periodontal tissue.

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

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

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

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

10 important participants in the destruction of periodontal tissues.

11 tory condition leading to the destruction of periodontal tissues.

12 rized by the inflammation and destruction of periodontal tissues.

13 acterized by inflammation and destruction of periodontal tissues.

14 cell proliferation and revascularization in periodontal tissues.

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

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

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

18 native treatment strategy to deliver BMPs to periodontal tissues.

19 design successful therapies for regenerating periodontal tissues.

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

21 mote significant anaplasis of the supporting periodontal tissues.

22 ion is significantly upregulated in inflamed periodontal tissues.

23 tions may be important during development of periodontal tissues.

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

25 e periodontal microvasculature or within the periodontal tissues.

26 gulating inflammatory responses in the human periodontal tissues.

27 gulating inflammatory responses in the human periodontal tissues.

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

29 evelopment, maintenance, and regeneration of periodontal tissues.

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

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

32 de trigger factors required for regenerating periodontal tissues.

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

34 ases between clinically healthy and inflamed periodontal tissues.

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

36 level reported as deleterious to pulpal and periodontal tissues.

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

38 propagation of T. denticola within inflamed periodontal tissues.

39 dult periodontitis and patients with healthy periodontal tissues.

40 ses necessary for repair and regeneration of periodontal tissues.

41 th factors that promotes restoration of lost periodontal tissues.

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

43 nomodulatory effects of PT in intestinal and periodontal tissues.

44 ately useful for the regenerative therapy of periodontal tissues.

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

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

47 eated mice because of reduced osteoclasts in periodontal tissues.

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

49 ost common esthetic concerns associated with periodontal tissues.

50 morbidities, possibly synergically affecting periodontal tissues.

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

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

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

54 Height of periodontal tissues also increased with the addition of

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

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

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

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

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

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

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

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

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

64 lationship with periodontopathic bacteria in periodontal tissue are examined.

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

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

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

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

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

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

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

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

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

74 Parstatin suppresses the periodontal tissue breakdown followed by experimental pe

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

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

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

78 rders may confer increased susceptibility to periodontal tissue breakdown.

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

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

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

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

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

84 Periodontal tissue destruction and local IL-6 synthesis

85 Periodontal tissue destruction and osteoclast numbers we

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

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

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

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

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

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

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

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

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

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

96 Periodontal tissue destruction, osteoclast number, and i

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

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

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

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

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

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

103 ify several molecules associated with active periodontal tissue destruction.

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

105 lar gingival enlargement with ulceration and periodontal tissue destruction.

106 Periodontal tissue dimensions were obtained by computed

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

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

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

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

111 A goal for periodontal tissue engineering/regenerative medicine is

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

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

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

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

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

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

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

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

120 Periodontal tissues have been recently evaluated, but th

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

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

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

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

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

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

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

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

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

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

131 930 and 1,325 nm, for structural analysis of periodontal tissue in porcine jaws.

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

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

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

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

136 onchial inflammation than those without such periodontal tissue infection.

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

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

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

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

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

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

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

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

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

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

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

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

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

150 >4,000 chemical components that could affect periodontal tissues, less is understood about the effect

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

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

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

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

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

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

157 This periodontal tissue-mimicking microenvironment is a poten

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 In periodontal tissue sections, a significantly reduced apo

184 Periodontal tissue specimens were harvested at baseline,

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

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

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

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

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

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

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

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

193 At periodontal tissues under repair, parstatin increased th

194 Then, periodontal tissue was collected and analyzed.

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

196 Revascularization of the periodontal tissues was studied following guided tissue

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

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