ライフサイエンスコーパス: gingiva

1 sion compared with those with thick and wide gingiva.

2 lative deepithelialization of hyperpigmented gingiva.

3 of obesity-induced insulin resistance in the gingiva.

4 of metastatic cells to chronically inflamed gingiva.

5 control sites regarding the thickness of the gingiva.

6 ration of melanocytes from the adjacent free gingiva.

7 n the modulation of inflammatory response in gingiva.

8 ially expressed between healthy and diseased gingiva.

9 r levels of MMP-9 and IL-1beta expression in gingiva.

10 h amounts of 15d-PGJ(2) were observed in the gingiva.

11 ptor 3-Ig (K14) mice that lack lymphatics in gingiva.

12 y responses after bacterial challenge of the gingiva.

13 xpressed by > 2-fold in diseased vs. healthy gingiva.

14 atched the color and texture of the adjacent gingiva.

15 erapy for augmenting the zone of keratinized gingiva.

16 highest values found in the buccal attached gingiva.

17 most up- and downregulated miRNAs in healing gingiva.

18 gingiva compared with the sites with thicker gingiva.

19 r levels in inflamed gingiva than in healthy gingiva.

20 al sulcular depth within healthy or inflamed gingiva.

21 type 1, a benign overgrowth condition of the gingiva.

22 ngival mass involving the anterior maxillary gingiva.

23 affects the oral cavity, most frequently the gingiva.

24 layer of inflamed gingiva but not in healthy gingiva.

25 er cytokines were similar to those in normal gingiva.

26 onse was present within chronically inflamed gingiva.

27 fusion was evaluated at labial LLLI attached gingiva.

28 ntribute to elevated NSAID levels in healthy gingiva.

29 enhancing their redistribution from blood to gingiva.

30 major source of IL-17-producing cells in the gingiva.

31 isions were initiated within the keratinized gingiva.

32 of fluoroquinolones and tetracyclines to the gingiva.

33 atients had a minimum of 4 mm of keratinized gingiva.

34 t galactose-deficient IgG-producing cells in gingiva.

35 lap design is carried out within keratinized gingiva.

36 sed concentrations of IL-12, within diseased gingiva.

37 cisional biopsy of the lesion on the lingual gingiva.

38 is is a case report of PSCC occurring on the gingiva.

39 roblasts could enhance their distribution to gingiva.

40 ent an unusual case of PSCC occurring on the gingiva.

41 eurofibromas in the connective tissue of the gingiva.

42 ment of maxillary and mandibular keratinized gingiva.

43 e review the literature on metastases to the gingiva.

44 nic scaler, hot food, and ice) injury to the gingiva.

45 rs of both the JSGH and that of the marginal gingiva.

46 ffected gingival tissues compared to healthy gingiva.

47 cated white lesions confined to the marginal gingiva.

48 cells and tones homeostatic immunity at the gingiva.

49 ed or generalized enlargement of keratinized gingiva.

50 e association of T. forsythia with the human gingiva.

51 upregulation of SERPINB1 and IL33 in healing gingiva.

52 data from healthy and periodontitis-affected gingiva.

53 udy, 17 had periodontitis and 15 had healthy gingiva.

54 s with normal blood sugar levels and healthy gingiva.

55 as it was 1.02 for the patients with healthy gingiva.

56 expressions of MMP-2, MMP-9, and EMMPRIN in gingiva.

57 pithelial-to-mesenchymal transition (EMT) in gingiva.

58 significant influence on the color of human gingiva.

59 ing inhibits beta-catenin degradation in the gingiva.

60 eir ability to augment keratinized tissue or gingiva.

61 al grafting to increase the zone of attached gingiva?

62 ncentrations in healthy control and inflamed gingiva (2.4 and 3.0 microg/g, respectively) were signif

63 ), spleen (7.3%), liver (5.3%), skin (4.5%), gingiva (4.4%), and CNS (1.1%).

64 surveillance at a specific oral barrier, the gingiva - a constantly stimulated and dynamic environmen

65 oclast activation, bacterial invasion of the gingiva, a greater propensity for the bacteria to dissem

66 gnals balance immunity and regulation at the gingiva, a key oral barrier, remains minimally explored.

67 ed a new population of stem cells from human gingiva, a tissue source easily accessible from the oral

68 concentrations were significantly greater in gingiva adjacent to > or = 6 mm pockets than in tissues

69 Within gingiva adjacent to >6 mm sulci, IL-6 concentrations wer

70 classified as "diseased, moderate" (DM); and gingiva adjacent to >6-mm sulci was classified as "disea

71 IFN-gamma concentrations were higher within gingiva adjacent to 3 to 6 mm diseased compared to norma

72 al sulcus) and diseased gingiva (hemorrhagic gingiva adjacent to a > or = 3 mm periodontal pocket) we

73 f both cytokines were significantly lower in gingiva adjacent to a > or = 6 mm pocket.

74 Biopsies from healthy (non-hemorrhagic gingiva adjacent to a < or = 3 mm gingival sulcus) and d

75 Gingiva adjacent to a <or=3-mm sulcus without BOP was cl

76 without BOP was classified as "normal" (N); gingiva adjacent to a 3-mm sulcus with BOP was classifie

77 P was classified as "diseased, slight" (DS); gingiva adjacent to a 4- to 6-mm sulcus featuring BOP wa

78 standard of care for increasing keratinized gingiva adjacent to teeth that do not require root cover

79 ession of no genes detectably changed in the gingiva after infection.

80 us (SIV) was nontraumatically applied to the gingiva after moderate gingivitis was identified through

81 te: 1) test site showing absence of attached gingiva (AG) associated with gingival recession (GR) tre

82 n lingual and buccal aspects of the attached gingiva, alveolar mucosa, and buccal mucosa to gain insi

83 gammadeltaT cells also reside in the gingiva, an oral tissue covered with specialized epithel

84 revealed generalized melanosis of the buccal gingiva and a lack of keratinized tissue around implants

85 al case of myeloid sarcoma presenting in the gingiva and affected by drug-induced gingival enlargemen

86 ucts (RAGE), are upregulated within inflamed gingiva and are responsible for initiation of detrimenta

87 associated with the thickness of both labial gingiva and bone.

88 ion of the clinical thickness of both labial gingiva and bone.

89 ial hyperplasia and inflammation of both the gingiva and esophagus.

90 phenotype according to the width of attached gingiva and gingival thickness.

91 utrophil defensin-1 (HNP-1) through HNP-3 in gingiva and in neutrophil extract-treated epithelial cel

92 junctional epithelium of clinically healthy gingiva and in the pocket epithelium of gingiva with per

93 gerin mRNAs are more highly expressed in the gingiva and interleukin-1 mRNA is more highly expressed

94 ratocyst localized to the maxillary anterior gingiva and its differential diagnosis.

95 ere were no differences between masticatory (gingiva and palate) and other mucosa (P >0.05).

96 it grafts (palatal tissue involving marginal gingiva and papillae) compared with conventional palatal

97 Human gingiva and periodontal fibroblasts were exposed to the

98 ct the expression of fibrogenic molecules in gingiva and promote gingival overgrowth.

99 e resistant mice, interleukin-15 mRNA in the gingiva and Selp mRNA in the spleen are present at highe

100 from patients with CP and those with healthy gingiva and show that MNC from CP subjects have a reduce

101 adrants and on the hard palate (eight on the gingiva and six on the palate).

102 eratinocytes were isolated from normal human gingiva and skin and grown in 3-D cultures for up to 42

103 We compared CD26 expression in human gingiva and skin and in gingival and hypertrophic-like s

104 y of immunological genes was measured in the gingiva and spleen of these mice by quantitative reverse

105 -expressing mast cells are present in normal gingiva and that their numbers are elevated in patients

106 nalysis, it is possible to identify the free gingiva and the attached gingiva, the calculus depositio

107 thoma affecting the maxillary and mandibular gingiva and the hard palate.

108 asminogen activation by fibroblasts from the gingiva and the periodontal ligament under basal conditi

109 al RNA transcription of a 48-gene set in the gingiva and the spleen and the subsequent changes in gen

110 -1 mRNA is more highly expressed in both the gingiva and the spleens of susceptible mice than resista

111 st to report on the miRNome of healing human gingiva and to provide an integrative analysis of miRNA/

112 losed six new pigmented lesions (four on the gingiva and two on the hard palate), clinically identica

113 study is to determine the dimensions of the gingiva and underlying alveolar bone in the maxillary an

114 lesion involving the free gingiva, attached gingiva, and alveolar mucosa.

115 hment level, GR height, width of keratinized gingiva, and assessment of gingival biotype.

116 GR dimensions, amount of keratinized gingiva, and clinical attachment level were evaluated.

117 Group 1 included 30 individuals with healthy gingiva, and group 2 included 30 patients with CP.

118 only cases metastasizing in the oral mucosa, gingiva, and periodontium were included.

119 pairs connective tissue formation in healing gingiva, and that impaired healing is associated with fa

120 ons were significantly higher than in normal gingiva, and the concentrations of the other cytokines w

121 OSF showed significant changes in affected gingiva, and the presence of comet cells in all the pati

122 focused on three mucosal sites: the gut, the gingiva, and the respiratory tree.

123 e body, including the skin, intestine, lung, gingiva, and uterus.

124 matory cytokines emanating from the inflamed gingiva are suspected mechanisms linking periodontitis a

125 Traumatic lesions of the gingiva are thought to be highly prevalent, yet the peri

126 was referred for augmentation of keratinized gingiva around implants at the right and left maxillary

127 technique to increase the amount of attached gingiva around teeth, but this technique requires the su

128 porting literature to understand the role of gingiva around teeth.

129 Gingiva as a functional unit is unique with a specific v

130 nty-five patients with insufficient attached gingiva associated with at least two teeth in contralate

131 wing absence or a reduced amount of attached gingiva associated with gingival recession (GR) at basel

132 64 sites (test group), with lack of attached gingiva associated with recessions, were treated with ma

133 adjacent tissue, a 1-mm width of keratinized gingiva at 6 months, patient treatment preference, surgi

134 of the LCC to regenerate >/=2 mm keratinized gingiva at 6 months.

135 The concentration of caspase-3 in female gingiva at all diseased sites was significantly greater

136 Spectral reflection of keratinized gingiva at upper central incisors was measured by spectr

137 ocalized pigmented lesion involving the free gingiva, attached gingiva, and alveolar mucosa.

138 rove patient quality of life, by keratinized gingiva augmentation and impact on physical disability,

139 with a round yellow nodule on the maxillary gingiva between the left canine and first premolar.

140 rochloride] (20 mug/mL) was dripped onto the gingiva between the mandibular incisors.

141 OSCC often affects upper and lower gingiva, buccal mucous membrane, the retromolar triangle

142 ed in the basal epithelial layer of inflamed gingiva but not in healthy gingiva.

143 ange and color distribution of healthy human gingiva by age, gender and ethnicity.

144 CsA could induce Type 2 EMT in gingiva by changing the morphology of epithelial cells a

145 n exuberant papillomatous enlargement of the gingiva by gestational day 110, with the most prominent

146 derived from periodontal ligament (PDL) and gingiva can be used for the development of cell-based re

147 variables -- changes in width of keratinized gingiva, changes in bucco-lingual width, and vertical bo

148 o analyze cases of metastatic lesions to the gingiva compared with cases metastasizing to other oral

149 recession was higher at the sites with thin gingiva compared with the sites with thicker gingiva.

150 To ascertain if the gingiva contained specific estrogen-sensitive cell popul

151 MSCs derived from PDL and gingiva demonstrated multipotent characteristics, sugges

152 ased sites was significantly greater than in gingiva derived from male sites (P <0.05).

153 n to determine whether substitution of human gingiva-derived mesenchymal stem cells (G-MSCs) would si

154 of extracellular vesicles (EVs) released by gingiva-derived mesenchymal stem cells (GMSC-EVs) on oxi

155 ily accessible from the oral cavity, namely, gingiva-derived mesenchymal stem cells (GMSCs), which ex

156 ell-like phenotypes, render oral mucosa- and gingiva-derived MSCs a promising alternative cell source

157 s study, we demonstrate that even though the gingiva develops after birth, the majority of gingival g

158 The gingiva displayed no signs of inflammation and was tight

159 vergrowth is the enlargement of the attached gingiva due to an increased number of cells.

160 tion and was found to be up-regulated in the gingiva during the resolution of periodontal inflammatio

161 patients, on selected neutral proteinases in gingiva, enzymes believed to mediate periodontal breakdo

162 n of MSCs derived from human oral mucosa and gingiva, especially their immunomodulatory and anti-infl

163 use pigmentation of the maxillary vestibular gingiva extending to the second premolar areas, without

164 ngival recession; and 5) band of keratinized gingiva for each of the six anterior mandibular teeth (#

165 e to support maintaining an adequate band of gingiva for intracrevicular margin restoration.

166 scribes a method for coronally repositioning gingiva for root coverage over the maxillary central inc

167 dominated the cellular immune compartment in gingiva from all groups, and B cells were relatively rar

168 The gingiva from around the molars was dissected and submitt

169 va, so we evaluated its concentration within gingiva from normal sites and sites of chronic periodont

170 After removing the mucosa and keratinized gingiva from the test site, either an LCC or FGG was app

171 isoforms were significantly increased in the gingiva from ZF rats compared with those from ZL rats.

172 of insulin on Akt and eNOS activation in the gingiva from ZF rats.

173 er time, progress to extensively involve the gingiva fulfilling the criteria for proliferative verruc

174 s of the periodontal ligament (PDLF) and the gingiva (GF) in monolayer and spheroid cultures were exp

175 es were collected from 223 dogs with healthy gingiva, gingivitis and mild periodontitis with 72 to 77

176 ulation of mesenchymal stem cells from human gingiva (GMSCs), which has many advantages over BMSCs, c

177 Thickness of the gingiva, GR, and percentage of root coverage (PRC) were

178 t may be less significant in palatal/lingual gingiva >3.0 mm.

179 e) that accumulates on teeth adjacent to the gingiva (gums).

180 In addition, the thickness of the labial gingiva had a moderate association with the underlying b

181 ity compositions: buccal mucosa, keratinized gingiva, hard palate; saliva, tongue, tonsils, throat; s

182 epth (RD), recession width (RW), keratinized gingiva height measured apico-coronally (KG), relative a

183 a < or = 3 mm gingival sulcus) and diseased gingiva (hemorrhagic gingiva adjacent to a > or = 3 mm p

184 ce of Th17 and Treg-related mediators in the gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-beta an

185 , the LCC regenerated >/=2 mm of keratinized gingiva in 95.3% of patients (81 of 85 patients; P <0.00

186 suggest that VEGF expression is increased in gingiva in experimentally induced diabetes.

187 we found that Th17 cells can develop at the gingiva independently of commensal microbiota colonizati

188 Histological assessment of HGF gingiva indicated increased numbers of fibroblasts (30%)

189 nd three-dimensional OCT images of the tooth/gingiva interface were performed, and measurements of th

190 The possible DNA damage on affected gingiva is also one of the objectives of the present stu

191 literature review of melanoacanthoma of the gingiva is also provided.

192 gingival augmentation when the dimension of gingiva is inadequate.

193 Our results show that healthy gingiva is infiltrated with cells expressing all HIV-1 r

194 ithelia, our knowledge on these cells in the gingiva is still incomplete.

195 Gingiva is supplied with lymphatics that drain interstit

196 The gingiva is the most common site for metastases to oral s

197 abeling, we show that the human oral mucosa (gingiva) is infiltrated by large numbers of TLR2(+) and

198 ared to the mean width of buccal keratinized gingiva (KG) of adjacent teeth.

199 Width of keratinized gingiva (KG) was determined at baseline and at 16 weeks.

200 ue thickness (GTT), and width of keratinized gingiva (KG) were assessed at baseline, and 3 and 6 mont

201 , recession width (RW), width of keratinized gingiva (KW), clinical attachment level (CAL), probing d

202 on that is abundant in human skin but not in gingiva may drive the profibrotic response leading to ex

203 Potentially malignant lesions of the gingiva may frequently present as well-demarcated white

204 biotype with an adequate band of keratinized gingiva, Miller Class I mucogingival defects, and a broa

205 olation of human stem cells from the PDL and gingiva, multilineage differentiation of those cells, an

206 0) were analyzed among patients with healthy gingiva (n = 176) and patients with CP (n = 177).

207 an mode of delivery in some body sites (oral gingiva, nares and skin; R(2) = 0.038), this was not tru

208 s multiple body sites, including stool, oral gingiva, nares, skin and vagina were collected for each

209 n of inflammatory and apoptotic mediators in gingiva obtained from normal and diseased sites of perio

210 sed MMP and other neutral proteinases in the gingiva of CP patients.

211 onocytes/macrophages in peripheral blood and gingiva of healthy individuals and patients with CP.

212 1 infection, we analyzed expression in human gingiva of HIV-1 receptors Langerin, DC-SIGN, MR, and Ga

213 performed on the furcation region and mesial gingiva of mandibular first molars to measure periodonta

214 ncreased DNA methylation was observed in the gingiva of mice infected with P. gingivalis in a periodo

215 zed the mucosal immune cells in the inflamed gingiva of mice with alveolar bone reduction.

216 ytes/macrophages in the peripheral blood and gingiva of patients with CP.

217 istribution profile of clarithromycin in the gingiva of patients with periodontitis compared to serum

218 n and function of immune cells isolated from gingiva of people who had PD and were systemically healt

219 and IgG locally produced by plasma cells in gingiva of periodontal disease patients, display altered

220 This study examines the hypothesis that the gingiva of rats fed a calorie-restriction (CR) diet expr

221 diet expresses lower levels of RAGE than the gingiva of rats fed an ad libitum (AL) diet.

222 f the susceptible BALB/cByJ mice than in the gingiva of resistant A/J mice.

223 dvanced glycation end products (RAGE) in the gingiva of smokers and triggers the proinflammatory effe

224 examination revealed a cystic lesion in the gingiva of the mandibular canine-premolar area.

225 is factor alpha (Tnf) mRNA was higher in the gingiva of the susceptible BALB/cByJ mice than in the gi

226 thickness wounds were created in the palatal gingiva of type 1 and type 2 diabetic and normoglycemic

227 ow estrogen affects cellular function in the gingiva of women.

228 nct clinicopathological entity of the buccal gingiva of young patients which has been related to seve

229 injection of CD40L and CpG into the palatal gingiva on days 3, 6, and 9.

230 ematous, papillary appearance of the lingual gingiva on teeth #27, #28, and #29.

231 Samples of the marginal gingiva on the contralateral side of the implant were ta

232 lly located in plaque, others in keratinized gingiva or buccal mucosa, and some oligotypes were chara

233 dental bone between individuals with healthy gingiva or moderate periodontitis using digital images.

234 showed differential basal expression in the gingiva or spleens (or both).

235 r within normal gingiva than within diseased gingiva (P <0.001).

236 re lower within diseased than within healthy gingiva (P <0.001).

237 al treatment and changes in the width of the gingiva (P = 0.481).

238 ts were analyzed based on anatomic location (gingiva, palate, and other mucosa), there was no differe

239 f RANKL(+)CD4(+) T-cells in GMCs of inflamed gingiva peaked 15 days after infection.

240 , a previously unrecognized lack of attached gingiva, pretibial hyperpigmentation, skin and vascular

241 ings showed that LCS-treated sites resembled gingiva rather than alveolar mucosa.

242 The gingiva regenerated with the LCC matched the color and t

243 ast to the skin and gut, we demonstrate that gingiva-resident T helper 17 (Th17) cells developed via

244 Microscopic examination of the thickened gingiva revealed surface stratified squamous epithelium

245 Analysis of the gingiva showed that insulin-induced phosphorylation of I

246 Width of keratinized gingiva significantly increased after IMITG (WDKG, 1.27

247 ase in this index (GIPI) at a given attached gingiva site could indicate, respectively, the clinical

248 IL)-23 has not been reported within inflamed gingiva, so we evaluated its concentration within gingiv

249 eeds and the reformation of the supraosseous gingiva (SOG).

250 , TRAP-5b, and calcium levels were measured, gingiva specimens were extracted for IL-1beta and IL-10

251 HGFs were primary cultured from human gingiva specimens.

252 tu studies performed on diseased and healthy gingiva suggest that a similar pattern of endotoxin tole

253 ely low IL-15 concentrations within diseased gingiva suggest that IL-15 might have anti-inflammatory

254 and matrix metalloproteinase 9 (Mmp9) in the gingiva; support and alveolar bone loss; connective tiss

255 indicates that subjects with thin and narrow gingiva tend to have more gingival recession compared wi

256 an serum and reach higher levels in inflamed gingiva than in healthy gingiva.

257 Clarithromycin can attain higher levels in gingiva than serum and reach higher levels in inflamed g

258 Clarithromycin can attain higher levels in gingiva than serum of patients with periodontitis.

259 expected, the FGG generated more keratinized gingiva than the LCC (4.57 +/- 1.0 mm versus 3.2 +/- 1.1

260 ons were significantly greater within normal gingiva than within diseased gingiva (P <0.001).

261 Gingiva that is prone to inflammation may serve as a pre

262 JSGH is a reactive tumor of the gingiva that may have an odontogenic etiology, whose ori

263 o identify the free gingiva and the attached gingiva, the calculus deposition over tooth surfaces, an

264 dantly CD26-positive fibroblasts, whereas in gingiva they were rare.

265 Because fibroblasts are prevalent in gingiva, they may help sustain therapeutic fluoroquinolo

266 received LPS injections to the palatal molar gingiva three times per week for 4 weeks to establish pe

267 als received injections to the palatal molar gingiva three times per week for 8 weeks.

268 of VX lesions from the oral cavity (six from gingiva, three from palate, and seven from other mucosa)

269 After tissue processing, interdental gingiva tissues were exhaustively sectioned into 4-mum-t

270 and verrucoid and spread along the marginal gingiva to encircle the tooth.

271 ously published genomes recovered from human gingiva to gain perspective on evolutionary relationship

272 -13 and -15 within healthy or inflamed human gingiva to gingival sulcular depth and the concentration

273 Results confirm the keratinized gingiva to have increased tensile strength (3.94 +/- 1.1

274 ractices that involve direct exposure of the gingiva to noxious chemicals and additives.

275 Accumulation of Th17 cells at the gingiva was driven in response to the physiological barr

276 Gingiva was grouped by the depth of the adjacent gingiva

277 Gingiva was obtained from 110 human donors before extrac

278 Gingiva was obtained prior to extraction of teeth.

279 Diseased gingiva was subdivided into 3, 4 to 6 and >6 mm groups.

280 The gingiva was the most common site (60.4%), followed by to

281 ndex score (WDPIS), and width of keratinized gingiva (WDKG) between initial and last measurements wer

282 ide synthase (iNOS) messenger (m)RNAs in the gingiva were determined by reverse-transcription polymer

283 Blood was then drawn, and samples of gingiva were harvested from both sites.

284 ing sufficient zones of attached keratinized gingiva were randomly assigned to soft tissue surgery pl

285 CP]) and 15 volunteers who exhibited healthy gingiva were recruited.

286 ex, age, and the apico-coronal height of the gingiva were related to buccal bone thickness.

287 al ridge dimension, and width of keratinized gingiva were the esthetic outcomes reviewed.

288 ut gingival recession (GR) and with attached gingiva, were left untreated.

289 f IL-10-producing CD4(+) T-cells in inflamed gingiva when compared with the control group.

290 = 50) consisted of individuals with healthy gingiva, whereas the other group consisted of patients w

291 of JSGH and the basal layer of the marginal gingiva, while expression of CK14 was present in all epi

292 and upper lip that readily reveal the upper gingiva, widely spaced teeth, and a broad nasal tip.

293 The samples were divided into two groups: gingiva with 1% taurine-hydrated collagen membrane (n =

294 s of IL-18 within diseased and healthy human gingiva with concentrations of other T(H)1 and T(H)2 cyt

295 s IL-6, MMP-1, and MMP-9 immunoexpression in gingiva with induced periodontal disease (PD).

296 lthy gingiva and in the pocket epithelium of gingiva with periodontitis.

297 All patients achieved >/=1 mm keratinized gingiva with the LCC treatment by 6 months, and more pat

298 detected both Wnt5a and sFRP5 mRNA in human gingiva, with Wnt5a dominating in diseased and sFRP5 in

299 recession height (RH), width of keratinized gingiva (WKG) and assessment of gingival biotype.

300 Clinical parameters (width of keratinized gingiva [WKG], facial soft tissue level [FST], papilla i