ライフサイエンスコーパス: gingiva

1 control sites regarding the thickness of the gingiva.

2 ration of melanocytes from the adjacent free gingiva.

3 n the modulation of inflammatory response in gingiva.

4 ially expressed between healthy and diseased gingiva.

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

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

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

8 y responses after bacterial challenge of the gingiva.

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

10 atched the color and texture of the adjacent gingiva.

11 erapy for augmenting the zone of keratinized gingiva.

12 highest values found in the buccal attached gingiva.

13 cells and tones homeostatic immunity at the gingiva.

14 ed or generalized enlargement of keratinized gingiva.

15 r levels in inflamed gingiva than in healthy gingiva.

16 al sulcular depth within healthy or inflamed gingiva.

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

18 ngival mass involving the anterior maxillary gingiva.

19 affects the oral cavity, most frequently the gingiva.

20 layer of inflamed gingiva but not in healthy gingiva.

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

22 er cytokines were similar to those in normal gingiva.

23 onse was present within chronically inflamed gingiva.

24 fusion was evaluated at labial LLLI attached gingiva.

25 ntribute to elevated NSAID levels in healthy gingiva.

26 enhancing their redistribution from blood to gingiva.

27 isions were initiated within the keratinized gingiva.

28 of fluoroquinolones and tetracyclines to the gingiva.

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

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

31 lap design is carried out within keratinized gingiva.

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

33 cisional biopsy of the lesion on the lingual gingiva.

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

35 roblasts could enhance their distribution to gingiva.

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

37 eurofibromas in the connective tissue of the gingiva.

38 ment of maxillary and mandibular keratinized gingiva.

39 e review the literature on metastases to the gingiva.

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

41 proliferation and differentiation within the gingiva.

42 ysical, and thermal injuries may involve the gingiva.

43 acerbation of reactive lesions involving the gingiva.

44 roblasts isolated from untreated oral mucosa/gingiva.

45 in the oral cavity, but rarely appear on the gingiva.

46 care for a swelling on his right mandibular gingiva.

47 hereby enhancing their redistribution to the gingiva.

48 o measure the apico-coronal dimension of the gingiva.

49 data from healthy and periodontitis-affected gingiva.

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

51 s with normal blood sugar levels and healthy gingiva.

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

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

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

55 significant influence on the color of human gingiva.

56 ing inhibits beta-catenin degradation in the gingiva.

57 eir ability to augment keratinized tissue or gingiva.

58 lative deepithelialization of hyperpigmented gingiva.

59 of obesity-induced insulin resistance in the gingiva.

60 of metastatic cells to chronically inflamed 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 leukin-11 concentrations were highest within gingiva adjacent to 3 mm diseased pockets (P < 0.001), a

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

73 of IL-11 and IL-17 are different in diseased gingiva adjacent to 3, 4 to 5, and > or = 6 mm pockets,

74 VEGF concentrations were highest within gingiva adjacent to 4 to 6 mm pockets and nearly equival

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

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

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

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

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

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

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

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

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

84 hment level (CAL), and width of the attached gingiva (AG) were measured.

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

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

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

88 The small lesion arose on the gingiva and alveolar mucosa.

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

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

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

92 esent within healthy and marginally inflamed gingiva and decreases in concentration as the adjacent p

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

94 minant cells of the periodontal ligament and gingiva and have important roles in the function and reg

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

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

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

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

99 solated and cultured fibroblasts from normal gingiva and overgrown gingiva from patients on cyclospor

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

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

102 Human gingiva and periodontal fibroblasts were exposed to the

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

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

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

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

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

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

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

110 gests that multiple DC subsets mature in the gingiva and that mature DCs engage in antigen presentati

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

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

113 l expression of interleukin-15 (Il15) in the gingiva and the basal expression of p-selectin (Selp) in

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

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

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

117 -1 mRNA is more highly expressed in both the gingiva and the spleens of susceptible mice than resista

118 lpha6 integrin, a 120-kDa protein present in gingiva and the tumor cell line.

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

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

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

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

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

124 y better root coverage, width of keratinized gingiva, and complete root coverage.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 64 sites (test group), with lack of attached gingiva associated with recessions, were treated with ma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 uggesting that leptin could be released from gingiva coincident to vascular expansion.

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

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

157 scopy, we show that, in addition to LCs, the gingiva contains dermal DCs (DDCs) in the lamina propria

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

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

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

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

162 The gingiva displayed no signs of inflammation and was tight

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

164 esigned to analyze the newly formed bone and gingiva during the consolidation period of mandibular os

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

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

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

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

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

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

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

172 The gingiva from around the molars was dissected and submitt

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

174 ibroblasts from normal gingiva and overgrown gingiva from patients on cyclosporine (CSA).

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

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

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

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

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

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

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

182 hy (< or =3 mm sulcus) and severely diseased gingiva (>6 mm sulcus).

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

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

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

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

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

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

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

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

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

192 The gingiva initially underwent mild inflammatory and reacti

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

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

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

196 gingival augmentation when the dimension of gingiva is inadequate.

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

198 Gingiva is supplied with lymphatics that drain interstit

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

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

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

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

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

204 ent root coverage, the amount of keratinized gingiva (KG), and probing depth (PD).

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

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

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

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

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

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

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

212 ection affecting the pharynx, lower lip, and gingiva of a healthy 19-year-old male is presented.

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

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

215 1 infection, we analyzed expression in human gingiva of HIV-1 receptors Langerin, DC-SIGN, MR, and Ga

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

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

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

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

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

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

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

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

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

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

226 more in the mandible on the labial attached gingiva of the anterior teeth.

227 plaque-induced inflammation relative to the gingiva of the dentition.

228 ft tissue response to plaque compared to the gingiva of the dentition.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 0 weeks after the distraction period and the gingiva responds favorably to increased length by regene

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

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

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

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

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

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

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

256 HGFs were primary cultured from human gingiva specimens.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 not affect the inflammatory response of the gingiva to dental plaque.

274 and IL-17 within healthy and diseased human gingiva to determine their possible role in the initiati

275 -13 and -15 within healthy or inflamed human gingiva to gingival sulcular depth and the concentration

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

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

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

279 Gingiva was grouped by the depth of the adjacent gingiva

280 Gingiva was obtained from 110 human donors before extrac

281 Gingiva was obtained prior to extraction of teeth.

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

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

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

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

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

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

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

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

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

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

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