ライフサイエンスコーパス: gingival

1 Gene expression of gingival adhesion molecules in periodontitis is regulate

2 expression in human gingiva and skin and in gingival and hypertrophic-like scar-forming skin wound h

3 ntal tissues; histopathologic examination of gingival and liver tissues; immunohistochemistry to cell

4 Both gingival and PDL fibroblasts displayed reduced cell viab

5 al grafts (DGG) placed for non-root coverage gingival augmentation by laser Doppler flowmetry (LDF).

6 periodontal conditions of sites treated with gingival augmentation procedures (GAPs) and untreated ho

7 Gingival augmentation procedures around natural teeth an

8 e GR defects not treated by root coverage or gingival augmentation procedures were considered eligibl

9 movement in thin biotype is high to justify gingival augmentation when the dimension of gingiva is i

10 CsA-enhanced gingival beta-catenin stability may be involved in gene

11 Wound fluid (WF) and gingival biopsies were analyzed for protein levels and g

12 Thirty healthy patients with thin gingival biotype (<1 mm) and history of periodontal dise

13 The gingival biotype also showed a thick biotype in 9 sites

14 of keratinized tissue, and thickness of the gingival biotype.

15 h of keratinized tissue and thickness of the gingival biotype.

16 = 0.07), and also had an indirect effect on gingival bleeding (beta = 0.011; P = 0.05).

17 was positively associated with the extent of gingival bleeding (beta = 0.24; P = 0.01).

18 affects estimates of the association between gingival bleeding (GB) and oral health-related quality o

19 al parameters of visible plaque index (VPI), gingival bleeding index (GBI), probing depth (PD), and b

20 The following parameters were evaluated: gingival bleeding index (GBI), probing depth (PD), myelo

21 by probing depth, clinical attachment level, gingival bleeding index, and the presence of calculus.

22 who maintain excellent oral hygiene and low gingival bleeding scores.

23 e oral hygiene (beta = -0.101; P = 0.01) and gingival bleeding status (beta = -0.024; P = 0.01).

24 ng had a deleterious effect on the extent of gingival bleeding via a worse oral hygiene status of chi

25 Prevalence of gingival bleeding was 92.4%.

26 rrence of periodontitis, visible plaque, and gingival bleeding was significantly higher among crack u

27 High levels of gingival bleeding were associated with the genera Prevot

28 so important for predicting oral hygiene and gingival bleeding.

29 Gingival blood perfusion after postextraction bone regen

30 nants, this prospective case series assesses gingival blood perfusion and tissue molecular responses

31 Gingival blood perfusion was measured by laser Doppler f

32 efit in using photometric analysis to assess gingival changes after therapy.

33 s (P <0.05) and maintenance of the amount of gingival collagen fibers.

34 ) mice demonstrate greater susceptibility to gingival colonization/infection, with severe gingival in

35 etric method is introduced for assessment of gingival condition and changes after periodontal therapy

36 ittle clinical significance, was observed in gingival conditions between the two groups, probably due

37 the precise effect of collagen glycation on gingival connective tissue biology is not fully understo

38 static balance and wound-healing response of gingival connective tissues affected by diabetes mellitu

39 al glycocalyx (ECG) in images of the healthy gingival crevice (GC).

40 pth (PD) and local inflammatory mediators in gingival crevicular fluid (GCF) among patients with untr

41 vels in peri-implant crevicular fluid (PICF)/gingival crevicular fluid (GCF) and a selection of subgi

42 onal flap surgery on growth factor levels in gingival crevicular fluid (GCF) and periodontal healing.

43 im of this study is to investigate levels of gingival crevicular fluid (GCF) and plasma TGM-2 and oxi

44 6, and tumor necrosis factor (TNF)-alpha, in gingival crevicular fluid (GCF) and serum samples betwee

45 Gingival crevicular fluid (GCF) and subgingival plaque w

46 e present study are to: 1) determine whether gingival crevicular fluid (GCF) chemerin is a novel pred

47 Aims of the study are to determine serum and gingival crevicular fluid (GCF) endocan levels in the pa

48 platelet-derived growth factor (PDGF-BB) in gingival crevicular fluid (GCF) from localized intrabony

49 m human gingival fibroblasts in vitro and in gingival crevicular fluid (GCF) in a randomized controll

50 he clinical parameters of disease and on the gingival crevicular fluid (GCF) inflammatory mediator in

51 ssessing clinical periodontal parameters and gingival crevicular fluid (GCF) levels of interleukin (I

52 Serum, saliva, and gingival crevicular fluid (GCF) levels of interleukin (I

53 Different gingival crevicular fluid (GCF) matrix metalloproteinase

54 pare them with their corresponding levels in gingival crevicular fluid (GCF) obtained from the same p

55 study is to determine visfatin levels in the gingival crevicular fluid (GCF) of healthy individuals a

56 l index (GI), bleeding on probing (BOP), PD, gingival crevicular fluid (GCF) volume, and total amount

57 Clinical evaluation was performed, and gingival crevicular fluid (GCF) was collected for select

58 The volume of gingival crevicular fluid (GCF) was quantified, and inte

59 Gingival crevicular fluid (GCF) was sampled for the anal

60 The aim of this study is to evaluate gingival crevicular fluid (GCF), saliva, and plasma leve

61 MMP-9, and TIMP-1 levels were determined in gingival crevicular fluid (GCF), saliva, and serum by im

62 Gingival crevicular fluid (GCF), serum, and saliva sampl

63 s with data on microbial plaque composition, gingival crevicular fluid (GCF)-interleukin (IL)-1beta l

64 ential amino acid, enters the oral cavity in gingival crevicular fluid (GCF).

65 unstimulated whole-mouth salivary flow rate, gingival crevicular fluid biomarkers).

66 rs could be used for measuring ions from the gingival crevicular fluid directly into the peri-odontal

67 pathogens) and local inflammatory response (gingival crevicular fluid IL-1beta) and derive periodont

68 ts in response to a major human salivary and gingival crevicular fluid LPA species, 18:1, and that th

69 In addition, gingival crevicular fluid was analyzed for an inflammati

70 ns of the genera of bacteria compatible with gingival disease.

71 The CsA-induced gingival EMT is dependent or at least partially dependen

72 confirm the notion that EMT occurs in human gingival epithelial (hGE) cells after CsA treatment and

73 (eATP)/P2X7-receptor mediated cell death in gingival epithelial cells (GECs) via eATP hydrolysis.

74 ssion, which was confirmed in cultured human gingival epithelial cells (HGECs).

75 In the case of periodontitis, gingival epithelial cells form the first line of defense

76 xpression of inflammatory cytokines in human gingival epithelial cells in response to microbial infec

77 Then, human gingival epithelial cells were seeded on the modified ti

78 to lipopolysaccharide stimulation in primary gingival epithelial cells, which is in the same directio

79 and fibrosis were regulated by phenytoin in gingival epithelial tissues and in connective tissues si

80 Wnt5a and sFRP5 protein colocalized in the gingival epithelium, suggesting epithelial cell expressi

81 one loss was significantly decreased and the gingival expression of IL-1beta, tumor necrosis factor a

82 23 axis, with a decreasing effect on ABL and gingival expressions of IL-17 and RORgammat.

83 ystemic T helper 17 (Th17) cell response; 2) gingival expressions of interleukin (IL)-17 and retinoic

84 and blocking Cx43 function in cultured human gingival fibroblasts (GFBLs) strongly regulated the expr

85 s with a profibrotic phenotype distinct from gingival fibroblasts (GFBLs).

86 and IL-8 on epithelial cells (ECs) and human gingival fibroblasts (GFs) in vitro.

87 s was used to test the hypothesis that human gingival fibroblasts (GFs) would show significant change

88 periodontal pathogenesis using primary human gingival fibroblasts (HGFs) and human periodontal ligame

89 eciphered the overall host response of human gingival fibroblasts (HGFs) to two featured isoforms of

90 ence of apoptosis, was demonstrated in human gingival fibroblasts (HGFs).

91 properties and remodeling capacity of human gingival fibroblasts (HGFs).

92 ractions on the cytokine profiles from human gingival fibroblasts in vitro and in gingival crevicular

93 d motility of periodontal ligament (PDL) and gingival fibroblasts in vitro.

94 deleterious to the function of both PDL and gingival fibroblasts than STE.

95 PDL and gingival fibroblasts were exposed to various concentrati

96 ear to be more sensitive to CSE and STE than gingival fibroblasts.

97 sensitive to both CSE and STE compared with gingival fibroblasts.

98 Hereditary gingival fibromatosis (HGF) is the most common genetic f

99 iciency associated with maternally inherited gingival fibromatosis is an allelic disorder with cardia

100 sis (HGF) is the most common genetic form of gingival fibromatosis that develops as a slowly progress

101 hormone deficiency and maternally inherited gingival fibromatosis.

102 Since many pathways are shared, the study of gingival fibrosis and comparisons with characteristics a

103 The increased expression of markers of gingival fibrosis, particularly CCN2 [also known as conn

104 nd tumor necrosis factor [TNF]-alpha) in the gingival fluid among individuals with and without period

105 Is a thick autogenous gingival graft more effective than a thin autogenous gin

106 ting from the de-epithelialization of a free gingival graft.

107 ure to predictably gain KT is the autogenous gingival graft.

108 graft more effective than a thin autogenous gingival graft?

109 3) What are the alternatives to autogenous gingival grafting to increase the zone of attached gingi

110 the early healing period of deepithelialized gingival grafts (DGG) placed for non-root coverage gingi

111 dontal dimensions of teeth treated with free gingival grafts (FGGs) compared with adjacent/untreated

112 re treated with marginal or submarginal free gingival grafts.

113 differential expression of these regulons in gingival health versus disease with a type 1 error betwe

114 iated mast cell degranulation contributes to gingival homeostasis but that sustained inflammation due

115 iated with Amelogenesis Imperfecta (AI) with gingival hyperplasia and nephrocalcinosis, while FAM20C

116 P = .34), nodal involvement ( P = .94), and gingival hypertrophy ( P = .24), was associated with a s

117 Gingival IL-10 mRNA expression was significantly increas

118 nd K2 alone or in combination did not affect gingival IL-1beta and IL-10, serum B-ALP and TRAP-5b lev

119 rmed at baseline and after 6 months were: 1) gingival index (GI), 2) probing depth (PD), 3) clinical

120 whole-mouth periodontal probing depth (PD), gingival index (GI), and plaque index (PI) were monitore

121 Outcome measures were plaque index (PI), gingival index (GI), bleeding on probing (BOP), PD, ging

122 rs were recorded, such as plaque index (PI), gingival index (GI), probing depth (PD), clinical attach

123 bleeding on probing, plaque index (PI), and gingival index (GI).

124 1) Plaque index (PI); 2) gingival index (GI); 3) oral hygiene index-simplified (O

125 chment level (CAL); 3) plaque index (PI); 4) gingival index (GI); 5) CRP; and 6) complete blood count

126 e reduction in both Plaque Index (TMQHI) and Gingival Index (mean MGI) at Day 3, Day 11 and Day 27 wa

127 sampled-site clinical attachment level, and gingival index (P <0.05).

128 data (probing depth [PD], plaque index [PI], gingival index [GI], bleeding on probing [BOP], and clin

129 probing depth (PD), bleeding on probing, and gingival index change after treatment.

130 d a greater reduction than placebo in PD and gingival index, along with increased gain in CAL.

131 depth, bleeding on probing, tooth mobility, gingival index, and plaque index was performed on the me

132 If complete examinations (plaque/gingival index, probing depth [PD], vertical clinical at

133 ng the simplified oral hygiene index and the gingival index, respectively.

134 Clinical parameters of plaque index, gingival index, vertical recession (VR), probing depth,

135 clinical attachment level, plaque index, and gingival index.

136 ere recorded, including: 1) plaque index; 2) gingival index; 3) bleeding on probing (BOP); 4) probing

137 nt and change in clinical parameters (plaque/gingival indices, unstimulated whole-mouth salivary flow

138 bial biofilm-induced inflammatory osteolytic gingival infection that results in orofacial implant fai

139 laque (HR = 3.30, [95% CI: 1.76-6.17]), high gingival inflammation (HR = 2.86, [95% CI: 1.71-4.79]),

140 and/or filled adult teeth [DMF-T] index); 2) gingival inflammation (papillary bleeding index [PBI]);

141 The present findings emphasize that PCOS and gingival inflammation are associated with each other, as

142 rhTSG-6 reduced postoperative gingival inflammation by reducing levels of proinflammat

143 outcome was the progression of the extent of gingival inflammation in children over time.

144 rtality risk were raised with dental plaque, gingival inflammation, >10 missing teeth and functional

145 gingival colonization/infection, with severe gingival inflammation, apical migration of the junctiona

146 The presence of gingival inflammation, calculus, and infectious dental d

147 positively associated with dental plaque and gingival inflammation.

148 e levels were both associated with increased gingival inflammation.

149 to assess dental plaque, dental calculus and gingival inflammation.

150 a positive effect on plaque accumulation and gingival inflammatory parameters after refraining from o

151 ne surface was significantly decreased after gingival injection of CD40L and CpG.

152 (+) cells were significantly increased after gingival injection of CD40L and CpG.

153 ed transcriptional regulatory network of the gingival interactome was subsequently interrogated with

154 ith various periodontal states (five biofilm-gingival interface [BGI] groups) abstained from oral hyg

155 Prevalence of severe periodontitis (biofilm-gingival interface P3 classification) was positively ass

156 eria on neutrophil location across the tooth/gingival interface.

157 therapy (scaling and root planing [SRP]) on gingival interleukin (IL)-1beta and IL-10, serum bone al

158 elium-derived, telomerase-immortalized human gingival keratinocytes (TIGKs) to microbial infection.

159 Weighted mean difference of mid-buccal gingival level (WDBGL), papilla index score (WDPIS), and

160 Mid-buccal gingival level (WDBGL, 0.07 mm; 95% confidence interval

161 = -0.44 to 0.59; P = 0.12) and interproximal gingival level did not significantly change after IMITG

162 Mid-buccal gingival level, interproximal gingival level, facial gingival thickness, gingival ridg

163 Mid-buccal gingival level, interproximal gingival level, facial gin

164 Treated sites ended with gingival margin (GM) 1.7 mm (P = 0.01) more coronal and

165 The aim of this study is to evaluate the gingival margin (GM) stability with the use of an oscill

166 CAL); 3) probing depth (PD); and 4) level of gingival margin (LGM).

167 lative clinical attachment level (rCAL), and gingival margin level (GML) at baseline and 9 months aft

168 ically detectable apical displacement of the gingival margin, and an increase in gingival width and t

169 ive clinical attachment level (rCAL); and 5) gingival marginal level were recorded at baseline before

170 h (PD), clinical attachment level (CAL), and gingival marginal level, included as parameters for clin

171 The gingival morphology after CsA treatment was evaluated by

172 The gingival mRNA and protein expression profiles for genes

173 In PDSG and PDCimG, gingival mucosa exhibited few collagen fibers among nume

174 MMP-1, and MMP-9-immunolabeled cells in the gingival mucosa were quantified.

175 ction of IL-6 immunolabeling in the inflamed gingival mucosa.

176 for the induction of Th17 cells at the oral/gingival mucosal barrier.

177 enrollment; at day 0, after reinstitution of gingival/mucosal health; at days 7, 14, and 21, during s

178 TRPV1 activation in gingival nerves induced production of the neuropeptide,

179 zontal cracks; Type II - vertically (occluso-gingival) oriented cracks; and Type III - hybrid or comp

180 arkers (OSMs) in cyclosporin A (CsA)-induced gingival overgrowth (GO).

181 mouse model to mimic human phenytoin-induced gingival overgrowth and assess the ability of a drug to

182 Drug-induced gingival overgrowth is caused by the antiseizure medicat

183 prevent or attenuate phenytoin-induced human gingival overgrowth, although specific human studies are

184 Gingival pain was more often reported by individuals in

185 Sub-gingival paper-point samples were taken at initial and r

186 and N. sicca, N. mucosa and N. elongata the gingival plaque.

187 Treatment also reduced gingival production of inflammatory mediators augmented

188 buccal SFA may support the stability of the gingival profile.

189 t the Lig + CsA group had significantly less gingival protein expression of gelatinases and EMMPRIN t

190 to limit the post-surgery increase in buccal gingival recession (bREC), effect of a connective tissue

191 ogous sites (control group), with or without gingival recession (GR) and with attached gingiva, were

192 d amount of attached gingiva associated with gingival recession (GR) at baseline were treated with FG

193 inical outcomes after treatment of localized gingival recession (GR) by a coronally advanced flap (CA

194 t patients presenting with 21 Miller Class I gingival recession (GR) defects (isolated or adjacent mu

195 s the long-term outcomes of untreated buccal gingival recession (GR) defects and the associated repor

196 TG) associated with LLLT in the treatment of gingival recession (GR) defects.

197 Gingival recession (GR) might be associated with patient

198 hip between toothbrushing and development of gingival recession (GR), but relevant GR data for the mu

199 Overall, data from 325 single gingival recession defects revealed a statistically sign

200 Management of gingival recession defects, a common periodontal conditi

201 duals with at least one Miller Class I or II gingival recession underwent a surgical root coverage pr

202 th at least one site of Miller Class I or II gingival recession were treated by a coronally advanced

203 y prevent the development and progression of gingival recession, especially when restorative margins

204 , despite many advantages, carries a risk of gingival recession, papilla loss, collapse of ridge cont

205 omes of clinical treatments in patients with gingival recession.

206 nship; 3) previous orthodontic treatment; 4) gingival recession; and 5) band of keratinized gingiva f

207 urface area (AERSA) as a prognostic test for gingival recessions (GRs) and to compare the predictive

208 ntal attachment apparatus when used to treat gingival recessions (GRs).

209 the RC, KMW, or CAL of Miller Class I and II gingival recessions compared with the other treatment mo

210 als in the treatment of Miller Class I or II gingival recessions.

211 advanced flap (CAF) procedures in localized gingival recessions.

212 After gingival resection in 120 Sprague-Dawley rats, 2 microg

213 Facial gingival thickness and gingival ridge dimension could be increased after IMITG.

214 l gingival level, facial gingival thickness, gingival ridge dimension, and width of keratinized gingi

215 ) mRNA were differentially expressed between gingival samples harvested from human healthy and chroni

216 (n = 70) or periodontitis-affected (n = 243) gingival sites.

217 For instance, tooth surfaces close to the gingival sulcus contact serum proteins that emanate via

218 nctional potential from microbes in the oral gingival sulcus of two bottlenose dolphins (Tursiops tru

219 indigenous oral spirochete that inhabits the gingival sulcus or periodontal pocket.

220 he tooth, leading to formation of a deepened gingival sulcus that is highly prone to pathologic chang

221 t numbers of serum proteins emanate from the gingival sulcus, their ability to participate in dental

222 calculus that enables the enlargement of the gingival sulcus.

223 nt promise as an anti-inflammatory agent for gingival surgery.

224 ctor T cell function, promoting increases in gingival Th17 cell numbers.

225 12 in the ECM group who completed the study, gingival thickness (GT) increased from 0.1 to 0.2 mm for

226 Facial gingival thickness and gingival ridge dimension could be

227 For the primary objective, the gingival thickness that best corresponded with probe inv

228 The gingival thickness that most closely corresponded with p

229 this study is to determine at what objective gingival thickness the probe becomes invisible through t

230 The study failed to identify a gingival thickness threshold that can discriminate relia

231 Gingival thickness was measured via transgingival soundi

232 level, interproximal gingival level, facial gingival thickness, gingival ridge dimension, and width

233 f CRC; however, the addition of CM increases gingival thickness.

234 s induced by LPS (1 mg/mL) injected into the gingival tissue (GT) of maxillary and mandibular first m

235 t abundant innate immune cell present in the gingival tissue and function to constrain the oral micro

236 olume of only PBS solution was injected into gingival tissue approximating the surgical wound.

237 Total RNA was extracted from gingival tissue biopsies collected from normal weight an

238 Gingival tissue biopsies from 23 patients with GAgP and

239 r-alpha, interleukin-1beta, and RANKL in the gingival tissue compared with the control site without l

240 differences in the transcriptome of healthy gingival tissue from edentulous sites from GAgP when com

241 study evaluated the transcriptome of healthy gingival tissue from edentulous sites in patients with a

242 Healthy gingival tissue from edentulous sites was taken from GAg

243 The expression of IL-33 in gingival tissue from healthy controls (n = 10) and patie

244 nd gene expression of leptin and visfatin in gingival tissue from patients with chronic periodontitis

245 ed amounts of tropoelastin were confirmed in gingival tissue from PD patients.

246 mini virus, named TTMV-222, was detected in gingival tissue from periodontitis patients using a vira

247 Lovastatin attenuated epithelial gingival tissue growth in phenytoin-treated mice and alt

248 yeloperoxidase activities were determined in gingival tissue homogenates, and ABL was evaluated with

249 Myeloperoxidase levels were determined in gingival tissue homogenates, and receptor activator of n

250 s in microRNA (miRNA) expression profiles of gingival tissue in periodontitis when obesity is present

251 lial desquamation, erythema, and erosions on gingival tissue is usually described in the literature a

252 The gingival tissue miRNA profile of obese patients, compare

253 vels of matrix metalloproteinase (MMP)-12 in gingival tissue of patients with the chronic inflammator

254 large gene expression profile data set (313 gingival tissue samples from a cross-sectional study of

255 lysis of secretions of adhesion molecules in gingival tissue samples from patients with periodontitis

256 ution of immature (im) and mature (m) DCs in gingival tissue samples obtained from patients diagnosed

257 Gingival tissue samples obtained from patients with: 1)

258 periodontitis (GAgP) are investigated using gingival tissue samples through omics-based whole-genome

259 n of IL-1beta, IL-17, TNF-alpha, and PAR2 in gingival tissue samples.

260 cally, A20 was modestly upregulated in human gingival tissue specimens from chronic periodontitis pat

261 The gingival tissue was used to quantify the myeloperoxidase

262 -STAMP gene expression is upregulated in the gingival tissue with periodontitis, its pathophysiologic

263 will prolong neutrophil traffic time in the gingival tissue, and subsequent degranulation will contr

264 Gingival tissue, hemimandibles, and oral biofilm were co

265 by direct injections of LPS into the palatal gingival tissues adjacent to the maxillary first molars

266 by direct injections of LPS into the palatal gingival tissues adjacent to the upper first molars 3 ti

267 nuclear factor kappaB ligand (RANKL) in the gingival tissues and T lymphocytes expressing RANKL in t

268 of TLR signaling, in ligated TLR9(-/-) mouse gingival tissues compared to its expression in the WT.

269 ced expression of Tnf, Il6, and Il1b mRNA in gingival tissues compared with wild-type mice.

270 ysis of IFI16 and AIM2 protein expression in gingival tissues from healthy individuals (n = 2) and in

271 Gingival tissues from patients with CP and T2DM had a si

272 The expression of Tnf mRNA in gingival tissues of Kit(W-sh/W-sh) mice was elevated fol

273 Gingival tissues of maxillary molars were subjected to r

274 y higher in recovered mononuclear cells from gingival tissues of the CD1d(hi) CD5(+) B cell transfer

275 Consistent with the disease phenotype, gingival tissues showed significantly more inflammatory

276 Expression of leptin and visfatin in the gingival tissues suggests a possible role for these adip

277 hronic inflammatory disease that affects the gingival tissues supporting the tooth.

278 Gingival tissues surrounding mandibular molars were coll

279 Moreover, reduction of LTB4 levels in the gingival tissues was associated with a significant decre

280 Moreover, reduction of LTB4 levels in gingival tissues was associated with a significant decre

281 Leptin and visfatin protein expression in gingival tissues was determined using enzyme-linked immu

282 expression levels of IL-17 and RORgammat in gingival tissues were evaluated immunohistochemically.

283 We combined RNA-seq data from gingival tissues with quantitative trait loci (QTLs) tha

284 sponse genes are differentially expressed in gingival tissues, comparing samples from experimental gi

285 ssion was observed in multiple cell types of gingival tissues, including inflammatory cells.

286 Gingival tissues, periodontal probing, and tooth mobilit

287 linically healthy and periodontitis-affected gingival tissues, we used miRNA inhibitors (sponges) in

288 performed according to Th cell responses in gingival tissues.

289 tor (TNF), interleukin (IL)-12, and IL-10 in gingival tissues.

290 t cells contributed to the Tnf transcript in gingival tissues.

291 ficantly reduced TNF and IL-12 levels in the gingival tissues.

292 ignificantly reduced TNF and IL-12 levels in gingival tissues.

293 LISAs quantified TNF, IL-12 and IL-10 in the gingival tissues.

294 The gingival transcriptome was evaluated by RNA sequencing o

295 Changes in diameter of the selected gingival venule were measured by vital microscopy combin

296 eceptor type 2 (VEGFR2) in the regulation of gingival venules in a rat model of experimental diabetes

297 t of the gingival margin, and an increase in gingival width and thickness.

298 HC function could promote fast and scarless gingival wound healing.

299 was strongly reduced in fibroblasts of human gingival wounds, and blocking Cx43 function in cultured

300 sitive cells were present in the regenerated gingival wounds.