ライフサイエンスコーパス: gingival

1 th APE when compared to patients with normal gingival anatomy.

2 The reduced scattering coefficients of the gingival and labial tissues are significantly different

3 neration of periodontal bone, attenuation of gingival and periodontal bone inflammation, and revertiv

4 gingivitis, aggressive periodontitis, acute gingival and periodontal conditions, conditions associat

5 ly healing index, probing depth and modified gingival and plaque indices and crestal bone loss (CBL)

6 This in vitro study evaluated the gingival attachment to zirconia implants and zirconia im

7 tes that have and have not been treated with gingival augmentation following free gingival graft (FGG

8 gene expression was also evaluated in human gingival biopsies using RT-qPCR.

9 During the periodontal surgery gingival biopsies were collected and processed for histo

10 Subgingival plaque samples and gingival biopsies were collected from healthy sites and

11 Gingival biopsies were obtained from 19 periodontitis pa

12 r oral biopsy services was performed for all gingival biopsies.

13 A gingival biopsy was obtained from one selected diseased

14 buccal bone dehiscence (P = 0.052) and thin gingival biotype (P = 0.054).

15 ime-point, gender, jaw, craniofacial growth, gingival biotype, buccal bone dehiscence after extractio

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

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

18 study was to assess the association between gingival bleeding and reports of verbal bullying among a

19 Adolescents who presented gingival bleeding had an 80% higher prevalence of verbal

20 ocket depth (PPD), attachment loss (AL), and gingival bleeding in addition to assessing their age, ge

21 s were recorded: visible plaque index (VPI), gingival bleeding index (GBI), probing depth (PD), clini

22 ses of the following periodontal parameters: gingival bleeding index (GBI), probing pocket depth (PPD

23 Gingival bleeding index (GI), probing depth (PD), clinic

24 Gingival bleeding index and oxidative stress parameters

25 Our results suggest that the presence of gingival bleeding negatively impacts the social life of

26 iance were used to evaluate the influence of gingival bleeding on the occurrence of verbal bullying.

27 beliefs and self-esteem indirectly predicted gingival bleeding via toothbrushing frequency and oral h

28 Gingival bleeding was assessed through adolescent self-p

29 norrhagia and one child aged 6-11 years with gingival bleeding).

30 ratified on baseline levels of pocket depth, gingival bleeding, ACH, and smoking status.

31 elationships include deficient oral hygiene, gingival bleeding, and bone and tooth loss.

32 ed probing depth, clinical attachment level, gingival bleeding, and radiographic alveolar crestal hei

33 health measurements included the presence of gingival bleeding, dental fracture, dental fluorosis, an

34 bserved between the percentage of sites with gingival bleeding, mean PPD, AL, F, and either gastritis

35 ic H. pylori in the percentage of sites with gingival bleeding, PPD, CAL, D, M, and F with adjustment

36 ral hygiene effectiveness directly predicted gingival bleeding.

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

38 ve lesion were significantly associated with gingival cancer in patients with PL.

39 Most gingival cancer occurred in areas with teeth and took th

40 Female sex was predominant in the group with gingival cancer, and simultaneous involvement of the buc

41 S. dentisani attached to gingival cells in vitro, inhibiting periodontal pathogen

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

43 Gingival clefts (GCs) develop frequently during orthodon

44 ce, its actions on alveolar bone resorption, gingival collagen content and key inflammatory mediators

45 ture + desipramine group (P < 0.05), whereas gingival collagen degradation was like the ligature grou

46 Alveolar bone resorption and gingival collagen fibers were histologically analyzed us

47 number of neutrophils that migrate into the gingival crevice to counteract its harmful effects.

48 S. dentisani is found at high levels in the gingival crevice.

49 n detached subgingival bacteria collected in gingival crevicular fluid (GCF) and RA parameters.

50 This study aimed to investigate the gingival crevicular fluid (GCF) and salivary HIF-1alpha,

51 This study aimed to investigate gingival crevicular fluid (GCF) and serum levels of LRG,

52 At baseline, gingival crevicular fluid (GCF) and subgingival plaque w

53 Subgingival plaque microbial profiles and gingival crevicular fluid (GCF) cytokine levels were det

54 atelet derived growth factor-BB (PDGF-BB) in gingival crevicular fluid (GCF) during early healing per

55 f matrix metalloproteinase (MMP)-8 and -9 in gingival crevicular fluid (GCF) during early pregnancy w

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

57 resence of human herpesviruses in saliva and gingival crevicular fluid (GCF) from patients with CKD.

58 ect of non-surgical periodontal treatment on gingival crevicular fluid (GCF) HIF-1alpha, VEGF, and TN

59 r aim was to determine levels of ADAMTS-1 in gingival crevicular fluid (GCF) in patients with advance

60 2) and matrix metalloproteinase-8 (MMP-8) in gingival crevicular fluid (GCF) in patients with periodo

61 study is to determine the serum, saliva and gingival crevicular fluid (GCF) levels of MT in smokers

62 of caspase-8, -9, and AIF were evaluated in gingival crevicular fluid (GCF) of all participants via

63 cation end products (AGEs) are higher in the gingival crevicular fluid (GCF) of chronic periodontitis

64 peptides 1 through 3 (HNP 1-3) levels in the gingival crevicular fluid (GCF) of patients with periodo

65 cig use on biological profiles in saliva and gingival crevicular fluid (GCF) was assessed and compare

66 mor necrosis factor-alpha (TNF-alpha) in the gingival crevicular fluid (GCF).

67 , 6, and 9 days) were compared with adjacent gingival crevicular fluid (GCF; at baseline, 1, and 4 mo

68 ival biofilm as well as on biomarkers in the gingival crevicular fluid after SRP.

69 of periodontal pockets, which are bathed in gingival crevicular fluid consisting of 70% of blood pla

70 Total RNA was extracted from gingival crevicular fluid samples and relative gene expr

71 plaque index (PlI), gingival index (GI), and gingival crevicular fluid volume (GCF) were evaluated fo

72 Samples of subgingival biofilm and gingival crevicular fluid were collected at baseline and

73 Gingival crevicular fluid, bleeding on probing (BOP), an

74 Saliva, gingival crevicular fluid, subgingival plaque, and blood

75 Excessive gingival display (EGD), or a gummy smile (GS), is a muco

76 ce differences among patients with different gingival display (GD) levels.

77 characterized by coarse facial features with gingival enlargement, intellectual disability (ID), hype

78 lead to compromised barrier function of the gingival epithelia.

79 hypotheses that infection of cultured human gingival epithelial (HGEp) cells with Porphyromonas ging

80 , causative of PD, efficiently invades human gingival epithelial and blood-dendritic cells.

81 s review, we highlight recent discoveries in gingival epithelial cell research in the context of bact

82 Gingival epithelial cells form an anatomic architecture

83 ously uncharacterized response mechanisms in gingival epithelial cells that are constructed to rapidl

84 red the barrier function of cultured primary gingival epithelial cells, which suggests a mechanism fo

85 to assess the toxicity of BNPs against human gingival epithelial cells.

86 iles from multi-cell computational models of gingival epithelial keratinocytes (GE KER), dendritic ce

87 Secondly, to mimic the interactions between gingival epithelium and immune cells in vivo, we integra

88 The gingival epithelium is a physical and immunological barr

89 toxicity and high viability were observed in gingival epithelium of NEGATIVE, GAS, CHX, and both LTP

90 Similarly, the gingival epithelium performs uniquely critical tasks in

91 The morphologic analysis of gingival epithelium revealed minor cell damage in the pl

92 ogical response of an in vitro reconstituted gingival epithelium tissue.

93 terface model using a commercially available gingival epithelium to study the tissue inflammatory res

94 These results suggest that gingival epithelium-derived soluble mediators may contro

95 n implant surfaces, while being safe for the gingival epithelium.

96 e immune cells that patrol the tissue at the gingival epithelium.

97 n the immune cells cultured with and without gingival epithelium.

98 ed into the center of full-thickness porcine gingival explants (n = 31).

99 on factor, and cytokines production in human gingival fibroblast cells (HGF) under inflammatory condi

100 on of CSF-1 and IL-34 in gingival tissue and gingival fibroblasts (GF) from patients with periodontit

101 Activation of gingival fibroblasts (GFs) significantly contributes to

102 recently observed in the coculture of human gingival fibroblasts (HGFs) and U937 human monocytic cel

103 the modulation of cytokine release by human gingival fibroblasts (HGFs) remains underexplored.

104 a-induced expression of IL1, IL6, and IL8 in gingival fibroblasts and the HSC-2 cell line.

105 Gingival fibroblasts and the oral human squamous carcino

106 PDL and gingival fibroblasts were exposed to various concentrati

107 ce inflammation-induced production of IL6 in gingival fibroblasts, HSC-2 and RAW 264.7 cells.

108 blocking of nuclear translocation of p65 in gingival fibroblasts.

109 ium nucleatum growth and attachment to human gingival fibroblasts.

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

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

112 hormone deficiency and maternally inherited gingival fibromatosis.

113 d higher levels of IL-6 and TNF-alpha in the gingival fluid (P <0.05).

114 elated to increased inflammatory activity in gingival fluid, which may become a risk indicator for fu

115 Notably, gingival gammadeltaT cell homeostasis is regulated by th

116 ingiva develops after birth, the majority of gingival gammadeltaT cells are fetal thymus-derived Vgam

117 eriments indicated that the main fraction of gingival gammadeltaT cells is radioresistant and tissue-

118 between the microbiome members and specific gingival genes showed a high number of significant bacte

119 notypes of the tooth or teeth region of free gingival graft (FGG) on the shrinkage ratio of graft at

120 PF-based approaches in combination with free gingival graft (FGG), CTG, CM, or ADM showed a significa

121 ed with gingival augmentation following free gingival graft (FGG).

122 investigated treatment groups (ADM, CM, free gingival graft [FGG], living cellular construct [LCC], i

123 e indications and predictability of the free gingival graft and connective tissue graft (CTG) techniq

124 g technique (TDT) or the epithelialized free gingival graft harvesting technique (FGGT).

125 ollowing soft tissue augmentation using free gingival grafts (FGG) at implant sites over a 3-month fo

126 ) group (n = 27), palatal wounds, after free gingival grafts (FGG) harvest, received sham application

127 A key component of gingival health is the regulation of the number of neutr

128 this pilot study, we compared the impact of gingival health, periodontitis (CP), CHD, or of both dis

129 m of this study was to analyze the impact of gingival health, periodontitis, and CHD on suPAR levels

130 ontrolling biofilm formation and maintaining gingival health; however, there is limited information o

131 versus thick gingival phenotype in terms of gingival health?

132 resolution displayed significantly increased gingival HIF-1alpha protein levels and bone regeneration

133 Juvenile spongiotic gingival hyperplasia (JSGH) is a distinct clinicopatholo

134 is by measuring alveolar bone resorption and gingival IL-17 expression as outcomes of Pg-induced infl

135 gnificant increase in alveolar bone loss and gingival IL-17 expression over sham-infected animals.

136 ata indicate that fundamental differences in gingival immune cell function between PD and T2D-potenti

137 resenting with probing depth (PD) >=4 mm and gingival index (GI) >=1 at >=4 sites distributed over >=

138 Gingival index (GI) and bleeding on probing (BOP) were e

139 h (PD), clinical attachment level (CAL), and gingival index (GI) were performed by calibrated masked

140 Interdental plaque score (IPS) and gingival index (GI) were recorded at baseline and 4-week

141 l attachment level (CAL), plaque index (PI), gingival index (GI), and bleeding on probing (BOP), were

142 14, 21, 28, 35, and 42, plaque index (PlI), gingival index (GI), and gingival crevicular fluid volum

143 Probing depth, gingival index (GI), plaque index (PI), and bleeding on

144 The plaque index (PI), gingival index (GI), probing depth (PD), clinical attach

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

146 ng probing depth, clinical attachment level, gingival index and plaque index were recorded at baselin

147 uration, implant mobility, plaque index, and gingival index) and radiographic bone level measurements

148 ay 42 bleeding on probing (primary outcome), gingival index, plaque control record, probing attachmen

149 inical periodontal parameters (plaque index, gingival index, sulcus bleeding index, probing depth, an

150 The following parameters were assessed: gingival index, tooth mobility; liver status, and portal

151 Plaque and gingival indices were measured at every visit whereas IP

152 phase (days 0 to 21), the rate of change in gingival inflammation (GI) was dramatically different be

153 The histometry results revealed less gingival inflammation and connective tissue loss in the

154 e immune defenses of the host; this leads to gingival inflammation and eventually to deepening period

155 ion of gammadeltaT cells results in elevated gingival inflammation and subsequent alterations of oral

156 dental gel improves oral health by reducing gingival inflammation at the local site in addition to b

157 ents, 41-70 years old, with evident signs of gingival inflammation but no attachment loss.

158 to examine the development and resolution of gingival inflammation in patients with APE when compared

159 CF children presented with higher gingival inflammation scores and salivary calprotectin l

160 development and resolution of plaque-induced gingival inflammation when compared to controls.

161 PPC stage V (Mild Tooth Loss/High Gingival Inflammation) was significant for fatal CHD (HR

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

163 re associated with CF or reflect concomitant gingival inflammation.

164 ation of AM251 and AM630 exacerbated ABL and gingival inflammatory mediators, increased by LPS, alter

165 ere we report that SCCs are present in mouse gingival junctional epithelium, where they express sever

166 M), was evaluated in telomerase immortalized gingival keratinocytes (TIGKs) by measuring cell viabili

167 study aims to raise awareness that marginal gingival leukoplakia may represent potentially malignant

168 A total of 30 cases of marginal gingival leukoplakia were included.

169 criteria included cases exhibiting marginal gingival leukoplakia, and with accompanying clinical ima

170 Some cases of marginal gingival leukoplakia, over time, progress to extensively

171 a by reporting a series of cases of marginal gingival leukoplakia.

172 (TNM) stage, and clinical characteristics of gingival malignancy between groups.

173 wed a significantly more apical shift of the gingival margin (almost two-fold).

174 ransparency of periodontal probe through the gingival margin at midfacial level.

175 gnificant predictor for the stability of the gingival margin at the ADM-treated, and the ADM-adjacent

176 , showed a higher apical displacement of the gingival margin compared with the ADM-treated sites, and

177 cket depth (PPD), bleeding on probing (BoP), gingival margin level, dentin hypersensitivity, and perc

178 were discussed based on the position of the gingival margin of the implant-supported crown in relati

179 ffective in maintaining the stability of the gingival margin over time, while EMD, acellular dermal m

180 ct length; new cementum (NC); new bone (NB); gingival margin position; total epithelium length; epith

181 may be defined as an apical migration of the gingival margin respective to the cementoenamel junction

182 A similar pattern toward apical shift of the gingival margin was noticed for the ADM-adjacent untreat

183 eukoplakias, either on the buccal or lingual gingival margin, or circumferentially forming a "ring ar

184 all were predictors for the stability of the gingival margin.

185 ubmucosa-extracellular matrix (SIS-ECM) with gingival mesenchymal stem cells (GMSCs) or their derivat

186 igament mesenchymal stem cells (PDLMSCs) and gingival mesenchymal stem cells (GMSCs).

187 Gingival mRNA expressions of interleukin (IL)-1beta, ind

188 ergrowth of colonizing microorganisms in the gingival mucosa can shift from homeostasis to dysbiosis

189 res (P = 0.015) and to patient perception of gingival/mucosal bleeding when performing oral hygiene (

190 smorphism, hypertrichosis, epilepsy, ID, and gingival overgrowth, we propose to combine the phenotype

191 1) What are the factors affecting gingival phenotype (e.g., age, sex, dental arch, race, c

192 oximal bone level, and (2) Assessment of the gingival phenotype according to the width of attached gi

193 tions were defined to understand the role of gingival phenotype around teeth.

194 Asian individuals tend to have thinner gingival phenotype compared with white subjects.

195 dence to support conversion of thin to thick gingival phenotype in sites without gingival recession o

196 conversion of gingivae from a thin to thick gingival phenotype in sites without mucogingival defects

197 there a difference between thin versus thick gingival phenotype in terms of gingival health?

198 mponents, overlying the bone, constitute the gingival phenotype.

199 are the effect of mesial and distal adjacent gingival phenotypes of the tooth or teeth region of free

200 , tobacco habit, clinical characteristics of gingival PL lesions, and location, tumor-node-metastasis

201 wo groups: group 1 included 33 patients with gingival PL that did not progress to cancer, and group 2

202 he clinical characteristics of patients with gingival PL with and without progression to oral squamou

203 sms to mimic the formation of supra- and sub-gingival plaque in vivo.

204 n of >=2 mm as compared with bi-weekly supra-gingival plaque removal.

205 pithelium (JE), is constantly exposed to sub-gingival plaque.

206 nce in regard to the utilized approaches for gingival PMT and assess their comparative efficacy in au

207 Changes in gingival recession (0.29 +/- 0.68 mm versus 0.15 +/- 0.5

208 ques in the treatment of localized maxillary gingival recession (GR) defects, 1 and 5 years after sur

209 or TUN in the treatment of single maxillary gingival recession (GR) defects.

210 Gingival recession (GR) might be associated with patient

211 nce of attached gingiva (AG) associated with gingival recession (GR) treated with FGG; and 2) contral

212 h (PPD), clinical attachment level (CAL) and gingival recession (GR) were evaluated at 3 and 6 months

213 attachment level (CAL), probing depth (PD), gingival recession (GR), bleeding on probing (BOP), plaq

214 can manifest loss of periodontal support and gingival recession (GR).

215 depth (PD), clinical attachment loss (CAL), gingival recession (REC), and bleeding on probing (BoP)

216 epth [PPD], clinical attachment level [CAL], gingival recession [GR]) and radiographic (defect Bone l

217 Gingival recession and a thin or absent buccal plate occ

218 ic parameters and other clinical findings to gingival recession and buccal bone conditions.

219 mine the association between the presence of gingival recession and the condition of radiographic buc

220 th thin and narrow gingiva tend to have more gingival recession compared with those with thick and wi

221 Gingival recession defect (GRD) may be defined as an api

222 .47 mm (P < 0.0001), and minimal increase in gingival recession of 0.23 +/- 0.62 mm (P = 0.168) were

223 to thick gingival phenotype in sites without gingival recession or mucogingival deformity.

224 and flap alone showed a similar tendency for gingival recession recurrence.

225 em, the 2017 classification of phenotype and gingival recession successfully incorporated the most re

226 two conditions is unclear and the ability of gingival recession to predict underlying buccal bone def

227 Accordingly, gingival recession was a significant predictor for bucca

228 Prevalence and severity of gingival recession was higher at the sites with thin gin

229 Gingival recession was present at 32.9% of maxillary ant

230 , maxillary anterior teeth with pre-existing gingival recession were more likely to have thin (<1 mm)

231 of the 2017 classification of phenotype and gingival recession, and to stress why it should be fully

232 ive tissue grafts (CTG) for the treatment of gingival recession, over a 3-month period.

233 PD, clinical attachment level (CAL), gingival recession, plaque index, GI, and bleeding on pr

234 s were related to the presence or absence of gingival recession, while patient sex, age, and the apic

235 Sixty RCTs with a total of 2,554 gingival recessions (1,864 patients) were included in th

236 ures in the treatment of single and multiple gingival recessions (GR).

237 ed flap (CAF) for treating multiple adjacent gingival recessions (MAGRs) remains to be determined.

238 5 pertaining to root coverage (3,539 treated gingival recessions [GRs]), and 10 for non-root coverage

239 nts with bilateral recession type 1 multiple gingival recessions after 6 months postoperatively.

240 l matrix (ADM) for the treatment of isolated gingival recessions has not yet been evaluated.

241 implementation of this new classification of gingival recessions, recent articles still report data b

242 te signaling molecules or genetic absence of gingival SCCs (gSCCs) increases the bacterial load, redu

243 Children with both diseases had 41.02% of gingival sites red whereas children with only obesity ha

244 Gingival status (bleeding on probing) and oral hygiene e

245 luence of social and psychosocial factors on gingival status in socially disadvantaged children is sc

246 oeconomic status and psychosocial factors on gingival status in underprivileged adolescents.

247 ssociations between psychosocial factors and gingival status.

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

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

250 morphotype, the keratinized tissue (KT), and gingival thickness (GT).

251 he probe transparency method and keratinized gingival thickness measurements; study groups were divid

252 e [mRC], keratinized tissue width [KTW], and gingival thickness) were evaluated and compared with the

253 Gingival thickness, keratinized tissue width, and bone m

254 cording to the width of attached gingiva and gingival thickness.

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

256 significance of keratinized mucosa (KM) and gingival tissue (KT) on peri-implant and adjacent period

257 The expression of CSF-1 and IL-34 in gingival tissue and fibroblasts suggests involvement in

258 valuate the expression of CSF-1 and IL-34 in gingival tissue and gingival fibroblasts (GF) from patie

259 dentified anti-inflammatory cytokines) in CP gingival tissue as compared with healthy tissue.

260 Gingival tissue attachment is known to be important for

261 ngly implicated in periodontal inflammation, gingival tissue destruction, and alveolar bone loss thro

262 CSF-1 was increased in gingival tissue from periodontitis patients compared wit

263 ological analysis support each other, so the gingival tissue is more strongly attached to sol-gel der

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

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

266 reased by LPS-induced EP, were diminished in gingival tissue of rats treated with Capz.

267 gnatures of chronic periodontitis (CP) using gingival tissue samples through omics-based whole-genome

268 Gingival tissue samples were obtained from all participa

269 Expression of CSF-1 and IL-34 in gingival tissue was assessed by western blot and localiz

270 osa tissues, including labial mucosa tissue, gingival tissue, and tongue dorsum tissue.

271 Oral gingival tissue, especially the junctional epithelium (J

272 a cells are the major immune cell type in CP gingival tissues and that these cells produce IL-35 and

273 gnificantly higher in periodontitis-affected gingival tissues compared to healthy gingiva.

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

275 Gingival tissues from 18 CP and 25 controls were analyze

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

277 Gingival tissues from mandibular molars were collected f

278 activities occurring in healthy and diseased gingival tissues in this human-like periodontitis model.

279 Gingival tissues of maxillary molars were subjected to r

280 in levels was significantly increased in the gingival tissues of the mice and in macrophages exposed

281 PDL and gingival tissues of third molar teeth were digested enzy

282 ans (Aa) was injected 3x/week (4 weeks) into gingival tissues of wild-type (WT), Nlrp3-KO and Caspase

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

284 Mandibles and gingival tissues were collected 3 or 15 days after ligat

285 Maxillary gingival tissues were processed for real-time polymerase

286 The outgrown cells derived from PDL and gingival tissues were similar, fibroblast-like, and spin

287 cultured on titanium discs and reconstituted gingival tissues were submitted to similar treatment con

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

289 of Wnt3a and Dvl3 in P. gingivalis-infected gingival tissues, and increases disease severity.

290 n was detected in healthy and inflamed human gingival tissues.

291 th RAGE and its antagonist AGER1 locally, in gingival tissues.

292 okine ligand 2 and interleukin 6 in diseased gingival tissues.

293 ections of lipopolysaccharide (LPS) into the gingival tissues.

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

295 performed according to Th cell responses in gingival tissues.

296 the relationship of the oral microbiome and gingival transcriptome in health and periodontitis in no

297 The gingival transcriptome was determined with a microarray

298 rty-one patients with inadequate keratinized gingival width (KGW) around mandibular incisors were inc

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

300 sitive cells were present in the regenerated gingival wounds.