ライフサイエンスコーパス: palatal

1 e measured at two points (mid-labial and mid-palatal).

2 macrocephaly, distinct facial dysmorphisms, palatal abnormalities, ventriculomegaly, and hypogonadis

3 ge epithelial (MEE) cells were necessary for palatal adhesion.

4 the factors related to the resorption of the palatal alveolar bone caused by tooth movement after the

5 Correlation analysis adopting the amount of palatal alveolar bone resorption as a dependent variable

6 The amount of palatal alveolar bone resorption was measured and variou

7 this study is to evaluate the changes in the palatal alveolar bone thickness and find the factors rel

8 Palatal alveolar bone thickness changes and resorption f

9 he changes of maxillary central incisors and palatal alveolar bone thickness were measured, and the c

10 and reduced cell proliferation levels in the palatal and dental mesenchyme.

11 In contrast, caBmprIb fails to rescue the palatal and mandibular defects including the lack of low

12 ilateral hypoesthesia on the left side, weak palatal and pharyngeal reflexes on both sides, paresthes

13 om conventional therapy had failed, combined palatal and tongue surgery, compared with medical manage

14 -induced bone loss (BL) was noted on buccal, palatal, and interproximal height (P <0.05) and ridge wi

15 ng a multivariate approach, we observed that palatal anomalies represent a risk factor for the develo

16 In the in situ test, volunteers wore a palatal appliance containing titanium discs.

17 lunteers wore, in 3 phases of 7 days each, a palatal appliance containing titanium specimens.

18 tively, were injected into the subperiosteal palatal area adjacent to maxillary second molars every o

19 The PRF-enriched palatal bandage significantly accelerates palatal wound

20 Palatal biofilm formation was commensurate with developm

21 Palatal biopsies, in the form of connective tissue graft

22 ovided standardized normal and 5-day healing palatal biopsies, used for next generation miRNA and mRN

23 oCT analysis showed significantly more bucco-palatal bone formation in furcations treated with PTG co

24 growth, elevation, adhesion and fusion, and palatal bone formation.

25 sation and osteoblast differentiation during palatal bone formation.

26 usal plane during treatment helps to prevent palatal bone loss.

27 nificantly correlated with the difference in palatal bone resorption.

28 length of the bone anterior to the canal; 3) palatal bone width and length; and 4) root width and len

29 s study is to evaluate the effects of buccal-palatal bone width on the presence of the interproximal

30 d in the condensed mesenchyme progenitors of palatal bone.

31 y completely occluded sinus that was missing palatal bone.

32 ine, vomer and pterygoid to be tooth-bearing palatal bones, but also observed heterodonty on the pter

33 ification along the fusion area of secondary palatal bones.

34 cleft palate is characterized by defects in palatal bones.

35 divisions that promote stratification of the palatal, buccogingival and ventral tongue epithelia.

36 expression, leading to formation of complete palatal cleft.

37 id not display cleft palate, suggesting that palatal clefting in Wnt1-Cre;Erk2(fl/fl) mice is a secon

38 Whether the composition of palatal connective tissue grafts (CTGs) varies depending

39 In addition, the variables related to palatal contour (PP to PAS, SN to PAS, palatal surface a

40 y assigned to have the implant placed at the palatal crest or 1 mm subcrestally.

41 Bucco-palatal cylindrical microCT cores demonstrated a median

42 revealed latent haploinsufficiency, causing palatal defects in approximately 62% of pdgfra heterozyg

43 Palatal defects were caused by increased mesenchymal pro

44 molecular explanation for the resolution of palatal defects, showing that Eda and Edar-related genes

45 xpression studies support a role for MAFB in palatal development.

46 ples were stained with 5% toluidine blue and palatal digital images were traced to include the enamel

47 The bucco-palatal distance (BPD) was measured at 8, 10, and 12 mm

48 healing, and postoperative complications at palatal donor area of subepithelial connective tissue gr

49 ded that when a collagen sponge is placed in palatal donor areas of SCTG harvest by means of the SIT

50 The palatal donor site of the epithelialized connective tiss

51 of PRF and gelatin sponge on the healing of palatal donor sites and the patient's morbidity.

52 llagen sponge with or without sutures in the palatal donor sites following connective tissue grafting

53 Both palatal donor sites healed with spontaneous pigmentation

54 Hemostasis was achieved at the palatal donor sites with moistened gauze, and an acrylic

55 oviding KT augmentation without the need for palatal donor tissue.

56 d we identify and describe the braincase and palatal elements as well the atlas-axis complex for the

57 r-beta3 (TGF-beta3) plays a critical role in palatal epithelial cells by inducing palatal epithelial

58 microdissection was used to collect selected palatal epithelial cells from embryonic mouse embryos at

59 calize with IRF6 in the cytoplasm of primary palatal epithelial cells in vivo, and their interaction

60 taneous abrogation of both Tak1 and Smad4 in palatal epithelial cells resulted in characteristic defe

61 alatal mesenchyme affected Shh expression in palatal epithelial cells, indicating that Pax9 plays a c

62 undantly to transduce TGF-beta3 signaling in palatal epithelial cells.

63 Using this technique, we demonstrate that palatal epithelial conditional loss of afadin (Afdn) - a

64 role in palatal epithelial cells by inducing palatal epithelial fusion, failure of which results in c

65 ys involving Smad4, Tak1 and Trim33 regulate palatal epithelial fusion.

66 e-1 (Tak1) and Smad4 interact genetically in palatal epithelial fusion.

67 We find prominent Noggin expression in the palatal epithelium along the anterior-posterior axis dur

68 expression of stabilized beta-catenin in the palatal epithelium also disrupts normal palatogenesis by

69 Signals from the palatal epithelium also play key roles via tissue-tissue

70 ctivating ectopic Tgfbeta3 expression in the palatal epithelium and causing an aberrant fusion betwee

71 the canonical Wnt signaling activity in the palatal epithelium and leads to an abnormal persistence

72 vidence that overexpression of Noggin in the palatal epithelium does not cause a cleft palate defect,

73 ion of Shh was downregulated in the anterior palatal epithelium in the Bmpr1a conditional mutant embr

74 senchymal cells in palate, palatal rugae and palatal epithelium in the fused palate.

75 modulation of BMP signaling is essential for palatal epithelium integrity and for normal palate devel

76 ve cell death in the epithelium disrupts the palatal epithelium integrity, which in turn leads to an

77 The mammalian palatal epithelium is a landmark-rich tissue, marked by

78 found that loss of TGFbeta signaling in the palatal epithelium led to soft palate muscle defects in

79 abel-retention assays, we show that the hard palatal epithelium of the oral cavity is unique in displ

80 veractive BMP signaling, particularly in the palatal epithelium.

81 rmation was commensurate with development of palatal erythema, which suggests a role for biofilm in t

82 After bonding open spring palatal expanders for 3-day, 5-day, 7-day, and retention

83 late osteoclasts at the early stage of rapid palatal expansion and further facilitate bone formation

84 clinically modulating T cells to improve the palatal expansion efficacy.

85 Palatal expansion has been widely used for the treatment

86 is study, we conducted the tooth borne rapid palatal expansion model on the mouse, and detect whether

87 y identifies that T cells participate in the palatal expansion procedure by regulating osteoclasts an

88 However, whether T cells participate in the palatal expansion process remains to be determined.

89 lated at the end of the early stage of rapid palatal expansion.

90 We show that wnt9a is required for palatal extension, wherein the chondrocytes form a proli

91 However, incubation of palatal fibroblasts with recombinant amelogenin did not

92 missions have higher post-operative odds of palatal fistula than do children treated by local physic

93 ate target genes of TGFbeta signaling during palatal formation.

94 e of the medial edge epithelium (MEE) during palatal fusion in mice.

95 y is responsible for MEE degeneration during palatal fusion in mice.

96 Following palatal fusion, Bmpr1a mRNA expression was upregulated i

97 as medial epithelial seam dissolution during palatal fusion.

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

99 ipopolysaccharide (LPS) were injected into 3 palatal gingival sites, and Omp29-specific T clone cells

100 /c mice by direct injections of LPS into the palatal gingival tissues adjacent to the maxillary first

101 /c mice by direct injections of LPS into the palatal gingival tissues adjacent to the upper first mol

102 osity and to compare it with the traditional palatal graft, while highlighting functional, esthetic,

103 ival unit grafts in group 1 (n = 8) and with palatal grafts in group 2 (n = 9).

104 iva and papillae) compared with conventional palatal grafts.

105 cal, and esthetic improvements compared with palatal grafts.

106 The bucco-palatal implant position was the most relevant factor re

107 odontitis was induced with three consecutive palatal injections of Porphyromonas gingivalis lipopolys

108 Clefting of the lip, with or without palatal involvement (CLP), is associated with a higher i

109 sed maxillae and premaxillae with facial and palatal laminae, and that these bones underwent divergen

110 terventions were identified and reviewed: 1) palatal/lingual implant position; 2) platform-switched a

111 absolute ILDs including skull, basicranial, palatal, mandibular, and toothrow lengths.

112 proteoglycans (CSPGs) on apical surfaces of palatal medial edge epithelial (MEE) cells were necessar

113 tants display reduced expression of Mmp13 in palatal medial edge epithelial cells, suggesting that bo

114 2, is dependent on Tak1 activity and that in palatal mesenchymal cells TGFbetaRI and Tak1 kinases med

115 from PDGF-AA-treated primary mouse embryonic palatal mesenchyme (MEPM) lysates and analyzed the pepti

116 that tissue-specific deletion of Pax9 in the palatal mesenchyme affected Shh expression in palatal ep

117 d Arhgap29(K326X/+) embryos showed confluent palatal mesenchyme and epithelium at e18.5 ( n = 16), an

118 st lineage or specifically in the developing palatal mesenchyme caused reduced palatal shelf size and

119 sed reduced palatal shelf size and increased palatal mesenchyme cell density prior to the time of nor

120 th factor (FGF) signaling in mouse embryonic palatal mesenchyme cells and that Srf neural crest condi

121 In this study, we isolated palatal mesenchyme cells from embryonic day 12.5 (E12.5)

122 d at both E12.5 and E13.5 in the Osr2(RFP/-) palatal mesenchyme cells, in comparison with Osr2(RFP/+)

123 th factor (FGF) signaling in mouse embryonic palatal mesenchyme cells.

124 ng plays critical roles in the regulation of palatal mesenchyme condensation and osteoblast different

125 fic inactivation of Bmpr1a in the developing palatal mesenchyme in mice caused reduced cell prolifera

126 , is ectopically activated in the developing palatal mesenchyme in Osr2(-/-) embryos.

127 ignificantly downregulated in the developing palatal mesenchyme in Pax9 mutant embryos.

128 rescues the cell proliferation defect in the palatal mesenchyme of Tgfbr2(fl/fl);Wnt1-Cre mice.

129 restoration of Osr2 expression in the early palatal mesenchyme through a Pax9(Osr2KI) allele rescued

130 Foxf2-dependent expression in the developing palatal mesenchyme, 88 contained or were located next to

131 which the Erk2 deletion is restricted to the palatal mesenchyme, did not display cleft palate, sugges

132 , in which Ift88 is lost specifically in the palatal mesenchyme, exhibit isolated cleft palate.

133 f canonical Wnt signaling, in the developing palatal mesenchyme, particularly in the posterior region

134 xtracellular glycosaminoglycan in developing palatal mesenchyme, plays a major role in palatal shelf

135 Adamts20 is expressed in palatal mesenchyme, whereas Adamts9 is expressed exclusi

136 loss of the primary cilia in the CNC-derived palatal mesenchyme.

137 restored hyaluronic acid accumulation in the palatal mesenchyme.

138 Bmp7, Mef2c, Sox6, and Sp7 in the developing palatal mesenchyme.

139 significantly upregulated in the Osr2 mutant palatal mesenchyme.

140 gulation of the Shh signaling pathway in the palatal mesenchyme.

141 the Sema3a and Sema3d genes in the embryonic palatal mesenchyme.

142 on and impaired protein glycosylation in the palatal mesenchyme.

143 T-beta-catenin signaling is disrupted in the palatal mesenchyme.

144 way; and defective cell proliferation in the palatal mesenchyme.

145 ng of extracellular matrix components in the palatal mesenchyme.

146 roitin sulfate accumulation in the posterior palatal mesenchyme.

147 s reduced in the corresponding region of the palatal mesenchyme.

148 eveal a novel role for Osr2 in regulation of palatal morphogenesis through preventing aberrant activa

149 alatogenesis revealed distinct mechanisms of palatal morphogenesis: extension, proliferation and inte

150 effect on the transcriptome of normal human palatal mucosa and seems to target genes important for i

151 ssociated gene expression changes in healthy palatal mucosa and to identify potentially implicated im

152 group I-Pg: heat-killed Pg injected into the palatal mucosa between the molars; and 6) group I-V: pho

153 DS presents as erythema of the palatal mucosa in areas where denture-surface associated

154 Test and control wounds were created on the palatal mucosa of 54 Sprague-Dawley rats.

155 phosphate-buffered saline injected into the palatal mucosa.

156 hronic oral infection of the denture-bearing palatal mucosa.

157 e microbiota of denture-fitting surfaces and palatal mucosae were similar.

158 Palatal mucosal thickness, ranging from 2.35 to 6.89 mm,

159 e anatomy, function, and development of soft palatal muscles are similar in humans and mice, renderin

160 crest lineage or specifically in developing palatal or mandibular mesenchyme, respectively, using Wn

161 tarI kinase inhibitor (SB431542) was used in palatal organ cultures to determine if blocking TFGbeta

162 palate and anterior secondary palate during palatal outgrowth.

163 s mesenchymal-epithelial interactions during palatal outgrowth.

164 d4 double conditional knockouts leads to the palatal phenotypes which are identical to those seen in

165 er the intact defect-associated papilla with palatal positioning suture.

166 the medial edge epithelia (MEE) of the fetal palatal processes for isolation of intact microRNA for e

167 In addition, formation of the palatal processes of the maxilla was blocked while forma

168 e maxilla was blocked while formation of the palatal processes of the palatine was significantly dela

169 y higher prevalence of apical delta than the palatal root or the distobuccal root.

170 EPs were found in an unusual location on the palatal roots of maxillary second molars.

171 presents CEPs in an unusual location in the palatal roots of maxillary secondary molars.

172 n of SULT2A1 in mesenchymal cells in palate, palatal rugae and palatal epithelium in the fused palate

173 epithelium disrupts palatal shelf extension, palatal rugae formation, tooth development, and periderm

174 This observational study compared palatal rugae morphology in adolescent subjects with nor

175 the oral epithelium blocks the formation of palatal rugae, which are a set of specialized ectodermal

176 f extension, as well as for the formation of palatal rugae, which are signaling centers that regulate

177 In each patient, a palatal shallow site (<=3 mm) and a residual site (>=5 m

178 e of how mesenchymal FGF signaling regulates palatal shelf development may ultimately lead to pharmac

179 lts in increased nasal septum width, delayed palatal shelf development, and subepidermal blebbing.

180 resulted from a temporally specific delay in palatal shelf elevation and growth towards the midline.

181 , most likely due to inhibition of posterior palatal shelf elevation by disrupted morphology of the d

182 se mice was associated with delay/failure of palatal shelf elevation caused by tongue malposition and

183 re) drivers, respectively, which resulted in palatal shelf elevation delay and clefting of the second

184 t culture assays indicate that disruption of palatal shelf elevation in Has2(f/f);Hand2-Cre mutant fe

185 Just prior to the developmental stage of palatal shelf elevation in wild-type littermates, Golgb1

186 Whereas the molecular mechanism controlling palatal shelf elevation is not well understood, a prevai

187 e cause of cleft palate is a delay of proper palatal shelf elevation that may result from the small m

188 MT2D mutant NCCs lead to defective secondary palatal shelf elevation with reduced expression of extra

189 and/or dynamic cellular processes underlying palatal shelf elevation, adhesion, and fusion.

190 e palatal shelf mesenchyme, thus controlling palatal shelf elevation, as well as mineralization of th

191 educed mandible size and complete failure of palatal shelf elevation, whereas Has2(f/f);Osr2-Cre fetu

192 n implicated in playing an important role in palatal shelf elevation-80% of Pax9(del/del);Wise(-/-) d

193 gb1 mutant embryos have intrinsic defects in palatal shelf elevation.

194 abnormal palate-mandible fusion and prevents palatal shelf elevation.

195 Cre fetuses had normal mandibles and delayed palatal shelf elevation.

196 of them had cleft palate with disruption of palatal shelf elevation.

197 yme cell density prior to the time of normal palatal shelf elevation.

198 ng palatal mesenchyme, plays a major role in palatal shelf elevation.

199 bular morphogenesis that secondarily affects palatal shelf elevation.

200 eas Pax9(del/del) embryos exhibit defects in palatal shelf elevation/reorientation and significant re

201 double-mutant mouse embryos exhibit rescued palatal shelf elevation/reorientation, accompanied by re

202 hyaluronan plays a crucial intrinsic role in palatal shelf expansion and timely reorientation to the

203 palate in bt mice, with a similar defect in palatal shelf extension as Adamts9(+/-);bt/bt mice.

204 thermore, we found that Sox2 is required for palatal shelf extension, as well as for the formation of

205 deletion of Sox2 in oral epithelium disrupts palatal shelf extension, palatal rugae formation, tooth

206 in the coordination of GSK3beta signaling in palatal shelf fusion.

207 ption factor as a key intrinsic regulator of palatal shelf growth and morphogenesis.

208 g, and multiple transcription factors during palatal shelf growth and patterning.

209 lts indicate that, in addition to regulating palatal shelf growth through the Fgf18-Shh signaling net

210 genetic and molecular mechanisms controlling palatal shelf growth, elevation, adhesion and fusion, an

211 or birth defect resulting from disruption of palatal shelf growth, elevation, or fusion during fetal

212 the cellular and morphogenetic processes of palatal shelf growth, patterning, elevation, adhesion, a

213 Foxf-Fgf18-Shh molecular network controlling palatal shelf growth.

214 We deleted Yap/Taz throughout the palatal shelf mesenchyme as well as specifically in the

215 in the ossification region in the posterior palatal shelf mesenchyme upon deletion of Yap/Taz.

216 AZ may regulate collagen crosslinking in the palatal shelf mesenchyme, thus controlling palatal shelf

217 yme as well as specifically in the posterior palatal shelf mesenchyme, using the Osr2(Cre) and Col2(C

218 egulating cell proliferation in the anterior palatal shelf mesenchyme.

219 n of Dickkopf (DKK) activity in utero during palatal shelf morphogenesis partly rescued secondary pal

220 Fgf18-Shh signaling network, Foxf2 controls palatal shelf morphogenesis through regulating expressio

221 hondroitin sulfate proteoglycan important in palatal shelf morphogenesis, was increased, whereas expr

222 te that ephrin-B1 plays an intrinsic role in palatal shelf outgrowth in the mouse by regulating cell

223 mp4, Fgf10, Shh and Osr2 pathways to control palatal shelf patterning and morphogenesis.

224 and by ADAMTS20 in palate mesenchyme drives palatal shelf sculpting and extension.

225 developing palatal mesenchyme caused reduced palatal shelf size and increased palatal mesenchyme cell

226 ression patterns in the developing tooth and palatal shelf.

227 dary palatogenesis occurs when the bilateral palatal shelves (PS), arising from maxillary prominences

228 embryos showed an incomplete closure of the palatal shelves accompanied by a delay in ossification a

229 glycan protein and mRNA levels peaked as the palatal shelves adhered.

230 f Wise, which is expressed in the developing palatal shelves and encodes another secreted antagonist

231 s needed for the proper growth and fusion of palatal shelves are presented.

232 nderlying tissue fusion, using the secondary palatal shelves as a model.

233 as expressed in the mesenchyme of the murine palatal shelves at E12.5, prior to palate closure.

234 bsequently adhesion and fusion of the paired palatal shelves at the midline to separate the oral cavi

235 ng which the embryonic primary and secondary palatal shelves develop as outgrowths from the medial na

236 xpressed in the developing palate and mutant palatal shelves elevate above the tongue, demonstrating

237 In addition, the anterior portion of the palatal shelves emerged from the mandibular arch instead

238 proliferation leading to early overgrowth of palatal shelves followed by defects in their horizontali

239 p process that includes the elevation of the palatal shelves from a vertical to horizontal position,

240 phogenetic processes, including outgrowth of palatal shelves from the oral side of the embryonic maxi

241 Alteration in palatal shelves growth resulted in clefting of the secon

242 Mesenchyme of Adamts9(+/-);bt/bt palatal shelves had reduced cell proliferation, a lower

243 ly decreased in the posterior regions of the palatal shelves in embryonic day 13.5 Pax9-deficent embr

244 cally upregulated in the posterior region of palatal shelves in Foxf2(-/-) mouse embryos.

245 me surrounding Meckel's cartilage and in the palatal shelves in Med23(fx/fx);Wnt1-Cre mutant embryos

246 lication of exogenous Tgfbeta3 to the mutant palatal shelves in organ culture rescues the midline sea

247 Palatal shelves isolated from Adamts9(+/-);bt/bt mice fu

248 lial stemness marker SOX2 was altered in the palatal shelves of Tmem107(-/-) animals, and differences

249 ycan and decorin, that were expressed in the palatal shelves prior to adhesion.

250 and cleft palate resulting from a failure of palatal shelves to appropriately elevate and fuse.

251 evation of the initially vertically oriented palatal shelves to the horizontal position above the emb

252 ignaling and led to the growth and fusion of palatal shelves, as marked by an increase in cell prolif

253 dge epithelium (MEE) of the developing mouse palatal shelves, consistent with the expression patterns

254 I3K)) exhibit skeletal defects affecting the palatal shelves, shoulder girdle, vertebrae, and sternum

255 efects in growth or fusion of the developing palatal shelves, submucous cleft palate is characterized

256 wnstream targets of YAP/TAZ in the posterior palatal shelves, which included Ibsp and Phex, genes inv

257 particularly in the posterior regions of the palatal shelves.

258 this region and prevent approximation of the palatal shelves.

259 riants, and 3) expression in mouse embryonic palatal shelves.

260 sterior axis and outgrowth of the developing palatal shelves.

261 cal for modulating the growth orientation of palatal shelves.

262 not associated with defects intrinsic to the palatal shelves.

263 nd mandible in addition to severely deformed palatal shelves.

264 all of which are expressed in the developing palatal shelves.

265 ptosis in the MEE of the beta-catenin mutant palatal shelves.

266 ession is drastically reduced in Irf6 mutant palatal shelves.

267 te attachment loss that was localized to the palatal side of the maxillary second molars.

268 te attachment loss that was localized to the palatal side of the maxillary secondary molars.

269 nstrated a trend for more leakage at thinner palatal sites for the FGGT group (P = 0.09), and a stati

270 ofacial defects that include the loss of the palatal skeleton and hypoplasia of the pharyngeal skelet

271 th soft tissue and bone thickness except the palatal soft tissue measurements.

272 ed to palatal contour (PP to PAS, SN to PAS, palatal surface angle) and occlusal planes (UOP/POP) wer

273 chemosensory neurons innervating lingual and palatal taste buds and somatosensory neurons innervating

274 treatment modalities that did not depend on palatal tissue harvesting appear to have reported more s

275 neered materials may offer viable options to palatal tissue harvesting for gingival augmentation.

276 al recessions by using gingival unit grafts (palatal tissue involving marginal gingiva and papillae)

277 However, thicker palatal tissue was associated with higher FGT content (P

278 ans to adhere to denture material and invade palatal tissue.

279 d Edar-related genes are expressed in normal palatal tissues and that the Eda/Edar signaling pathway

280 Analysis of palatal tissues from 12 non-smokers and 10 smokers ident

281 Tgfa was not expressed in the palatal tissues of Irf6 knockout mice.

282 get loci, including Fgf18, in the developing palatal tissues was verified by ChIP-polymerase chain re

283 No pigmentation was noted on the palatal tissues.

284 In this study, we compared global palatal transcriptomes of wild type (WT) and Tgf-beta3 -

285 Additionally, a shallow palatal vault height (PVH) was associated with a higher

286 ditionally been considered homologous to the palatal vomer-dermopalatine series of osteichthyans.

287 mean loss in vertical ridge height (lingual/palatal) was less in the test sites but was not signific

288 for the complete re-epithelialization of the palatal wound (CWE), the alteration of sensitivity aroun

289 J/cm(2) LED light irradiation on the opened palatal wound and were euthanized after 4 to 28 days; th

290 nsity electrotherapy protocol may accelerate palatal wound healing and decrease patient discomfort af

291 ed palatal bandage significantly accelerates palatal wound healing and reduces the patient's morbidit

292 LED light irradiation at 660 nm accelerated palatal wound healing, potentially via reducing reactive

293 d outcomes of microcurrent electrotherapy on palatal wound healing.

294 y, the first one to report on topical PHT as palatal wound treatment, suggest that PHT application on

295 d treatment, suggest that PHT application on palatal wounds could result in improved healing outcomes

296 ols, 10%), whereas at the end of week 3, all palatal wounds in the test patients epithelialized compl

297 ectrotherapy treatment [EE]) group (n = 26), palatal wounds, after FGG harvest, received application

298 In the control (sham) group (n = 27), palatal wounds, after free gingival grafts (FGG) harvest

299 al phenytoin (PHT) treatment of experimental palatal wounds.

300 atients), a PRF membrane was placed over the palatal wounds; conversely, the 20 control group patient