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 follows: mean buccal, 0.51 mm; mean lingual/palatal, 0.61 mm; overall mean, 0.56 mm.

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

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

5 which is essential for ensuring appropriate palatal adhesion.

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

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

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

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

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

11 The PRF-enriched palatal bandage significantly accelerates palatal wound

12 Palatal biofilm formation was commensurate with developm

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

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

15 sation and osteoblast differentiation during palatal bone formation.

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

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

18 d in the condensed mesenchyme progenitors of palatal bone.

19 y completely occluded sinus that was missing palatal bone.

20 cleft palate is characterized by defects in palatal bones.

21 ification along the fusion area of secondary palatal bones.

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

23 expression, leading to formation of complete palatal cleft.

24 aterality defects and, surprisingly, induces palatal clefting in Cited2-deficient embryos.

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

26 c Snai1 deletion on a Snai2(-/-) background, palatal clefting results from a failure of Meckel's cart

27 for how disruption of Pdgf signaling causes palatal clefting.

28 he lip, cheek, periorbital soft tissues, and palatal competence present a challenging dilemma for rec

29 gration and apoptosis to generate immaculate palatal confluency during palatogenesis in response to r

30 moved by a two-stage procedure using grafted palatal connective tissue and laser deepithelialization.

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

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

33 Bucco-palatal cylindrical microCT cores demonstrated a median

34 This technique involves partial palatal deepithelialization and procurement of a layer o

35 This approach, involving partial palatal deepithelialization and the applied tunnel surgi

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

37 Palatal defects were caused by increased mesenchymal pro

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

39 cular mechanisms through which Shh regulates palatal development in vivo have not been directly analy

40 0 negatively regulates Pdgf signaling during palatal development, and we provide a mechanism for how

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

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

43 m H(2)O) and demonstrated abnormal two-point palatal discrimination compared with control subjects.

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

45 The palatal donor site of the epithelialized connective tiss

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

47 Both palatal donor sites healed with spontaneous pigmentation

48 PC-treated palatal donor sites were 1.10 mm thicker than control si

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

50 wound healing and hasten the regeneration of palatal donor tissue.

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

52 In food processing, palatal elevation was less frequent and its displacement

53 t pathological adhesion between the oral and palatal epithelia while permitting adhesion and subseque

54 in the palatal mesenchyme indirectly affects palatal epithelial cell proliferation.

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

56 Ablation of Tgfbr2 in the palatal epithelial cells causes soft palate cleft, submu

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

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

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

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

61 lly and to ablate Tgfbr2 specifically in the palatal epithelial cells.

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

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

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

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

66 veloping palatal mesenchyme induced aberrant palatal epithelial invaginations that resembled early to

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

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

71 ents revealed that signals from the anterior palatal epithelium are responsible for the restricted me

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

73 n isoform-specific role for TGF-beta3 in the palatal epithelium during palate formation, which cannot

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

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 mesenchymally expressed Fgf10 signals to the palatal epithelium to regulate Shh mRNA expression and c

80 Tgfb3 is strongly expressed in the prefusion palatal epithelium, and mice lacking Tgfb3 display a cle

81 veractive BMP signaling, particularly in the palatal epithelium.

82 tion of rugae and inter-rugae domains in the palatal epithelium.

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

84 anded Shh signaling is sufficient to restore palatal expansion and fusion in mice with compromised pa

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

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

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

88 ate target genes of TGFbeta signaling during palatal formation.

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

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

91 Palatal fusion is a complex, multi-step developmental pr

92 ion of the medial edge epithelium (MEE) upon palatal fusion is required for this process, and TGF-bet

93 Following palatal fusion, Bmpr1a mRNA expression was upregulated i

94 as medial epithelial seam dissolution during palatal fusion.

95 naling plays an important role in regulating palatal fusion.

96 l edge epithelium (MEE) disappearance during palatal fusion.

97 th the persistence of the MEE and failure of palatal fusion.

98 e interaction between TGFbeta3 and dioxin in palatal fusion.

99 Extensive analyses of palatal gene expression in wild-type and Mn1(-/-) mutant

100 Full-thickness wounds were created in the palatal gingiva of type 1 and type 2 diabetic and normog

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

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

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

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

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

106 iva and papillae) compared with conventional palatal grafts.

107 cal, and esthetic improvements compared with palatal grafts.

108 Palatal growth depends on reciprocal interactions betwee

109 n important epithelial signal for regulating palatal growth.

110 n shown to preferentially regulate posterior palatal growth.

111 1 have defects in posterior but not anterior palatal growth.

112 Blocking SFRP1 results in improvement of palatal healing outcomes.

113 s of the AMSA injection included outstanding palatal hemostatic control, avoidance of undesirable col

114 iately loaded miniscrews and osseointegrated palatal implants that are placed to control tooth moveme

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

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

117 ever, this effect may be less significant in palatal/lingual gingiva >3.0 mm.

118 ed and non-exposed cases were compared, only palatal/lingual gingival thickness showed a significant

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

120 Gingival excess in this and other palatal locations has the potential to alter linguopalat

121 Clinical overall (facial and palatal) maxillary SOG dimensions for zones 1, 2, and 3

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

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

124 required for complete disintegration of the palatal medial edge seam, that progresses between 14 and

125 Understanding the cellular mechanism of palatal MES disintegration in response to TGFbeta3 signa

126 xpansion and fusion in mice with compromised palatal mesenchymal cell proliferation, such as Msx1-nul

127 2, is dependent on Tak1 activity and that in palatal mesenchymal cells TGFbetaRI and Tak1 kinases med

128 idase staining gave extensive signals in the palatal mesenchymal region during and after palate fusio

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

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

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

132 Bmp4 and Fgf10 expression in the developing palatal mesenchyme and that specific inactivation of Smo

133 rectly to the palatal mesenchyme to regulate palatal mesenchyme cell proliferation through maintenanc

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

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

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

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

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

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

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

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

142 and that specific inactivation of Smo in the palatal mesenchyme indirectly affects palatal epithelial

143 bilization of beta-catenin in the developing palatal mesenchyme induced aberrant palatal epithelial i

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

145 pression of Fgf10 and Fgfr2c in the anterior palatal mesenchyme of the mutants.

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

147 lially expressed Shh signals directly to the palatal mesenchyme to regulate palatal mesenchyme cell p

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

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

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

151 s severely reduced after condensation of the palatal mesenchyme, resulting from a delay in the matura

152 the smoothened (Smo) gene in the developing palatal mesenchyme, we show that the epithelially expres

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

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

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

156 decreased level of cell proliferation in the palatal mesenchyme.

157 t Dlx5 is required for the O-N patterning of palatal mesenchyme.

158 tion rescue in the Msx1/Dlx5 double knockout palatal mesenchyme.

159 ors Foxf1a, Foxf2 and Osr2 in the developing palatal mesenchyme.

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

161 significantly upregulated in the Osr2 mutant palatal mesenchyme.

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

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

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

165 on and impaired protein glycosylation in the palatal mesenchyme.

166 restored hyaluronic acid accumulation in the palatal mesenchyme.

167 e-Dawley rats received LPS injections to the palatal molar gingiva three times per week for 4 weeks t

168 All animals received injections to the palatal molar gingiva three times per week for 8 weeks.

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

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

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

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

173 phosphate-buffered saline injected into the palatal mucosa.

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

175 In this report, we present the case of a palatal neurofibroma with radiographic involvement in a

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

177 in the anterior and posterior regions during palatal outgrowth, previous studies have identified seve

178 palate and anterior secondary palate during palatal outgrowth.

179 s mesenchymal-epithelial interactions during palatal outgrowth.

180 thelial-mesenchymal interactions controlling palatal outgrowth.

181 n in the middle and posterior regions during palatal outgrowth.

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

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

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

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

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

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

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

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

190 n factors is spatially organized relative to palatal rugae.

191 orphological changes that MES undergo during palatal seam disintegration.

192 tion elevated Pdgfra protein levels, altered palatal shape and caused neural crest cells to accumulat

193 lium, triggering abnormal fusion between the palatal shelf and mandible and preventing palatal shelf

194 Rather than having a major role in palatal shelf closure, we show that Tbx22 is an importan

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

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

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

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

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

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

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

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

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

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

205 he palatal shelf and mandible and preventing palatal shelf elevation.

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

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

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

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

210 h activity prevents apoptosis and subsequent palatal shelf fusion.

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

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

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

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

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

216 egulating cell proliferation in the anterior palatal shelf mesenchyme.

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

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

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

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

221 system, in which a Rosa26-originated ;blue' palatal shelf was paired with a C57BL/6-derived ;white'

222 ression patterns in the developing tooth and palatal shelf.

223 ssion from the oral to the nasal side of the palatal shelf.

224 lf was paired with a C57BL/6-derived ;white' palatal shelf.

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

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

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

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

229 g the anteroposterior axis of the developing palatal shelves and its expression is specifically downr

230 ociated with the expansion and fusion of the palatal shelves and that Dlx5 is required for the O-N pa

231 ate as a consequence of adhesion between the palatal shelves and the tongue.

232 ted in absence of the anterior region of the palatal shelves and, subsequently, cleft palate.

233 In mammals, adhesion and fusion of the palatal shelves are essential mechanisms during the deve

234 t relates to the expansion and fusion of the palatal shelves are unknown.

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

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

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

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

239 During embryonic development, palatal shelves display oronasal (O-N) and anteroposteri

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

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

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

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

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

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

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

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

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

249 Palatal shelves of Tgfb1 knockin homozygote mice adhere,

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

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

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

253 to extend the mandible and thereby allow the palatal shelves to elevate, defects similar to those see

254 embryos is due to a failure of the elevated palatal shelves to fuse.

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

256 itting adhesion and subsequent fusion of the palatal shelves via their medial edge epithelia remain o

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

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

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

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

261 sterior axis and outgrowth of the developing palatal shelves.

262 particularly in the posterior regions of the palatal shelves.

263 cal for modulating the growth orientation of palatal shelves.

264 not associated with defects intrinsic to the palatal shelves.

265 nd mandible in addition to severely deformed palatal shelves.

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

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

268 signaling centers to pattern the elongating palatal shelves.

269 to allow merging of the mesenchyme from both palatal shelves.

270 evelopment is not dependent on fusion of the palatal shelves.

271 this region and prevent approximation of the palatal shelves.

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

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

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

275 ody fragments thereof were injected into the palatal sites in each rat (days -1, 1, and 3).

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

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

278 necessary in establishing confluence of the palatal stroma.

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

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

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

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

283 of gingival abscesses secondary to excessive palatal tissue presented for treatment.

284 Palatal tissue thickness, post-surgical complications, a

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

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

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

288 Bilateral gingivectomies of palatal tissues were performed with inverse bevel incisi

289 No pigmentation was noted on the palatal tissues.

290 tively tested with buccal mucosal sticks and palatal transgingival probing.

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

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

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

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

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

296 le for the poorer healing performance of the palatal wounds compared with dermal wounds.

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

298 ibody experiments aimed at blocking SFRP1 in palatal wounds resulted in promotion of wound closure, e

299 did not harbor SFRP1, but healed faster than palatal wounds which expressed significant levels of SFR

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