OBJECTIVEThis study aims to test the accuracy and precision of iWitness photogrammetry for measuring the facial tissues of mannequin head.

METHODSUnder ideal circumstances, the 3D landmark coordinates were repeatedly obtained from a mannequin head using iWitness photogrammetric system with different parameters, to examine the precision of this system. The differences between the 3D data and their true distance values of mannequin head were computed.

RESULTSOperator error of 3D system in non-zoom and zoom status were 0.20 mm and 0.09 mm, and the difference was significant (P 0.05). Image captured error of 3D system was 0.283 mm, and there was no significant difference compared with the same group of images (P>0.05). Error of 3D systen with recalibration was 0.251 mm, and the difference was not statistically significant compared with image captured error (P>0.05). Good congruence was observed between means derived from the 3D photos and direct anthropometry, with difference ranging from -0.4 mm to +0.4 mm.

CONCLUSIONThis study provides further evidence of the high reliability of iWitness photogrammetry for several craniofacial measurements, including landmarks and inter-landmark distances. The evaluated system can be recommended for the evaluation and documentation of the facial surface.

Anthropometry ; Cephalometry ; Face ; Humans ; Image Processing, Computer-Assisted ; Imaging, Three-Dimensional ; Manikins ; Photogrammetry ; Reproducibility of Results

Objective:To explore the biological activities of interferon-? on the fibroblasts from rat palatal scar.Methods:Fibroblasts were cultured from rat palatal scar.The cells of pasage 4-6 were suspended into culture medium at (2.5)?105 cells/ml.Then the cells were cultured as fibroblasts-populated collagen latice(FPCL) with the final cell density of 5?104/ml.The cultures were exposed to IFN-?(U/ml) at 0,40, 400 and 4 000 for 24 h respectively.The cell proliferation was studied by MTT assay and FPCL contraction was studied by diameter measuring.Results:The absorbance of the cells treated with IFN-?(U/ml) at 0,40,400 and 4 000 was 0.247?0.014,0.235?0.014,0.190?(0.024) and 0.184?0.021 respectively,the contraction idex(%) of FPCL treated with above concentrations of IFN-? was 88.53,64.47,46.00 and 23.63 respectively.Conclusion:IFN-? may inhibit the proliferation of fibroblasts and the contraction of FPCL.

OBJECTIVEThe purpose of this study was to observe the healing process of palate wound with denuded bone restored with transplanted buccal or palatal mucosa and to elucidate the mechanism of maxillary growth inhibition following palate repair.

METHODS32 Japan white rabbits, 5 weeks old, were selected as the subjects for this study. They were divided into 4 groups at random. The rabbits in group I was the control without receiving any treatment. The rabbits in group II, III, IV was surgically denuded the bone of palate, and afterwards, the rabbits in group II were not received further restoration, but rabbits in group III and IV were restored with transplanted buccal and palatal mucosa respectively. From 2 to 14 weeks after surgery, at regular intervals, palatal wounds were observed by using a light microscope. Histological changes were also compared among different groups.

RESULTSIt was found in group II that dense connective tissue was formed 2 weeks after the surgery, and Sharpey's fibers was formed between the scar and bone tissue 4 weeks after the surgery. However, no Sharpey's fiber was found in group III and group IV, and in the latter two groups, the histological character of tissue was similar to that of the control.

CONCLUSIONPrevention of the attachment of Sharpey's fibers to the palatal bone could be effectively accomplished by covering the denuded palatal bone with the transplanted buccal or palatal mucosa.

Animals ; Cleft Palate ; pathology ; surgery ; Female ; Mouth Mucosa ; transplantation ; Palate, Hard ; pathology ; surgery ; Rabbits ; Random Allocation ; Surgical Flaps ; Wound Healing

OBJECTIVETo observe the effectiveness of prevention and cure for maxillary growth deformity following tissue engineered oral mucosa implantation on mucoperiosteal denuded palate process in young rat.

METHODSHard palate mucoperiosteum of a SD baby rat were excised and oral keratinocytes were isolated and cultured. Tissue engineered oral mucosa was fabricated with the cultured oral keratinocytes and the membrane made of sodium alginate (SA). 80 female three-week-old SD rats were used as subjects in this study. The animals were divided randomly into a normal control group and 3 experimental groups, each group included 20 rats. Normal control group (NG) were not operated. Hard palate mucoperiosteum on left side in all experimental groups were excised, exposed bone were not treated in denuded group (DG), but repaired with membrane in material group (MG) and repaired with the tissue engineered oral mucosa in mucosal group (MUG). All the animals were sacrificed at 9th week postoperatively (12 weeks old), and the clean widths of right and left hard palatal were measured under a dissection microscope. The difference between palatal widths of two sides and the asymmetry ratio between the different groups were compared and analyzed.

RESULTSNo significant difference in asymmetry was discovered between the DG and the MG, but the asymmetry in MUG was less than DG or MG.

CONCLUSIONTissue engineered oral mucosal implantation in palatoplasty is an effective method in preventing and curing secondary maxilla deformity by repairing denuded bone wound.

Animals ; Animals, Newborn ; Cleft Palate ; physiopathology ; surgery ; Keratinocytes ; cytology ; Maxilla ; growth & development ; Mouth Mucosa ; transplantation ; Oral Surgical Procedures ; methods ; Palate, Hard ; surgery ; Periosteum ; surgery ; Rats ; Rats, Sprague-Dawley ; Tissue Engineering

Normal embryonic development is regulated by different genes and related signaling pathways. In recent years, the association between different genes and genes, genes and signaling pathways in the same organization has been widely concerned by scholars at home and abroad. Sp and Wnt gene deletion or mutation can lead to abnormal embryonic development. The results of this review indicate that abnormal embryonic development is due to Sp gene deletion/mutation The zinc finger protein superfamily member Sp1-9 is involved in the development of various tissues and organs , such as the hematopoietic system, respiratory system and skeletal system, and its deletion or mutation can lead to developmental abnormalities in embryonic tissues. In addition, the Sp8 gene is associated with the occurrence of cleft palate. By summarizing the observations about the relationship between the Wnt gene and cleft lip and palate in recent years, we can understand the abnormal expression of Wnt3, Wnt3A, Wnt5A, Wnt9B, Wnt10A and Wnt11 in humans. The occurrence of cleft lip and palate is closely related; Sp5/8 is a key downstream effector of the Wnt signaling pathway during embryonic development and participates in the Wnt signaling pathway. Sp5/8 and the Wnt signaling pathway are involved in the regulation of normal neural crest development and the self-renewal of embryonic stem cells in embryonic mice. In summary, this paper proposes that the Sp and Wnt genes may be involved in the regulation of the formation and occurrence of embryonic cleft palate and provides a reference for further study of the associated mechanisms between the two genes in the cleft palate model.

OBJECTIVE: The purpose of this study is to observe the affection of different clinical surgeries on alar nasal cartilages' growth and development. The experimental results can provide some theory basis for clinical surgeries. METHOD: Twenty-eight New Zealand immature rabbits were used in this study, and divided into normal control group, hidden dissection group and cutting off alar nasal cartilages group randomly, which included 4,12 and 12 rabbits, separately. Arc incision were made on the mucous membrane of nasal cavity,and then dissect the alar nasal cartilages hidden or cut off the alar nasal cartilages, separately. The growth and development of the alar cartilage were observed at different stages after the surgery using histological and immuno-histochemical methods. RESULT: Four weeks, eight weeks, twelve weeks and sixteen weeks after surgery, there were no significant differences in the indexes of chondrocytes between hidden dissection group and control group. In cutting off alar nasal cartilages group, fiber tissue were observed in the vacancy left after being cut off cartilages, and even mucous membrane tissue could be seen in some slices. CONCLUSION There is no adverse influence on the growth and development of the alar cartilage after being hidden dissected. Contrarily, the restoring capability of transparent cartilage cannot counteract the injury resulted form the surgery after the alar nasal cartilages being cut off.
Animals ; Nasal Cartilages ; growth & development ; surgery ; Nose ; surgery ; Rabbits ; Rhinoplasty ; methods

Congenital cleft lip and/or palate (CL/P) is a common malformation of maxillofacial development. At present, it is believed that the etiology of congenital cleft lip and palate mainly results from genetic factors and environmental factors. Epigenetic changes induced by environmental factors may be the key factor in the occurrence of fetal congenital malformations. As one of the important epigenetic modifications, DNA methylation has been widely and deeply studied in many fields, but as a link between the individual and the environment, its application in CL/P is limited. Existing studies have shown that DNA methylation is closely related to the occurrence of cleft lip and palate. Stimulation of folate deficiency, smoking, pollutant exposure and other environmental factors can induce changes in the state of DNA methylation, thus affecting gene expression in the development of lip and palate and leading to the occurrence of deformities.

Objective To investigate the effect of transcription factor specific protein5(Sp5)silencing on Wnt signaling pathway correlated factors and cell proliferation ability in mouse embryo palatal mesenchymal cells(mEPMCs).Methods mEPMCs of 14.5 d pregnant C57BL/6J mice were isolated and cultured in vitro.Cell source was identified by immunofluorescence staining.Lentivirus transfection technique was used to silence the expression of Sp5 gene in mEPMCs,and the transfection efficiency was verified by Western blot assay.Follow-up experiments were set up with the blank control group,the no-load virus group and the slience group(the Sp5-shRNA group).The protein and mRNA expression levels of β-catenin,GSK-3β,Wnt3a and CyclinD1 were detected by Western blot assay and RT-qPCR after transfection for 72 h in each group.Cell proliferation capacity was detected by CCK-8.The proliferation rate of 5-Ethynyl-2'-deoxyuridine(EdU)positive cells was detected by immunofluorescence assay.Cell cycle was detected by flow cytometry.Results mEPMCs were successfully isolated,and Sp5 expression was silenced.Western blot and RT-qPCR results showed that the protein and mRNA expressions of β-catenin,GSK-3β,Wnt3a and CyclinD1 were significantly higher in the Sp5-shRNA group than those in the blank control group and the no-loaded virus group(P<0.05).The proliferative ability and the proliferative rate of EdU positive cells were higher in the Sp5-shRNA group than those in the blank control group and the no-loaded virus group(P<0.05).The proportion of mEPMCs in S phase was higher in the Sp5-shRNA group than that in the blank control group and the no-loaded virus group(P<0.05).Conclusion Sp5 in silenced mEPMCs can participate in palate development and promote the proliferation of mEPMCs by regulating Wnt signaling pathway.

Objective??This?study?aims?to?test?the?accuracy?and?precision?of?iWitness?photogrammetry?for?measuring?the?facial?tissues?of?mannequin?head. Methods??Under?ideal?circumstances,?the?3D?landmark?coordinates?were?repeatedly?obtained?from?a?mannequin?head?using?iWitness?photogrammetric?system?with?different?parameters,?to?examine?the?precision?of?this?system.?The?differences?between?the?3D?data?and?their?true?distance?values?of?mannequin?head?were?computed.?Results??Ope-rator?error?of?3D?system?in?non-zoom?and?zoom?status?were?0.20?mm?and?0.09?mm,?and?the?difference?was?significant?(P<0.05).?Image?captured?error?of?3D?system?was?0.283?mm,?and?there?was?no?significant?difference?compared?with?the?same?group?of images?(P>0.05).?Error?of?3D?system?with?recalibration?was?0.251?mm,?and?the?difference?was?not?statistically?significant?compared?with?image?captured?error?(P>0.05).?Good?congruence?was?observed?between?means?derived?from?the?3D?photos?and direct anthropometry, with difference ranging from ?0.4 mm to +0.4 mm.Conclusion??This?study?provides?further?evi-dence?of?the?high?reliability?of?iWitness?photogrammetry?for?several?craniofacial?measurements,?including?landmarks?and?inter-landmark?distances.?The?evaluated?system?can?be?recommended?for?the?evaluation?and?documentation?of?the?facial?surface.

Objective:To investigate the effect of the trace element zinc (Zn) on apoptosis and cell proliferation in palate shelvesduring the fusion phase, and to screen candidate genes of the Zn-finger special protein (Sp) family that were differentially expressed between the cleft palate and the normal palate to explore the mechanism of Zn in the development of cleft palate.Methods:Zn-rich, normal-Zn, low-Zn, and Zn-deficient diets were fed to female mice and, for the resultant fetuses, paraffin slices of their heads were made at embryonicdays 14.5 and 16.5. Using terminaldeoxynucleotidyltransferase-mediated dUTP nick-end labeling, the number of apoptotic cells in the palatal shelves was counted, and cell proliferation activity was detected using proliferating cell nuclear antigen staining. Total RNA from the palatal shelves of fetal mice was extracted from the Zn-rich diet, normal Zn-diet, and Zn-deficient-diet groups. We used microarray analysis to examine the expression of genes to identify intergroup differential gene expression and polymerase chain reaction tests to validate the results.Results:At ED14.5, the incidence of cleft palate in the regular zinc group, zinc rich group, low zinc group, and zinc deficient group was 8% (3/36), 2% (1/39), 29% (12/41), and 39% (15/38), respectively. The HE staining results at ED14.5 showed that both the left and right palatal processes in the zinc group had been lifted up and were in contact and connected with each other. In the zinc deficiency group, the left and right palatine processes remained vertically downwards on both sides of the tongue, ultimately forming cleft palate; In the low zinc group, the left and right palatine processes were raised but not in contact, ultimately resulting in cleft palate. There is no significant difference between the zinc rich group and the regular zinc group. At ED14.5, the positive rates of proliferative cells in the palatal process of fetal mice in the regular zinc group (80.29% ± 7.39%) and the zinc rich group (87.69% ± 6.62%) were significantly higher than those in the zinc deficient group (56.05% ± 16.13%) and the low zinc group (56.22% ± 9.61%) ( t=4.32, P<0.05). The apoptosis index of fetal rat palatal process cells in the zinc deficient group (38.80% ± 3.10%) and the low zinc group (28.80% ± 6.19%) were significantly higher than those in the regular zinc group (16.80% ± 1.82%) ( t=19.35, P<0.001; t=5.81, P<0.001). There were 663 differentially expressed genes in the zinc rich group and the zinc deficient group, with 513 up-regulated genes and 150 down-regulated genes, among which Sp5 was found to be located. The real time PCR results showed that compared with the regular zinc group (2.22 ± 0.36), the expression level of Sp5mRNA in the palatal process tissue of the zinc deficient group (1.23 ± 0.38) significantly increased ( P<0.05), while the zinc rich group (3.68 ± 0.90) significantly decreased ( P<0.05). Conclusions:Trace element Zn content was found to be closely related to the occurrence of cleft palate in mice offspring, with a lack of Zn leading to cleft palate.