FAM20A条件性基因敲除小鼠牙龈增生的组织测量学分析

›› 2020, Vol. 40 ›› Issue (12): 1084-1087.

FAM20A条件性基因敲除小鼠牙龈增生的组织测量学分析

刘静,李丽丽,刘培红,马肃

哈尔滨医科大学附属第一医院

收稿日期:2019-11-01 修回日期:2019-12-10 出版日期:2020-12-28 发布日期:2020-12-22
通讯作者: 马肃 E-mail:putiner365@163.com
基金资助:
哈尔滨市科技局应用技术研究与开发项目科技创新人才基金

Tissue measurement analysis of gingival hyperplasia in FAM20A conditioned knockout mice

Received:2019-11-01 Revised:2019-12-10 Online:2020-12-28 Published:2020-12-22

摘要/Abstract

摘要： 摘要：目的：分析Fam20A条件性基因敲除对小鼠牙龈组织形态的影响。方法：k14-Cre;Fam20Aflox/flox条件性基因敲除小鼠及同窝正常小鼠各20只，分别于出生后4、6、8、12周随机处死每组中的5只；体式显微镜下观察下颌磨牙区牙龈的大体形态；常规法获得下颌第一磨牙近远中向中点部位的颊舌向石蜡切片，行HE染色，光学显微镜下分别测量颊侧牙龈总面积、牙龈上皮面积和牙龈结缔组织面积；析因设计的方差分析和费舍尔最小显著性差异确定显著性水平。结果：基因敲除小鼠牙龈增生，颊侧牙龈总面积、牙龈上皮面积和牙龈结缔组织面积均大于对照组（P＜0.05）。结论：敲除小鼠牙龈上皮组织内的Fam20A基因后，导致牙龈组织增生，牙龈组织增生涉及牙龈上皮组织和结缔组织。

关键词: Fam20A, 条件性基因敲除, 形态计量学, 牙龈增生, 小鼠 

Abstract: [Abstract] Objective To analyze the morphometric changes on gingival tissue when FAM20A is conditional knock out (cKO) in mice. Methods Brood k14-Cre;Fam20Aflox/flox cKO mice and normal control mice each had 20, at the ages of 4, 6, 8, 12 weeks after birth, be put to death five in each group. Serial paraffin section was cut in a bucco-lingual direction throughout the mandibular first molars, and make haematoxylin and eosin staining. The area of buccal total gingival, gingival epithelial and connective tissue, were measured under optical microscope with the image analysis system. Data were analyzed by two-way analysis of variance of factorial design, and determined the significance level by fisher least significant difference. Results The area of total buccal gingival, gingival epithelium and gingival connective tissue of the cKO mice were all increased significantly than the control group one’s (P < 0.05). Conclusion Loss of epithelial FAM20A in mice causes the area of buccal gingival overgrowth, including gingival epithelial and connective tissue.

Key words: Fam20A, condition knockout, morphometry, gingival hyperplasia, mice 

中图分类号:

R394.114

刘静李丽丽刘培红马肃. FAM20A条件性基因敲除小鼠牙龈增生的组织测量学分析[J]. 口腔医学, 2020, 40(12): 1084-1087.

参考文献 17

[1]	Nalbant D, Youn H, Nalbant SI, et al.FAM20: an evolutionarily conserved family of secreted proteins expressed in hematopoietic cells[J].[J].BMC Genomics, 2005, 6(1):11-21
[2]	Cui J, Xiao J, Tagliabracci VS, et al.A secretory kinase complex regulates extracellular protein phosphorylation[J][J].Elife, 2015, 1(4):e06120-e06130
[3]	Jaureguiberry G,De la Dure-Molla M, Parry D, Quentric M, Himmerkus, N, Koike T. et al..Nephrocalcinosis (enamel renal syndrome) caused by autosomal recessive FAM20A mutations[J][J].Nephron Physiol., 2012, 122(1-2):1-6
[4]	Ooya K, Nalbandian J, Noikura T.Autosomal recessive rough hypoplastic amelogenesis imperfecta: a case report with clinical,light microscopic,radiographic,and electron microscopic observations[J][J].Oral surgery, oral medicine, oral pathology, 1988, 65(4):449-458
[5]	Martelli-Júnior H, Bonan P R F, dos Santos L A N, et al.Case reports of a new syndrome associating gingival fibromatosis and dental abnormalities in a consanguineous family[J][J].Journal of periodontology, 2008, 79(7):1287-1296
[6]	Muriel de la Dure-Molla M, Quentric M, Yamaguti P M, et al.Pathognomonic oral profile of Enamel Renal Syndrome (ERS) caused by recessive FAM20A mutations[J][J].Orphanet journal of rare diseases, 2014, 9(1):84-90
[7]	Piranit Nik Kantaputra, Chotika Bongkochwilawan, Mark Lubinsky, et al.Periodontal disease and FAM20A mutations[J] [J]. Journal of Human Genetics, 2017, 62(7):679-686
[8]	James O’Sullivan, Carolina C, Bitu, Sarah B. Daly, et al..Whole-Exome Sequencing Identifies FAM20A Mutations as a Cause of Amelogenesis Imperfecta and Gingival Hyperplasia Syndrome[J][J].The American Journal of Human Genet, 2011, 88(5):616-620
[9]	Wang X, Wang S, Li C, et al.Inactivation of a novel FGF23 regulator,FAM20C,leads to hypophosphatemic rickets in mice[J][J].PLoS Genet, 2012, 8(5):e1002708-E1002710
[10]	Wang X, Wang S, Lu Y, et al.FAM20C plays an essential role in the formation of murine teeth[J] [J].J Biol Chem, 2012, 287(43):35934-35942
[11]	Simpson MA, Hsu R, Keir LS, et al.Mutations in FAM20C are associated with lethal osteosclerotic bone dysplasia (Raine syndrome), highlighting a crucial molecule in bone development[J][J].Am J Hum Genet, 2007, 81(5):906-912
[12]	Ababneh FK, AlSwaid A, Youssef T, et al.Hereditary deletion of the entire FAM20C gene in a patient with Raine syndrome[J] [J]. Am J Med Genet A , 2013, 161A(12):3155-3160
[13]	Takeyari S, Yamamoto T, Kinoshita Y, et al.Hypophosphatemic osteomalacia and bone sclerosis caused by a novel homozygous mutation of the FAM20C gene in an elderly man with a mild variant of Raine syndrome[J] [J].Bone, 2014, 67(oct):56-62
[14]	Simpson MA, Scheuerle A, Hurst J, et al.Mutations in FAM20C also identified in non-lethal osteosclerotic bone dysplasia[J][J].Clin Genet, 2009, 75(3):271-276
[15]	Li-Li Li, Pei-Hong Liu, Xiao-Hua Xie，et al.Loss of epithelial FAM20A in mice causes amelogenesis imperfecta, tooth eruption delay and gingival overgrowth[J][J].International Journal of Oral Science , 2016, 8(2):98-109
[16]	Weinberg MA, Bral M.Laboratory animal models in periodontology[J][J].J Clin Periodontol, 1999, 26(6):335-340
[17]	Qiao B, Gopalan V, Chen Z, et al.Epithelial-mesenchymal transition and mesenchymal-epithelial transition are essential for the acquisition of stem cell properties in hTERT-immortalised oral epithelial cells[J][J].Biol Cell, 2012, 104(8):476-489