{"id":15800,"date":"2017-09-25T11:54:17","date_gmt":"2017-09-25T11:54:17","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=15800"},"modified":"2020-04-24T11:03:52","modified_gmt":"2020-04-24T11:03:52","slug":"role-of-msx1-gene-in-orofacial-clefting-a-systematic-review","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol10no3\/role-of-msx1-gene-in-orofacial-clefting-a-systematic-review\/","title":{"rendered":"Role of MSX1 Gene in Orofacial Clefting : A Systematic Review"},"content":{"rendered":"

Introduction <\/strong><\/p>\n

Orofacial clefting has always been the bane of the human race. It affects the overall wellbeing of the affected individual both phycological as well as physical. The Incidence of orofacial clefts have been around 1:500.4<\/sup>\u00a0Orofacial clefts can occur from an isolated cleft palate to a bilateral cleft lip and palate. Severe facial deformation gives the affected individuals a psychological set back. In developing countries like India where the cleft care does not reach to the rural population, the severity of unoperated clefting becomes more evident.
\nThe search for cause of orofacial clefting has been under research for a while now . While two forms of orofacial clefting , syndromic and non syndromic clefting have been researched extensively . The interest in Non syndromic clefting has grown more as it is a condition where an apparently healthy individual\u00a0 shows orofacial clefting without any other systemic condition.<\/p>\n

In\u00a0 1969 Carter proposed a model (MF\/T)\u00a0 multifactorial clefting\u00a0 inheritance,where he stated that non syndromic clefting was caused by the additive effects of minor abnormal genes and environmental factors.1<\/sup><\/p>\n

MSX Ggenes<\/strong><\/p>\n

The MSX group of genes in vertebrates comprise of a small family of chromosomally unlinked homeobox genes related to the Drosophilia muscle segment homeobox (MSH). MSX genes are expressed in vertebrate specific\u00a0 tissues , including sensory placodes , neural crest , bone and teeth. The MSX genes are classified into MSX1 and MSX2. MSX 3 found in mice is placed as a subclass of MSX1 subclass.
\nKnockout experiments with mice have shown a link to MSX 1 to failure to form teeth , and craniofacial abnormalities including absence alveolar bone in the jaws and disturbances in the formation of the parietal, nasal, frontal, cleft palate and malleus of middle ear.<\/p>\n

Objective<\/strong><\/p>\n

To test the null hypothesis<\/p>\n

MSX 1 gene mutation causes orofacial clefting.<\/p>\n

Methodology<\/strong><\/p>\n

Three search bases, Pubmed, Science direct and Cochrane were searched using the key words.<\/p>\n

The Inclusion criteria for the study was<\/p>\n

Direct association of MSX 1 gene mutation to orofacial clefting<\/p>\n

Human subjects with Cleft<\/p>\n

Results<\/strong><\/p>\n

Pub med showed 5, Science direct 79 and Cochrane 1 articles.<\/p>\n

Further using the inclusion criteria, 5 articles were selected<\/p>\n

Discussion<\/strong><\/p>\n

The Role of MSX 1 gene\u00a0 in Human orofacial clefting has always been debated , this systematic review was designed to find if there were any human studies that implicated orofacial clefting to the MSX 1 gene . In all 4 studies have implicated a direct relation to orofacial clefting. These studies have covered most of the populations around the world. AC Lidral and BC Reising2<\/sup>\u00a0 found \u00a0a Met61Lys substitution\u00a0 in two siblings in a big\u00a0 family with autosomal-dominant tooth agenesis. Venkatesh S Prasad and Venkatesh Shivani3<\/sup> found a novel\u00a0 mutation (414G to T) in a south Indian population . Seishi Yamaguchi et al 5<\/sup> found two \u00a0MSX1<\/em>\u00a0variants with an amino acid substitution ; Thr174Ile (T174I) of a\u00a0 hypodontia case and Leu205Arg of a\u00a0\u00a0 familial oligodontia case in a Japanese Population. Derya Ceyhan , Zuhal Kirzioglu and Nilufer Sahin Calapoglu6<\/sup> reported mutations in the MSX 1 gene from a predominant Turkish population.<\/p>\n

Conclusion<\/strong><\/p>\n

MSX1 gene which is a homeobox gene has been implicated in the formation of orofacial clefting. Several human studies have shown mutations in different populations.<\/p>\n

Acknowledgement<\/strong><\/p>\n

The Authors would like to thank Bharath University for providing the facility for the study.<\/p>\n

Conflict of Interest<\/strong><\/p>\n

There is no conflict of Interest.<\/p>\n

References <\/strong><\/p>\n

    \n
  1. Carte C. O.\u00a0 Genetics of Common Disorders. Br. Med. Bul.<\/em> 1969;25:52.
    \nCrossRef<\/a><\/li>\n
  2. Lidral A. C\u00a0 and\u00a0 Reising\u00a0 B. C. The Role of MSX1 in Human tooth agenesis. J Dent Res<\/em>. 2002;81(4):274-278.
    \n    CrossRef<\/a><\/li>\n
  3. Prasad S. V., Shivani V.\u00a0 Genetic significance of muscle segment homeo box1 gene in South Indian population for cleft lip and palate. Indian Journal of Human genetics<\/em>. 2012;18(3):332-339.
    \n    CrossRef<\/a><\/li>\n
  4. Ankola A. V., Nagesh L., Hedge P., Karibasappa G. N. Primary dentition status and treatment needs of children with cleft lip and\/or palate. J Indian Soc Pedod Prev Dent.<\/em> 2005;23:80\u201382.
    \n    CrossRef<\/a><\/li>\n
  5. Yamaguchi S., Machida J., Kamamoto M., Kimura M., Shibata A., Tatematsu T., et al. Characterization of Novel MSX1 Mutations Identified in Japanese Patients with Nonsyndromic Tooth Agenesis.\u00a0PLoS ONE<\/em>. 2014;9(8):102944.
    \n    CrossRef<\/a><\/li>\n
  6. Ceyhan D.,\u00a0 Kirzioglu Z and\u00a0Calapoglu S.\u00a0 N. Mutations in the Msx1 gene in Turkish Children with non \u2013syndromic tooth agenesis and other dental anomalies.Indian J Dental<\/em>. 2014;5 (4):172-182.
    \n    CrossRef<\/a><\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Introduction Orofacial clefting has always been the bane of the […]<\/p>\n","protected":false},"author":9,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[51],"tags":[],"class_list":["post-15800","post","type-post","status-publish","format-standard","hentry","category-vol10no3"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/15800","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/9"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=15800"}],"version-history":[{"count":6,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/15800\/revisions"}],"predecessor-version":[{"id":32727,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/15800\/revisions\/32727"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=15800"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=15800"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=15800"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}