De Coster Peter J, Martens Luc C, De Paepe Anne
Department of Paediatric Dentistry, Centre for Special Care, Paecamed Research, University of Ghent, Belgium.
Pediatr Dent. 2004 Nov-Dec;26(6):535-7.
Mutations in the genes encoding fibrillin, an extracellular matrix protein involved in providing elastic properties to the connective tissues, may result in specific craniofacial and oral anomalies. A number of craniofacial (retrognathia, dolichocephaly, high palate) and dental (root deformity, pulp calcification) manifestations are considered pathognomic for the Marfan syndrome (MFS), a condition caused by congenital fibrillin-1 deficiency. Reports on similar features in congenital contractural arachnodactyly (CCA), caused by fibrillin-2 deficiency, support the hypothesis that fibrillin deficiency might result in a number of morphological anomalies by influencing tissue interaction during growth and development. Hence, clinical manifestations can be related to specific aspects of fibrillin deficiency pathogenesis, and may be adopted as diagnostic tools in the outlook for affected individuals.
编码原纤维蛋白的基因突变可能导致特定的颅面和口腔异常,原纤维蛋白是一种细胞外基质蛋白,参与赋予结缔组织弹性特性。一些颅面(下颌后缩、长头畸形、高腭)和牙齿(牙根畸形、牙髓钙化)表现被认为是马凡综合征(MFS)的特征性表现,这是一种由先天性原纤维蛋白-1缺乏引起的疾病。关于由原纤维蛋白-2缺乏引起的先天性挛缩性蜘蛛指(趾)症(CCA)的类似特征的报道支持了这样一种假说,即原纤维蛋白缺乏可能通过影响生长发育过程中的组织相互作用而导致多种形态异常。因此,临床表现可能与原纤维蛋白缺乏发病机制的特定方面相关,并且可以作为受影响个体诊断的工具。