Where adult tissue is damaged, a complex repair process is taking place involving regeneration and acute phase immunological response. Unlike embryonic tissues, adult repair always leads to the formation of a fibrotic scar where the wound has healed, which ultimately can disable proper tissue function [1]. In recent years, research was able to link several genes to the event of scar formation . Knockdown of Ostepontin (OPN) in mice for example resulted in reduced granulation tissue formation and scarring [2]. It also has been indicated that TGF-beta1 in conjunction with Connective tissue growth factor (CTGF) is promoting scar formation [3]. Most of this data comes from mouse model studies, in humans however, less is known.

Using ALSPAC data we want to perform both a candidate driven analysis and a non-hypothesis driven GWAS (the latter being determined by the sample sizes generated from available phenotypic data) comparing individuals involved in an accident developing a scar compared to individuals involved in an accident who did not develop a scar. Where possible, we will attempt to assess differing types of scar

tissue and healing related phenotype, however this will again be contingent upon available phenotypic data).

Analysis plan:

(i) assess the depth of data pertinent to scarring phenotypes and establish cases

control series according to differential scarring patterns.

(ii) perform bioinformatic work up of select genes (LIST) to establish likely

functional variants across the coding region and surrounding region.

(iii) unite both genetic and phenotypic data to undertake tests of association

between genetic variation and phenotypic characterisation.