Investigation of matrix metalloproteinase-1 1607 1G/2G polymorphism in a Turkish population with periodontitis Ustun K, Alptekin NO ¨ , Hakki SS, Hakki EE. Investigation of matrix metalloproteinase- 1 1607 1G/2G polymorphism in a Turkish population with periodontitis. J Clin Periodontol 2008; 35: 1013–1019. doi: 10.1111/j.1600-051X.2008.01313.x. Abstract Aim: Matrix metalloproteinase-1 (MMP-1) is a proteolytic enzyme that degrades extracellular matrix and plays a fundamental role during destruction of periodontal tissues. The aim of this study was to examine the association between MMP-1 1607 1G/2G polymorphism and chronic periodontitis susceptibility in a Turkish population. Material and Methods: A total of 180 subjects were enrolled in this study. All the subjects received a periodontal examination including full-mouth clinical attachment loss measurements, probing depths, plaque index scores, gingival index scores and radiographic bone loss ratios. Three groups formed according to periodontal conditions were healthy, moderate periodontitis and severe periodontitis groups. MMP-1 1607 1G/2G gene promoter polymorphism was genotyped using a polymerase chain reaction-restriction fragment length polymorphism method. Results:Analysis of the polymorphism showed no differences in distribution of the MMP-1 1607 1G/2G polymorphism among healthy, moderate periodontitis and severe periodontitis groups (p40.05). When the groups were further stratified by smoking status, we found no significant differences in genotype distributions, allele frequencies and carriage rates among any groups either (p40.05). Conclusions:On the basis of the results, no significant association is found for the MMP-1 1607 1G/2G polymorphism with susceptibility to periodontitis. Moreover, smoking status did not seem to affect this result. Key words:genetics; MMP-1; periodontitis susceptibility; polymorphism Accepted for publication 31 July 2008 Chronicperiodontitis is an infectious disease resulting in inflammation within the supporting tissues of the teeth, pro- gressive attachment loss,bone resorp- tion andcharacterizedby pocket formationand/or gingival recession (Armitage 1999). Current understanding of the aetiology of periodontitis impli- cates that bacterial infection is the pri- mary causeof thedisease(Flemmig 1999), while the pathology is the result of the interactions between pathogens and host. Host responseinvolves immune mechanisms that are under the influence of genetic and environmental factorsknown as risk determinants (Kornman & Newman 2000). Role of these risk factors is not clearly under- stood, while data have been accumulat- ing on the involvement of genetic determinants in the initiation and pro- gression of periodontitis (Kornman et al. 1997, Kornman & Newman 2000, Michalowiczet al. 2000). Multiple aspects of periodontitiscould be affected by genetic mechanisms such as the predisposal of the individual to develop the disease or experience its more severeforms (Shapiroet al. 1997).A genetic predisposal to perio- dontitismay exhibitpopulation-based variations (Kinane & Hart 2003), while somehuman groups are significantly more prone to various forms suggesting a chromosomal specificity (Fujita et al. 2005).In addition to the chromosome- based linkage studies, single nucleotide polymorphisms (SNPs) have also been studied in detail and shown to be linked to certain types of periodontitis (Kornman & Newman 2000). Disease forms linked Kemal Ustun 1 , Nilgu ¨n O ¨ zlem Alptekin 2 , Sema S. Hakki 2 and Erdogan E. Hakki 3 1 Oral and Dental Health Center, Selc¸uklu, Konya, Turkey; 2 Department of Periodontology, Faculty of Dentistry, Selcuk University, Konya, Turkey; 3 Department of Field Crops, Faculty of Agriculture, Selcuk University, Konya, Turkey Conflict of interest and source of funding statement There is no conflict of interests. This study is supported by a grant for scientific research from Selcuk University (2003–203). J Clin Periodontol 2008; 35: 1013–1019 doi: 10.1111/j.1600-051X.2008.01313.x 1013 r 2008 The Authors Journal compilation r 2008 Blackwell Munksgaard