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Analysis of two common α 1 ‐antitrypsin deficiency alleles ( PI * Z and PI * S ) in subjects with periodontitis
Author(s) -
Scott D. A.,
Von Ahsen N.,
Palmer R. M.,
Wilson R. F.
Publication year - 2002
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1034/j.1600-051x.2002.291212.x
Subject(s) - periodontitis , genotyping , genotype , allele , alpha 1 antitrypsin deficiency , medicine , immunology , polymerase chain reaction , pi , biology , genetics , gene , biochemistry
Background: πα 1 ‐Antitrypsin deficiency is a genetically determined condition resulting in predisposition to certain inflammatory diseases due to a protease: antiprotease imbalance that is exacerbated by tobacco smoking. Limited evidence suggests that there may be a significant enrichment of mild α 1 ‐antitrypsin deficiency phenotypes in subjects with chronic inflammatory periodontal disease. Objective: To examine the prevalence of two common α 1 ‐antitrypsin deficiency alleles ( PI * Z and PI * S ) in a UK population of subjects with periodontitis . Subjects and methods: The prevalence of PI * M , PI * S and PI * Z allele combinations was determined in 31 subjects with periodontitis and compared with 31 healthy control subjects matched for smoking status, ethnicity, age and gender. α 1 ‐Antitrypsin genotyping was performed by multiplex real‐time fluorescence polymerase chain reaction (PCR) using DNA extracted from whole blood. Results: There was no difference in the proportion of any α 1 ‐antitrypsin genotype found in the diseased and control populations. Conclusions: We did not find evidence to support an association between mutant PI * alleles and periodontitis in a small, controlled study. Larger studies will be required to clarify the relationship between α 1 ‐antitrypsin genotype and susceptibility to inflammatory periodontal disease.