Association of gene polymorphisms for plasminogen activators with alveolar bone loss.
OBJECTIVE
The plasminogen activating system is a protease/inhibitor system central to extracellular matrix remodeling with a suggested role in periodontal disease pathology. A few studies have reported polymorphisms in the genes of plasminogen activator inhibitors to be associated with periodontal disease severity. Two gene polymorphisms - a BamHI restriction fragment length polymorphism in the urokinase plasminogen activator gene (uPA) and a HindIII restriction fragment length polymorphism in the plasminogen activator inhibitor type 1 gene (PAI-1) - have been associated with conditions having a vascular component, and our objective was to assess the association of these gene polymorphisms with alveolar bone loss in chronic periodontal disease of adults.


METHODS
Genotype was determined by polymerase chain reaction amplification of whole blood, pertinent histories were obtained by interview, and alveolar bone loss was assessed from current radiographs.


RESULTS
In 77 elderly patients with a normal distribution of alveolar bone loss, we demonstrated a significant association between levels of alveolar bone loss and these polymorphisms in the uPA and PAI-1 genes. Controlling for the contributions of smoking or diabetes to periodontal bone loss, estimated odds ratios for predicting lower levels of alveolar bone loss, associated with a greater degree of periodontal health, were strongest when defined by the concurrent presence of a homozygous urokinase plasminogen activator genotype and the nuclease-sensitive plasminogen activator inhibitor type 1 (HindIII) allele (odds ratio = 2.6; 95% confidence interval: 5.8-1.3).


CONCLUSIONS
The urokinase plasminogen activator (BamHI) and plasminogen activator inhibitor type 1 (HindIII) genotypes may serve as useful markers for heritability of bone loss associated with periodontal disease.
DeCarlo
A A
AA
Department of Periodontology, College of Dental Medicine, Nova Southeastern University, Fort Lausderdale, FL, USA. DeCarlo@angentabiotechnologies.com
Grenett
H
H
Park
J
J
Balton
W
W
Cohen
J
J
Hardigan
P
P
D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D016301:Alveolar Bone Loss / Q000000981:diagnostic imaging / Q000235:genetics*; D002908:Chronic Disease; D015245:Deoxyribonuclease BamHI / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000150:complications; D004812:Epidemiologic Methods; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis / Q000235:genetics*; D011110:Polymorphism, Genetic; D011859:Radiography; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific) / Q000032:analysis; D012907:Smoking / Q000009:adverse effects; D014568:Urokinase-Type Plasminogen Activator / Q000032:analysis / Q000235:genetics*
D017395:Plasminogen Activator Inhibitor 1; C090528:DNA modification methylase HindIII; D015265:Site-Specific DNA-Methyltransferase (Adenine-Specific); D015245:Deoxyribonuclease BamHI; D014568:Urokinase-Type Plasminogen Activator