Literature DB >> 17559626

Association of gene polymorphisms for plasminogen activators with alveolar bone loss.

A A DeCarlo1, H Grenett, J Park, W Balton, J Cohen, P Hardigan.   

Abstract

BACKGROUND AND
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.
MATERIAL AND 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).
CONCLUSION: 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.

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Year:  2007        PMID: 17559626     DOI: 10.1111/j.1600-0765.2006.00949.x

Source DB:  PubMed          Journal:  J Periodontal Res        ISSN: 0022-3484            Impact factor:   4.419


  4 in total

1.  Porphyromonas gingivalis-derived RgpA-Kgp Complex Activates the Macrophage Urokinase Plasminogen Activator System: IMPLICATIONS FOR PERIODONTITIS.

Authors:  Andrew J Fleetwood; Neil M O'Brien-Simpson; Paul D Veith; Roselind S Lam; Adrian Achuthan; Andrew D Cook; William Singleton; Ida K Lund; Eric C Reynolds; John A Hamilton
Journal:  J Biol Chem       Date:  2015-05-15       Impact factor: 5.157

2.  GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.

Authors:  Roselind S Lam; Neil M O'Brien-Simpson; John A Hamilton; Jason C Lenzo; James A Holden; Gail C Brammar; Rebecca K Orth; Yan Tan; Katrina A Walsh; Andrew J Fleetwood; Eric C Reynolds
Journal:  Immunol Cell Biol       Date:  2015-03-10       Impact factor: 5.126

3.  Plasminogen activator inhibitor-1 polymorphisms as a risk factor for chronic periodontitis in North Indian population.

Authors:  Puja Debnath; Jayant Dewangan; Divya Tandon; Vivek Govila; Mona Sharma; Virendra Kumar; Smita Govila; Srikanta Kumar Rath
Journal:  J Oral Biol Craniofac Res       Date:  2018-04-18

4.  Plasmin inhibition by bacterial serpin: Implications in gum disease.

Authors:  Alicja Sochaj-Gregorczyk; Miroslaw Ksiazek; Irena Waligorska; Anna Straczek; Malgorzata Benedyk; Danuta Mizgalska; Ida B Thøgersen; Jan J Enghild; Jan Potempa
Journal:  FASEB J       Date:  2019-11-26       Impact factor: 5.191

  4 in total

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