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Degenerative periodontal-diseases and oral osteonecrosis: The role of gene-environment interactions

Abstract

Chronic-degenerative dentistry diseases, including periodontal diseases and oral osteonecrosis, are widespread in human populations and represent a significant problem for public health. These diseases result from pathogenic mechanisms created by the interaction between environmental genotoxic risk-factors and genetic assets conferring individual susceptibility. Osteonecrosis occurs in subjects undergoing exposure to high doses of DNA-damaging agents for chemo- and radiotherapy of neoplastic diseases. In susceptible patients, ionizing radiation and biphosphonate-chemotherapy induce severe, progressive, and irreversible degeneration of facial bones, resulting in avascular necrosis of the jaw. This may also occur in patients receiving biphosphonate for osteoporosis therapy. Periodontal diseases include chronic, aggressive, and necrotizing periodontitis, often resulting in severe alteration of periodontal tissues and tooth loss. Cigarette smoking and chronic inflammation caused by specific bacteria are the main risk factors for periodontitis. Oxidative damage plays a fundamental pathogenic role, as established by detection of mitochondrial DNA damage in the gingival tissue of patients with periodontitis. Endogenous risk factors in dental diseases include polymorphisms for metabolic enzymes such as glutathione transferases M1 and T1, N-acetyl transferase 2, and CYP 1A1. Other genetic polymorphisms that confer susceptibility to dentistry diseases affect genes encoding metalloproteases (involved in periodontal tissue remodeling and degradation), cytokines (involved in  More>>
Authors:
Baldi, D.; [1]  Izzotti, A.; [2]  Bonica, P.; Pera, P.; [1]  Pulliero, A., E-mail: alessandra.pulliero@unige.it [2] 
  1. Department of Medical, Biophysical, and Dentistry Sciences and Technologies, University of Genoa (Italy)
  2. Department of Health Sciences, University of Genoa, Via A. Pastore 1 (Italy)
Publication Date:
Jul 10, 2009
Product Type:
Journal Article
Resource Relation:
Journal Name: Mutation Research; Journal Volume: 667; Journal Issue: 1-2; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS; BACTERIA; CHEMOTHERAPY; DENTISTRY; DNA REPAIR; GENETIC RADIATION EFFECTS; GLUTATHIONE; HEALTH HAZARDS; INFLAMMATION; IONIZING RADIATIONS; JAW; LYMPHOKINES; OSTEOPOROSIS; PROTHROMBIN; RADIATION DOSES; RADIOTHERAPY; TOBACCO SMOKES; TRANSFERASES
OSTI ID:
22142944
Country of Origin:
Netherlands
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 0027-5107; Other: PII: S0027-5107(08)00280-7; TRN: NL09S2675097644
Availability:
Available from http://dx.doi.org/10.1016/j.mrfmmm.2008.11.005
Submitting Site:
NLN
Size:
page(s) 118-131
Announcement Date:
Oct 31, 2013

Citation Formats

Baldi, D., Izzotti, A., Bonica, P., Pera, P., and Pulliero, A., E-mail: alessandra.pulliero@unige.it. Degenerative periodontal-diseases and oral osteonecrosis: The role of gene-environment interactions. Netherlands: N. p., 2009. Web. doi:10.1016/J.MRFMMM.2008.11.005.
Baldi, D., Izzotti, A., Bonica, P., Pera, P., & Pulliero, A., E-mail: alessandra.pulliero@unige.it. Degenerative periodontal-diseases and oral osteonecrosis: The role of gene-environment interactions. Netherlands. doi:10.1016/J.MRFMMM.2008.11.005.
Baldi, D., Izzotti, A., Bonica, P., Pera, P., and Pulliero, A., E-mail: alessandra.pulliero@unige.it. 2009. "Degenerative periodontal-diseases and oral osteonecrosis: The role of gene-environment interactions." Netherlands. doi:10.1016/J.MRFMMM.2008.11.005. https://www.osti.gov/servlets/purl/10.1016/J.MRFMMM.2008.11.005.
@misc{etde_22142944,
title = {Degenerative periodontal-diseases and oral osteonecrosis: The role of gene-environment interactions}
author = {Baldi, D., Izzotti, A., Bonica, P., Pera, P., and Pulliero, A., E-mail: alessandra.pulliero@unige.it}
abstractNote = {Chronic-degenerative dentistry diseases, including periodontal diseases and oral osteonecrosis, are widespread in human populations and represent a significant problem for public health. These diseases result from pathogenic mechanisms created by the interaction between environmental genotoxic risk-factors and genetic assets conferring individual susceptibility. Osteonecrosis occurs in subjects undergoing exposure to high doses of DNA-damaging agents for chemo- and radiotherapy of neoplastic diseases. In susceptible patients, ionizing radiation and biphosphonate-chemotherapy induce severe, progressive, and irreversible degeneration of facial bones, resulting in avascular necrosis of the jaw. This may also occur in patients receiving biphosphonate for osteoporosis therapy. Periodontal diseases include chronic, aggressive, and necrotizing periodontitis, often resulting in severe alteration of periodontal tissues and tooth loss. Cigarette smoking and chronic inflammation caused by specific bacteria are the main risk factors for periodontitis. Oxidative damage plays a fundamental pathogenic role, as established by detection of mitochondrial DNA damage in the gingival tissue of patients with periodontitis. Endogenous risk factors in dental diseases include polymorphisms for metabolic enzymes such as glutathione transferases M1 and T1, N-acetyl transferase 2, and CYP 1A1. Other genetic polymorphisms that confer susceptibility to dentistry diseases affect genes encoding metalloproteases (involved in periodontal tissue remodeling and degradation), cytokines (involved in inflammation), prothrombin, and DNA repair activities. These findings provide evidence that dentistry diseases are related to risk factors associated with environmental mutagenesis. This issue warrants future investigations aimed at improving oral health and preventing oral degenerative diseases using molecular and experimental approaches currently utilized in mutagenicity studies.}
doi = {10.1016/J.MRFMMM.2008.11.005}
journal = {Mutation Research}
issue = {1-2}
volume = {667}
journal type = {AC}
place = {Netherlands}
year = {2009}
month = {Jul}
}