POSSIBLE INVOLVEMENT OF ADVANCED GLYCATION END PRODUCTS IN PERIODONTAL DISEASES

被引:30
作者
Pietropaoli, D. [1 ]
Tatone, C. [1 ]
D'Alessandro, A. M. [1 ]
Monaco, A. [1 ]
机构
[1] Univ Aquila, Dept Hlth Sci, Sch Dent, I-67100 Laquila, Italy
关键词
periodontal ligament; periodontal diseases; advanced glycation end products; AGE; ROS; oxidative stress; METABOLIC DISEASES; OXIDATIVE STRESS; LIGAMENT; ASSOCIATION; DYSFUNCTION; INDUCTION; COLLAGEN; RECEPTOR; THERAPY; RAGE;
D O I
10.1177/039463201002300301
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Periodontal diseases are considered as multifactorial conditions initiated by infection with pathogenic bacteria, promoted by inflammation and immune response against bacteria and modified by different environmental and genetic factors. Recently, interest in periodontal diseases has been increasing due to the awareness that the hyperinflammatory status associated with this disorder could impose a significant increase of reactive oxygen species (ROS) relevant to numerous systemic diseases driven by a pro-oxidant profile. A highly complex interplay occurs between oxidative stress and AGEs (Advanced Glycation End products), a group of heterogeneous compounds that form constantly under physiologic conditions, although their rate of formation is markedly increased in hyperglycemia and oxidizing conditions. Starting from the most relevant hypotheses on the pathogenesis of periodontal diseases, the present review outlines their relationship with oxidative stress and inflammation response in order to make a critical evaluation of the potential role of AGEs in periodontal deterioration. Although direct evidence for the presence of AGEs in the periodontal ligament is still lacking, valuable approaches based on the use of periodontal cells along with genetic and biochemical studies in animal models and chronic periodontal patients support a potential role for protein glycation in the aetiology and severity of this disease. Following a review of the current literature, the present study highlights the need for further investigation on the presence of AGEs in the periodontal ligament as a means for the comprehension of the pathogenic mechanisms underlying periodontal diseases in order to develop prevention and treatment modalities for this dysfunction.
引用
收藏
页码:683 / 691
页数:9
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共 50 条
[1]   Periodontitis and Type 2 Diabetes: Is Oxidative Stress the Mechanistic Link? [J].
Allen, E. M. ;
Matthews, J. B. ;
O'Connor, R. ;
O'Halloran, D. ;
Chapple, I. L. C. .
SCOTTISH MEDICAL JOURNAL, 2009, 54 (02) :41-47
[2]  
AUKHIL I, 1990, Critical Reviews in Oral Biology and Medicine, V1, P101
[3]   Tobacco-induced alterations to Porphyromonas gingivalis-host interactions [J].
Bagaitkar, Juhi ;
Williams, Lisa R. ;
Renaud, Diane E. ;
Bemakanakere, Manjunatha R. ;
Martin, Mike ;
Scott, David A. ;
Demuth, Donald R. .
ENVIRONMENTAL MICROBIOLOGY, 2009, 11 (05) :1242-1253
[4]   In vitro stem cell cultures from human dental pulp and periodontal ligament:: New prospects in dentistry [J].
Ballini, A. ;
De Frenza, G. ;
Cantore, S. ;
Papa, F. ;
Grano, M. ;
Mastrangelo, F. ;
Tete, S. ;
Grassi, F. R. .
INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY, 2007, 20 (01) :9-16
[5]   The role of AGEs in aging: causation or correlation [J].
Baynes, JW .
EXPERIMENTAL GERONTOLOGY, 2001, 36 (09) :1527-1537
[6]   The periodontal ligament: A unique, multifunctional connective tissue [J].
Beertsen, W ;
McCulloch, CAG ;
Sodek, J .
PERIODONTOLOGY 2000, 1997, 13 :20-40
[7]  
Beisswenger P, 2003, DIABETES METAB, V29, pS95
[8]   Advanced glycation end products and the kidney [J].
Bohlender, JM ;
Franke, S ;
Stein, G ;
Wolf, G .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2005, 289 (04) :F645-F659
[9]   The role of reactive oxygen and antioxidant species in periodontal tissue destruction [J].
Chapple, Iain L. C. ;
Matthews, John B. .
PERIODONTOLOGY 2000, 2007, 43 :160-232
[10]   Potential mechanisms underpinning the nutritional modulation of periodontal inflammation [J].
Chapple, Iain L. C. .
JOURNAL OF THE AMERICAN DENTAL ASSOCIATION, 2009, 140 (02) :178-184