TY - JOUR
T1 - Characterization of progressive periodontal lesions in chronic periodontitis patients
T2 - Levels of chemokines, cytokines, matrix metalloproteinase-13, periodontal pathogens and inflammatory cells
AU - Silva, Nora
AU - Dutzan, Nicolas
AU - Hernandez, Marcela
AU - Dezerega, Andrea
AU - Rivera, Oriana
AU - Aguillon, Juan Carlos
AU - Aravena, Octavio
AU - Lastres, Pedro
AU - Pozo, Patricia
AU - Vernal, Rolando
AU - Gamonal, Jorge
PY - 2008/3
Y1 - 2008/3
N2 - Background and aims: Periodontitis is an infection with an episodic nature of tissue support destruction. The aim of this work was to determine the levels of chemokines, cytokines, matrix metalloproteinase-13, periodontal pathogens and inflammatory cells in periodontal sites characterized by active periodontal connective tissue destruction. Material and Method: Fifty-six patients with moderate or advanced severity of chronic periodontitis were selected. Periodontitis was characterized by at least six sites with probing depth ≥5 mm, clinical attachment level ≥3 mm and radiographic bone loss. Periodontitis progression was determined by the tolerance method. Receptor activator for nuclear factor κ B-ligand (RANK-L), monocyte chemoattractant protein-1 (MCP-1), tumour necrosis factor-α (TNF-α), IL-1β, MMP-13, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsithia and inflammatory cells levels were determined. Statistical analysis was performed using the Stata® 7.0 software. Data were expressed as mean±SD and paired samples t-test and χ2 tests were used. Results: Higher RANK-L, IL-1β and MMP-13 activity levels were observed in active sites (p<0.05). The proportion of P. gingivalis, A. actinomycetemcomitans, T. forsythia and the number of CD4+ T were higher in active than in inactive sites (p>0.05). Conclusion: The detection of periodontopathic bacteria, host matrix metalloproteinases and cytokines in periodontitis patients with lesions undergoing episodic attachment loss could partially explain the mechanisms associated with the destruction of the supporting tissues of the tooth.
AB - Background and aims: Periodontitis is an infection with an episodic nature of tissue support destruction. The aim of this work was to determine the levels of chemokines, cytokines, matrix metalloproteinase-13, periodontal pathogens and inflammatory cells in periodontal sites characterized by active periodontal connective tissue destruction. Material and Method: Fifty-six patients with moderate or advanced severity of chronic periodontitis were selected. Periodontitis was characterized by at least six sites with probing depth ≥5 mm, clinical attachment level ≥3 mm and radiographic bone loss. Periodontitis progression was determined by the tolerance method. Receptor activator for nuclear factor κ B-ligand (RANK-L), monocyte chemoattractant protein-1 (MCP-1), tumour necrosis factor-α (TNF-α), IL-1β, MMP-13, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsithia and inflammatory cells levels were determined. Statistical analysis was performed using the Stata® 7.0 software. Data were expressed as mean±SD and paired samples t-test and χ2 tests were used. Results: Higher RANK-L, IL-1β and MMP-13 activity levels were observed in active sites (p<0.05). The proportion of P. gingivalis, A. actinomycetemcomitans, T. forsythia and the number of CD4+ T were higher in active than in inactive sites (p>0.05). Conclusion: The detection of periodontopathic bacteria, host matrix metalloproteinases and cytokines in periodontitis patients with lesions undergoing episodic attachment loss could partially explain the mechanisms associated with the destruction of the supporting tissues of the tooth.
KW - Cytokines
KW - Inflammatory cells
KW - Matrix metalloproteinases
KW - Periodontal pathogens
KW - Progressive periodontitis
UR - http://www.scopus.com/inward/record.url?scp=38849108128&partnerID=8YFLogxK
U2 - 10.1111/j.1600-051X.2007.01190.x
DO - 10.1111/j.1600-051X.2007.01190.x
M3 - Article
C2 - 18269660
AN - SCOPUS:38849108128
SN - 0303-6979
VL - 35
SP - 206
EP - 214
JO - Journal of Clinical Periodontology
JF - Journal of Clinical Periodontology
IS - 3
ER -