Induction of osteoclastogenesis-inducing cytokines and invasion by alive Aggregatibacter actinomycetemcomitans in osteoblasts.
10.5051/jkape.2007.37.3.553
- Author:
Ho Kil CHOI
1
;
Yang Sin LEE
;
Min Young KIM
;
Kyoung Dae KIM
;
Jeong Heon CHA
;
Yun Jung YOO
Author Information
1. Department of Oral Biology, Brain Korea 21 project, College of Dentistry, Yonsei University, Korea.
- Publication Type:Original Article
- Keywords:
Aggregatibacter actinomycetemcomitans;
osteoblast;
osteoclastogenesis-inducing cytokine;
invasion
- MeSH:
Aggregatibacter actinomycetemcomitans*;
Aggregatibacter*;
Animals;
Bacteria;
Bone Resorption;
Chemokine CCL3;
Cytokines*;
Immune System;
Interleukins;
Macrophages;
Mice;
Osteoblasts*;
Periodontitis;
RNA, Messenger;
Skull;
Tumor Necrosis Factor-alpha;
United Nations
- From:The Journal of the Korean Academy of Periodontology
2007;37(3):553-562
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Osteoblasts regulate osteoclastogenesis by production of various cytokines. Aggregatibacter(A) actinomycetemcomitans is one of periodontopathogens which invades gingival tissue. Therefore, clarifying the effect of alive A. actinomycetemcomitans on osteoblasts is important to understand the mechanism of alveolar bone resorption in periodontitis. We investigated induction of osteoclastogenesis- inducing cytokines, adherence, and invasion by A. actinomycetemcomitans in osteoblasts. Osteoblasts were isolated from mouse calvaria and expression of cytokines was determined by RT-PCR. When the ratio of the number of A. actinomycetemcomtians to the number of osteoblasts was 10:1, 50:1 and 100:1, RANKL mRNA expression was increased. A. actinomycetemcomitans also increased expression of macrophage inflammatory protein (MIP)-1alpha, interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha. A. actinomycetemcomitans attached to and invaded osteoblasts at ratio of 1000:1. These results suggest that A. actinomycetemcomitans increases osteoclastogenesis-inducing ability of osteoblasts by stimulating the expression of RANKL, MIP-1alpha, IL-1beta, and TNF-alpha and that invasion of A. actinomycetemcomitans provides a means by which the bacteria escape from immune system and antibiotic therapy.
