Initial apical migration of junctional epithelium in rats following application of lipopolysaccharide and proteases

被引:42
作者
Ekuni, D [1 ]
Tomofuji, T [1 ]
Yamanaka, R [1 ]
Tachibana, K [1 ]
Yamamoto, T [1 ]
Watanabe, T [1 ]
机构
[1] Okayama Univ, Grad Sch Med & Dent, Dept Oral Hlth, Okayama 7008525, Japan
关键词
animal studies; antigens; nuclear; apical migration; apoptosis; epithelial attachment; fibroblasts; periodontal;
D O I
10.1902/jop.2005.76.1.43
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Background: Apical migration of junctional epithelium (JE) occurs in association with periodontal pocket formation. The aim of this study was to investigate the gingival changes occurring during apical migration of the JE following application of factors associated with inflammatory periodontal disease pathogenesis. Methods: Six-week-old male Wistar rats were divided into six groups: three experimental groups to investigate gingival changes following 2, 4, and 8 weeks topical application of lipopolysaccharide (LPS) and proteases and three control groups using pyrogen-free water. After 2, 4 or 8 weeks, nuclear DNA fragmentation was detected in periodontal ligament (PDL) fibroblasts using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method, and proliferative activities of the basal cells and fibroblasts were evaluated through expression of proliferating cell nuclear antigen (PCNA). Collagen destruction was examined histologically. Results: Gingiva treated with LPS and proteases showed an increase in PCNA-positive basal cells but not the fibroblasts. Collagen destruction was observed at 2 weeks; apical migration of the JE and TUNEL-positive fibroblasts was seen at 4 weeks. Conclusions: Following application of LPS and proteases to rat gingival sulci, the apical migration of the JE appears to occur simultaneously with the apoptosis of PDL fibroblasts, which in turn follows proliferation of the basal cells and collagen destruction.
引用
收藏
页码:43 / 48
页数:6
相关论文
共 28 条
[1]   A NEW CONCEPT OF POCKET FORMATION [J].
AISENBERG, MS ;
AISENBERG, AD .
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS, 1948, 1 (11) :1047-1055
[2]  
Berkovitz B.K., 1995, PERIODONTAL LIGAMENT, P9
[3]  
BREX MC, 1987, J PERIODONTAL RES, V22, P50
[4]  
CARRANZA FA, 2002, CARRANZAS CLIN PERIO, P336
[5]   Induction of cell proliferation and collagen synthesis in human small intestinal lamina propria fibroblasts by lipopolysaccharide: Possible involvement of nitric oxide [J].
Chakravortty, D ;
Kumar, KSN .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 240 (02) :458-463
[6]  
COHEN JJ, 1992, ANNU REV IMMUNOL, V10, P267, DOI 10.1146/annurev.iy.10.040192.001411
[7]   FINE-STRUCTURAL OBSERVATIONS ON THE MECHANISM OF LOSS OF ATTACHMENT DURING EXPERIMENTAL PERIODONTAL-DISEASE IN THE RAT [J].
DEPORTER, DA ;
BROWN, DY .
JOURNAL OF PERIODONTAL RESEARCH, 1980, 15 (03) :304-313
[8]   Proteases augment the effects of lipopolysaccharide in rat gingiva [J].
Ekuni, D ;
Yamamoto, T ;
Yamanaka, R ;
Tachibana, K ;
Watanabe, T .
JOURNAL OF PERIODONTAL RESEARCH, 2003, 38 (06) :591-596
[9]   IDENTIFICATION OF PROGRAMMED CELL-DEATH INSITU VIA SPECIFIC LABELING OF NUCLEAR-DNA FRAGMENTATION [J].
GAVRIELI, Y ;
SHERMAN, Y ;
BENSASSON, SA .
JOURNAL OF CELL BIOLOGY, 1992, 119 (03) :493-501
[10]   GRANULOCYTE APOPTOSIS AND THE CONTROL OF INFLAMMATION [J].
HASLETT, C ;
SAVILL, JS ;
WHYTE, MKB ;
STERN, M ;
DRANSFIELD, I ;
MEAGHER, LC .
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES, 1994, 345 (1313) :327-333