scholarly journals Irsogladine maleate regulates neutrophil migration and E-cadherin expression in gingival epithelium stimulated by Aggregatibacter actinomycetemcomitans

2010 ◽  
Vol 79 (10) ◽  
pp. 1496-1505 ◽  
Author(s):  
Tsuyoshi Fujita ◽  
Akiyoshi Kishimoto ◽  
Hideki Shiba ◽  
Kouichi Hayashida ◽  
Mikihito Kajiya ◽  
...  
2006 ◽  
Vol 77 (5) ◽  
pp. 832-839 ◽  
Author(s):  
Hsiao-Pei Tu ◽  
Yen-Teen Chen ◽  
Yi-Shing Shieh ◽  
Yu-Tang Chin ◽  
Ren-Yeong Huang ◽  
...  

2012 ◽  
Vol 80 (6) ◽  
pp. 2247-2256 ◽  
Author(s):  
Jun Kang ◽  
Beatriz de Brito Bezerra ◽  
Sandra Pacios ◽  
Oelisoa Andriankaja ◽  
Yu Li ◽  
...  

ABSTRACTThe purpose of this study was to test the hypothesis that diabetes aggravates periodontal destruction induced byAggregatibacter actinomycetemcomitansinfection. Thirty-eight diabetic and 33 normal rats were inoculated withA. actinomycetemcomitansand euthanized at baseline and at 4, 5, and 6 weeks after inoculation. Bone loss and the infiltration of polymorphonuclear leukocytes (PMNs) in gingival epithelium were measured in hematoxylin-eosin-stained sections. The induction of tumor necrosis factor alpha (TNF-α) was evaluated by immunohistochemistry and of apoptotic cells by a TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay. AfterA. actinomycetemcomitansinfection, the bone loss in diabetic rats was 1.7-fold and the PMN infiltration 1.6-fold higher than in normoglycemic rats (P< 0.05). The induction of TNF-α was 1.5-fold higher and of apoptotic cells was up to 3-fold higher in diabetic versus normoglycemic rats (P< 0.05). Treatment with a caspase-3 inhibitor significantly blocked noninflammatory cell apoptosis induced byA. actinomycetemcomitansinfection in gingival epithelium and connective tissue (P< 0.05). These results provide new insight into how diabetes aggravatesA. actinomycetemcomitans-induced periodontal destruction in rats by significantly increasing the inflammatory response, leading to increased bone loss and enhancing apoptosis of gingival epithelial and connective tissue cells through a caspase-3-dependent mechanism. Antibiotics had a more pronounced effect on many of these parameters in diabetic than in normoglycemic rats, suggesting a deficiency in the capacity of diabetic animals to resist infection.


Author(s):  
C.N. Sun

The present study demonstrates the ultrastructure of the gingival epithelium of the pig tail monkey (Macaca nemestrina). Specimens were taken from lingual and facial gingival surfaces and fixed in Dalton's chrome osmium solution (pH 7.6) for 1 hr, dehydrated, and then embedded in Epon 812.Tonofibrils are variable in number and structure according to the different region or location of the gingival epithelial cells, the main orientation of which is parallel to the long axis of the cells. The cytoplasm of the basal epithelial cells contains a great number of tonofilaments and numerous mitochondria. The basement membrane is 300 to 400 A thick. In the cells of stratum spinosum, the tonofibrils are densely packed and increased in number (fig. 1 and 3). They seem to take on a somewhat concentric arrangement around the nucleus. The filaments may occur scattered as thin fibrils in the cytoplasm or they may be arranged in bundles of different thickness. The filaments have a diameter about 50 A. In the stratum granulosum, the cells gradually become flatted, the tonofibrils are usually thin, and the individual tonofilaments are clearly distinguishable (fig. 2). The mitochondria and endoplasmic reticulum are seldom seen in these superficial cell layers.


Author(s):  
J. Roemer ◽  
S.R. Simon

We are developing an in vitro interstitial extracellular matrix (ECM) system for study of inflammatory cell migration. Falcon brand Cyclopore membrane inserts of various pore sizes are used as a support substrate for production of ECM by R22 rat aortic smooth muscle cells. Under specific culture conditions these cells produce a highly insoluble matrix consisting of typical interstitial ECM components, i.e.: types I and III collagen, elastin, proteoglycans and fibronectin.


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