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Bacterial Infection Increases Periodontal Bone Loss in Diabetic Rats through Enhanced Apoptosis
Pacios, Sandra1; Andriankaja, Oelisoa1,2; Kang, Jun3; Alnammary, Maher1; Bae, Jason1; Bezerra, Beatriz de Brito4; Schreiner, Helen5; Fine, Daniel H.5; Graves, Dana T.1
刊名AMERICAN JOURNAL OF PATHOLOGY
2013-12-01
DOI10.1016/j.ajpath.2013.08.017
183期:6页:1928-1935
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pathology
研究领域[WOS]Pathology
关键词[WOS]CASPASE-3 ACTIVATION ; OXIDATIVE STRESS ; IN-VIVO ; INFLAMMATION ; GENES ; ACTINOMYCETEMCOMITANS ; FIBROBLASTS ; OSTEOBLASTS ; OSTEOCLASTS ; RESORPTION
英文摘要

Periodontal disease is the most common osteolytic disease in humans and is significantly increased by diabetes mellitus. We tested the hypothesis that bacterial infection induces bone loss in diabetic animals through a mechanism that involves enhanced apoptosis. Type II diabetic rats were inoculated with Aggregatibacter actinomycetemcomitans and treated with a caspase-3 inhibitor, ZDEVD-FMK, or vehicle alone. Apoptotic cells were measured with TUNEL; osteoblasts and bone area were measured in H&E sections. New bone formation was assessed by labeling with fluorescent dyes and by osteocalcin mRNA levels. Osteoclast number, eroded bone surface, and new bone formation were measured by tartrate-resistant acid phosphatase staining. Immunohistochemistry was performed with an antibody against tumor necrosis factor-alpha. Bacterial infection doubled the number of tumor necrosis factor-alpha-expressing cells and increased apoptotic cells adjacent to bone 10-fold (P < 0.05). Treatment with caspase inhibitor blocked apoptosis, increased the number of osteoclasts, and eroded bone surface (P < 0.05); yet, inhibition of apoptosis resulted in significantly greater net bone area because of an increase in new bone formation, osteoblast numbers, and an increase in bone coupling. Thus, bacterial infection in diabetic rats stimulates periodontitis, in part through enhanced apoptosis of osteoblastic cells that reduces osseous coupling through a caspase-3 dependent mechanism.

语种英语
WOS记录号WOS:000327829000023
项目编号DE017732 ; P30AR050950
资助机构NIH ; Penn Center for Musculoskeletal Disorders from NIAMS ; Coordination for the Improvement of Higher Education Personnel (CAPES) Foundation in Brazil
引用统计
被引频次:19[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/63016
专题北京大学口腔医学院_牙周科
作者单位1.Univ Penn, Dept Periodont, Sch Dent Med, Philadelphia, PA 19104 USA
2.Univ Puerto Rico, Sch Dent Med, Ctr Clin Res & Hlth Promot, San Juan, PR 00936 USA
3.Peking Univ, Sch & Hosp Stomatol, Dept Periodontol, Beijing 100871, Peoples R China
4.Univ Estadual Campinas, Piracicaba Dent Sch, Prosthodont & Periodont Dept, Piracicaba, Brazil
5.Univ Med & Dent New Jersey, New Jersey Dent Sch, Dept Oral Biol, Newark, NJ 07103 USA
推荐引用方式
GB/T 7714
Pacios, Sandra,Andriankaja, Oelisoa,Kang, Jun,et al. Bacterial Infection Increases Periodontal Bone Loss in Diabetic Rats through Enhanced Apoptosis[J]. AMERICAN JOURNAL OF PATHOLOGY,2013,183(6):1928-1935.
APA Pacios, Sandra.,Andriankaja, Oelisoa.,Kang, Jun.,Alnammary, Maher.,Bae, Jason.,...&Graves, Dana T..(2013).Bacterial Infection Increases Periodontal Bone Loss in Diabetic Rats through Enhanced Apoptosis.AMERICAN JOURNAL OF PATHOLOGY,183(6),1928-1935.
MLA Pacios, Sandra,et al."Bacterial Infection Increases Periodontal Bone Loss in Diabetic Rats through Enhanced Apoptosis".AMERICAN JOURNAL OF PATHOLOGY 183.6(2013):1928-1935.
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