help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
This version published online on October 2, 2003
Endocrinology, doi:10.1210/en.2003-1239
A more recent version of this article appeared on January 1, 2004
This Article
Right arrow Author Manuscript (PDF)
Right arrow All Versions of this Article:
145/1/447    most recent
Author Manuscript (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by He, H.
Right arrow Articles by Graves, D. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by He, H.
Right arrow Articles by Graves, D. T.

Submitted on September 18, 2003
Accepted on September 22, 2003

Diabetes Causes Decreased Osteoclastogenesis, Reduced Bone Formation and Enhanced Apoptosis of Osteoblastic Cells in Bacteria Stimulated Bone Loss

Hongbing He1, Rongkun Liu1, Tesfahun Desta1, Cataldo Leone1, Louis C. Gerstenfeld1, and Dana T. Graves1*

1 Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118 Department of Orthopedics, School of Medicine, 700 Albany Street, Boston Medical Center, Boston, MA 02118

* To whom correspondence should be addressed. E-mail: dgraves{at}bu.edu.

The most common cause of inflammatory bone loss is periodontal disease. Following bacterial insult inflammation induces bone resorption which is followed by new reparative bone formation. Since diabetics have a higher incidence and more severe periodontitis, we examined mechanisms by which diabetes alters the response of bone to bacterial challenge. This was accomplished with db/db mice, which naturally develop type 2 diabetes. Following inoculation of bacteria osteoclastogenesis and bone resorption was measured. Both parameters were decreased in the diabetic group. Diabetes also suppressed reparative bone formation measured histologically and by the expression of osteocalcin. The impact of diabetes on new bone formation coincided with the effect of diabetes on apoptosis of bone lining cells. Within 5 days of bacterial challenge, apoptosis declined in the wild-type animals yet remained significantly higher in the diabetic group. Thus, diabetes may cause a net loss of bone because the suppression of bone formation is greater than the suppression of bone resorption. The diminished formation may be due in part to prolonged apoptosis of bone lining cells.
Key words: apoptosis • bone formation • bone resorption • diabetes • inflammation • osteoclast




This article has been cited by other articles:


Home page
 EndocrinologyHome page
R. Irwin, H. V. Lin, K. J. Motyl, and L. R. McCabe
Normal Bone Density Obtained in the Absence of Insulin Receptor Expression in Bone
Endocrinology, December 1, 2006; 147(12): 5760 - 5767.
[Abstract] [Full Text] [PDF]

Home page
 J. Dent. Res.Home page
R. Liu, H.S. Bal, T. Desta, N. Krothapalli, M. Alyassi, Q. Luan, and D.T. Graves
Diabetes Enhances Periodontal Bone Loss through Enhanced Resorption and Diminished Bone Formation.
J. Dent. Res., June 1, 2006; 85(6): 510 - 514.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
C. W. Leone, H. Bokhadhoor, D. Kuo, T. Desta, J. Yang, M. F. Siqueira, S. Amar, and D. T. Graves
Immunization Enhances Inflammation and Tissue Destruction in Response to Porphyromonas gingivalis
Infect. Immun., April 1, 2006; 74(4): 2286 - 2292.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
R. Liu, H. S. Bal, T. Desta, Y. Behl, and D. T. Graves
Tumor Necrosis Factor-{alpha} Mediates Diabetes-Enhanced Apoptosis of Matrix-Producing Cells and Impairs Diabetic Healing
Am. J. Pathol., March 1, 2006; 168(3): 757 - 764.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
H. A. Al-Mashat, S. Kandru, R. Liu, Y. Behl, T. Desta, and D. T. Graves
Diabetes Enhances mRNA Levels of Proapoptotic Genes and Caspase Activity, Which Contribute to Impaired Healing
Diabetes, February 1, 2006; 55(2): 487 - 495.
[Abstract] [Full Text] [PDF]

Home page
 J. Dent. Res.Home page
D.T. Graves, R. Liu, M. Alikhani, H. Al-Mashat, and P.C. Trackman
Diabetes-enhanced Inflammation and Apoptosis--Impact on Periodontal Pathology
J. Dent. Res., January 1, 2006; 85(1): 15 - 21.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
K. M. Thrailkill, C. K. Lumpkin Jr., R. C. Bunn, S. F. Kemp, and J. L. Fowlkes
Is insulin an anabolic agent in bone? Dissecting the diabetic bone for clues
Am J Physiol Endocrinol Metab, November 1, 2005; 289(5): E735 - E745.
[Abstract] [Full Text] [PDF]

Home page
 J. Dent. Res.Home page
D.T. Graves, G. Naguib, H. Lu, C. Leone, H. Hsue, and E. Krall
Inflammation is More Persistent in Type 1 Diabetic Mice
J. Dent. Res., April 1, 2005; 84(4): 324 - 328.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
R. Liu, T. Desta, H. He, and D. T. Graves
Diabetes Alters the Response to Bacteria by Enhancing Fibroblast Apoptosis
Endocrinology, June 1, 2004; 145(6): 2997 - 3003.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2003 by The Endocrine Society