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Infection and Immunity, June 2002, p. 3143-3148, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3143-3148.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Bacteria Induce Osteoclastogenesis via an Osteoblast-Independent Pathway

Yanling Jiang,* Chetan K. Mehta, Tun-Yi Hsu, and Fahad F. H. Alsulaimani

Department of Endodontics, Boston University School of Dental Medicine, Boston, Massachusetts 02118

Received 20 August 2001/ Returned for modification 5 December 2001/ Accepted 14 March 2002

Bacteria or their products may cause chronic inflammation and subsequent bone loss. This inflammation and bone loss may be associated with significant morbidity in chronic otitis media, periodontitis, endodontic lesions, and loosening of orthopedic implants caused by lipopolysaccharide (LPS)-contaminated implant particles. Currently, it is not clear how bacteria or endotoxin-induced bone resorption occurs and what cell types are involved. Here we report that Porphyromonas gingivalis, a periodontal pathogen, and Escherichia coli LPS induce osteoclastic cell formation from murine leukocytes in the absence of osteoblasts. In contrast, stimulation with parathyroid hormone had no effect. These multinucleated, tartrate-resistant acid phosphatase-positive cells were positive for receptor activator of NF-{kappa}B (RANK), the receptor for osteoprotegerin ligand (OPGL), also known as RANK ligand (RANKL). Blocking antibodies demonstrated that their formation was dependent upon expression of OPGL and, to a lesser extent, on tumor necrosis factor alpha. Mononuclear cells represented a significant source of OPGL production. In vivo, P. gingivalis injection stimulated OPGL expression in both mononuclear leukocytes and osteoblastic cells. Thus, these findings describe a pathway by which bacteria could enhance osteolysis independently of osteoblasts and suggest that the mix of cells that participate in inflammatory and physiologic bone resorption may be different. This may give insight into new targets of therapeutic intervention.

* Corresponding author. Mailing address: 700 Albany St., Rm. W-201, Boston University Medical Center, Boston, MA 02118. Phone: (617) 638-4987. Fax: (617) 638-4924. E-mail: yljiang{at}bu.edu.

Editor: R. N. Moore

Infection and Immunity, June 2002, p. 3143-3148, Vol. 70, No. 6
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.6.3143-3148.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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