Open AccessBacteria Induce Osteoclastogenesis via an Osteoblast-Independent Pathway
Author(s) -
Yanling Jiang,
Chetan K. Mehta,
Tun-Yi Hsu,
Fahad F. H. Alsulaimani
Publication year - 2002
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.70.6.3143-3148.2002
Subject(s) - rankl , bone resorption , osteoprotegerin , osteoclast , porphyromonas gingivalis , osteoblast , biology , bone remodeling , inflammation , osteolysis , periodontitis , rank ligand , tumor necrosis factor alpha , lipoteichoic acid , cytokine , cancer research , immunology , medicine , receptor , endocrinology , activator (genetics) , in vitro , bacteria , staphylococcus aureus , dentistry , biochemistry , genetics
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-kappaB (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.