Topic
Physiologic bone resorption
About: Physiologic bone resorption is a research topic. Over the lifetime, 3 publications have been published within this topic receiving 137 citations.
Papers
TL;DR: Five novel RANKL-induced, NFATc1-dependent transcripts in the osteoclast are described: Nhedc2, Rhoc, Serpind1, Adcy3 and Rab38, and despite reasonable hypotheses for the importance of these molecules in the bone resorption pathway, the analysis of mice with mutations in these genes failed to reveal a function in osteooclast biology.
39 citations
TL;DR: Daily subcutaneous injections of parathyroid extract, beginning within 24 hr of birth, significantly increased the incidence of molar teeth eruption in grey lethal mice.
6 citations
TL;DR: It is reported that Porphyromonas gingivalis, a periodontal pathogen, and Escherichia coli LPS induce osteoclastic cell formation from murine leukocytes in the absence of osteoblasts, and suggested that the mix of cells that participate in inflammatory and physiologic bone resorption may be different.
Abstract: 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-κB (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.
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2012 | 1 |
| 2002 | 1 |
| 1972 | 1 |