The British Journal of Rheumatology, Vol 37, 1095-1101, Copyright © 1998 by British Society for Rheumatology
S Meghji, SJ Crean, PA Hill, M Sheikh, SP Nair, K Heron, B Henderson, EB Mawer and M Harris
OBJECTIVE: Staphylococcus aureus is the cause of bone destruction in
osteomyelitis, bacterial arthritis and orthopaedic implant failure. We have
previously shown that gentle saline extraction of S. aureus has revealed
the presence of an extremely potent stimulator of osteoclast activation in
both the murine calvarial bone resorption assay and the isolated chick
osteoclast resorption assay. In order to investigate the mechanism of
action of this surface-associated material (SAM), we have investigated its
capacity to recruit osteoclasts. METHODS: The murine bone marrow osteoclast
recruitment assay was used. The ability of the recruited cells to resorb
dentine slices was also investigated. Results. The SAM from S. aureus dose
dependently stimulated tartrate- resistant acid phosphatase (TRAP)-positive
osteoclast formation and pit formation on dentine slices. Neutralization of
the cytokines tumour necrosis factor alpha and interleukin (IL)-6 totally
inhibited, but antagonism of IL-1 only partially blocked, the stimulated
maturation of osteoclast-like cells. CONCLUSION: These findings suggest
that bone destruction associated with local infection by S. aureus is due
to the stimulation of osteoclast formation induced by the action of the
easily solubilized SAM, and could explain the large numbers of osteoclasts
found in infarcted bone in osteomyelitis.
ORIGINAL PAPERS
Surface-associated protein from Staphylococcus aureus stimulates osteoclastogenesis: possible role in S. aureus-induced bone pathology
Department of Oral and Maxillofacial Surgery, Eastman Dental Institute for Oral Health Care Sciences, London.
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