Effect of streptococcal cell wall components on bone metabolism in vitro

Meikle, Murray C.; Gowen, Maxine; Reynolds, John J.

doi:10.1007/bf02411268

Cited by 20 publications

(3 citation statements)

References 20 publications

(10 reference statements)

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“…The high potency of the B. gingivalis LPS fractions in stimulating bone resorption confirms findings previously reported (5,13). While previous studies have demonstrated that cell wall fractions from gram-positive organisms such as Streptococcus mutants and Streptococcus sanguis (10) and muramyl dipeptide (25) have been shown to inhibit bone protein synthesis in calvarial systems (10), this is the first report to indicate that LPS can inhibit bone collagen formation. Interestingly, the higher-molecular-weight species ofB.…”

Section: Discussionmentioning

confidence: 69%

Modulation of bone metabolism by two chemically distinct lipopolysaccharide fractions from Bacteroides gingivalis

Millar¹,

Goldstein²,

Levine³

et al. 1986

Infect Immun

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Section: Discussionmentioning

confidence: 69%

Modulation of bone metabolism by two chemically distinct lipopolysaccharide fractions from Bacteroides gingivalis

Millar¹,

Goldstein²,

Levine³

et al. 1986

Infect Immun

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“…Many of these non-LPS components are also potent inducers of cytokine synthesis (38,39). Examination of gram-positive bacteria has revealed that unspecified cell wall components from Streptococcus mutans and Streptococcus sanguis (62,82) and sonicated extracts of Staphylococcus aureus and Staphylococcus epidermidis (63) stimulate bone resorption. Lipoteichoic acid (31), muramyl dipeptide (13), and an amphipathic antigen from Actinomyces viscosus also have been reported to induce bone resorption (32).…”

Section: Fig 3 the Possible Points Of Interaction Between Osteolytimentioning

confidence: 99%

Bacterially induced bone destruction: mechanisms and misconceptions

et al. 1996

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Normal bone remodelling requires the coordinated regulation of the genesis and activity of osteoblast and osteoclast lineages. Any interference with these integrated cellular systems can result in dysregulation of remodelling with the consequent loss of bone matrix. Bacteria are important causes of bone pathology in common conditions such as periodontitis, dental cysts, bacterial arthritis, and osteomyelitis. It is now established that many of the bacteria implicated in bone diseases contain or produce molecules with potent effects on bone cells. Some of these molecules, such as components of the gram-positive cell walls (lipoteichoic acids), are weak stimulators of bone resorption in vitro, while others (PMT, cpn60) are as active as the most active mammalian osteolytic factors such as cytokines like IL-1 and TNF. The complexity of the integration of bone cell lineage development means that there are still question marks over the mechanism of action of many well-known bone-modulatory molecules such as parathyroid hormone. The key questions which must be asked of the now-recognized bacterial bone-modulatory molecules are as follows: (i) what cell population do they bind to, (ii) what is the nature of the receptor and postreceptor events, and (iii) is their action direct or dependent on the induction of secondary extracellular bone-modulating factors such as cytokines, eicosanoids, etc. In the case of LPS, this ubiquitous gram-negative polymer probably binds to osteoblasts or other cells in bone through the CD14 receptor and stimulates them to release cytokines and eicosanoids which then induce the recruitment and activation of osteoclasts. This explains the inhibitor effects of nonsteroidal and anticytokine agents on LPS-induced bone resorption. However, other bacterial factors such as the potent toxin PMT may act by blocking the normal maturation pathway of the osteoblast lineage, thus inducing dysregulation in the tightly regulated process of resorption and replacement of bone matrix. At the present time, it is not possible to define a general mechanism by which bacteria promote loss of bone matrix. Many bacteria are capable of stimulating bone matrix loss, and the information available would suggest that each organism possesses different factors which interact with bone in different ways. With the rapid increase in antibiotic resistance, particularly with Staphylococcus aureus and M. tuberculosis, organisms responsible for much bone pathology in developed countries only two generations ago, we would urge that much greater attention should be focused on the problem of bacterially induced bone remodelling in order to define pathogenetic mechanisms which could be therapeutic targets for the development of new treatment modalities.

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“…Thus, the active moiety in this fraction could be a major factor in the pathogenesis of bone resorption in LJP. A number of bacterial components including LPS, teichoic acids, muramyl dipeptide, and certain protein fractions have been shown to be capable of stimulating bone resorption (10)(11)(12)(13). However, with the possible exception of a toxin from the bacterium Pasteurella multocida (14), the SAM from A. actinomycetemcomitans is the most potent bacterial osteolytic agent reported.…”

Section: Introductionmentioning

confidence: 99%

The potent bone-resorbing mediator of Actinobacillus actinomycetemcomitans is homologous to the molecular chaperone GroEL.

Kirby¹,

Meghji²,

Nair³

et al. 1995

J. Clin. Invest.

126

112

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Actinobacillus actinomycetemcomitans is a Gram-negative bacterium implicated in the pathology of localized juvenile periodontitis, a condition involving rapid destruction of alveolar bone. We have established that gentle extraction of this bacterium in saline releases a proteinaceous fraction (which we have termed surface-associated material [SAM]) which has potent osteolytic activity in the murine calvarial bone resorption assay. Fractionation of the SAM has now revealed that activity is associated with a 62-kD protein. This bone-resorbing activity can be blocked by a monoclonal antibody (raised to the whole bacterium) that is claimed to recognize a protein homologous to the Escherichia coil molecular chaperone GroEL. Purification of this bone-resorbing protein to homogeneity has been achieved by a combination of anion exchange, gel filtration, and ATP-affinity chromatography and the NH2-terminal sequence shows > 95% homology to E.

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Effect of streptococcal cell wall components on bone metabolism in vitro

Cited by 20 publications

References 20 publications

Modulation of bone metabolism by two chemically distinct lipopolysaccharide fractions from Bacteroides gingivalis

Modulation of bone metabolism by two chemically distinct lipopolysaccharide fractions from Bacteroides gingivalis

Bacterially induced bone destruction: mechanisms and misconceptions

The potent bone-resorbing mediator of Actinobacillus actinomycetemcomitans is homologous to the molecular chaperone GroEL.

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