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LPS and Health Maintenance

(5) Osteoporosis and LPS

LPS can promote bone metabolism; a previous study showed that ingesting LPS-containing beverages can curb bone density decrease (*1).

One age-related disease is osteoporosis. Women have an especially high risk of developing osteoporosis because they experience a rapid postmenopausal decline in the female hormone estrogen. Osteoporosis and resulting fractures can cause a person to become bedridden and affect dementia development and progression.

In addition to forming the skeleton that supports the body, bones serve as calcium reservoirs. Since bone stores and releases calcium as necessary, bone always produce and grind itself for metabolism. In order to produce bone, bone has to grind itself, so both need to be performed in a balanced manner. Bone-producing cells are called osteoblasts, whereas bone-grinding cells are called osteoclasts.

It is known that LPS activates macrophages. Stimulated by LPS, bone tissue macrophages secrete a substance called oncostatin M, which in turn promotes the differentiation of mesenchymal stem cells into osteoblasts (*2). Similarly, bone-grinding osteoclasts, which are macrophage-like cells, are also activated by LPS (*3). Thus, it appears that LPS promotes normal bone metabolism by activating the two types of cell required for bone metabolism.

Mechanism of bone density maintenance

(*1) Pantoea agglomerans lipopolysaccharide maintains bone density in premenopausal women: a randomized, double-blind, placebo-controlled trial, Food science & nutrition 2 (6): 638-646 (2014)
(*2) Induction of Osteogenesis in Mesenchymal Stem Cells by Activated Monocytes/Macrophages Depends on Oncostatin M Signaling, STEM CELLS 30: 762–772 (2012)
(*3) Lipopolysaccharide Promotes the Survival of Osteoclasts Via Toll-Like Receptor 4, but Cytokine Production of Osteoclasts in Response to Lipopolysaccharide Is Different from That of Macrophages, J Immunol 170: 3688-3695 (2003)

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