Lutein Maintains Bone Mass In Vitro and In Vivo Against Disuse-Induced Bone Loss in Hindlimb-Unloaded Mice.

Background: Lutein, a carotenoid, exhibits various biological activities such as maintaining the health of the eye, skin, heart, and bone. Recently, we found that lutein has dual roles in suppressing bone resorption and promoting bone formation. In this study, we examined the effects of lutein in a disuse-induced osteoporosis model using hindlimb-unloaded (HLU) mice.

Roles of Toll-like Receptor Signaling in Inflammatory Bone Resorption.

Toll-like receptors (TLRs) are pattern recognition receptors expressed in immune cells, including neutrophils, macrophages, and dendritic cells. Microbe-associated molecular patterns, including bacterial components, membranes, nucleic acids, and flagella are recognized by TLRs in inflammatory immune responses. Periodontal disease is an inflammatory disease known to cause local infections associated with gingival inflammation, subsequently leading to alveolar bone resorption.

Prostate cancer expressing membrane-bound TGF-α induces bone formation mediated by the autocrine effect of prostaglandin E in osteoblasts.

Prostate cancer highly metastasizes to bone, and such cancer is associated with severe bone resorption and bone formation at the site of metastasis. Prostaglandin E (PGE) promotes bone resorption in inflammatory diseases; however, the roles in prostate cancer-induced bone formation are still unclear. In the present study, we investigated the effects of membrane-bound TGF-α on prostate cancer-induced bone formation through autocrine PGE signaling in osteoblasts.