Liver–bone crosstalk implicated in osteoporosis progression

Osteoporosis is a disease characterized by a low level of bone formation (by osteoblasts) and an excess of bone resorption (by osteoclasts), in part due to increased differentiation of

osteoclasts from their precursor cells, bone marrow-derived monocytes (BMDMs). A new study finds that deficiency in the deacetylase SIRT2 in hepatocytes reduces bone loss in mouse models of

osteoporosis.

They then generated a liver-specific knockout of SIRT2 (SIRT2-KOhep mice). Aged SIRT2-KOhep mice had statistically significantly higher bone mass than age-matched controls. Additionally,

SIRT2-KOhep mice had lower serum levels of C-terminal telopeptide for type 1 collagen, a marker of bone turnover, and lower numbers of osteoclasts than controls. The researchers then

co-cultured BMDMs in vitro with plasma from either SIRT2-KOhep mice or control mice; the culture was treated with the cytokines M-CSF and RANKL to induce osteoclast differentiation. Plasma

from SIRT2-KOhep mice suppressed RANKL-induced osteoclastogenesis, as shown by the reduced number and size of osteoclasts and reduced expression of key markers of osteoclastogenesis compared

with the control co-cultures.

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