Investigating Osteoblast Deficiencies in Aspects of Osteopenia

Bone density declines with aging, a condition known as osteopenia, and which leads to the serious frailties of osteoporosis. One of the possible reasons for this is a growing deficiency in osteoblasts, the cells that lay down bone structure, or perhaps a widening mismatch between the behavior of osteoblasts and osteoclasts, the cells responsible for breaking down bone structure when needed. Here, researchers look into some of the details of osteoblast deficiency, and find it is complex, with differing mechanisms between the genders:

Bones adjust their mass and architecture to be sufficiently robust to withstand functional loading by adapting to their strain environment. This mechanism appears less effective with age resulting in low bone mass. In male and female young adult (17 week) and old (19 month) mice we investigated the effect of age in vivo on bones' adaptive response to loading and in vitro in primary cultures of osteoblast-like cells derived from bone cortices.

Right tibiae were axially loaded on alternate days for 2 weeks. Left tibiae were non-loaded controls. In a separate group, the number of sclerostin positive osteocytes and the number of periosteal osteoblasts were analyzed 24 hours after a single loading episode. In young male and female mice loading increased trabecular thickness and the number of trabecular connections. Increase in the number of trabecular connections was impaired with age but trabecular thickness was not. In old mice the loading-related increase in periosteal apposition of the cortex was less than in young ones. Age was associated with a lesser loading-related increase in osteoblast number on the periosteal surface but had no effect on loading-related reduction in the number of sclerostin positive osteocytes. In vitro, strain-related proliferation of osteoblast-like cells was lower in cells from old than young mice. Cells from aged female mice demonstrated normal entry into the cell cycle but subsequently arrested in G2-phase, reducing strain-related increases in cell number.

Thus in both male and female mice loading-related adaptive responses are impaired with age. This impairment is different in females and males. The deficit appears to occur in osteoblasts' proliferative responses to strain rather than earlier strain-related responses in the osteocytes.


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