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Disruption of this balance leads to osteoporosis characterized by decline in bone function and skeletal rigidity.
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Examining whole bones revealed that bone allometry is strongly affected by regional variations in bone function, presumably through mechanical effects on bone modelling.
The distinct subsets of expressed genes associated with glycobiology are consistent with the underlying age-related decline in bone marrow function.
In mice, it has been suggested that JTT improves the decline in bone marrow function induced by anticancer therapy or radiotherapy and that the effect is mediated, at least partly, by enhancing the proliferation of hematopoietic stem cells.
Women who experience chemotherapy-induced amenorrhea have been shown to experience a rapid decline in bone density compared to women who retain their menstrual function [ 82].
In summary, we propose that the systemic environment crucially contributes to the age-related decline in bone regeneration by increasing intracellular ROS levels, hence compromising viability and function of mesenchymal (progenitor) cells.
More importantly, previous investigations showed an age-related decline in bone regeneration, which can be traced back to a decline in both the number and function of bone marrow MSC.
This important role is quite helpful reduce the age-related decline in bone mass.
Poor bone marrow is also associated with a decline in bone architectural quality.
Metabolic bone diseases such as osteoporosis usually cause a decrease in bone mass and a deterioration of bone microarchitecture leading to a decline in bone strength.
Pregnancy and lactation have been associated with decline in bone mineral density (BMD).
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