Drug therapy and pathological changes of bone microarchitecture in osteoporosis / 中华骨科杂志

ABSTRACT

Destruction of bone microarchitecture is one of the most important pathological changes of osteoporosis; it will result in the decrease of bone strength and the increase of fracture risk. Imbalance occurring in bone remodeling is the main cause of microarchitecture destruction. Anti-osteoporosis drugs are able to regulate bone remodeling and therefore improve declined bone microarchitecture. So far, there are mainly two types of anti-osteoporosis drugs antiresorptive agents and anabolic agents. The antiresorptive agents, including bisphosphonates and receptor activator of nuclear factor kappa-B ligand (RANKL) inhibitors, can improve microarchitecture in two ways (1) preventing further loss of trabecular bone volume, trabecula number and connectivity; and (2) suppressing activation of remodeling, giving the remodeling unit more time to improve bone mineralization. The anabolic agents include teriparatide and abaloparatide, which can stimulate bone remodeling and some extent of bone modeling thus lead to a positive bone metabolism balance. Therefore, anabolic agents can increase the number of trabecula and improve trabecular bone structure. Except for the two types of agents, sclerostin antibodies, a new type of anti-osteoporosis drug, can neutralize sclerostin to bilaterally promote bone formation and inhibit bone resorption, leading to an improvement in microarchitecture in both cortical bone and trabecular bone. Although many studies have proved the efficacy of anti-osteoporosis drugs in the improvement of bone microarchitecture and quality, further research is still needed for specific topics, such as the mechanism of RANKL inhibitor to improve bone modeling and the effect of bisphosphonate on porosity of cortical bone.