The objective of this systematic review was to examine the influence of 
treatments for postmenopausal osteoporosis (parathyroid hormone [PTH], 
bisphosphonates, strontium ranelate, and denosumab) on bone quality and discuss 
the clinical implications. Most bone-quality data for PTH is from teriparatide. 
Teriparatide results in a rapid increase in bone-formation markers, followed by 
increases in bone-resorption markers, opening an "anabolic window," a period of 
time when PTH is maximally anabolic. Teriparatide reverses the structural damage 
seen in osteoporosis and restores the structure of trabecular bone. It has a 
positive effect on cortical bone, and any early increases in cortical porosity 
appear to be offset by increases in cortical thickness and diameter. 
Bisphosphonates are antiresorptive agents which reduce bone turnover, improve 
trabecular microarchitecture, and mineralization. Concerns have been raised that 
the prolonged antiresorptive action of bisphosphonates may lead to failure to 
repair microdamage, resulting in microcracks and atypical fragility. Strontium 
ranelate is thought to have a mixed mode of action, increasing bone formation 
and decreasing bone resorption. Strontium ranelate improves cortical thickness, 
trabecular number, and connectivity, with no change in cortical porosity. 
Denosumab exerts rapid, marked, and sustained effects on bone resorption, 
resulting in falls in the markers of bone turnover. Evidence from bone-quality 
studies suggests that treatment-naive women, aged 60-65 years, with very low BMD 
T scores may benefit from PTH as primary therapy to improve bone substrate and 
build bone. Post-PTH treatment with bisphosphonates will maintain improvements 
in bone quality and reduce the risk of fracture.