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The improvement of cortical bone strength may be limited by an increase in cortical porosity. The results of clinical and experimental studies are consistent with the mode of action of strontium involving dissociation between bone formation and resorption leading to a stimulation both trabecular and cortical bone formation without increasing cortical porosity. The aim of the pharmacological treatment of osteoporosis is to balance bone formation and bone resorption.
Unbalanced bone metabolism, resulting in bone loss, starts during the transition to menopause perimenopause. Even bone quality degenerates during perimenopause and subsequent menopause 1. Bone mass builds up during the first twenty years of life 2.
The Strength of Bone
Once skeletal growth has been completed, bone health is preserved by the coupled processes of old bone resorption by osteoclasts and of new bone formation led by osteoblasts, together called bone remodeling, taking place throughout life 3. This process requires a constant flow of communication between osteoclast and osteoblast cells, in order to keep constantly synchronized bone resorption and bone formation 3. A disproportion, resulting in a greater osteoclast activity, would end up causing bone loss, decreased bone mass and subsequent increased fracture risk 4.
Therefore therapeutic strategies in order to reduce the risk of fracture would consist in reducing applied load or increasing bone strength. Strategies to reduce bone failure load consist in the prevention of falls through physiatric approach, nutritional approach, vitamin D supplementation and in biomechanical interventions such as hip pads, preventive hip surgery, vertebral body augmentation.
On other hand, therapeutic strategies to increase bone strength consist in improving both bone quantity and quality through physiatric interventions e. Antiresorptive agents, however, do not increase bone tissue mass.
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The gain in bone mineral density observed in clinical trials of antiresorptive drugs is the result of a more complete secondary mineralization of the existing but reduced bone tissue mass. Bisphosphonates may prevent the decay of cancellous bone and cortical thinning, although an improvement of bone microstructure above baseline has never been demonstrated with these drugs. Antiresorptive treatment results in partial correction of the principal bone quality defect in osteoporosis, the disruption in bone microarchitecture, but cannot completely restore mechanical integrity because of the absence of an anabolic effect.
The main goal of antiosteoporotic treatments is to improve bone quality and strength, thereby reducing the risk of fracture. Antifracture efficacy would therefore be expected to be linked to the effect of treatment on bone microarchitecture. Restoration of bone tissue mass and bone structure requires the use of anabolic agents. Anabolic agents, like PTH or Teriparatide, promote bone formation at both trabecular and endocortical surfaces, resulting in an increase of cancellous bone volume and cortical thickness.
PTH treatment was associated with higher cancellous bone formation and bone volume in the iliac crest without affecting bone resorption. There was tendency for cortical porosity to be higher and there was no effect on cortical thickness 7 Figure 2.
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Biopsies were obtained from 42 patients. Histomorphometry indices of bone formation were significantly higher after 6 or 18 months of teriparatide compared with alendronate treatment 8. Treatment with an antiresorptive agent appears to preserve baseline trabecular microarchitecture, to have no impact on cortical bone, and to increase mineralization of bone.
On the other hand, the bone-forming agent teriparatide produce an overall improvement in trabecular microarchitecture and increases cortical thickness, even if it tends to decrease bone mineralization and to increase cortical porosity. Strontium ranelate is an orally active agent consisting of two atoms of stable strontium and an organic moiety ranelic acid , now considered effective in managing osteoporosis and reducing fracture risk in postmenopausal women. By its dual mode of action, strontium ranelate stimulates bone formation and decreases bone resorption, and therefore rebalances bone turnover in favor of new bone formation 9.
In numerous studies this drug has demonstrated to improve all parameters linked to bone quality and bone strength 10 — Strontium ranelate increases lumbar spine BMD by A similar effect was measured at the level of hip, with an increase of femoral neck BMD by 8. The cortical solid bone on the outside forms the shaft of the long bone.
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This xray of a femur shows the thick cortical bone, and the trabecular bone which is arranged to withstand the stresses from usual standing and walking. Compressive stresses are those of the body weight pushing the bone down, and tensile stresses are from the muscles, pulling the bone apart.
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Photo courtesy of Clint Rubin Move mouse over image for labels Click image for a new window with larger view Magnified view of a cut surface of bone, showing the cortical bone and trabecular bone surrounded by marrow tissue M. This is from the iliac crest, part of the pelvic bone. The actual width is about 1 cm. Move mouse over image for labels Further magnification demonstrates the organization of the cortical bone into Haversian systems, consisting of concentric layers of bone and a central canal which supplies blood. The small black dots are spaces that contain osteocytes.
The Strength of Bone by Lucie Wilk
The boundaries between Haversian systems are the cement lines. Move mouse over image for labels Mineral reservoir In addition to its mechanical functions, the bone is a reservoir for minerals a "metabolic" function. Changes with aging This graph shows values for bone mineral density at the hip in Caucasian men and women and African-American men and women. With aging, bone density decreases in all groups.