Review on January 07, 2010
This investigation was intended to verify the safety and efficacy of fluoride in increasing spinal bone mass and lowering spinal fractures in older women with established osteoporosis. A combination of sustained-release sodium fluoride, calcium citrate, and cholecalciferol (SR-NaF group) was compared to calcium and cholecalciferol alone (control group). Because estrogen use is popularly suggested for postmenopausal women for various reasons, current estrogen use was allowed but patients with osteoporosis were stratified to ensure equal distribution between groups.
Osteoporosis is a prevalent condition affecting older members of society, particularly post-menopausal women who may be receiving Hormone Replacement Therapy. Bone turnover may also enhance with aging. At present, there are no official anabolic or bone-forming agents to remedy osteoporosis. Such therapies influence bone mass through prompting osteoblastic activity, leading to increased bone mass. Sodium fluoride is known to stimulate bone formation and when given in low doses, bone mass is augmented and risk for vertebral fractures is lowered in osteoporosis sufferers, including post-menopausal women who may be using Hormone Replacement Therapy. Yet, the efficacy and safety of sodium fluoride is inexact.
Reviews of patients with osteoporosis who may be using Hormone Replacement Therapy treated with constant and/or high-dose sodium fluoride have revealed that risk for vertebral fractures was unaltered compared with that of controls, despite increases in spinal bone mass in the sodium fluoride-treated category. Additionally, increased numbers of nonvertebral fractures in sodium fluoride-treated patients caused concern about impaired bone quality and reduced bone strength. Furthermore, serious side effects have been associated with sodium fluoride.
Data from this study show that the combination therapy comprising sustained-release sodium fluoride, calcium, and cholecalciferol in elderly women with established osteoporosis who may be using Hormone Replacement Therapy largely reduced the risk for subsequent vertebral fractures compared with cholecalciferol and calcium therapy alone. The redistribution of bone mass from other sites to the spine has been a general concern with sodium fluoride therapy. These results also demonstrate considerable biochemical changes in markers of bone turnover and resorption in osteoporosis sufferers who may be using Hormone Replacement Therapy, receiving only calcium citrate and cholecalciferol.
It would be worthwhile investigating whether or not a stronger antiresorptive agent, such as a bisphosphonate or estrogen, possibly as a Hormone Replacement Therapy, would have had more therapeutic significance. The small subgroup of patients already receiving estrogen, possibly as a Hormone Replacement Therapy, did not appear to change response to therapy. When parathyroid hormone (PTH) was distributed with estrogen in postmenopausal women with osteoporosis, urinary N-telopeptide and serum osteocalcin levels quickly rose compared with an estrogen-only group. This suggests that anabolic bone agents such as fluoride and PTH could influence bone metabolism by augmenting bone turnover via osteoblastic stimulation or recruitment, directly or indirectly.
Conclusion 2: The above data supports the use of sustained-release sodium fluoride with calcium and cholecalciferol in treating older women with established osteoporosis. These results indicate that this combination of therapy safely lowers the risk for vertebral fractures by stimulating new bone formation by fluoride-mediated increased osteoblastic activity. These findings also back earlier findings on the use of combining bone-forming and antiresorptive agents in the treatment of osteoporosis.