Osteoporosis sodium fluoride

In extensive studies of the effect of fluoride In patients with osteoporosis carried out In this Research Unit, a therapeutic dally dose of 45 mg fluoride per day was used as sodium fluoride. The main effect of fluoride on calcium metabolism was a decrease of the urinary calcium, while the fecal calcium did not change and the calcium balance also remained unchanged. Also, the Intestinal absorption of calcium remained unchanged during the high fluoride Intake (Table I), The decrease In urinary calcium, Induced by sodium fluoride, may be due to decreased bone resorption, a very desirable effect for patients with osteoporosis. 

Alternatives to steroid hormone therapy for osteoporosis include raloxifene, bisphosphonates, sodium fluoride, vitamin D and calcium supplementation, calcitonin, and parathyroid hormone. Tamoxifen has estrogenic effects on bone and delays bone loss in postmenopausal women. However as a result of estrogenic activity in the uterus, long-term tamoxifen administration has been associated with an increased risk of... 

M. Kleerekoper, D.B. Mendlovic, Sodium fluoride therapy of postmenopausal osteoporosis, Endocr. Rev. 14 (1993) 312-323. 

C.Y.C. Pak, K. Sakheee, B. Adams-Huet, V. Piziak, R.D. Peterson, J.R. Poindexter, Treatment of postmenopausal osteoporosis with slow-release sodium fluoride Final report of a randomized controlled trial, Ann. Intern. Med. 123 (1995) 401-408. 

Osteoporosis is of two forms- primary i.e. idiopathic and secondary. Primary osteoporosis is classified into type I and type II osteoporosis. Type I is referred to post menopausal osteoporosis which is the main type affecting women, characterized by rapid bone loss and affects women after the menopause, mainly in trabecular bone and is associated with vertebrae and distal radio fractures whereas type II also termed as senile osteoporosis occurs due to chronic deficiency of calcium, increase in parathormone activity and decrease in bone formation and is associated with aging. On the other hand secondary type results from inflammatory processes, endocrine changes, multiple myeloma, sedentariness and the use of drugs such as heparin, corticoid and alcohol [3]. Prevention is the main treatment of osteoporosis, for which bone mass peak and the prevention of postmenopausal reabsorption are critical elements. The common treatment of osteoporosis includes calcium consumption as calcium salts, vitamin D supplements, and hormone reposition [4], the use of calcitonin to modulate serum levels of calcium and phosphorous [5], the use of bisphosphonate, mainly alendronates [6], use of ipriflavone and sodium fluoride [7], besides physical activity to strengthen muscles, stimulate osteoblasts formation and prevent reabsorption. 

Calcitonin therapy results in decreased bone resorption. Osteoclasts have calcitonin receptors and calcitonin inhibits their activity. Sodium fluoride stimulates bone formation by unknown mechanisms. In women with osteoporosis, fluoride therapy produced an increased bone mineral density but no reduction in the rate of vertebral fractures. Other drugs known as selective estrogen receptor modulators (raloxifene, droloxifene, idoxifene, and levormeloxifene) may provide an alternative to estrogen replacement therapy (Chapter 34). Administration of low doses of PTH [or recombinant PTH( 1 -34)] does not affect serum calcium concentration, promotes bone formation, and increases mineral density. This anabolic action of PTH is probably mediated by decreasing osteoblast apoptosis. 

HUMAN TOXICITY DATA (Note Toxicity data for sodium fluoride (NaF) will be used for illustrative purposes). Oral human LDLo 71 mg/kg toxic effect central nervous system, musculo-skeletal effects, such as osteoporosis and muscular degeneration intradermal-human TDLo 14pg/kg toxic effect peripheral nervous system effects, mucous membrane effects oral-man TDLo 1662 mg/kg toxic effect cardiovascular system, pulmonary effects, gastrointestinal tract oral-woman LDLo 90 mg/kg oral-woman LDLo 360 mg/kg toxic effect pulmonary effects, gastrointestinal tract oral-woman TDLo 7 mg/kg toxic effect eye, pulmonary effects unreported-man LDLo 75 mg/kg. 

Sodium fluoride (NaF) promotes the proliferation and activity of osteoblasts and is classified as a nonhormonal bone-forming agent. Because treatment with NaF induces bone formation, it is essential that this therapy be coupled with oral calcium supplementation (1,000 mg/day). Additionally, NaF exhibits moderate antiresorptive activity, because it inhibits osteoclastic activity when it is absorbed into the bone matrix. In the treatment of osteoporosis, the therapeutic window for this agent is fairly narrow Doses less than 45 mg/day are subtherapeutic, and doses in excess of 75 mg/day impair bone mineralization. In addition, the bone that is formed in the presence of NaF is neither as well mineralized nor as strong as normal bone tissue. In fact, some... 

The client with osteoporosis is ptesctibed sodium fluoride, a minetal. Which infot-mation should the nutse discuss with the client ... 

Jowsey, J., et al, "Effect of Combined Therapy with Sodium Fluoride, Vitamin D and Calcium in Osteoporosis," American lournal of Medicine, Vol.53,1972, p.43. 

Fluoride is a potent stimulator of trabecular bone formation. Sodium monofluorophosphate was given to 48 patients with osteoporosis due to glucocorticoids (more than 10 mg of prednisone equivalents/day). Patients were randomly allocated to 1 g of calcium carbonate (control) or 200 mg of sodium monofluorophosphate plus 1 g of... 

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