Treatment

Estrogen: Estrogen replacement therapy stops early bone loss through the inhibition of bone remodeling processes 12,39. Replacement therapy could result in increases of bone mineral density of 5 to 10 percent 39,12. These results could further be enhanced through the use of calcium supplements 12. The most effective use of estrogen is to begin early in menopause and continue its use throughout life 39.  If estrogen therapy is stopped, bone loss will resume at the same rate as after menopause 12,6. Maintaining estrogen levels is still considered the most important way to maintain bone density 46,39,6. 

Calcitonin: Calcitonin is a hormone which directly inhibits the osteoclastic (bone resorption) activity in bone remodeling 39,6. Calcitonin is a good alternative for people who can not take estrogen 1,39. It produces an analgesic effect with regard to bone pain so it is often prescribed to those who have had an osteoporotic fracture 39,6. This hormone decreases the loss of trabecular bone in the early years after menopause but it is unclear if cortical bone loss is decreased 39,6. Calcitonin can be used in two forms; nasal form and injection form 12,39.  

Bisphosphonates: These antiresorptive agents can be used in preventing bone loss that is associated with low estrogen, glucocorticoid treatments, and immobilization 39,46,50.  Bisophosphonates work by permanently binding to mineralized bone surfaces and inhibiting the activity of the osteoclasts 12,46,4. Less osteoclastic activity decreases the amount of bone degraded during the remodeling cycle 46,39,6. Vertebral and hip fractures have been reduced by 50-60 percent in postmenopausal women following use of these bisphosphonates 33. Three bisphosphonates are currently approved by the FDA for treatment and prevention of osteoporosis.  They include, alendronate, risedronate, and ibandronate 33.

Fluoride: Fluoride stimulates osteoblasts, which increases bone formation 46,39. This compound is incorporated into the hydroxyapitite part of the bone and stimulates osteoblast activity increasing the rate of bone formation 12,14. Sodium fluoride increases bone mineral density linearly with time in the spine but has little effect at the hip 3. Fluoride is not recommended to treat postmenopausal osteoporosis 12. 

Parathyroid Hormone: Bone loss is decreased with excess secretion and intravenous infusion of parathyroid hormone 12. This hormone restores bone strength through the formation of new bone at the periosteal (outer) and endosteal (inner) regions of the bone surface 12. High doses cause nausea and headache 12.

Gene Therapy: Potential exists for gene therapy to induce bone formation by providing sustained protein production and delivery of protein to fractured bones in the body 29.  Gene transfer of the bone morphogenetic protein-2 (BMP-2), enhances fracture healing in animals.  Osteoprotegerin, is a naturally occurring protein that prevents bone resorption in the body by hindering osteoclast formation, function, and survival 29. Osteopenia was reversed in mice treated with osteoprotegerin 29.  Growth factors may act as agents to improve fracture healing in bone 16.

Nutrition: Nutrition is important in both the treatment and prevention of osteoporosis. A balanced diet with adequate calories will allow the body to achieve peak bone mass 46,12,19. Adequate amounts of both vitamin D and calcium are needed to build stronger bones 12,19,48,11,41.

Exercise: Similar to nutrition, when done throughout life, exercise allows the body to achieve peak bone mass 12,46,1. Load bearing exercise is the most effective and the exercise program should focus on maintaining both strength and flexibility 12,1.

Decisions on the type of treatment method to use should be based on an assessment of the patient’s risk of fracture, efficacy of drug therapy, and the possible side effects that pertain to certain drugs 12,32. A treatment plan for osteoporosis should be put in place, as well as a strategy to decrease the risk of falls 12,14.

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