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Risedronate is an osteoporosis medication, proven to reduce the risk of bone fractures in elderly patients, and used widely by doctors to treat osteoporosis and osteopenia.
Risedronate hit the market in 1997 as a third-generation bisphosphonate. It was developed by Procter and Gamble and Sanofi-Aventis. Risedronate is indicated for treatment and prevention postmenopausal women with osteoporosis by reducing the risk of bone fractures. A second indication is in men with osteoporosis to increase bone mass. The third indication is the treatment and prevention in men and women who are being treated with glucocorticoids such as of prednisone or similar products for chronic diseases. These patients should also receive additional amounts of calcium and vitamin D to prevent bone loss. The fourth indication is for the treatment of Paget's Disease of both men and women.
The bisphosphonate drugs, of which risedronate is one, have become the mainstay medicine in attempts to forestall the progress of osteoporosis in patients with thinning bones. Risedronate reduces the incidence of non-vertebral and hip fractures as well as breaks in the vertebrae bones.
To understand the way risedronate acts on the bones, it is important to understand the composition and structure of bone. Bone is composed of three components: protein matrix, a mineral phase and bone cells. Osteonectin is a protein found only in bone that binds to hydroxyapatite crystals (mineral) and bone collagen (a protein fiber). There are three types of bone cells: osteoblasts, osteocytes and osteoclasts.
Osteoblasts are the cells that control the mineralization and produce the bone matrix. Osteocytes are connected to each other by cytoplasm extensions. This allows controls the rate of ions transported into and out of the bone and regulate the mineralization of new bone matrix. Risedronate works on the orthoclast cellular level. Osteoclasts are large cells found on the resorbing surface of mineralized bone. Osteoclasts primary responsibility is removal of bone matrix. Risedronate works by acting as an antiresorptive agent. At the cellular level risedronate inhibits osteoclasts. The osteoclasts attach normally to the bone surface. This reduces the active bone resorption, and prevents bone loss by reducing bone turn over and bone resorption. Biochemical studies suggest the drug "up-regulates" the cyclooxygenase 2 enzyme and this contributes to the bone building.
Although risedronate is not routinely used in treatment of cancer, recent research shows it can be effective in treatment of a bone cancer called osteosarcoma.
Although estrogen is commonly thought of as a woman’s hormone, it is present in men’s bodies as well and plays a part in the onset of at least some osteoporosis cases. It has been found that men with a deficiency of aromatase, the enzyme that converts testosterone to estrogen, have a higher tendency to develop osteoporosis. Giving these men estrogen supplements results in an increase in bone mass. Testosterone injections can result in an increase in bone mass, but only in men with sufficient serum estrogen levels.
Androgen deficiency also increases the risk of osteoporosis in both men and women. Androgen levels decline with age.
Approximately 1.5 million bone fractures occur every year in the US as a result of osteoporosis. Almost half of these are vertebrae (spinal) fractures, resulting in pain and disability. Wrist and hip fractures due to osteopenia are also common.
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