Alendronate
Bone Density Conservation Agents
Osteoporosis, Postmenopausal
Etidronic Acid
Diphosphonates
Bone Density
Osteoporosis
Bone Remodeling
Teriparatide
Bone and Bones
Raloxifene
Hydroxycholecalciferols
Fractures, Spontaneous
Collagen Type I
Tibia
Drugs, Generic
Bone Demineralization Technique
Lumbar Vertebrae
Geranyltranstransferase
Alendronate gastric ulcers. (1/413)
BACKGROUND: It appears likely that drugs other than NSAIDs may cause ulcers and ulcer complications (e.g. potassium chloride). Alendronate (Fosamax) is used in the treatment and prevention of metabolic bone disease and has also been associated with severe oesophageal damage and stricture. We have previously shown that the dose of alendronate used for Paget's disease (40 mg) causes gastric damage similar to NSAIDs. The usual dose for the treatment of postmenopausal osteoporosis is 10 mg per day. AIM: To investigate whether the 10 mg dose of alendronate causes gastric ulcers. METHODS: We performed an endoscopist-blind, crossover, randomized, single-centre comparison of 10 mg of alendronate/day and placebo in volunteers aged 40 years or more. Video-endoscopy was used to evaluate the presence and degree of mucosal damage to the oesophagus, stomach, or duodenal bulb after 7 and 14 days of treatment. RESULTS: Twenty-four healthy volunteers participated, including 15 women and nine men, ranging in age from 41 to 52 years. Visible gastric mucosal damage was present in nine (38%) who received alendronate compared to three (13%) in the placebo group. There was a marked difference in the severity of mucosal damage; there were no ulcers or large erosions in those receiving placebo. In contrast, potentially clinically significant gastric mucosal injury was seen in six subjects receiving alendronate (two developed antral ulcers and four had large (4-8 mm) superficial antral erosions) compared to none in the placebo group (P = 0.0219). One subject developed oesophageal damage in the form of multiple linear superficial erosions in the mid and distal oesophagus. Duodenal injury was not seen. CONCLUSION: Alendronate causes gastric ulceration, suggesting that alendronate use may be associated with ulcer complications such as acute upper gastrointestinal bleeding. The results of this study suggest the need for post-marketing surveillance to clarify the nature, frequency and magnitude of any potential gastrointestinal side-effects associated with the use of this drug. (+info)Clinic visits and hospital admissions for care of acid-related upper gastrointestinal disorders in women using alendronate for osteoporosis. (2/413)
CONTEXT: About 1 in 3 women taking alendronate for osteoporosis report gastrointestinal symptoms, a rate much higher than that found during clinical trials. OBJECTIVE: To establish the frequency of outpatient visits and hospital admissions for acid-related upper gastrointestinal disorder (ARD) among women taking alendronate and to identify potential risk factors. METHODS: A retrospective database analysis identified 812 women with osteoporosis who had filled one or more 10-mg alendronate prescriptions from October 1995 through October 1996. RESULTS: One hundred (12.3%) of the 812 women received healthcare for ARD, a clinical encounter rate of 28.5 per 100 person-years. A reference group of 362,109 women from the same health plan had 17.6 ARD encounters per 100 person-years. Excluding women who had ARDs before receiving alendronate, alendronate users were 1.6 (95% CI = 1.2, 2.7) times more likely to have an ARD encounter than nonusers. Risk of having ARD increased with age [users aged 70 years and older had a relative risk of 1.5 (95% confidence interval (CI) 1.0-2.30) compared with younger women] and with concurrent use of nonsteroidal anti-inflammatory drugs (NSAIDS) (relative risk 1.7, 95% CI 1.1-2.6). CONCLUSIONS: Elderly alendronate users or those concurrently taking NSAIDS should be carefully monitored because of their high risk of having ARD. Cost/benefit analyses of alendronate treatment for osteoporosis should include costs of treating ARD. (+info)Alendronate induces antinociception in mice, not related with its effects in bone. (3/413)
The antinociceptive effect of alendronate was studied. The bisphosphonate was i.p. administered and two tests were carried out: acetic acid in mice and formalin test in rats. In the acetic acid test, alendronate induced a dose-dependent antinociceptive effect that was statistically significant for the doses of 10, 20 and 40 mg/kg, and could be detected 48 hr after its administration. In the formalin test, however, alendronate, at the doses of 10 and 20 mg/kg, did not modify the pain score nor the number of flinches, when it was administered either 30 or 60 min before the test. However it must be noted that doses inducing analgesic effect are close to those inducing toxicity. (+info)Larger increases in bone mineral density during alendronate therapy are associated with a lower risk of new vertebral fractures in women with postmenopausal osteoporosis. Fracture Intervention Trial Research Group. (4/413)
OBJECTIVE: To investigate whether the incidence of vertebral fractures is related to the magnitude of change in bone mineral density (BMD) during alendronate treatment. METHODS: Women in this study were age 55-81 years (n = 2,984). While participating in the Fracture Intervention Trial, they received 5 mg/day of alendronate for 2 years followed by 10 mg/day for the remaining 12-30 months of the study. Their BMD was measured at baseline and at 12 and 24 months, and spine radiographs were obtained at baseline and again at 36 or 48 months to identify new vertebral fractures. RESULTS: After 12 months of alendronate treatment, 35% of participants had increases of > or =3% in total hip BMD, and 21% had either decreased total hip BMD or no change. Women who had larger increases in total hip BMD during the first 12 months had a lower incidence of new vertebral fractures during the entire followup period. Only 3.2% of women with increases of > or =3% in total hip BMD experienced new vertebral fractures, whereas twice as many women (6.3%) whose BMD declined or stayed the same experienced new fractures (adjusted odds ratio 0.45, 95% confidence interval 0.27-0.72). Similar patterns were observed for spine BMD at 12 months, and for both sites using change in BMD at 24 months. CONCLUSION: Women with increases of > or =3% in BMD during the first 1 or 2 years of alendronate treatment had the lowest incidence of new vertebral fractures. These findings suggest that, among women taking antiresorptive agents, greater increases in BMD are associated with lower risk of new vertebral fractures. (+info)Farnesol and geranylgeraniol prevent activation of caspases by aminobisphosphonates: biochemical evidence for two distinct pharmacological classes of bisphosphonate drugs. (5/413)
Recently, advances have been made in understanding the molecular mechanisms by which bisphosphonate drugs inhibit bone resorption. Studies with the macrophage-like cell line J774 have suggested that alendronate, an amino-containing bisphosphonate, causes apoptosis by preventing post-translational modification of GTP-binding proteins with isoprenoid lipids. However, clodronate, a nonaminobisphosphonate, does not inhibit protein isoprenylation but can be metabolized intracellularly to a cytotoxic, beta-gamma-methylene (AppCp-type) analog of ATP. These observations raise the possibility that bisphosphonates can be divided into two groups with distinct molecular mechanisms of action depending on the nature of the R2 side chain. We addressed this question by directly comparing the ability of three aminobisphosphonates (alendronate, ibandronate, and pamidronate) and three nonaminobisphosphonates (clodronate, etidronate, and tiludronate) to inhibit protein isoprenylation and activate caspase-3-like proteases or to be metabolized to AppCp-type nucleotides by J774 cells. All three aminobisphosphonates inhibited protein isoprenylation and activated caspase-3-like proteases. Apoptosis and caspase activation after 24-h treatment with the aminobisphosphonates could be prevented by addition of farnesol or geranylgeraniol, confirming that these bisphosphonates inhibit the metabolic mevalonate pathway. No AppCp-type metabolites of the aminobisphosphonates could be detected by mass spectrometry. The three nonaminobisphosphonates did not inhibit protein isoprenylation or cause activation of caspase-3-like proteases, but were incorporated into AppCp-type nucleotides. Taken together, these observations clearly demonstrate that bisphosphonate drugs can be divided into two pharmacological classes: the aminobisphosphonates, which act by inhibiting protein isoprenylation, and the less potent nonaminobisphosphonates, which act through the intracellular accumulation of AppCp-type metabolites. (+info)Use of bone alkaline phosphatase to monitor alendronate therapy in individual postmenopausal osteoporotic women. (6/413)
BACKGROUND: Biochemical bone markers are sensitive to the changes in bone turnover that result from treatment of postmenopausal osteoporotic women with antiresorptive therapies. Although information is available on the use of bone markers in monitoring therapy in groups of subjects, less is known regarding how these markers perform in individual patients. METHODS: Serum bone alkaline phosphatase (bone ALP) concentrations, measured with the Tandem(R) Ostase(R) assay, were used to monitor the biochemical response of bone in postmenopausal women with osteoporosis receiving either 10 mg/day alendronate therapy (n = 74) or calcium supplementation (n = 148) for 24 months. RESULTS: Bone ALP decreased significantly from baseline at 3 months (P +info)Prevention of osteoporosis and fractures. (7/413)
Osteoporosis and low bone density are associated with a risk of fracture as a result of even minimally traumatic events. The estimated lifetime risk of osteoporotic fracture is as high as 50 percent, especially in white and Asian women. The use of caffeine, tobacco and steroids is associated with a decrease in bone density. Cognitive impairment, vision problems and postural instability increase the risk of falling and sustaining a fracture. Medications such as long-acting sedative hypnotics, anticonvulsants and tricyclic antidepressants also increase this risk. Combinations of clinical and radiographic findings can predict fracture risk more effectively than bone densitometry, but often only after the first fracture has occurred. The addition of dietary calcium and/or vitamin D is clearly both cost-effective and significant in reducing the likelihood of fractures. Bisphosphonates reduce fracture risk but at a cost that may be prohibitive for some patients. Estrogen and estrogen-receptor modulators have not been well studied in randomized trials evaluating the reduction of fractures, but they are known to increase bone density. Pharmacologic therapy and the reduction of sensory and environmental hazards can prevent osteoporotic fractures in some patients. (+info)Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin. (8/413)
Glucocorticoid-induced osteoporosis may be due, in part, to increased apoptosis of osteocytes and osteoblasts, and bisphosphonates (BPs) are effective in the management of this condition. We have tested the hypothesis that BPs suppress apoptosis in these cell types. Etidronate, alendronate, pamidronate, olpadronate, or amino-olpadronate (IG9402, a bisphosphonate that lacks antiresorptive activity) at 10(-9) to 10(-6) M prevented apoptosis of murine osteocytic MLO-Y4 cells, whether it was induced by etoposide, TNF-alpha, or the synthetic glucocorticoid dexamethasone. BPs also inhibited apoptosis of primary murine osteoblastic cells isolated from calvaria. Similar antiapoptotic effects on MLO-Y4 and osteoblastic cells were seen with nanomolar concentrations of the peptide hormone calcitonin. The antiapoptotic effect of BPs and calcitonin was associated with a rapid increase in the phosphorylated fraction of extracellular signal regulated kinases (ERKs) and was blocked by specific inhibitors of ERK activation. Consistent with these in vitro results, alendronate abolished the increased prevalence of apoptosis in vertebral cancellous bone osteocytes and osteoblasts that follows prednisolone administration to mice. These results suggest that the therapeutic efficacy of BPs or calcitonin in diseases such as glucocorticoid-induced osteoporosis may be due, in part, to their ability to prevent osteocyte and osteoblast apoptosis. (+info)During menopause, the levels of estrogen in the body decrease significantly, which can lead to a loss of bone density and an increased risk of developing osteoporosis. Other risk factors for postmenopausal osteoporosis include:
* Family history of osteoporosis
* Early menopause (before age 45)
* Poor diet or inadequate calcium and vitamin D intake
* Sedentary lifestyle or lack of exercise
* Certain medications, such as glucocorticoids and anticonvulsants
* Other medical conditions, such as rheumatoid arthritis and liver or kidney disease.
Postmenopausal osteoporosis can be diagnosed through a variety of tests, including bone mineral density (BMD) measurements, which can determine the density of bones and detect any loss of bone mass. Treatment options for postmenopausal osteoporosis typically involve a combination of medications and lifestyle changes, such as:
* Bisphosphonates, which help to slow down bone loss and reduce the risk of fractures
* Hormone replacement therapy (HRT), which can help to replace the estrogen that is lost during menopause and improve bone density
* Selective estrogen receptor modulators (SERMs), which mimic the effects of estrogen on bone density but have fewer risks than HRT
* RANK ligand inhibitors, which can help to slow down bone loss and reduce the risk of fractures
* Parathyroid hormone (PTH) analogues, which can help to increase bone density and improve bone quality.
It is important for women to discuss their individual risks and benefits with their healthcare provider when determining the best course of treatment for postmenopausal osteoporosis. Additionally, lifestyle changes such as regular exercise, a balanced diet, and avoiding substances that can harm bone health (such as smoking and excessive alcohol consumption) can also help to manage the condition.
There are several types of osteoporosis, including:
1. Postmenopausal osteoporosis: This type of osteoporosis is caused by hormonal changes that occur during menopause. It is the most common form of osteoporosis and affects women more than men.
2. Senile osteoporosis: This type of osteoporosis is caused by aging and is the most common form of osteoporosis in older adults.
3. Juvenile osteoporosis: This type of osteoporosis affects children and young adults and can be caused by a variety of genetic disorders or other medical conditions.
4. secondary osteoporosis: This type of osteoporosis is caused by other medical conditions, such as rheumatoid arthritis, Crohn's disease, or ulcerative colitis.
The symptoms of osteoporosis can be subtle and may not appear until a fracture has occurred. They can include:
1. Back pain or loss of height
2. A stooped posture
3. Fractures, especially in the spine, hips, or wrists
4. Loss of bone density, as determined by a bone density test
The diagnosis of osteoporosis is typically made through a combination of physical examination, medical history, and imaging tests, such as X-rays or bone density tests. Treatment for osteoporosis can include medications, such as bisphosphonates, hormone therapy, or rANK ligand inhibitors, as well as lifestyle changes, such as regular exercise and a balanced diet.
Preventing osteoporosis is important, as it can help to reduce the risk of fractures and other complications. To prevent osteoporosis, individuals can:
1. Get enough calcium and vitamin D throughout their lives
2. Exercise regularly, especially weight-bearing activities such as walking or running
3. Avoid smoking and excessive alcohol consumption
4. Maintain a healthy body weight
5. Consider taking medications to prevent osteoporosis, such as bisphosphonates, if recommended by a healthcare provider.
Open fracture: The bone breaks through the skin, exposing the bone to the outside environment.
Closed fracture: The bone breaks, but does not penetrate the skin.
Comminuted fracture: The bone is broken into many pieces.
Hairline fracture: A thin crack in the bone that does not fully break it.
Non-displaced fracture: The bone is broken, but remains in its normal position.
Displaced fracture: The bone is broken and out of its normal position.
Stress fracture: A small crack in the bone caused by repetitive stress or overuse.
The symptoms of a femoral fracture may include:
* Severe pain in the thigh or groin area
* Swelling and bruising around the affected area
* Difficulty moving or straightening the leg
* A visible deformity or bone protrusion
Femoral fractures are typically diagnosed through X-rays, CT scans, or MRIs. Treatment for these types of fractures may involve immobilization with a cast or brace, surgery to realign and stabilize the bone, or in some cases, surgical plate and screws or rods may be used to hold the bone in place as it heals.
In addition to surgical intervention, patients may also require physical therapy to regain strength and mobility in the affected leg after a femoral fracture.
There are several factors that can contribute to bone resorption, including:
1. Hormonal changes: Hormones such as parathyroid hormone (PTH) and calcitonin can regulate bone resorption. Imbalances in these hormones can lead to excessive bone resorption.
2. Aging: As we age, our bones undergo remodeling more frequently, leading to increased bone resorption.
3. Nutrient deficiencies: Deficiencies in calcium, vitamin D, and other nutrients can impair bone health and lead to excessive bone resorption.
4. Inflammation: Chronic inflammation can increase bone resorption, leading to bone loss and weakening.
5. Genetics: Some genetic disorders can affect bone metabolism and lead to abnormal bone resorption.
6. Medications: Certain medications, such as glucocorticoids and anticonvulsants, can increase bone resorption.
7. Diseases: Conditions such as osteoporosis, Paget's disease of bone, and bone cancer can lead to abnormal bone resorption.
Bone resorption can be diagnosed through a range of tests, including:
1. Bone mineral density (BMD) testing: This test measures the density of bone in specific areas of the body. Low BMD can indicate bone loss and excessive bone resorption.
2. X-rays and imaging studies: These tests can help identify abnormal bone growth or other signs of bone resorption.
3. Blood tests: Blood tests can measure levels of certain hormones and nutrients that are involved in bone metabolism.
4. Bone biopsy: A bone biopsy can provide a direct view of the bone tissue and help diagnose conditions such as Paget's disease or bone cancer.
Treatment for bone resorption depends on the underlying cause and may include:
1. Medications: Bisphosphonates, hormone therapy, and other medications can help slow or stop bone resorption.
2. Diet and exercise: A healthy diet rich in calcium and vitamin D, along with regular exercise, can help maintain strong bones.
3. Physical therapy: In some cases, physical therapy may be recommended to improve bone strength and mobility.
4. Surgery: In severe cases of bone resorption, surgery may be necessary to repair or replace damaged bone tissue.
There are several types of spinal fractures, including:
1. Vertebral compression fractures: These occur when the vertebrae collapses due to pressure, often caused by osteoporosis or trauma.
2. Fracture-dislocations: This type of fracture occurs when the vertebra is both broken and displaced from its normal position.
3. Spondylolysis: This is a type of fracture that occurs in the spine, often due to repetitive stress or overuse.
4. Spondylolisthesis: This is a type of fracture where a vertebra slips out of its normal position and into the one below it.
5. Fracture-subluxation: This type of fracture occurs when the vertebra is both broken and partially dislocated from its normal position.
The diagnosis of spinal fractures typically involves imaging tests such as X-rays, CT scans, or MRI to confirm the presence of a fracture and determine its severity and location. Treatment options for spinal fractures depend on the severity of the injury and may include pain management, bracing, physical therapy, or surgery to stabilize the spine and promote healing. In some cases, surgical intervention may be necessary to realign the vertebrae and prevent further damage.
Overall, spinal fractures can have a significant impact on an individual's quality of life, and it is important to seek medical attention if symptoms persist or worsen over time.
Examples of spontaneous fractures include:
1. Pathological fractures: Fractures that occur in the presence of a bone-weakening condition such as osteoporosis, Paget's disease, or bone cancer.
2. Stress fractures: Small cracks in the bone that occur due to repetitive stress or overuse, often seen in athletes or individuals engaged in high-impact activities.
3. Osteogenesis imperfecta: A genetic disorder characterized by brittle bones and an increased risk of fractures.
4. Osteoporotic fractures: Fractures that occur due to bone loss and weakening associated with osteoporosis.
5. Frailty fractures: Fractures that occur in individuals who are frail or have a low bone mineral density, often seen in older adults.
Symptoms of spontaneous fractures may include pain, swelling, and difficulty moving the affected limb. Treatment for these fractures depends on the underlying cause and may involve immobilization, medication, or surgery.
* Osteogenesis imperfecta (OI): A genetic disorder that affects the formation of bone tissue, leading to fragile bones and an increased risk of fractures.
* Rickets: A vitamin D-deficient disease that causes softening of the bones in children.
* Osteomalacia: A condition similar to rickets, but affecting adults and caused by a deficiency of vitamin D or calcium.
* Hyperparathyroidism: A condition in which the parathyroid glands produce too much parathyroid hormone (PTH), leading to an imbalance in bone metabolism and an increase in bone resorption.
* Hypoparathyroidism: A condition in which the parathyroid glands produce too little PTH, leading to low levels of calcium and vitamin D and an increased risk of osteoporosis.
Bone diseases, metabolic are typically diagnosed through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests to evaluate bone metabolism. Treatment depends on the specific underlying cause of the disease and may include medications, dietary changes, or surgery.
Alendronic acid
Effervescent tablet
Mevalonate kinase deficiency
Teriparatide
Gideon Rodan
Discovery and development of bisphosphonates
Hajdu-Cheney syndrome
Romosozumab
Paget's disease of bone
Bisphosphonate
Feline odontoclastic resorptive lesion
Etidronic acid
William H. Harris (orthopaedic surgeon)
Osteoporosis
Mouth ulcer
Avascular necrosis
Merck & Co.
Menopause
Geranyltranstransferase
Osteosarcoma
Abaloparatide
Senile osteoporosis
Fibrous dysplasia of bone
Osteogenesis imperfecta
Chest pain
Hematopoietic stem cell niche
Bone biopsy
Medication-related osteonecrosis of the jaw
Jane A. Cauley
Parish Sedghizadeh
Alendronate: MedlinePlus Drug Information
Alendronate - Janusinfo.se
Hip Fracture Risk Up With Drug Holiday From Risedronate Versus Alendronate - Consumer Health News | HealthDay
Fluoride Action Network | Effects of sodium fluoride and alendronate on the bone mineral in minipigs: a small-angle X-ray...
Clinical trial: Safety/Efficacy of Zoledronic Acid and Alendronate on Bone Metabolism in Postmenopausal Women With Osteoporosis
Alendronate disturbs vesicular trafficking in osteoclasts - OncoBone Ltd
Alendronate improves fasting plasma glucose and insulin sensitivity and decreases insulin resistance in prediabetic osteopenic...
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Effectiveness of Etidronate and Alendronate in the Treatment of Osteoporosis in Males (…) - Osteoporoza.pl
Evaluation of sodium alendronate activity on bone repair under hormones absence
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Added effect of 1% topical alendronate in intra-bony and inter-radicular defects as part of step II periodontal therapy: a...
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An initial investigation of the effect of a bisphosphonate, alendronate, on medullary and trabecular bone in egg laying fowl,...
Efficacy of a combined alendronate and calcitriol agent (Maxmarvil®) in Korean postmenopausal women with early breast cancer...
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Medicines for osteoporosis Information | Mount Sinai - New York
Bone Markers in Osteoporosis: Bone Turnover Markers, Bone Formation Markers, Bone Resorption Markers
Osteoporosis14
- Alendronate is used to treat and prevent osteoporosis (a condition in which the bones become thin and weak and break easily) in women who have undergone menopause (''change of life,'' end of menstrual periods) and to treat osteoporosis in men. (medlineplus.gov)
- Alendronate is also used to treat osteoporosis in men and women who are taking corticosteroids (a type of medication that may cause osteoporosis in some patients). (medlineplus.gov)
- Alendronate controls osteoporosis and Paget's disease of bone but does not cure these conditions. (medlineplus.gov)
- Alendronate helps to treat and prevent osteoporosis only as long as it is taken regularly. (medlineplus.gov)
- Data from placebo-controlled clinical trials in primary and glucocorticoid-induced osteoporosis show an increase in lumbar spine BMD in men and women after 12 months of treatment with alendronate 10 mg/day [12, 14, 15]. (janusinfo.se)
- The aim of this study was to examine the effect of zoledronic acid and alendronate on bone metabolism as measured by biomarkers in postmenopausal women with osteoporosis. (druglib.com)
- Etidronate (E) and alendronate (A) are two bisphosphosates available in most countries for the treatment of osteoporosis (OP). From CANDOO, our prospective observasional database of patients with OP or osteopenia who are being followed at our academic tertiary care centre, we extracted the records of males who had had an initial bone mineral density (BMD) determination (immediately prior to any bisphosphonate therapy) and a follow- up BMD after 1 yr. (osteoporoza.pl)
- This study used histomorphometric analysis to investigate the effect of sodium alendronate, used for the treatment of osteoporosis, on the repair of surgically-induced bone defects in the tibia of castrated rats. (bvsalud.org)
- Medicamento no hormonal para el tratamiento de la osteoporosis postmenopáusica en mujeres. (bvsalud.org)
- Therapeutic equivalence of alendronate 70 mg once-weekly and alendronate 10 mg daily in the treatment of osteoporosis. (bvs.br)
- Patients with osteoporosis prefer once weekly to once daily dosing with alendronate. (bvs.br)
- LRP5 polymorphisms and response to alendronate treatment in Chinese postmenopausal women with osteoporosis. (cdc.gov)
- The effect of raloxifene after discontinuation of long-term alendronate treatment of postmenopausal osteoporosis. (medscape.com)
- Black DM, Bilezikian, Ensrud KE et al One year of alendronate after one year of parathyroid hormone (1-84) for osteoporosis. (medscape.com)
Bisphosphonate2
- In this study, using small-angle X-ray scattering and backscattered electron imaging, we analyzed the bone mineral in the vertebrae of minipigs treated with fluoride, with the bisphosphonate alendronate (ALN), or with vehicle. (fluoridealert.org)
- The bisphosphonate-related osteonecrosis of the bisphosphonates (ONBP) est un effet indésirable décrit jaw (BRONJ) is an undesirable effect which was pour la 1 ère fois en 2003. (who.int)
Long-term alendronate1
- THURSDAY, Jan. 13, 2022 (HealthDay News) -- Drug holidays after long-term risedronate are associated with a small increase in the risk for hip fracture compared with drug holidays after long-term alendronate, according to a study published online Jan. 11 in the Annals of Internal Medicine . (healthday.com)
Fosamax4
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Sodium alendronate6
- This research proposes to study sodium alendronate effect on bone repair of ovarectomized rats. (unesp.br)
- The histhologic analysis of the tibia material showed a more marked bone deposition in the groups treated with higher doses of sodium alendronate. (unesp.br)
- The most mature bone repair process was observed in the 14-days/0.5 mg/kg group, with bone spindles and remodeling in a higher degree of development, showing a dose-dependency regarding sodium alendronate. (unesp.br)
- At 16, 30 and 44 days after the first injection of sodium alendronate, the animals were sacrificed and the right tibias were removed and processed for histomorphometric analysis. (bvsalud.org)
- The results revealed that sodium alendronate stimulated bone formation in castrated rats in all occasions, mainly at 16 and 30 days. (bvsalud.org)
- Sodium alendronate affects mineral homeostasis, promoting bone repair. (bvsalud.org)
Risedronate4
- Kaleen N. Hayes, Pharm.D., Ph.D., from the Brown University School of Public Health in Providence, Rhode Island, and colleagues conducted a population-based, matched, cohort study to examine the comparative risks for fracture during a drug holiday after long-term (three or more years) risedronate versus alendronate therapy among persons aged 66 years or older. (healthday.com)
- We emphasize that our results do not indicate that alendronate therapy should be preferred over risedronate therapy,' the authors write. (healthday.com)
- The decision to initiate alendronate or risedronate therapy is driven by the prescriber and may be influenced by many patient-specific considerations. (healthday.com)
- Risedronate, with its shorter half-life compared with alendronate, is associated with a somewhat higher risk of hip fracture during a drug holiday. (hcn.health)
Decreases2
- A meta-analysis (in total 375 men) reports that alendronate 10 mg/day decreases the risk of vertebral fractures in men to a similar extent as previously observed in postmenopausal women (in total 12698 women) [16, 17]. (janusinfo.se)
- calcium acetate decreases levels of alendronate by inhibition of GI absorption. (medscape.com)
Osteoclasts2
- Signaling studies show that lovastatin and alendronate activate in purified osteoclasts a 34 kDa kinase. (elsevier.com)
- Together, these findings support the hypothesis that alendronate, acting directly on osteoclasts, inhibits a rate-limiting step in the cholesterol biosynthesis pathway, essential for osteoclast function. (elsevier.com)
Therapy8
- Results from one study showed that the effect of 5 and 10 mg alendronate in women with postmenopausal hormonal replacement therapy (HRT) and men did not differ. (janusinfo.se)
- One clinical trial (141 men, 336 women) showed similar efficacy on increased BMD (bone mineral density) with 5 and 10 mg of alendronate in men and postmenopausal women with hormonal replacement therapy [12]. (janusinfo.se)
- Added effect of 1% topical alendronate in intra-bony and inter-radicular defects as part of step II periodontal therapy: a systematic review with meta-analysis and trial sequential analysis. (bvsalud.org)
- This systematic review and meta-analysis aimed to investigate the role of alendronate combined with step 2 of periodontal therapy in reducing probing pocket depth, improving clinical attachment level, and reducing bone defect depth in intra-bony and inter-radicular defects. (bvsalud.org)
- Topical application of alendronate during second step of periodontal therapy significantly improved PD and CAL. (bvsalud.org)
- Local application of alendronate may confer a beneficial effect when applied during step II of periodontal therapy even if long term studies are needed to confirm these results. (bvsalud.org)
- CLINICAL RELEVANCE Considering the emerging role of host-inflammatory response in treatment of periodontitis and the antiresorptive and osteostimulative properties of bisphosphonates , several studies are focusing on the role of alendronate as an addition to non-surgical periodontal therapy . (bvsalud.org)
- Effects of denosumab on bone mineral density and bone turnover in postmenopausal women transitioning from alendronate therapy. (medscape.com)
Rats1
- 18 female rats were distributed into the following groups: 1) control healthy, 2) LASER-healthy (890nm, 80Hz, 1.5J/cm 2 , three days weekly, 60days), 3) control OVX, 4) LASER-OVX, 5) Alendronate (Alen. (nih.gov)
Tablets3
- If you are taking the alendronate tablets, swallow the tablet with a full glass (6 to 8 ounces [180 to 240 mL]) of plain water. (medlineplus.gov)
- If you are taking the alendronate effervescent tablets, dissolve one effervescent tablet in a full glass (4 ounces [120 milliliters]) of plain, non-carbonated drinking water before drinking. (medlineplus.gov)
- Blümel JE, Castelo-Branco C, de la Cuadra G, Maciver L, Moreno M, Haya J. Alendronate daily, weekly in conventional tablets and weekly in enteric tablets: preliminary study on the effects in bone turnover markers and incidence of side effects. (bvs.br)
Effect2
- We aimed to determine the effect of alendronate on plasma glucose, insulin indices of postmenopausal women with prediabetes and osteopenia. (shu.ac.uk)
- In addition stimulatory effect of LASER+alendronate on viability and cell proliferation of OVX-BMMSCs compared to those of control-OVX, alendronate-OVX, and LASER-OVX groups were found. (nih.gov)
Zoledronic1
- Intravenous zoledronic acid 5 mg in the treatment of postmenopausal women with low bone density previously treated with alendronate. (medscape.com)
Bisphosphonates1
- Alendronate is in a class of medications called bisphosphonates. (medlineplus.gov)
Effectiveness1
- The effectiveness and safety of alendronate sodium are dependent on patient adherence to very specific guidelines regarding use. (bvsalud.org)
Medications2
- After you take alendronate, do not eat, drink, or take any other medications (including vitamins or antacids) for at least 30 minutes. (medlineplus.gov)
- tell your doctor and pharmacist if you are allergic to alendronate or any other medications. (medlineplus.gov)
Intervention1
- They were randomly enrolled in intervention (70 mg/week alendronate for 12 week) and control (placebo tablet per week for 12 weeks) groups. (shu.ac.uk)
Products1
- A.-A prescription is NOT required to order Alendronate Sodium and other of our products. (your-onlinepharmacy.net)
Tablet1
- Alendronate comes as a tablet, an effervescent tablet, and a solution (liquid) to take by mouth. (medlineplus.gov)
Study4
- There was statistically significant more reductions in FPG (‐8.2 (8.63) mg/dl vs. ‐2.5 (14.26) mg/dl, P=0.002) and HbA1c (‐0.2 (0.23) % vs. ‐0.09 (0.26) %, P=0.015) were observed in alendronate‐treated group than placebo group during the study course, respectively. (shu.ac.uk)
- This study aims to estimate the rational use of alendronate sodium in the elderly. (bvsalud.org)
- This is a cross-sectional study carried out with a structured questionnaire containing form of use and occurrence of adverse events related to alendronate sodium. (bvsalud.org)
- Alendronate Once-Weekly Study Group. (bvs.br)
Drug1
- www.re-indian.com Around charterable carotinemia www.patosz.hu indocin drug feeds unconfiscatory acetonation https://www.re-indian.com/reind-actonel-no-rx-fed-ex.html up How to buy alendronate australia purchase unerring, intentionally failing sulfonated an earplugs. (re-indian.com)
Patients2
- Prescribing intravenous or intraosseous BP to cile en rapport avec la gravité de cette pathologie et la patients has become more and more frequent these complexité de ses lésions. (who.int)
- The prevalence of irrational use of alendronate sodium in the elderly is high, and this use is associated with patients' sociodemographic factors. (bvsalud.org)
Week1
- Conclusions Administration of 70 mg/week alendronate improves fasting plasma glucose, HbA1c and insulin indices in postmenopausal women. (shu.ac.uk)
Results1
- Results Mean (SD) FPG (102.43 (1.46) mg/dl vs. 94.23)1.17) mg/dl, P=0.001), 120‐minutes insulin concentration (101.86)15.70) mU/l vs. 72.60 (11.36), P=0.026), HbA1c (5.60 (0.06) % vs. 5.40 (0.05)%, P=0.001), HOMA‐IR (3.57 (0.45) vs. 2.62 (0.24), P=0.021) and Matsuda index (7.7 (0.41) vs. 9.2 (0.4), P=0.001) significantly improved in the alendronate‐treated group. (shu.ac.uk)
Effects2
- Lovastatin effects are blocked fully by mevalonate and less effectively by geranylgeraniol whereas alendronate effects are blocked partially by mevalonate and more effectively by geranylgeraniol. (elsevier.com)
- The lovastatin effects are prevented by mevalonate or geranylgeraniol, and alendronate effects are prevented by geranylgeraniol. (elsevier.com)
Solution1
- If you are taking the alendronate oral solution, drink at least 2 ounces (60 milliliters [1/4 cup]) of water after taking alendronate oral solution. (medlineplus.gov)
Local1
- Save yourself the embarrassment of buying Alendronate Sodium at your local pharmacy, and simply order online Alendronate Sodium in the dose that you require. (your-onlinepharmacy.net)
Cheap2
Activity1
- Furthermore, rabbit osteoclast formation and activity also are inhibited by lovastatin and alendronate. (elsevier.com)
Similar1
- A series of clinical trials (in total 16 men, 132 women) found that the bioavailability of alendronate is similar in men and postmenopausal women [11]. (janusinfo.se)
Formation1
- We report that murine osteoclast formation in culture is inhibited by both lovastatin, an inhibitor of hydroxymethylglutaryl CoA reductase, and alendronate. (elsevier.com)
Time2
- Do not stop taking alendronate without talking to your doctor, but talk to your doctor from time to time about whether you still need to take alendronate. (medlineplus.gov)
- Q.-What is the minimum and maximum amount I can order Alendronate Sodium at one time? (your-onlinepharmacy.net)
Order3
- Q.-Do I need a prescription to order Alendronate Sodium? (your-onlinepharmacy.net)
- A.-We have no limits to how much you can order Alendronate Sodium. (your-onlinepharmacy.net)
- Simply press the BUY Alendronate Sodium button and order Alendronate Sodium online. (your-onlinepharmacy.net)
Control1
- Pulse wave (PW) PBM significantly stimulated viability and cell proliferation of healthy BMMSCs compared to those of control-OVX, OVX-alendronate, OVX-LASER, and LASER+alendronate-OVX. (nih.gov)