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 Diseases, Metabolic
Bone Demineralization Technique
Lumbar Vertebrae
Geranyltranstransferase
Clodronic Acid
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)Alendronate is a medication that falls under the class of bisphosphonates. It is commonly used in the treatment and prevention of osteoporosis in postmenopausal women and men, as well as in the management of glucocorticoid-induced osteoporosis and Paget's disease of bone.
Alendronate works by inhibiting the activity of osteoclasts, which are cells responsible for breaking down and reabsorbing bone tissue. By reducing the activity of osteoclasts, alendronate helps to slow down bone loss and increase bone density, thereby reducing the risk of fractures.
The medication is available in several forms, including tablets and oral solutions, and is typically taken once a week for osteoporosis prevention and treatment. It is important to follow the dosing instructions carefully, as improper administration can reduce the drug's effectiveness or increase the risk of side effects. Common side effects of alendronate include gastrointestinal symptoms such as heartburn, stomach pain, and nausea.
Bone density conservation agents, also known as anti-resorptive agents or bone-sparing drugs, are a class of medications that help to prevent the loss of bone mass and reduce the risk of fractures. They work by inhibiting the activity of osteoclasts, the cells responsible for breaking down and reabsorbing bone tissue during the natural remodeling process.
Examples of bone density conservation agents include:
1. Bisphosphonates (e.g., alendronate, risedronate, ibandronate, zoledronic acid) - These are the most commonly prescribed class of bone density conservation agents. They bind to hydroxyapatite crystals in bone tissue and inhibit osteoclast activity, thereby reducing bone resorption.
2. Denosumab (Prolia) - This is a monoclonal antibody that targets RANKL (Receptor Activator of Nuclear Factor-κB Ligand), a key signaling molecule involved in osteoclast differentiation and activation. By inhibiting RANKL, denosumab reduces osteoclast activity and bone resorption.
3. Selective estrogen receptor modulators (SERMs) (e.g., raloxifene) - These medications act as estrogen agonists or antagonists in different tissues. In bone tissue, SERMs mimic the bone-preserving effects of estrogen by inhibiting osteoclast activity and reducing bone resorption.
4. Hormone replacement therapy (HRT) - Estrogen hormone replacement therapy has been shown to preserve bone density in postmenopausal women; however, its use is limited due to increased risks of breast cancer, cardiovascular disease, and thromboembolic events.
5. Calcitonin - This hormone, secreted by the thyroid gland, inhibits osteoclast activity and reduces bone resorption. However, it has largely been replaced by other more effective bone density conservation agents.
These medications are often prescribed for individuals at high risk of fractures due to conditions such as osteoporosis or metabolic disorders that affect bone health. It is essential to follow the recommended dosage and administration guidelines to maximize their benefits while minimizing potential side effects. Regular monitoring of bone density, blood calcium levels, and other relevant parameters is also necessary during treatment with these medications.
Postmenopausal osteoporosis is a specific type of osteoporosis that occurs in women after they have gone through menopause. It is defined as a skeletal disorder characterized by compromised bone strength, leading to an increased risk of fractures. In this condition, the decline in estrogen levels that occurs during menopause accelerates bone loss, resulting in a decrease in bone density and quality, which can lead to fragility fractures, particularly in the hips, wrists, and spine.
It's important to note that while postmenopausal osteoporosis is more common in women, men can also develop osteoporosis due to other factors such as aging, lifestyle choices, and medical conditions.
Etidronic acid is a type of medication known as a bisphosphonate. It is used to treat conditions such as Paget's disease, osteoporosis, and certain types of cancer that have spread to the bones.
Etidronic acid works by inhibiting the activity of cells called osteoclasts, which are responsible for breaking down bone tissue. This helps to slow down the process of bone loss and can increase bone density, making bones stronger and less likely to break.
The medication is available in the form of a solution that is given intravenously (through a vein) in a hospital or clinic setting. It may be given as a single dose or as multiple doses over a period of time, depending on the condition being treated and the individual patient's needs.
As with any medication, etidronic acid can have side effects, including nausea, vomiting, diarrhea, and bone pain. It is important for patients to discuss the potential risks and benefits of this medication with their healthcare provider before starting treatment.
Diphosphonates are a class of medications that are used to treat bone diseases, such as osteoporosis and Paget's disease. They work by binding to the surface of bones and inhibiting the activity of bone-resorbing cells called osteoclasts. This helps to slow down the breakdown and loss of bone tissue, which can help to reduce the risk of fractures.
Diphosphonates are typically taken orally in the form of tablets, but some forms may be given by injection. Commonly prescribed diphosphonates include alendronate (Fosamax), risedronate (Actonel), and ibandronate (Boniva). Side effects of diphosphonates can include gastrointestinal symptoms such as nausea, heartburn, and abdominal pain. In rare cases, they may also cause esophageal ulcers or osteonecrosis of the jaw.
It is important to follow the instructions for taking diphosphonates carefully, as they must be taken on an empty stomach with a full glass of water and the patient must remain upright for at least 30 minutes after taking the medication to reduce the risk of esophageal irritation. Regular monitoring of bone density and kidney function is also recommended while taking these medications.
Bone density refers to the amount of bone mineral content (usually measured in grams) in a given volume of bone (usually measured in cubic centimeters). It is often used as an indicator of bone strength and fracture risk. Bone density is typically measured using dual-energy X-ray absorptiometry (DXA) scans, which provide a T-score that compares the patient's bone density to that of a young adult reference population. A T-score of -1 or above is considered normal, while a T-score between -1 and -2.5 indicates osteopenia (low bone mass), and a T-score below -2.5 indicates osteoporosis (porous bones). Regular exercise, adequate calcium and vitamin D intake, and medication (if necessary) can help maintain or improve bone density and prevent fractures.
Osteoporosis is a systemic skeletal disease characterized by low bone mass, deterioration of bone tissue, and disruption of bone architecture, leading to increased risk of fractures, particularly in the spine, wrist, and hip. It mainly affects older people, especially postmenopausal women, due to hormonal changes that reduce bone density. Osteoporosis can also be caused by certain medications, medical conditions, or lifestyle factors such as smoking, alcohol abuse, and a lack of calcium and vitamin D in the diet. The diagnosis is often made using bone mineral density testing, and treatment may include medication to slow bone loss, promote bone formation, and prevent fractures.
Bone remodeling is the normal and continuous process by which bone tissue is removed from the skeleton (a process called resorption) and new bone tissue is formed (a process called formation). This ongoing cycle allows bones to repair microdamage, adjust their size and shape in response to mechanical stress, and maintain mineral homeostasis. The cells responsible for bone resorption are osteoclasts, while the cells responsible for bone formation are osteoblasts. These two cell types work together to maintain the structural integrity and health of bones throughout an individual's life.
During bone remodeling, the process can be divided into several stages:
1. Activation: The initiation of bone remodeling is triggered by various factors such as microdamage, hormonal changes, or mechanical stress. This leads to the recruitment and activation of osteoclast precursor cells.
2. Resorption: Osteoclasts attach to the bone surface and create a sealed compartment called a resorption lacuna. They then secrete acid and enzymes that dissolve and digest the mineralized matrix, creating pits or cavities on the bone surface. This process helps remove old or damaged bone tissue and releases calcium and phosphate ions into the bloodstream.
3. Reversal: After resorption is complete, the osteoclasts undergo apoptosis (programmed cell death), and mononuclear cells called reversal cells appear on the resorbed surface. These cells prepare the bone surface for the next stage by cleaning up debris and releasing signals that attract osteoblast precursors.
4. Formation: Osteoblasts, derived from mesenchymal stem cells, migrate to the resorbed surface and begin producing a new organic matrix called osteoid. As the osteoid mineralizes, it forms a hard, calcified structure that gradually replaces the resorbed bone tissue. The osteoblasts may become embedded within this newly formed bone as they differentiate into osteocytes, which are mature bone cells responsible for maintaining bone homeostasis and responding to mechanical stress.
5. Mineralization: Over time, the newly formed bone continues to mineralize, becoming stronger and more dense. This process helps maintain the structural integrity of the skeleton and ensures adequate calcium storage.
Throughout this continuous cycle of bone remodeling, hormones, growth factors, and mechanical stress play crucial roles in regulating the balance between resorption and formation. Disruptions to this delicate equilibrium can lead to various bone diseases, such as osteoporosis, where excessive resorption results in weakened bones and increased fracture risk.
A bone fracture is a medical condition in which there is a partial or complete break in the continuity of a bone due to external or internal forces. Fractures can occur in any bone in the body and can vary in severity from a small crack to a shattered bone. The symptoms of a bone fracture typically include pain, swelling, bruising, deformity, and difficulty moving the affected limb. Treatment for a bone fracture may involve immobilization with a cast or splint, surgery to realign and stabilize the bone, or medication to manage pain and prevent infection. The specific treatment approach will depend on the location, type, and severity of the fracture.
Teriparatide is a synthetic form of parathyroid hormone (PTH), which is a natural hormone produced by the parathyroid glands in the body. The medication contains the active fragment of PTH, known as 1-34 PTH, and it is used in medical treatment to stimulate new bone formation and increase bone density.
Teriparatide is primarily prescribed for the management of osteoporosis in postmenopausal women and men with a high risk of fractures who have not responded well to other osteoporosis therapies, such as bisphosphonates. It is administered via subcutaneous injection, typically once daily.
By increasing bone formation and reducing bone resorption, teriparatide helps improve bone strength and structure, ultimately decreasing the risk of fractures in treated individuals. The medication's effects on bone metabolism can lead to improvements in bone mineral density (BMD) and microarchitecture, making it an essential tool for managing severe osteoporosis and reducing fracture risk.
A femoral fracture is a medical term that refers to a break in the thigh bone, which is the longest and strongest bone in the human body. The femur extends from the hip joint to the knee joint and is responsible for supporting the weight of the upper body and allowing movement of the lower extremity. Femoral fractures can occur due to various reasons such as high-energy trauma, low-energy trauma in individuals with weak bones (osteoporosis), or as a result of a direct blow to the thigh.
Femoral fractures can be classified into different types based on their location, pattern, and severity. Some common types of femoral fractures include:
1. Transverse fracture: A break that occurs straight across the bone.
2. Oblique fracture: A break that occurs at an angle across the bone.
3. Spiral fracture: A break that occurs in a helical pattern around the bone.
4. Comminuted fracture: A break that results in multiple fragments of the bone.
5. Open or compound fracture: A break in which the bone pierces through the skin.
6. Closed or simple fracture: A break in which the bone does not pierce through the skin.
Femoral fractures can cause severe pain, swelling, bruising, and difficulty walking or bearing weight on the affected leg. Diagnosis typically involves a physical examination, medical history, and imaging tests such as X-rays or CT scans. Treatment may involve surgical intervention, including the use of metal rods, plates, or screws to stabilize the bone, followed by rehabilitation and physical therapy to restore mobility and strength.
Bone resorption is the process by which bone tissue is broken down and absorbed into the body. It is a normal part of bone remodeling, in which old or damaged bone tissue is removed and new tissue is formed. However, excessive bone resorption can lead to conditions such as osteoporosis, in which bones become weak and fragile due to a loss of density. This process is carried out by cells called osteoclasts, which break down the bone tissue and release minerals such as calcium into the bloodstream.
The femur is the medical term for the thigh bone, which is the longest and strongest bone in the human body. It connects the hip bone to the knee joint and plays a crucial role in supporting the weight of the body and allowing movement during activities such as walking, running, and jumping. The femur is composed of a rounded head, a long shaft, and two condyles at the lower end that articulate with the tibia and patella to form the knee joint.
A spinal fracture, also known as a vertebral compression fracture, is a break in one or more bones (vertebrae) of the spine. This type of fracture often occurs due to weakened bones caused by osteoporosis, but it can also result from trauma such as a car accident or a fall.
In a spinal fracture, the front part of the vertebra collapses, causing the height of the vertebra to decrease, while the back part of the vertebra remains intact. This results in a wedge-shaped deformity of the vertebra. Multiple fractures can lead to a hunched forward posture known as kyphosis or dowager's hump.
Spinal fractures can cause pain, numbness, tingling, or weakness in the back, legs, or arms, depending on the location and severity of the fracture. In some cases, spinal cord compression may occur, leading to more severe symptoms such as paralysis or loss of bladder and bowel control.
"Bone" is the hard, dense connective tissue that makes up the skeleton of vertebrate animals. It provides support and protection for the body's internal organs, and serves as a attachment site for muscles, tendons, and ligaments. Bone is composed of cells called osteoblasts and osteoclasts, which are responsible for bone formation and resorption, respectively, and an extracellular matrix made up of collagen fibers and mineral crystals.
Bones can be classified into two main types: compact bone and spongy bone. Compact bone is dense and hard, and makes up the outer layer of all bones and the shafts of long bones. Spongy bone is less dense and contains large spaces, and makes up the ends of long bones and the interior of flat and irregular bones.
The human body has 206 bones in total. They can be further classified into five categories based on their shape: long bones, short bones, flat bones, irregular bones, and sesamoid bones.
Raloxifene is a selective estrogen receptor modulator (SERM) that is used in the prevention and treatment of osteoporosis in postmenopausal women. It works by mimicking the effects of estrogen on some tissues, such as bones, while blocking its effects on others, such as breast tissue. This can help to reduce the risk of fractures and breast cancer in postmenopausal women with osteoporosis.
Raloxifene is available in tablet form and is typically taken once a day. Common side effects include hot flashes, leg cramps, and sweating. It may also increase the risk of blood clots, so it is important to discuss any history of blood clots or other medical conditions with your healthcare provider before starting treatment with raloxifene.
It's important to note that Raloxifene should not be used in premenopausal women or in men, and it should not be taken during pregnancy or while breastfeeding. It is also important to follow the dosage instructions carefully and to discuss any concerns with your healthcare provider before taking this medication.
Hydroxycholecalciferols are metabolites of vitamin D that are formed in the liver and kidneys. They are important for maintaining calcium homeostasis in the body by promoting the absorption of calcium from the gut and reabsorption of calcium from the kidneys.
The two main forms of hydroxycholecalciferols are 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D). 25-hydroxyvitamin D is the major circulating form of vitamin D in the body and is used as a clinical measure of vitamin D status. It is converted to 1,25-dihydroxyvitamin D in the kidneys by the enzyme 1α-hydroxylase, which is activated in response to low serum calcium or high phosphate levels.
1,25-dihydroxyvitamin D is the biologically active form of vitamin D and plays a critical role in regulating calcium homeostasis by increasing intestinal calcium absorption and promoting bone health. Deficiency in hydroxycholecalciferols can lead to rickets in children and osteomalacia or osteoporosis in adults, characterized by weakened bones and increased risk of fractures.
Spontaneous fractures are bone breaks that occur without any identifiable trauma or injury. They are typically caused by underlying medical conditions that weaken the bones, making them more susceptible to breaking under normal stress or weight. The most common cause of spontaneous fractures is osteoporosis, a condition characterized by weak and brittle bones. Other potential causes include various bone diseases, certain cancers, long-term use of corticosteroids, and genetic disorders affecting bone strength.
It's important to note that while the term "spontaneous" implies that the fracture occurred without any apparent cause, it is usually the result of an underlying medical condition. Therefore, if you experience a spontaneous fracture, seeking medical attention is crucial to diagnose and manage the underlying cause to prevent future fractures and related complications.
Collagen Type I is the most abundant form of collagen in the human body, found in various connective tissues such as tendons, ligaments, skin, and bones. It is a structural protein that provides strength and integrity to these tissues. Collagen Type I is composed of three alpha chains, two alpha-1(I) chains, and one alpha-2(I) chain, arranged in a triple helix structure. This type of collagen is often used in medical research and clinical applications, such as tissue engineering and regenerative medicine, due to its excellent mechanical properties and biocompatibility.
The tibia, also known as the shin bone, is the larger of the two bones in the lower leg and part of the knee joint. It supports most of the body's weight and is a major insertion point for muscles that flex the foot and bend the leg. The tibia articulates with the femur at the knee joint and with the fibula and talus bone at the ankle joint. Injuries to the tibia, such as fractures, are common in sports and other activities that put stress on the lower leg.
A generic drug is a medication that contains the same active ingredients as an originally marketed brand-name drug, known as its "innovator" or "reference listed" drug. The active ingredient is the component of the drug that is responsible for its therapeutic effect. Generic drugs are required to have the same quality, strength, purity, and stability as their brand-name counterparts. They must also meet the same rigorous Food and Drug Administration (FDA) standards regarding safety, effectiveness, and manufacturing.
Generic drugs are typically less expensive than their brand-name equivalents because generic manufacturers do not have to repeat the costly clinical trials that were required for the innovator drug. Instead, they demonstrate through bioequivalence studies that their product is therapeutically equivalent to the reference listed drug. This means that the generic drug delivers the same amount of active ingredient into a patient's bloodstream in the same timeframe as the brand-name drug.
In summary, generic drugs are copies of brand-name drugs with the same active ingredients, dosage forms, strengths, routes of administration, and intended uses. They must meet FDA regulations for safety, efficacy, and manufacturing standards, ensuring that they provide patients with the same therapeutic benefits as their brand-name counterparts at a more affordable price.
Metabolic bone diseases are a group of conditions that affect the bones and are caused by disorders in the body's metabolism. These disorders can result in changes to the bone structure, density, and strength, leading to an increased risk of fractures and other complications. Some common examples of metabolic bone diseases include:
1. Osteoporosis: a condition characterized by weak and brittle bones that are more likely to break, often as a result of age-related bone loss or hormonal changes.
2. Paget's disease of bone: a chronic disorder that causes abnormal bone growth and deformities, leading to fragile and enlarged bones.
3. Osteomalacia: a condition caused by a lack of vitamin D or problems with the body's ability to absorb it, resulting in weak and soft bones.
4. Hyperparathyroidism: a hormonal disorder that causes too much parathyroid hormone to be produced, leading to bone loss and other complications.
5. Hypoparathyroidism: a hormonal disorder that results in low levels of parathyroid hormone, causing weak and brittle bones.
6. Renal osteodystrophy: a group of bone disorders that occur as a result of chronic kidney disease, including osteomalacia, osteoporosis, and high turnover bone disease.
Treatment for metabolic bone diseases may include medications to improve bone density and strength, dietary changes, exercise, and lifestyle modifications. In some cases, surgery may be necessary to correct bone deformities or fractures.
The spine, also known as the vertebral column, is a complex structure in the human body that is part of the axial skeleton. It is composed of 33 individual vertebrae (except in some people where there are fewer due to fusion of certain vertebrae), intervertebral discs, facet joints, ligaments, muscles, and nerves.
The spine has several important functions:
1. Protection: The spine protects the spinal cord, which is a major component of the nervous system, by enclosing it within a bony canal.
2. Support: The spine supports the head and upper body, allowing us to maintain an upright posture and facilitating movement of the trunk and head.
3. Movement: The spine enables various movements such as flexion (bending forward), extension (bending backward), lateral flexion (bending sideways), and rotation (twisting).
4. Weight-bearing: The spine helps distribute weight and pressure evenly across the body, reducing stress on individual vertebrae and other structures.
5. Blood vessel and nerve protection: The spine protects vital blood vessels and nerves that pass through it, including the aorta, vena cava, and spinal nerves.
The spine is divided into five regions: cervical (7 vertebrae), thoracic (12 vertebrae), lumbar (5 vertebrae), sacrum (5 fused vertebrae), and coccyx (4 fused vertebrae, also known as the tailbone). Each region has unique characteristics that allow for specific functions and adaptations to the body's needs.
I'm not able to directly access real-time medical databases or search functions, but I can provide you with some information on the topic.
Bone demineralization is a process often associated with various medical and scientific techniques. It generally refers to the reduction of mineral content in bones, which can occur due to certain medical conditions, aging, or as part of laboratory procedures.
A bone demineralization technique in a laboratory setting typically involves the use of chemical solutions to remove minerals, mainly calcium and phosphate, from bone samples. This process is often used in research and scientific studies to isolate the organic matrix of bones, allowing for the study of its properties and components, such as collagen.
The demineralization process usually involves soaking bone specimens in a weak acid solution, like ethylenediaminetetraacetic acid (EDTA) or acetic acid, for several days to weeks, depending on the size and density of the bones. The procedure must be carefully controlled to avoid damaging the organic matrix while ensuring complete demineralization.
Keep in mind that this is a simplified explanation, and specific techniques and protocols may vary based on the research question and bone type being studied.
The lumbar vertebrae are the five largest and strongest vertebrae in the human spine, located in the lower back region. They are responsible for bearing most of the body's weight and providing stability during movement. The lumbar vertebrae have a characteristic shape, with a large body in the front, which serves as the main weight-bearing structure, and a bony ring in the back, formed by the pedicles, laminae, and processes. This ring encloses and protects the spinal cord and nerves. The lumbar vertebrae are numbered L1 to L5, starting from the uppermost one. They allow for flexion, extension, lateral bending, and rotation movements of the trunk.
Geranyltranstransferase is not a commonly used medical term, but it is a type of enzyme involved in the biosynthesis of various compounds in the body. According to biochemistry and molecular biology resources, Geranyltranstransferase (GTT) is an enzyme that catalyzes the head-to-tail condensation of geranyl diphosphate with isopentenyl diphosphate to form farnesyl diphosphate.
Farnesyl diphosphate is a key intermediate in the biosynthesis of steroids, sesquiterpenes, and other isoprenoid compounds. These compounds have diverse functions in the body, including serving as components of cell membranes, hormones, and signaling molecules.
In summary, Geranyltranstransferase is a biochemical term that refers to an enzyme involved in the biosynthesis of various isoprenoid compounds through the condensation of geranyl diphosphate with isopentenyl diphosphate.
Clodronic acid is a medication that belongs to a class of drugs called bisphosphonates. It is used to treat and prevent osteoporosis in postmenopausal women and men with a high risk of fracture, as well as to treat Paget's disease of bone.
Clodronic acid works by inhibiting the activity of bone-resorbing cells called osteoclasts, which helps to slow down bone loss and increase bone density. This can help reduce the risk of fractures in people with osteoporosis.
The medication is available in several forms, including tablets and intravenous solutions. It is usually taken or administered once a day or once a week, depending on the specific formulation and the individual patient's needs.
Like all medications, clodronic acid can have side effects, including gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as muscle pain, joint pain, and headaches. In rare cases, it can also cause more serious side effects such as esophageal ulcers and bone necrosis of the jaw. It is important for patients to follow their doctor's instructions carefully when taking this medication and to report any unusual symptoms or side effects promptly.
The calcaneus is the largest tarsal bone in the human foot, and it is commonly known as the heel bone. It articulates with the cuboid bone anteriorly, the talus bone superiorly, and several tendons and ligaments that help to form the posterior portion of the foot's skeletal structure. The calcaneus plays a crucial role in weight-bearing and movement, as it forms the lower part of the leg's ankle joint and helps to absorb shock during walking or running.
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
Octacalcium phosphate
Osteogenesis imperfecta
Chest pain
Hematopoietic stem cell niche
Bone biopsy
Medication-related osteonecrosis of the jaw
Jane A. Cauley
DailyMed - ALENDRONATE SODIUM tablet
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Osteoporosis21
- Alendronate sodium tablets, USP are indicated for the treatment of osteoporosis in postmenopausal women. (nih.gov)
- Alendronate is used to prevent and treat certain types of bone loss ( osteoporosis ) in adults. (rxlist.com)
- The aim of this study was to evaluate the effect of a 3-year alendronate treatment on bone mineral density (BMD) and quantitative ultrasound (QUS) in men with primary osteoporosis. (nih.gov)
- In conclusion, this study confirms that alendronate represents an important therapeutic advance in the management of male osteoporosis. (nih.gov)
- By making bones stronger, alendronate can help to reduce the incidence of osteoporosis-related fractures. (medbroadcast.com)
- Alendronate is approved for the treatment and prevention of postmenopausal osteoporosis, male osteoporosis, and glucocorticoid-induced osteoporosis. (medscape.com)
- The safety and effectiveness of alendronate sodium tablets for the treatment of osteoporosis are based on clinical data of four years duration. (medlibrary.org)
- Alendronate sodium is a nitrogen-containing bisphosphonate medication that is most commonly used in the treatment of osteoporosis because it inhibits the resorption of osteoclast-mediated bone. (icoi.org)
- Effect of alendronate on HIV-associated osteoporosis: a randomized, double-blind, placebo-controlled, 96-week trial (ANRS 120). (pasteur.fr)
- Bisphosphonates such as alendronate potently inhibit bone resorption and are effective against osteoporosis. (pasteur.fr)
- El alendronate para el tratamiento del osteoporosis masculina en Suecia. (sogacot.org)
- Rentabilidad del alendronate para el tratamiento del osteoporosis masculino en Suecia. (sogacot.org)
- There are also results demonstrating alendronate to be cost-effective in the treatment of osteoporosis in women. (sogacot.org)
- Objective: To investigate the cost effectiveness of alendronate for male osteoporosis in Sweden by assuming the same relative risk reduction of fractures in men as for women, based on the FIT trial. (sogacot.org)
- Design: A Markov model earlier used to analyze cost effectiveness of alendronate in treatment of postmenopausal osteoporosis in Sweden was adapted to fit a cohort of Swedish men. (sogacot.org)
- Fosamax is a trade name for Alendronate drug primarily used for treating osteoporosis and Paget's disease. (womenhealthjournal.com)
- Fosamax or Alendronate is prescribed for treating osteoporosis in women in menopause. (womenhealthjournal.com)
- She began treatment with alendronate weekly 5 years ago after dual-energy x-ray absorptiometry (DEXA) revealed a T score in the osteoporosis range (T = -2.60). (medscape.com)
- 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)
- 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)
Fosamax8
- One of the most well-known alendronate sodium medications is Fosamax. (icoi.org)
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- In this article, we will tell you about the usage, dosage, and side effects of Fosamax or Alendronate. (womenhealthjournal.com)
- Contraindications: When Should You Avoid Fosamax (Alendronate) Pills? (womenhealthjournal.com)
- You should not use Fosamax pills if you are allergic to alendronate drug or any other component of this medicine. (womenhealthjournal.com)
- Does generic Fosamax (alendronate) work just as well as Prolia (Denosumab)? (med-head.com)
Bisphosphonates1
- Alendronate belongs to a class of drugs called bisphosphonates. (rxlist.com)
Tablets22
- These highlights do not include all the information needed to use ALENDRONATE SODIUM TABLETS safely and effectively. (nih.gov)
- See full prescribing information for ALENDRONATE SODIUM TABLETS. (nih.gov)
- o Not lie down for at least 30 minutes after taking alendronate sodium tablets and until after food. (nih.gov)
- In postmenopausal women, alendronate sodium tablets, USP increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). (nih.gov)
- In postmenopausal women, alendronate sodium tablets increase bone mass and reduce the incidence of fractures, including those of the hip and spine (vertebral compression fractures). (medlibrary.org)
- Alendronate sodium tablets are indicated for the treatment of Paget's disease of bone in men and women. (medlibrary.org)
- Re-treatment with alendronate sodium tablets may be considered, following a six-month post-treatment evaluation period in patients who have relapsed, based on increases in serum alkaline phosphatase, which should be measured periodically. (medlibrary.org)
- Waiting less than 30 minutes, or taking alendronate sodium tablets with food, beverages (other than plain water) or other medications will lessen the effect of alendronate sodium tablets by decreasing its absorption into the body. (medlibrary.org)
- Take alendronate sodium tablets upon arising for the day. (medlibrary.org)
- Alendronate sodium tablets should not be taken at bedtime or before arising for the day. (medlibrary.org)
- If a once-weekly dose of alendronate sodium tablets is missed, instruct patients to take one dose on the morning after they remember. (medlibrary.org)
- Anwita Drugs & Chemicals Pvt Ltd offers a wide range of tablets which includes (alendronate sodium) effervescent tablets. (cphi-online.com)
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- 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)
20232
- On September 29, 2023 Alendronate plus D3 Cal (DRLA) was not listed on the Australian Register of Therapeutic Goods (ARTG). (healthdirect.gov.au)
- On August 30, 2023 Alendronate (AN) was not listed on the Australian Register of Therapeutic Goods (ARTG). (healthdirect.gov.au)
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Bisphosphonate2
- In clinical trials, both treatments increase bone density, although sodium fluoride (NaF) increases and alendronate (bisphosphonate, ALN) decreases bone turnover. (fluoridealert.org)
- The Fracture Intervention Trial (FIT) showed that the bisphosphonate alendronate reduces the risk of fractures and increases bone mineral density (BMD) in osteoporotic women. (sogacot.org)
Dose of alendronate1
- The recommended dose of alendronate - cholecalciferol is one tablet once weekly. (medbroadcast.com)
Effects of alendronate1
- Similar effects of alendronate were observed in men in some other trials. (sogacot.org)
Absorption of alendronate1
- Food and drugs containing large amounts of calcium, magnesium or aluminium (antacids) decrease the absorption of alendronate. (wikipedia.org)
Denosumab6
- To investigate patient characteristics and changes in bone mineral density (BMD) after transitioning from denosumab to alendronate. (edu.au)
- This post hoc analysis evaluated women randomized to subcutaneous denosumab 60 mg every 6 months in year 1 followed by once-weekly oral alendronate 70 mg in year 2. (edu.au)
- Of 126 participants randomized to denosumab, 115 (91%) transitioned to alendronate in year 2. (edu.au)
- BMD increased by 3% to 6% with denosumab in year 1 and by 0% to 1% with alendronate in year 2. (edu.au)
- Women who lost BMD with alendronate in year 2 also showed a greater percent change in BMD with denosumab in year 1. (edu.au)
- Alendronate can effectively maintain the BMD gains accrued after 1 year of denosumab in most patients, regardless of baseline characteristics. (edu.au)
Sodium is not1
- Alendronate sodium is not indicated for use in pediatric patients. (nih.gov)
Tablet2
- Each white-to-off-white, oval, biconvex tablet, engraved 'APO' on one side, 'A-D28' on the other side, contains 91.37 mg of alendronate sodium, equivalent to 70 mg of alendronate and 28 mg of cholecalciferol concentrate, equivalent to 70 µg (2800 IU) of cholecalciferol. (medbroadcast.com)
- To facilitate delivery to the stomach and thus reduce the potential for esophageal irritation, an alendronate sodium tablet should be swallowed with a full glass of water (6 to 8 ounces). (medlibrary.org)
Fractures1
- Bone: alendronate has been linked in long-term users to the development of low-impact femoral fractures. (wikipedia.org)
Alendronic acid1
- The second product, Alendronate Sodium [the trihydrate monosodium salt of alendronic acid (CAS-66376-36-1), which is listed in Table 1 of the Pharmaceutical Appendix to the Tariff Schedule], is indicated for use as a bone resorption inhibitor. (faqs.org)
Osteoporotic4
- We studied 77 osteoporotic men (aged 57.1 +/- 10.8 yrs) who completed a 3-year treatment with alendronate (10 mg/day) plus calcium (1000 mg/day) (n = 39), or calcium alone (n = 38). (nih.gov)
- BMD at the lumbar spine appears to be the best method for monitoring the effect of alendronate on bone mass in osteoporotic men. (nih.gov)
- Conclusions: The results in this study indicate that treating osteoporotic men with alendronate was projected to be cost-effective, under the assumption of the same fracture-risk-reducing effect of alendronate for men as for women. (sogacot.org)
- The most common types are alendronate and zoledronate which aim to strengthen osteoporotic bones by slowing down the activity of bone cells. (diamond.ac.uk)
Generic4
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Cholecalciferol2
- This is a combination medication that contains alendronate and cholecalciferol. (medbroadcast.com)
- The overall appropriate dosage of alendronate - cholecalciferol for you is determined by your doctor and is based on how much vitamin D you require. (medbroadcast.com)
Calcium1
- By binding to calcium salts, alendronate blocks the transformation of calcium phosphate into hydroxyapatite and inhibits the formation, aggregation, and dissolution of hydroxyapatite crystals in bone. (medscape.com)
Inhibits2
- Alendronate inhibits osteoclast activity and bone resorption. (medscape.com)
- But while pyrophosphate inhibits both osteoclastic bone resorption and the mineralization of the bone newly formed by osteoblasts, alendronate specifically inhibits bone resorption without any effect on mineralization at pharmacologically achievable doses. (wikipedia.org)
Trihydrate4
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Vitamin1
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Treatment4
- Alendronate treatment had significantly increased lumbar spine BMD by 4.2% at year 1, by 6.3% at year 2, and 8.8% at year 3. (nih.gov)
- Alendronate is an anti-inflammatory molecule and may therefore be of benefit in the treatment of the inflammation associated with spinal cord injury. (en-journal.org)
- Taken together, these results suggest that alendronate treatment can inhibit the inflammatory response in spinal cord injury thus improving functional responses. (en-journal.org)
- Cost effectiveness of alendronate vs. no treatment was assessed by transitioning men in the model over time between different health states. (sogacot.org)
Osteonecrosis2
- Alendronate sodium dental extraction patients have a risk osteonecrosis of the jawbone or jawbone death. (icoi.org)
- All rats treated with alendronate developed osteonecrosis , presenting as ulcers and necrotic bone , associated with a significant infection process, especially at the inter-alveolar septum area and crestal regions. (bvsalud.org)
Https2
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Rats1
- The results revealed that sodium alendronate stimulated bone formation in castrated rats in all occasions, mainly at 16 and 30 days. (bvsalud.org)
Fracture1
- Results: Taking a societal perspective treating a 71-year-old man (mean age in the FIT) with low BMD and prior vertebral fracture (VFA) with alendronate was found to be associated with a cost of 14,843 per quality adjusted life year (QALY) gained. (sogacot.org)
Significantly2
- The two-year study of alendronate revealed that the drug was safe and significantly improves bone mineral density. (catie.ca)
- Neuro-behavioral assessments, including the Basso, Beattie, and Bresnahan scale for locomotor function, the von Frey filament test, the hot plate test, and the cold stimulation test for sensory function, and the horizontal ladder test for sensorimotor function improved significantly in the alendronate-treated group at D28PI. (en-journal.org)
Evaluate2
- This study aimed to evaluate whether alendronate attenuates motor/sensory dysfunction and the inflammatory response in a thoracic spinal cord clip injury model. (en-journal.org)
- The aim of the ANRS 120 Fosivir trial was to evaluate the effect of alendronate on low BMD in HIV-infected patients. (pasteur.fr)
Medication1
- This means that after having a tooth extracted, a patient taking alendronate sodium medication may not heal properly after the extraction procedure. (icoi.org)
Pills1
- Gathers embeds Cheap alendronate pills online his sal exogenote, few buy paypal alendronate hardhack specializes his discriminantal upbeats yet resolving kenogenetically. (algec.org)
Ulcers1
- The combination of NSAIDs and alendronate may increase the risk of gastric ulcers. (wikipedia.org)
Ponstel2
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Effectiveness1
- Be careful about inadvertently mixing the dosage with any other medicine, since it can substantially affect the effectiveness of alendronate. (womenhealthjournal.com)
Effect1
- selenium will decrease the level or effect of alendronate by cation binding in GI tract. (medscape.com)
Once weekly1
- Alendronate Once-Weekly Study Group. (bvs.br)
Baseline3
- The BMD change in year 2 was similar regardless of baseline characteristics or adherence to oral alendronate. (edu.au)
- Baseline characteristics were well balanced between the alendronate (n=20) and placebo (n=24) groups. (pasteur.fr)
- At baseline, 15 patients (75%) in the alendronate group and 17 patients (71%) in the placebo group had a t-score≤-2.5 at the lumbar spine. (pasteur.fr)
Additionally1
- Additionally, the 70.3% decline of TOC in the activated sludge indicates that alendronate also undergoes some ultimate biodegradation by converting to CO 2 . (janusinfo.se)
Side effects1
- What Are Side Effects Associated with Using Alendronate? (rxlist.com)
Primarily2
- Therefore, alendronate can be classified as inherently, primarily biodegradable, without pre-adaption to the inoculum according to the OECD Guidelines and is not expected to persist in the environment. (janusinfo.se)
- Justification of chosen degradation phrase: Alendronate is classified as inherently, primarily biodegradable, therefore the phrase "Alendronate is slowly degraded in the environment" is thus chosen. (janusinfo.se)
Participants1
- A 3% BMD threshold identified participants who lost, maintained, or gained BMD in year 2 on alendronate. (edu.au)
Patients1
- Alendronate 70 mg weekly for 96 weeks improves BMD in HIV-1-infected patients on antiretroviral therapy. (pasteur.fr)