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Journal of Nanobiotechnology May 2023Large-scale skin damage brings potential risk to patients, such as imbalance of skin homeostasis, inflammation, fluid loss and bacterial infection. Moreover, multidrug...
Large-scale skin damage brings potential risk to patients, such as imbalance of skin homeostasis, inflammation, fluid loss and bacterial infection. Moreover, multidrug resistant bacteria (MDRB) infection is still a great challenge for skin damage repair. Herein, we developed an injectable self-healing bioactive nanoglass hydrogel (FABA) with robust antibacterial and anti-inflammatory ability for normal and Methicillin-resistant Staphylococcus aureus (MRSA) infected skin wound repair. FABA hydrogel was fabricated facilely by the self-crosslinking of F127-CHO (FA) and alendronate sodium (AL)-decorated Si-Ca-Cu nanoglass (BA). FABA hydrogel could significantly inhibit the growth of Staphylococcus aureus, Escherichia coli and MRSA in vitro, while showing good cytocompatibility and hemocompatibility. In addition, FABA hydrogel could inhibit the expression of proinflammatory factor TNF-α and enhance the expression of anti-inflammatory factor IL-4/ IL-10. Based on its versatility, FABA hydrogel could complete wound closure efficiently (75% at day 3 for normal wound, 70% at day 3 for MRSA wound), which was almost 3 times higher than control wound, which was related with the decrease of inflammatory factor in early wound. This work suggested that FABA hydrogel could be a promising dressing for acute and MRSA-infected wound repair.
Topics: Humans; Methicillin-Resistant Staphylococcus aureus; Hydrogels; Staphylococcus aureus; Alendronate; Anti-Bacterial Agents; Escherichia coli
PubMed: 37211601
DOI: 10.1186/s12951-023-01929-9 -
Medicine Jun 2016Glucocorticoid-induced osteoporosis (GIOP) is a serious problem for patients with rheumatic diseases requiring long-term glucocorticoid treatment. Alendronate, a... (Meta-Analysis)
Meta-Analysis Review
Glucocorticoid-induced osteoporosis (GIOP) is a serious problem for patients with rheumatic diseases requiring long-term glucocorticoid treatment. Alendronate, a bisphosphonate, has been recommended in the prevention of GIOP. However, the efficacy and safety of alendronate in preventing GIOP remains controversial. We performed a meta-analysis to investigate the efficacy and safety of alendronate in preventing GIOP in patients with rheumatic diseases.We retrieved randomized controlled trials from PubMed, EMBASE, and the Cochrane Library. Two reviewers extracted the data and evaluated the risk of bias and quality of the evidence. We calculated the risk ratio (RR) with a 95% confidence interval (CI) for dichotomous outcomes, and the mean difference (MD) with a 95% CI for continuous outcomes using Review Manager, version 5.3.A total of 339 studies were found, and 9 studies (1134 patients) were included. Alendronate was not able to reduce the incidence of vertebral fractures (RR = 0.63, 95% CI: 0.10-4.04, P = 0.62) and nonvertebral fractures (RR = 0.40, 95% CI: 0.15-1.12, P = 0.08). Alendronate significantly increased the percent change in bone mineral density (BMD) at the lumbar spine (MD = 3.66, 95% CI: 2.58-4.74, P < 0.05), total hip (MD = 2.08, 95% CI: 0.41-3.74, P < 0.05), and trochanter (MD = 1.68, 95% CI: 0.75-2.61, P < 0.05). Significant differences were not observed in the percent change in BMD at the femoral neck (MD = -0.33, 95% CI: -2.79 to 2.13, P = 0.79) and total body (MD = 0.64, 95% CI: -0.06 to 1.34, P = 0.07). No significant differences in the adverse events were observed in patients treated with alendronate versus the controls (RR = 1.00, 95% CI: 0.94-1.07, P = 0.89). The odds of gastrointestinal adverse events were significantly reduced (RR = 0.77, 95% CI: 0.62-0.97, P < 0.05).Our analysis suggests that alendronate can increase the percent change in BMD at the lumbar spine, total hip, and trochanter, and is not associated with an increased incidence of gastrointestinal adverse events; however, the vertebral and nonvertebral fractures cannot be reduced. However, the results should be interpreted with caution due to the poor statistical power.
Topics: Alendronate; Bone Density; Bone Density Conservation Agents; Glucocorticoids; Humans; Osteoporosis; Rheumatic Diseases
PubMed: 27336902
DOI: 10.1097/MD.0000000000003990 -
Journal of Postgraduate Medicine 2016We present a case of polyarticular synovitis following alendronate treatment for osteoporosis. The patient had no evidence of rheumatoid arthritis, pyrophosphate...
We present a case of polyarticular synovitis following alendronate treatment for osteoporosis. The patient had no evidence of rheumatoid arthritis, pyrophosphate arthropathy, or seronegative/seropositive arthritis. Our main aim in this study is to highlight the potential adverse effects of alendronate and to warn orthopedic surgeons about the possibility of such a side effect that might lead orthopedic surgeons to administer wrong and unnecessary treatments like arthrocentesis. The withdrawal of alendronate is found to be the treatment of choice. Alendronate should be considered as a possible cause of synovitis or polyarthritis in patients treated with this agent in the absence of any other pathology. An association between alendronate and synovitis has rarely been described in the literature. We present a patient who developed polyarticular synovitis after treatment with alendronate and responded to its withdrawal.
Topics: Alendronate; Arthritis; Bone Density Conservation Agents; Drug Administration Schedule; Drug-Related Side Effects and Adverse Reactions; Female; Humans; Middle Aged; Osteoporosis, Postmenopausal; Pain; Synovitis
PubMed: 26767974
DOI: 10.4103/0022-3859.174160 -
Aging Jan 2022To explore the anti-osteoporosis and anti-diabetes effects and potential underlying mechanisms of treatment with metformin and alendronate in diabetes mellitus mice.
BACKGROUND
To explore the anti-osteoporosis and anti-diabetes effects and potential underlying mechanisms of treatment with metformin and alendronate in diabetes mellitus mice.
METHODS
Eight-week-old C57 BL/KS db/db and db/+ female mice were evaluated according to the following treatment group for 12 weeks: control group, diabetes mellitus group, diabetes mellitus with metformin group, diabetes mellitus with Alendronate group, diabetes mellitus with metformin plus alendronate group. Glucose level, glucose tolerance test, bone mineral density, bone microarchitecture, bone histomorphometry, serum biomarkers, and qPCR analysis.
RESULTS
Combined metformin and alendronate can improve progression in glucose metabolism and bone metabolism, including blood glucose levels, blood glucose levels after 4 and 16 hours fasting, glucose tolerance test results, insulin sensitivity and reduces bone loss than the diabetes group. The use of alendronate alone can increase significantly serum glucagon-like peptide-1 levels than the diabetes group. The use of metformin alone can improve bone microstructure such as Tb.Sp and Tb.N of spine in diabetic mice.
CONCLUSION
The combined use of alendronate and metformin has an anti-diabetes and anti-osteoporotic effect compared with diabetic mice, but they appear to act no obvious synergistically between alendronate and metformin.
Topics: Alendronate; Animals; Blood Glucose; Bone Demineralization, Pathologic; Bone Density; Bone Density Conservation Agents; Diabetes Mellitus; Drug Therapy, Combination; Female; Glucose; Hypoglycemic Agents; Metformin; Mice; Mice, Inbred NOD
PubMed: 35027504
DOI: 10.18632/aging.203729 -
Alimentary Pharmacology & Therapeutics Apr 1999It 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... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
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.
Topics: Adult; Alendronate; Cross-Over Studies; Double-Blind Method; Esophagus; Female; Gastric Mucosa; Humans; Male; Middle Aged; Stomach Ulcer
PubMed: 10215737
DOI: 10.1046/j.1365-2036.1999.00488.x -
Cleveland Clinic Journal of Medicine Nov 2001Alendronate and risedronate, the two oral bisphosphonates approved in the United States for preventing and treating osteoporosis, have never been compared in direct... (Review)
Review
Alendronate and risedronate, the two oral bisphosphonates approved in the United States for preventing and treating osteoporosis, have never been compared in direct head-to-head trials, but they appear to have similar pharmacokinetics, drug interactions, adverse effect profiles, and efficacy. Alendronate, however, can be given as a once-weekly dose, whereas risedronate is not yet available in this dosage form. On the other hand, alendronate is not approved for preventing glucocorticoid-induced osteoporosis, whereas risedronate carries this indication.
Topics: Alendronate; Cost-Benefit Analysis; Diphosphonates; Dose-Response Relationship, Drug; Etidronic Acid; Female; Humans; Male; Osteoporosis; Osteoporosis, Postmenopausal; Practice Guidelines as Topic; Risedronic Acid; United States
PubMed: 11718433
DOI: 10.3949/ccjm.68.11.945 -
Archives of Oral Biology Dec 2021This study aimed to compare alveolar healing after tooth extraction in two experimental rat models using continuous or discontinuous dosing of sodium alendronate (ALN).
OBJECTIVE
This study aimed to compare alveolar healing after tooth extraction in two experimental rat models using continuous or discontinuous dosing of sodium alendronate (ALN).
DESIGN
Forty-eight male Wistar rats were divided into eight experimental groups (n = 6/group) and administered ALN (2.5, 5.0, or 7.5 mg/kg) by gavage, weekly, either intermittently or following a continuous regimen (2.5, 5.0, or 7.5 mg/kg) before tooth extraction. The positive control rats were administered zoledronic acid (ZA; 0.2 mg/kg, intravenous), whereas negative control rats received sterile saline (0.9% NaCl, gavage).
RESULTS
Only the ZA-treated animals showed a larger radiolucent extraction site area compared to the saline group (p = 0.007). Small areas of bone tissue filling the alveoli were visualized in the 7.5 mg/kg continuous ALN group and compared with the saline group (p < 0.001). Increased amounts of empty osteocyte lacunae (p < 0.001) and osteoclasts with signs of apoptosis (p = 0.004) were observed in the continuous ALN groups (2.5, 5.0, and 7.5 mg/kg) compared with the saline group. Increased immunolabeling for TNF-α was observed in the 7.5 mg/kg discontinuous ALN group and all continuous ALN groups compared with the saline group (p < 0.001). The number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts was higher in the two continuous ALN groups (5.0 and 7.5 mg/kg) than in the saline group (p < 0.001).
CONCLUSIONS
Continuous administration of ALN impaired post-extraction alveolar bone healing in rats; however, discontinuation of ALN administration before tooth extraction allowed for adequate post-dental extraction alveolar healing.
Topics: Alendronate; Animals; Bone Density Conservation Agents; Diphosphonates; Male; Rats; Rats, Wistar; Sodium; Tooth Extraction; Wound Healing
PubMed: 34700193
DOI: 10.1016/j.archoralbio.2021.105291 -
Arteriosclerosis, Thrombosis, and... Jul 2019Osteoporosis and cardiovascular diseases are major public health issues. Bone and cardiovascular remodeling share multiple biological markers and pathways. Medical... (Review)
Review
Osteoporosis and cardiovascular diseases are major public health issues. Bone and cardiovascular remodeling share multiple biological markers and pathways. Medical intervention, such as using romosozumab, an antisclerostin antibody, improves the clinical outcome of osteoporosis. However, blocking sclerostin leads to Wnt (wingless/integrated) activation and participation in the cardiovascular remodeling process, which could potentially lead to adverse events. Based on the opposing roles of bisphosphonates and the Wnt pathway on endothelial dysfunction, lipid accumulation and calcification of the vessel walls, the combination of romosozumab and bisphosphonates could be a new therapeutic approach to reducing the risks of adverse cardiovascular events in romosozumab receivers. Visual Overview- An online visual overview is available for this article.
Topics: Adaptor Proteins, Signal Transducing; Alendronate; Antibodies, Monoclonal; Cardiovascular Diseases; Humans; Osteoporosis; Wnt Signaling Pathway
PubMed: 31242037
DOI: 10.1161/ATVBAHA.119.312371 -
Circulation Jun 2021Valvular calcification is central to the pathogenesis and progression of aortic stenosis, with preclinical and observational studies suggesting that bone turnover and... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Valvular calcification is central to the pathogenesis and progression of aortic stenosis, with preclinical and observational studies suggesting that bone turnover and osteoblastic differentiation of valvular interstitial cells are important contributory mechanisms. We aimed to establish whether inhibition of these pathways with denosumab or alendronic acid could reduce disease progression in aortic stenosis.
METHODS
In a single-center, parallel group, double-blind randomized controlled trial, patients >50 years of age with calcific aortic stenosis (peak aortic jet velocity >2.5 m/s) were randomized 2:1:2:1 to denosumab (60 mg every 6 months), placebo injection, alendronic acid (70 mg once weekly), or placebo capsule. Participants underwent serial assessments with Doppler echocardiography, computed tomography aortic valve calcium scoring, and F-sodium fluoride positron emission tomography and computed tomography. The primary end point was the calculated 24-month change in aortic valve calcium score.
RESULTS
A total of 150 patients (mean age, 72±8 years; 21% women) with calcific aortic stenosis (peak aortic jet velocity, 3.36 m/s [2.93-3.82 m/s]; aortic valve calcium score, 1152 AU [655-2065 AU]) were randomized and received the allocated trial intervention: denosumab (n=49), alendronic acid (n=51), and placebo (injection n=25, capsule n=25; pooled for analysis). Serum C-terminal telopeptide, a measure of bone turnover, halved from baseline to 6 months with denosumab (0.23 [0.18-0.33 µg/L] to 0.11 µg/L [0.08-0.17 µg/L]) and alendronic acid (0.20 [0.14-0.28 µg/L] to 0.09 µg/L [0.08-0.13 µg/L]) but was unchanged with placebo (0.23 [0.17-0.30 µg/L] to 0.26 µg/L [0.16-0.31 µg/L]). There were no differences in 24-month change in aortic valve calcium score between denosumab and placebo (343 [198-804 AU] versus 354 AU [76-675 AU]; P=0.41) or alendronic acid and placebo (326 [138-813 AU] versus 354 AU [76-675 AU]; =0.49). Similarly, there were no differences in change in peak aortic jet velocity or F-sodium fluoride aortic valve uptake.
CONCLUSIONS
Neither denosumab nor alendronic acid affected progression of aortic valve calcification in patients with calcific aortic stenosis. Alternative pathways and mechanisms need to be explored to identify disease-modifying therapies for the growing population of patients with this potentially fatal condition. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02132026.
Topics: Aged; Aged, 80 and over; Alendronate; Aortic Valve Stenosis; Bone Density Conservation Agents; Denosumab; Disease Progression; Double-Blind Method; Female; Humans; Male; Middle Aged; Positron Emission Tomography Computed Tomography; Treatment Outcome; Vascular Calcification
PubMed: 33913339
DOI: 10.1161/CIRCULATIONAHA.121.053708 -
MedGenMed : Medscape General Medicine Jul 2004The objective of this review is to present the clinical profiles of the once-weekly and once-daily dosing formulations of alendronate and risedronate, the 2... (Review)
Review
OBJECTIVE
The objective of this review is to present the clinical profiles of the once-weekly and once-daily dosing formulations of alendronate and risedronate, the 2 bisphosphonates currently available in the United States for the prevention and treatment of postmenopausal osteoporosis. DATA SOURCE/STUDY SELECTION: Data were obtained from a MEDLINE literature search of all English language articles published between January 1996 and April 2004 using generic names of the bisphosphonates alendronate and risedronate. Results were refined by incorporating terms such as "osteoporosis," "bone mineral density," "fracture risk," and "adverse events." Randomized, controlled trials of once-daily and once-weekly bisphosphonate therapies were selected. Also selected for review were post hoc analyses and extension studies of the original controlled trials, including more recent data from published abstracts from scientific meetings.
DATA EXTRACTION
Relevant portions of articles obtained from the literature search were used to summarize the efficacy and tolerability of the 2 therapies.
CONCLUSIONS
In prospective trials, both bisphosphonates were effective in reducing vertebral and hip fractures in women with postmenopausal osteoporosis. In the only prospective trial evaluating hip fracture risk reduction as the primary end point, risedronate was effective at reducing hip fracture vs placebo. Both alendronate and risedronate are available in once-weekly formulations that have efficacy and tolerability profiles similar to the once-daily doses. Clinicians should review all available data for both agents as well as the medical history of the patient to make the most appropriate treatment choice.
Topics: Alendronate; Bone Density Conservation Agents; Drug Administration Schedule; Etidronic Acid; Female; Humans; Osteoporosis, Postmenopausal; Risedronic Acid
PubMed: 15520628
DOI: No ID Found