Relevant bibliographies by topics / Bone fracture targeted drugs

Academic literature on the topic 'Bone fracture targeted drugs'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Bone fracture targeted drugs"

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De Martinis, Massimo, Maria Maddalena Sirufo, and Lia Ginaldi. "Osteoporosis: Current and Emerging Therapies Targeted to Immunological Checkpoints." Current Medicinal Chemistry 27, no. 37 (November 6, 2020): 6356–72. http://dx.doi.org/10.2174/0929867326666190730113123.

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: Osteoporosis is a skeletal pathology characterized by compromised bone strength leading to increased risk of fracture, mainly the spine and hip fractures. Osteoporosis affects more than 200 million people worldwide and because of the skeletal fractures it causes, represents a major cause of morbidity, disability and mortality in older people. Recently, the new discoveries of osteoimmunology have clarified many of the pathogenetic mechanisms of osteoporosis, helping to identify new immunological targets for its treatment opening the way for new and effective therapies with biological drugs. Currently, there are basically two monoclonal antibodies for osteoporosis therapy: denosumab and romosozumab. Here, we focus on the modern approach to the osteoporosis management and in particular, on current and developing biologic drugs targeted to new immunological checkpoints, in the landscape of osteoimmunology.
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Hampson, Geeta, Grahame J. Elder, Martine Cohen-Solal, and Bo Abrahamsen. "A review and perspective on the assessment, management and prevention of fragility fractures in patients with osteoporosis and chronic kidney disease." Endocrine 73, no. 3 (May 11, 2021): 509–29. http://dx.doi.org/10.1007/s12020-021-02735-9.

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AbstractThis article aims to review the methods used for the assessment of fracture risk and the use of osteoporosis medications for fracture prevention in the population with CKD, and highlights the difficulties faced by clinicians in the management of these patients and the latest recommendations and guidelines. Chronic kidney disease (CKD) and osteoporosis often co-exist in older adults, and they present a major healthcare challenge. CKD mineral and bone disorder (CKD-MBD) occurs as renal function declines and this syndrome affects most patients in CKD stages 4 and 5. The biochemical abnormalities of CKD-MBD, renal bone disease and risk factors associated with age-related bone loss and osteoporosis lead to a cumulative effect on fracture risk and mortality. There is a need for routine evaluation of fracture risk and fracture prevention in this population. Measurement of bone mineral density (BMD) and the use of the FRAX tool have predictive value for incident fractures in the general population and in CKD. This enables physicians to identify CKD patients most at risk of sustaining a fragility fracture and allows a more targeted approach to fracture prevention. Data analysis from the pivotal trials of therapeutic agents used in osteoporosis show that these drugs can be considered in mild and moderate CKD (stages 1–3 CKD). Off-label drug use in patients with CKD-MBD and more severe renal impairment (CKD stages 4 and 5) could offer significant benefits to sub-groups of patients when carefully tailored to each individual’s bone turnover and calcium and phosphate balance. However, this requires a selective approach and treatment decisions based on inference from pathophysiology while we await further trials. Guidelines advocate the correction and/or reduction of the biochemical abnormalities of CKD-MBD before initiation of treatment with osteoporosis drugs and close monitoring during treatment.
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Adjei, Isaac, Madison Temples, Shannon Brown, and Blanka Sharma. "Targeted Nanomedicine to Treat Bone Metastasis." Pharmaceutics 10, no. 4 (October 25, 2018): 205. http://dx.doi.org/10.3390/pharmaceutics10040205.

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Bone metastases are common complications of solid tumors, particularly those of the prostate, breast, and lungs. Bone metastases can lead to painful and devastating skeletal-related events (SREs), such as pathological fractures and nerve compressions. Despite advances in treatment for cancers in general, options for bone metastases remain inadequate and generally palliative. Anticancer drugs (chemotherapy and radiopharmaceuticals) do not achieve therapeutic concentrations in the bone and are associated with dose-limiting side effects to healthy tissues. Nanomedicines, with their tunable characteristics, have the potential to improve drug targeting to bone metastases while decreasing side effects for their effective treatment. In this review, we present the current state of the art for nanomedicines to treat bone metastases. We also discuss new treatment modalities enhanced by nanomedicine and their effects on SREs and disease progression.
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Ferracini, Riccardo, Isabel Martínez Herreros, Antonio Russo, Tommaso Casalini, Filippo Rossi, and Giuseppe Perale. "Scaffolds as Structural Tools for Bone-Targeted Drug Delivery." Pharmaceutics 10, no. 3 (August 8, 2018): 122. http://dx.doi.org/10.3390/pharmaceutics10030122.

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Although bone has a high potential to regenerate itself after damage and injury, the efficacious repair of large bone defects resulting from resection, trauma or non-union fractures still requires the implantation of bone grafts. Materials science, in conjunction with biotechnology, can satisfy these needs by developing artificial bones, synthetic substitutes and organ implants. In particular, recent advances in materials science have provided several innovations, underlying the increasing importance of biomaterials in this field. To address the increasing need for improved bone substitutes, tissue engineering seeks to create synthetic, three-dimensional scaffolds made from organic or inorganic materials, incorporating drugs and growth factors, to induce new bone tissue formation. This review emphasizes recent progress in materials science that allows reliable scaffolds to be synthesized for targeted drug delivery in bone regeneration, also with respect to past directions no longer considered promising. A general overview concerning modeling approaches suitable for the discussed systems is also provided.
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Salave, Sagar, Dhwani Rana, and Derajram Benival. "Peptide Functionalised Nanocarriers for Bone Specific Delivery of PTH (1-34) in Osteoporosis." Current Nanomedicine 11, no. 3 (September 2021): 142–48. http://dx.doi.org/10.2174/2468187312666211220112324.

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: Osteoporosis represents a major public health burden especially considering the aging population worldwide. Treatment modalities for osteoporosis are classified into two categories based on the effect on bone remodelling: anabolic drugs and antiresorptive drugs. Anabolic drugs are preferred as it stimulates new bone formation. Currently, PTH (1-34) is the only peptide-based drug approved as an anabolic agent for the treatment of osteoporosis by both USFDA as well as EMA. However, its non-specific delivery results in prolonged kidney exposure, causing hypercalcemia. Nanotechnology-based drug delivery systems functionalized by conjugating it with homing moieties, such as peptides, offer an advantage of targeted delivery with reduced off-target effects. Here, we propose an innovative and targeted nanovesicle approach to efficiently deliver PTH (1-34) to the bone surface using peptides as a homing moiety. The proposed innovative delivery approach will augment the specific interaction between the drug and bone surface without producing side effects. This will reduce the off-target effects of PTH (1-34), and at the same time, it will also improve the outcome of anabolic therapy. Therefore, we postulate that the proposed innovative drug delivery approach for PTH (1-34) will establish as a promising therapy for osteoporotic patients, specifically in postmenopausal women who are at greater risk of bone fracture.
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Harris, Kira B., Kimberly L. Nealy, Delilah J. Jackson, and Phillip L. Thornton. "The Clinical Use of Denosumab for the Management of Low Bone Mineral Density in Postmenopausal Women." Journal of Pharmacy Practice 25, no. 3 (May 1, 2012): 310–18. http://dx.doi.org/10.1177/0897190012442061.

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Osteoporosis is a leading cause of debility and declining quality of life in postmenopausal women worldwide. Treatment of osteoporosis has been ubiquitous throughout the developed world since the mid-1990s, most notably with the introduction of bisphosphonates in 1995. Nonetheless, the incidence of hip fractures increased by 25% between 1990 and 2000, despite advances in osteoporosis therapy. Studies indicate that bone density increases over the first 3 years of bisphosphonate therapy and then plateaus or perhaps even declines, placing these patients at greater risk of fracture. Since hip fractures are associated with increased morbidity, mortality, and increased cost of health care, improvements in treating osteoporosis are critical. Denosumab is a novel monoclonal antibody targeted against the receptor activator of nuclear factor-κB ligand (RANKL) that inhibits osteoclast activity. Initial data suggest that denosumab increases bone mineral density for greater than 3 years. Of greater importance, denosumab has been shown to decrease vertebral fractures by 68%, nonvertebral fractures by 19%, and hip fractures by 42% for at least 36 months. Data also indicate that the safety profile of denosumab is equivalent to other drugs used in osteoporosis management, but potential risks of immunosuppression and cancer have been hypothesized.
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Genah, Shirley, Monica Monici, and Lucia Morbidelli. "The Effect of Space Travel on Bone Metabolism: Considerations on Today’s Major Challenges and Advances in Pharmacology." International Journal of Molecular Sciences 22, no. 9 (April 27, 2021): 4585. http://dx.doi.org/10.3390/ijms22094585.

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Microgravity-induced bone loss is currently a significant and unresolved health risk for space travelers, as it raises the likelihood for irreversible changes that weaken skeletal integrity and the incremental onset of fracture injuries and renal stone formation. Another issue related to bone tissue homeostasis in microgravity is its capacity to regenerate following fractures due to weakening of the tissue and accidental events during the accomplishment of particularly dangerous tasks. Today, several pharmacological and non-pharmacological countermeasures to this problem have been proposed, including physical exercise, diet supplements and administration of antiresorptive or anabolic drugs. However, each class of pharmacological agents presents several limitations as their prolonged and repeated employment is not exempt from the onset of serious side effects, which limit their use within a well-defined range of time. In this review, we will focus on the various countermeasures currently in place or proposed to address bone loss in conditions of microgravity, analyzing in detail the advantages and disadvantages of each option from a pharmacological point of view. Finally, we take stock of the situation in the currently available literature concerning bone loss and fracture healing processes. We try to understand which are the critical points and challenges that need to be addressed to reach innovative and targeted therapies to be used both in space missions and on Earth.
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Henriksen, K., DJ Leeming, C. Christiansen, and MA Karsdal. "Use of Bone Turnover Markers in Clinical Osteoporosis Assessment in Women: Current Issues and Future Options." Women's Health 7, no. 6 (November 2011): 689–98. http://dx.doi.org/10.2217/whe.11.74.

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Monitoring bone turnover of the adult and aging skeleton is essential for optimal treatment of bone metabolic diseases, such as postmenopausal osteoporosis. Diagnosis of osteoporosis is based solely on dual-emission x-ray absorptiometry-based measurements of bone mineral density. However, within the last 20 years, biochemical markers of bone turnover have been implemented to a larger degree, and especially within the field of drug development. Numerous clinical studies have underscored that the markers have promise in terms of predicting patients at high risk of losing bone, future fracture events and importantly also the fracture efficacy of drugs in development. Furthermore, while classical methods often require years to monitor the changes, the bone turnover markers do so within a shorter time span. The aims of this article are to provide an update on the different biochemical markers of bone turnover, and to give an overview of their applications in epidemiological and clinical research especially in women. The main emphasis will be on their utility in clinical trials testing the efficacy of drugs for the treatment of osteoporosis, and their ability to supplement bone mass measurements. Finally, recent evidence suggests that biochemical markers may provide information on bone age that may indirectly relate to bone quality, and this is discussed together with future possibilities for measuring bone quality using bone turnover markers. In summary, a more targeted use of biomarkers could assist in the identification of high-risk patients, the process of drug discovery and monitoring of the efficacy of osteoporosis treatment in clinical settings.
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Brailova, N. V., V. A. Kuznetsova, E. N. Dudinskaya, and O. N. Tkacheva. "Aging bone." Russian Journal of Geriatric Medicine, no. 2 (May 26, 2020): 147–53. http://dx.doi.org/10.37586/2686-8636-2-2020-147-153.

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This review article deals with the topic of changes in bone tissue in the process of aging of the body. Adipogenesis and osteogenesis are affected at the molecular level, proteins and genes are described, in which somatic mutation can occur during the aging process, resulting in both minor changes and an active loss of bone mineral density. The factors that affect the change in bone mineral density mainly in the elderly, and existing drugs that can slow down osteoporosis are listed. Knowledge of the cellular and molecular mechanisms underlying the aging of bone tissue will contribute to the creation of targeted therapy for osteoporosis, which slows down bone aging and prevents falls and fractures in the elderly people.
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Andrews, Rebecca E., Janet E. Brown, Michelle A. Lawson, and Andrew D. Chantry. "Myeloma Bone Disease: The Osteoblast in the Spotlight." Journal of Clinical Medicine 10, no. 17 (September 2, 2021): 3973. http://dx.doi.org/10.3390/jcm10173973.

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Lytic bone disease remains a life-altering complication of multiple myeloma, with up to 90% of sufferers experiencing skeletal events at some point in their cancer journey. This tumour-induced bone disease is driven by an upregulation of bone resorption (via increased osteoclast (OC) activity) and a downregulation of bone formation (via reduced osteoblast (OB) activity), leading to phenotypic osteolysis. Treatments are limited, and currently exclusively target OCs. Despite existing bone targeting therapies, patients successfully achieving remission from their cancer can still be left with chronic pain, poor mobility, and reduced quality of life as a result of bone disease. As such, the field is desperately in need of new and improved bone-modulating therapeutic agents. One such option is the use of bone anabolics, drugs that are gaining traction in the osteoporosis field following successful clinical trials. The prospect of using these therapies in relation to myeloma is an attractive option, as they aim to stimulate OBs, as opposed to existing therapeutics that do little to orchestrate new bone formation. The preclinical application of bone anabolics in myeloma mouse models has demonstrated positive outcomes for bone repair and fracture resistance. Here, we review the role of the OB in the pathophysiology of myeloma-induced bone disease and explore whether novel OB targeted therapies could improve outcomes for patients.
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Dissertations / Theses on the topic "Bone fracture targeted drugs"

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Mercatali, Laura <1977&gt. "Evaluation of Antitumoral activity of bone targeted drugs/conventional chemotherapies and identification of biomarkers for the selection of patients with breast cancer for the bone targeted therapy in adjuvant setting." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6394/.

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Bone metastases are responsible for different clinical complications defined as skeletal-related events (SREs) such as pathologic fractures, spinal cord compression, hypercalcaemia, bone marrow infiltration and severe bone pain requiring palliative radiotherapy. The general aim of these three years research period was to improve the management of patients with bone metastases through two different approaches of translational research. Firstly in vitro preclinical tests were conducted on breast cancer cells and on indirect co-colture of cancer cells and osteoclasts to evaluate bone targeted therapy singly and in combination with conventional chemotherapy. The study suggests that zoledronic acid has an antitumor activity in breast cancer cell lines. Its mechanism of action involves the decrease of RAS and RHO, as in osteoclasts. Repeated treatment enhances antitumor activity compared to non-repeated treatment. Furthermore the combination Zoledronic Acid + Cisplatin induced a high antitumoral activity in the two triple-negative lines MDA-MB-231 and BRC-230. The p21, pMAPK and m-TOR pathways were regulated by this combined treatment, particularly at lower Cisplatin doses. A co-colture system to test the activity of bone-targeted molecules on monocytes-breast conditioned by breast cancer cells was also developed. Another important criticism of the treatment of breast cancer patients, is the selection of patients who will benefit of bone targeted therapy in the adjuvant setting. A retrospective case-control study on breast cancer patients to find new predictive markers of bone metastases in the primary tumors was performed. Eight markers were evaluated and TFF1 and CXCR4 were found to discriminate between patients with relapse to bone respect to patients with no evidence of disease. In particular TFF1 was the most accurate marker reaching a sensitivity of 63% and a specificity of 79%. This marker could be a useful tool for clinicians to select patients who could benefit for bone targeted therapy in adjuvant setting.
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Davidson, Melissa Anne. "A Pharmacovigilance Approach for Assessing Cardiovascular, Osteological, and Carcinogenic Risk Associated with Thiazolidinedione Drugs Used in the Treatment of Type 2 Diabetes Mellitus." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38062.

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Diabetes is a chronic and debilitating disease that affects nearly half a billion people worldwide with the vast majority of diabetics suffering from Type 2 diabetes mellitus (T2DM), a disease characterized by insulin insensitivity that often requires pharmacotherapy to effectively maintain target blood sugar levels. The thiazolidinedione (TZD) class of drugs consists of oral hypoglycaemic agents used alone or in combination with other antidiabetic drugs to treat T2DM. The drugs within this class, which include rosiglitazone and pioglitazone, were originally heralded as providing novel first and second-line treatment of T2DM with glycaemic control and physiological effects comparable to, and in some cases, better than, first-line treatments such as metformin. However, over time they have also been associated with adverse cardiovascular, osteological, and carcinogenic effects in some, but not all clinical trials, observational studies, and meta-analyses. Given the conflicting evidence to date on the safety of TZD drugs, their role in the treatment of T2DM continues to be debated and epidemiological gaps remain. The objectives of this doctoral research are fourfold: 1) to conduct an in-depth review of the epidemiology of TZD pharmacotherapy including pharmacokinetics and modes of action, the results of previous studies investigating health risks and benefits associated with TZD treatment, and new and future uses for this class of drugs; 2) to determine whether diabetic patients treated with TZDs are at increased risk of adverse cardiovascular outcomes; 3) to assess whether TZD pharmacotherapy is associated with an increased risk of bone fractures and whether risks differ depending on fracture site and patient sex; and, 4) to investigate associations between TZD use and risk of bladder cancer. Specific research questions were investigated using nested case-control analyses designed to capture incident users of antidiabetic drugs and electronic health data from Cerner Health Facts®, an electronic medical record database that stores time-stamped patient records from more than 480 contributing hospitals throughout the United States. Findings from this work are reported in a series of manuscripts, including a published review paper. Key findings include: 1) TZD use was associated with an increased risk of incident myocardial infarction and congestive heart failure compared to never use of TZD drugs with a trend towards a potential early treatment effect within the first year of exposure to pioglitazone; 2) TZD use was associated with an increased risk of closed bone fractures among Type 2 diabetics with use of pioglitazone or rosiglitazone associated with an increased risk across multiple fracture sites in women, but only rosiglitazone use in men and only at peripheral fracture sites; 3) use of either pioglitazone or rosiglitazone were associated with an increased risk of incident bladder cancer compared to never users, however, a low number of bladder cancer cases resulted in underpowered analyses; and, 4) insulin use in a hospital setting may replace a patient's normal course of antidiabetic therapy which, when combined with other potential sources of bias in traditional nested case-control studies using hospital-based data, may lead to overestimation or underestimation of adverse health risks associated with non-insulin antidiabetic therapies. Although these findings warrant replication, the results of the research contained within this dissertation suggest that caution should be exercised when prescribing diabetic patients TZD drugs if they have cardiovascular, osteological, or carcinogenic risk factors. Additional pharmacovigilance studies should also continue to strive to better understand the health risks related to TZD therapy, especially as new therapeutic roles for TZDs in the prevention and treatment of some cancers, inflammatory diseases, and other conditions in non-diabetic populations are being explored.
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Güell, Parnau Sílvia. "Estudi de la incidència de fractura per fragilitat en dones amb càncer de mama: factors associat." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/456578.

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(6624113), Mingding Wang. "TARGETED DELIVERY OF DASATINIB FOR ACCELERATED BONE FRACTURE REPAIR." Thesis, 2020.

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Approximately 6.3 million bone fractures occur annually in the USA, resulting in considerable morbidity, deterioration in quality of life, loss of productivity and wages, and sometimes death (e.g. hip fractures). Although anabolic and antiresorptive agents have been introduced for treatment of osteoporosis, no systemically-administered drug has been developed to accelerate the fracture healing process. To address this need, we have undertaken to target a bone anabolic agent selectively to fracture surfaces in order to concentrate the drug’s healing power directly on the fracture site. We report here that conjugation of dasatinib to a bone fracture-homing oligopeptide via a releasable linker reduces fractured femur healing times in mice by ~60% without causing overt off-target toxicity or remodeling of nontraumatized bones. Thus, achievement of healthy bone density, normal bone volume, and healthy bone mechanical properties at the fracture site is realized after only 3-4 weeks in dasatinib-targeted mice, but requires ~8 weeks in PBS-treated controls. Moreover, optimizations have been implemented to the dosing regimen and releasing mechanisms of this targeted-dasatinib therapy, which has enabled us to cut the total doses by half, reduce the risk of premature release in circulation, and still improve upon the therapeutic efficacy. These efforts might reduce the burden associated with frequent doses on patients with broken bones and lower potential toxicity brought by drug degradation in the blood stream. In addition to dasatinib, a few other small molecules have also been targeted to fracture surfaces and identified as prospective therapeutic agents for the acceleration of fracture repair. In conclusion, in this dissertation, we have successfully targeted dasatinib to bone fracture surfaces, which can significantly accelerate the healing process at dasatinib concentrations that are known to be safe in oncological applications. A modular synthetic method has also been developed to allow for easy conversion of a bone-anabolic warhead into a fracture-targeted version for improved fracture repair.

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Murphy, Matthew Brian. "Targeted delivery of osteogenic drugs for bone tissue engineering." Thesis, 2008. http://hdl.handle.net/1911/22207.

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To create a more efficient and effective method of osteogenic drug delivery in vivo, drugs were modified with high calcium affinity moieties including pamidronate, poly(aspartic acid), and poly(glutamic acid). To test the initial hypothesis that modified drugs can demonstrate the same bone binding capabilities of pamidronate, poly(aspartic acid), and poly(glutamic acid), these motifs were conjugated to model peptides and exhibited high affinity to hydroxyapatite (HA). An in vitro controlled release experiment was conducted for native and modified TP508. Native and modified TP508 drugs were loaded in PLGA-PEG microparticles. Porous PPF scaffolds were injected with these drug-loaded particles, and in some instances with HA microparticles (20-50 or 50-100 mum). Less mineral surface resulted in less binding of drugs after release from the PLGA-PEG carriers and therefore a greater release than with the large HA particles. A final study was performed in the presence of 383 ng/mL collagenase, which cleaved the TP508 from the bone-binding domains at the point of the degradable peptide linker sequence. The dose effect of TP508 was established by delivering 0, 25, 50, and 100 mug TP508 loaded into PPF scaffolds and implanted in a sized rat cranial defect. After 4 weeks, microCT analysis of the skulls revealed a statistically significant increase in bone formation for the 50 mug dose compared to controls and the 25 mug dose. Based on these findings, an equivalent of 50 mug TP508 or modified drugs were delivered from PLGA-PEG microspheres in the presence of 20-50 mum HA microparticles in the PPF scaffolds' pore network, which revealed no significant differences between drug groups. These results were promising in that this strategy of drug modification had no apparent negative effect on the bioactivity of TP508. Another finding of this work was that the incorporation of HA into PPF composites resulted in significantly greater bone formation, even after subtraction of the initial amount of HA. The addition of this osteoconductive material stimulated an increase in new bone over 4 weeks for both the control and 50 mug TP508 groups.
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Books on the topic "Bone fracture targeted drugs"

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Elder, Grahame J. Metabolic bone disease after renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0288.

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Patients who undergo kidney transplantation have laboratory, bone, and soft tissue abnormalities that characterize chronic kidney disease mineral and bone disorder (CKD-MBD). After successful transplantation, abnormal values of parathyroid hormone, fibroblast growth factor 23, calcium, phosphate, vitamin D sterols, and sex hormones generally improve, but abnormalities often persist. Cardiovascular risk remains high and is influenced by prevalent vascular calcification, and fracture risk increases due to a combination of abnormal bone ‘quality’, compounded by immunosuppressive drugs and reductions in bone mineral density. Patients with well managed CKD-MBD before transplantation generally have a smoother post-transplant course, and it is useful to assess patients soon after transplantation for risk factors relevant to the general population and to patients with CKD. Targeted laboratory assessment, bone densitometry, and X-ray of the spine are useful for guiding therapy to minimize post-transplant effects of CKD-MBD. To reduce fracture risk, general measures include glucocorticoid dose minimization, attaining adequate 25(OH)D levels, and maintaining calcium and phosphate values in the normal range. Calcitriol or its analogues and antiresorptive agents such as bisphosphonates may protect bone from glucocorticoid effects and ongoing hyperparathyroidism, but the efficacy of these therapies to reduce fractures is unproven. Alternate therapies with fewer data include denosumab, strontium ranelate, teriparatide, oestrogen or testosterone hormone replacement therapy, tibolone, selective oestrogen receptor modulators, and cinacalcet. Parathyroidectomy may be necessary, but is generally avoided within the first post-transplant year. A schema is presented in this chapter that aims to minimize harm when allocating therapy.
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Healey, John H., and David McKeown. Orthopaedic surgery in the palliation of cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0125.

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Metastatic spread of cancer to bone is frequent and causes pain, disability, and functional limitation. New understanding of the homing method of cancer cells to bone and the mechanism of cancer production of pain raise possible new treatment strategies. Non-surgical treatments such as chemotherapy and hormone therapy are effective in early disease. Bisphosphonates and inhibition of osteoprotegerin prevent progression of bone lesions and avoid pain, radiation, and surgery. Radiotherapy arrests disease and relieves pain in many cases. Surgery is needed when the bone is weak or fractured. It effectively relieves pain and preserves function. It usually requires replacing or bypassing the deficient bone with site-specific reconstructive surgery. Surgery should be selected based on projections of patient survival. New tools to make these projections have been validated and are now available. New targeted drug therapies appear to be changing metastatic bone disease into a more chronic condition. This will alter the management of local disease in many histological subtypes of metastatic cancers.
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Shepherd, Angela J., and Juliet M. Mckee. Osteoporosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190466268.003.0015.

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Osteoporotic fractures are major causes of suffering and death. Dual-energy x-ray absorptiometry (DEXA) is the standard of care for diagnosis (T-score ≤ –2.5) of osteoporosis. Prevention of fractures requires addressing bone and muscle strength and balance. Physical exercise, good nutrition (fruits, vegetables, adequate calcium), adequate vitamin intake (C, D, and K), tobacco cessation, and no more than moderate alcohol intake enhance bone health and decrease fracture risk. Long-term treatment with glucocorticoids, certain drugs used in breast or prostate cancer treatment, and proton pump inhibitors used for gastroesophageal reflux disease may increase the risk for osteoporosis. Pharmacologically, bisphosphonates are the mainstay of osteoporosis treatment.
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McDougall, Jason J., and Joel A. Vilensky. The innervation of the joint and its role in osteoarthritis pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0007.

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Diarthrodial joints possess an extensive network of sensory and sympathetic nerve fibres whose physiological functions are varied and complex. Nerves are primarily located in the synovium but also innervate the subchondral bone, the outer third of menisci, and the superficial surface of tendons and ligaments. Large-diameter, myelinated neurons are involved in joint position sense while small-diameter neurons with thin or no myelin typically sense pain. The small-diameter nerves in conjunction with sympathetic fibres control synovial blood flow and maintain joint homeostasis. In patients with osteoarthritis (OA), the sensory nerves become sensitized and increase their firing rate in response to normal movement. This peripheral sensitization is mediated by numerous algogenic agents released into the OA knee including neuropeptides, eicosanoids, and proteinases. A portion of joint afferents fire in the absence of mechanical stimuli and encode pain at rest. Interestingly, the firing rate of joint afferents does not correlate with OA severity, indicating that pain is a poor predictor of joint pathology. Evidence is accumulating to suggest that a subpopulation of OA patients who are unresponsive to classical non-steroidal anti-inflammatory drugs may be suffering from neuropathic pain in which there is damage to the joint nerves themselves. Better understanding of the biology of joint nerves could help in the development of patient-targeted therapies to alleviate OA pain and inflammation.
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Book chapters on the topic "Bone fracture targeted drugs"

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Yakoub, Mohamed, and John Healey. "Orthopaedic surgery in the palliation of cancer." In Oxford Textbook of Palliative Medicine, edited by Nathan I. Cherny, Marie T. Fallon, Stein Kaasa, Russell K. Portenoy, and David C. Currow, 839–48. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198821328.003.0080.

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Metastatic spread of cancer to bone is frequent and causes pain, disability, and functional limitation. Non-surgical treatments such as chemotherapy and hormone therapy are effective in early disease. Administration of bisphosphonates or osteoprotegerin inhibitors prevent new ‘bone events’, thereby avoiding pain, radiation, and surgery. Radiotherapy arrests disease and relieves pain in many cases. Surgery is needed when the bone is weak or fractured. It effectively relieves pain and preserves function by bypassing the deficient bone with site-specific reconstructive surgery. Surgery should be selected based on projections of patient survival. New tools to make these projections are now available (https://www.pathfx.org/). New targeted drug therapies appear to be changing metastatic bone disease into a more chronic condition. This will alter the management of local disease in many histological subtypes of metastatic cancers.
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Ziv, Adi, and Catherine M. Gordon. "Bone Health and Eating Disorders." In AM:STARs: Advances in Adolescent Eating Disorders, 302–22. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/9781610021883-bone.

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As the incidence of eating disorders continues to rise, secondary bone disease is increasingly being diagnosed among affected children and adolescents. Wide evidence-based data support the long-lasting deleterious effect of eating disorders that arise during adolescence on bone accretion and fracture risk. Although novel treatment strategies show promising results, early recognition and management of eating disorders and their consequences on bone health are essential for preservation of skeletal integrity among adolescents. This review summarizes recent data regarding the various factors contributing to impaired bone health, the appropriate clinical assessment, and the available imaging modalities for evaluation of bone health and targeted therapeutic strategies.
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Eastell, Richard. "Osteoporosis." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 727–38. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0088.

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Osteoporosis is an important public health problem. It is defined in the individual by a low bone mineral density and a high risk of fracture. It is a consequence of a low peak bone mass or accelerated bone loss, or both. Oestrogen deficiency and ageing are important causes of accelerated bone loss as are a number of drugs and diseases. Treatments for osteoporosis are effective at reducing the risk of further fracture and these include drugs that work by inhibiting bone resorption or stimulating bone formation. Bisphosphonates are the drugs most commonly used for osteoporosis and most guidelines recommend a drug holiday after treatment for 5 years.
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Bishop, Nick. "Paediatric metabolic bone disease." In Oxford Textbook of Rheumatology, 1245–51. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0145.

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Childhood metabolic bone disease is developing as a specialty in its own right, but many skeletal diseases will present to the general paediatrician as well as those with an interest or specialism in endocrinology, genetics, neonatology, nephrology, or rheumatology. As well as de-novo presentations of skeletal disease, the adverse effects of inflammation, immobilization, altered nutrition, and drugs on the skeleton can become apparent during the management of childhood rheumatological conditions. Childhood metabolic bone diseases typically present with fracture, bony deformity, bone pain, or short stature, either alone or in combination. It is important to distinguish disorders that result in the loss of bone tissue—osteoporoses—from those where mineral is lost but matrix preserved—rickets and osteomalacia. Both have reduced bone density, but treatment is directed in the former group to arresting bone loss and increasing, where possible, bone formation and in the latter group to the appropriate provision of vitamin D or its active metabolites, often with calcium and phosphate supplementation. High bone mass disorders are much less common; in such situations it is again important to distinguish those in which there is reduced bone resorption as opposed to increased bone formation, as treatment options are very different. Treatment options often reflect those in adult practice, but there are important differences in the management of bone disease in the growing skeleton that are detailed here.
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"Nursing patients with rheumatologic problems and connective tissue disorders." In Oxford Handbook of Adult Nursing, edited by George Castledine and Ann Close, 549–68. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780199231355.003.0015.

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Metabolic bone disease 550 Osteoarthritis 554 Rheumatoid arthritis 556 Systemic lupus erythematosus 560 Other connective tissue diseases 562 Crystal arthropathy gout 564 Bone infections 565 Common drugs used for rheumatologic problems and connective tissue disorders 566 Osteoporosis is a systemic skeletal disease characterized by low bone density and micro-architectural deterioration of bone tissue that causes skeletal fragility and increases the risk of fracture. In the UK, one in three women and one in twelve men are likely to have a fracture due to osteoporosis by the age of 90 years. Osteoporosis can affect the whole skeleton but the wrist, hip, and spine are most frequently affected. It is estimated that it costs the NHS and government in the UK over £1.7 billion each year. Bone density can help to determine the risk of fracture and is measured by dual energy x-ray absorptiometry (DEXA)....
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Sanguineti, V. Ana, Jason R. Wild, Bellal Joseph, and Mindy J. Fain. "Management of common fractures in older adults." In Oxford Textbook of Geriatric Medicine, 539–44. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198701590.003.0070.

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Falls account for nearly 75% of all geriatric trauma, and are the most common cause of fractures in older people. Most falls occur from standing height or less, resulting in fragility fractures in older adults who often have multiple comorbidities and functional impairments. These fractures can lead to functional decline, institutionalization, and death. Fragility fractures are seen in the hip, spine, and wrist, pelvis, humerus, rib, and ankle. This fracture pattern identifies groups at increased risk for future falls and fractures, and those who can benefit from targeted programmes to prevent falls and optimize bone health. Management depends upon the site of fracture, the risks and benefits of non-surgical versus surgical intervention, and the patient’s goals of care.
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Gupta, Ruchir. "Orthopedics: Hip Surgery in Aortic Stenosis." In Anesthesiology Applied Exam Board Review, edited by Ruchir Gupta and Minh Chau Joe Tran, 75–80. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190852474.003.0011.

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In this chapter the essential aspects of aortic stenosis are discussed. Specifically, the hemodynamic consequences of this disease as well as which drugs should be used or avoided are explored. The case discussed is of an older patient needing emergent open reduction internal fixation of a hip fracture. The chapter is divided into preoperative, intraoperative, and postoperative sections with important subtopics related to the main topic in each section. Preoperative issues addressed include evaluation of the patient’s hypertension and cardiac status. Intraoperative topics include spinal versus epidural anesthesia, management of a difficult airway, and treatment of bone cement implantation syndrome and atrial fibrillation. Postoperative issues involve extubation and, in this case, managing hypertension.
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Emmett, Stevan R., Nicola Hill, and Federico Dajas-Bailador. "Musculoskeletal medicine." In Clinical Pharmacology for Prescribing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780199694938.003.0015.

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Osteoarthritis (OA) is best described as a chronic pain syndrome affecting one, or more frequently, multiple joints. It most commonly affects the knees, hips, hands, neck and lower back, although any joint can be affected. Defining OA by pathological changes is no longer con­sidered best practice, as the correlation between path­ology and symptoms is frequently discordant, i.e. patients with severe structural changes may present with min­imum symptoms and vice versa. For this reason, patients should be assessed using a biopsychosocial model, which takes into consideration impact on social and psycho­logical well- being, alongside pathological changes. OA can create substantial mobility problems and is the most common cause of disability in elderly people in the devel­oped world. Prevalence rises with age such that approxi­mately one- third of people in the UK over 45 have sought treatment for OA compared with 40– 50% of people over the age of 75. In the pathological conditions of OA, there are specific hallmarks of damage that affect load- bearing articular cartilage, the formation of new bone at the joint mar­gins (osteophytosis), subchondral bone changes (scler­osis), thickening of the joint capsule, loss of cartilage, and joint space narrowing (Figure 7.1B). In general, struc­tural changes seen on X- ray or CT do not correlate with the pain of OA, but an association does occur between the presence of synovitis, subchondral bone oedema and osteophytes. In OA the vasculature of the osteochondral junction also expresses higher levels of nerve growth fac­tors (NGF) so pain sensitization associated with inflam­mation is likely to occur. OA is considered by some to be the result of physio­logical processes originally targeted at joint repair that, over time, cause tissue damage resulting in symptomatic OA. In many cases, severe trauma or pathological repair processes may be contributory factors. Other risk factors for OA include genetic and patient factors, such as age and obesity (see Box 7.1). Anti- NGF drugs may be of benefit, primarily via pain modulation, but OA is not considered to be a disease of inflammation and the mainstay of treatment relies on effective analgesia. The presence of synovitis in late disease is controversial and the presence of joint crys­tals may confound inflammation in OA. It is clear that wear, tear, and damage is associated with the break­down of collagen and increased presence of proteo­lytic enzymes called matrix metalloproteinases (MMPs).
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Conference papers on the topic "Bone fracture targeted drugs"

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Scheiner, Stefan, Peter Pivonka, David W. Smith, and Colin R. Dunstan. "Computer Simulation-Based Modeling of the Pharmaceutical Intervention of Postmenopausal Osteoporosis by Denosumab." In ASME 2012 11th Biennial Conference on Engineering Systems Design and Analysis. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/esda2012-82990.

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Postmenopausal osteoporosis (PMO), leading to a higher bone fracture risk, is characterized by a significantly increasing bone porosity. Recently, denosumab, which is able to efficiently interfere with bone resorption, has been approved for the treatment of PMO. In order to optimize the design of drug administration regimes, we propose a computational methodology, based on mechanistic mathematical modeling of bone remodeling, considering the governing biochemical and biomechanical regulation mechanisms, and the targeted action of denosumab. The time-dependent serum concentration of denosumab, obtained from a pharmacokinetics model, is fed into a bone cell population model, allowing for prediction of porosity evolution in PMO patients. In order to account for the mechanobiology of bone remodeling, we utilize the concept of continuum micromechanics, which accurately provides the actual (microscopic) strain state of the investigated bone. Finally, different drug administration regimes are simulated, and their effect on the bone microarchitecture is discussed.
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Freier, Desiree, Edgar Wiebe, Kim Zeiner, Robert Biesen, Thomas Buttgereit, Sandra Hermann, and Frank Buttgereit. "FRI0433 EFFECTS OF DISEASE MODIFYING DRUGS ON BONE MINERAL DENSITY, FRACTURE INCIDENCE, BACK PAIN AND PHYSICAL ACTIVITY IN PATIENTS WITH PSORIASIS AND PSORIATIC ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4792.

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Altman, Allison R., Beom Kang Huh, Abhishek Chandra, Wei-Ju Tseng, Ling Qin, and X. Sherry Liu. "3D In Vivo Bone Dynamic Imaging of PTH’s Anabolic Action." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14671.

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Aging shifts bone remodeling toward a negative balance between bone formation and resorption, causing bone loss and increased fracture risk. Anti-resorptive agents are commonly used to inhibit bone resorption and stabilize bone mass. While they are effective to prevent further bone loss, there is also a great need for anabolic agents which can reverse bone deterioration and regain lost skeletal integrity. Intermittent parathyroid hormone (PTH) treatment is the only FDA-approved anabolic treatment for osteoporosis, which greatly stimulates bone formation. Combined therapy of anti-resorptive drugs, such as alendronate (ALN), and PTH have been proposed and are expected to further stimulate bone formation. However, studies show conflicting results regarding the effectiveness of combined treatments: some have reported the addition of ALN to impair PTH function [1, 2], while others suggest an improvement over PTH monotherapy [3, 4]. The first objective of this study is to document the immediate changes of individual trabecular structures due to PTH and combined therapy within 12 days using in vivo micro computed tomography (μCT). As PTH is typically prescribed for 1 to 3 years to osteoporotic patients, a treatment of 12 days for rats (approximately equivalent to one year of human life) may be more clinically relevant than long-term treatment studies on rats. The secondary purpose of this study was to gain insight into the mechanism of combined versus PTH treatments through a bone dynamic imaging strategy to track events over an individual remodeling site. We hypothesized that PTH and combined treatments would immediately enhance bone formation on the trabecular surface.
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Turner, Charles H., and Alexander G. Robling. "Genetic Effects on Skeletal Mechanosensitivity in Mice." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32596.

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The accumulation of bone mass during growth can be enhanced by environmental factors such as mechanical loading (exercise) or calcium intake, but 60–70% of the variance in adult bone mineral density (BMD) is explained by heredity. Consequently, understanding the signaling pathways targeted by the genes governing bone accumulation holds perhaps the greatest potential in reducing fracture incidence later in life. Rodent models are particularly useful for studying the genetics of skeletal traits. Of the available inbred mouse strains, three in particular have been studied extensively in skeletal genetics: C57BL/6, DBA/2, and C3H/He. The C57BL/6 strain is characterized by low BMD and large total cross-sectional area (CSA) in the midshaft femur; the C3H/He strain exhibits very high femoral BMD and a smaller femoral CSA than the C57BL/6 mice; and DBA/2 mice have moderately high femoral BMD and a very small midshaft femur CSA. Mechanical loading of the skeleton during growth can substantially enhance periosteal bone apposition, and ultimately produce a diaphyseal cross section with enlarged area. Therefore we hypothesized that the mouse strain with greater femoral cross-sectional area (C57BL/6) might have a genetic predisposition for greater mechanosensitivity than mice with smaller cross sections (C3H/He and DBA/2).
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Reports on the topic "Bone fracture targeted drugs"

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Alman, Benjamin. Discovery of Novel Drugs To Improve Bone Health in Neurofibromatosis Type 1: The Wnt/Beta-Catenin Pathway in Fracture Repair and Pseudarthrosis. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada608932.

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