Teriparatide Research & Studies

Osteogenesis imperfecta causes multiple fractures throughout life, causing substantial morbidity.

The purpose of this observational study was to investigate the effectiveness and safety of romosozumab (ROMO) and teriparatide (TPTD) in a clinical setting.

Accumulating evidence highlights the critical role of circadian rhythms in regulating bone turnover. Bone turnover markers, including parathyroid hormone, C-terminal telopeptide of type I collagen, and N-terminal propeptide of type I procollagen, all exhibit distinct diurnal variations. Teriparatide, a recombinant parathyroid hormone analog, demonstrates time-dependent efficacy influenced by these endogenous rhythms. However, the impact of administration timing on bone metabolism remains underexplored.

In the management of osteoporosis, anti-resorptive agents serve as a primary therapeutic approach. However, in cases where individuals exhibit an increased susceptibility to fractures, such as those characterized by severe low bone mass or a history of vertebral or hip fractures that markedly diminish life expectancy, the immediate reduction of fracture risk through the administration of osteoanabolic agents could be beneficial. Teriparatide, available in daily, once-weekly, or twice-weekly dosages, along with abaloparatide and romosozumab, constitutes a trio of such agents. Each of these medications is defined by unique characteristics, distinct efficacy profiles, and specific adverse effects. There is growing evidence to suggest that these agents have a superior effect on enhancing bone mineral density and reducing fracture incidence when compared to traditional bisphosphonate therapies. Nonetheless, their employment demands thorough consideration of clinical indications, which includes evaluating economic factors, the frequency of injections required, and the potential for adverse effects. The objective of this review is to consolidate the current evidence focusing primarily on the efficacy of these agents, with the goal of enhancing understanding and aiding in making more informed treatment decisions, particularly for those individuals who are at an elevated risk of fractures.

Parathyroid hormone (PTH) is thought to induce remodeling-based bone formation by promoting osteoclastic activity, a process known as cellular coupling. Our research has shown that the frequency of PTH administration affects trabecular number and thickness. High-frequency PTH administration induced remodeling-based bone formation, while less frequent administration induced both remodeling-based and modeling-based bone formation. Additionally, we found that specific bone sites influence whether remodeling-based or modeling-based bone formation is more likely to occur. Additionally, while PTH significantly increases trabecular bone, it also causes cortical porosis. Our research on the femoral diaphysis showed that PTH administration resulted in the invasion of blood vessels and osteoclasts into the cortical bone. Abaloparatide acts similarly to teriparatide through the parathyroid hormone receptor type 1 (PTH1R) but may have a wider anabolic window due to its lesser impact on bone resorption. Our mouse studies with abaloparatide showed similar results to those seen in human patients, with increased preosteoblastic cell populations and wider anabolic windows when compared with teriparatide. Abaloparatide-induced bone formation cannot be explained solely by remodeling-based bone formation, indicating the need for further research into modeling-based bone formation.

The effectiveness of combining romosozumab (ROMO) with denosumab (Dmab) remains uncertain. We compare the six-month effects of Dmab plus monthly ROMO versus Dmab plus daily teriparatide (TPTD) on bone mineral density (BMD) in treatment-naïve postmenopausal women with osteoporosis.

The landscape of osteoporosis management has evolved significantly over the years, witnessing a paradigm shift from conventional therapies to the emergence of biologic agents. This chapter delves into the intricate mechanisms, potential applications, and future directions of biologic interventions in osteoporosis care. Biologic agents, with their targeted approach to bone health, have revolutionized the field by offering precision-driven strategies that address the underlying mechanisms of bone fragility. This chapter explores the mechanisms of action of various biologics, including Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL) inhibitors, monoclonal antibodies targeting sclerostin, parathyroid hormone (PTH) analogues, and cathepsin K inhibitors. It discusses their potential benefits, limitations, and safety considerations, while shedding light on the promise of combination therapies that merge biologic agents with traditional approaches. Furthermore, the chapter delves into the potential applications of biologic agents in specific patient populations, the role of biomarkers in predicting treatment responses, and the influence of emerging biological targets. It also explores the advancements in novel targets and drug delivery systems that aim to enhance treatment convenience and effectiveness. By tailoring treatments based on patient characteristics and exploring novel therapeutic targets, the chapter envisions a future of precision medicine in osteoporosis care. As research continues to evolve, the chapter anticipates a transformative impact on bone health outcomes, fracture prevention, and overall quality of life for individuals at risk of osteoporosis-related fractures. Through comprehensive insights into the mechanisms, applications, and future directions of biologic agents, this chapter offers a holistic perspective on the evolving landscape of osteoporosis management.

Calciphylaxis is a rare and potentially fatal small-vessel occlusive disease in which the tunica media becomes calcified, endothelial cells proliferate, and the tunica intima becomes thickened and fibrotic. Calciphylaxis typically occurs in the setting of end-stage renal disease with secondary hyperparathyroidism and elevated calcium-phosphorus product. The estimated incidence of calciphylaxis in dialysis or kidney transplant patients is 1 to 4%; however, the incidence of non-uremic calciphylaxis is unknown. We assessed postmarketing adverse event reports to further characterize cases of calciphylaxis associated with teriparatide. We searched for cases of teriparatide-associated calciphylaxis in the literature (EMBASE, PubMed) and those reported to FDA, including the FDA Adverse Event Reporting System, through March 31, 2021. We included calciphylaxis cases following teriparatide exposure of < 2 years. Twelve cases described teriparatide-associated calciphylaxis. The median age was 81 (range 47-86) years. Eleven cases reported confirmatory biopsy and/or imaging. The median time-to-onset of calciphylaxis following teriparatide initiation was 3.5 (range 1-20) months. Three cases reported hospitalization, of which one resulted in death due to progression of the lesions. All cases had multiple risk factors (mean (SD), 4.5 (1.0)) including concomitant medications associated with calciphylaxis (12), female sex (11), and/or underlying autoimmune disease or other inflammatory disorder (10). We believe that exposure to teriparatide, coupled with underlying risk factors, may have triggered new-onset calciphylaxis. Expedited diagnosis and management by a clinician are important because calciphylaxis may be life-threatening and early intervention may improve outcomes.

Teriparatide belongs to osteo-anabolic compounds and has been used in recent years to treat patients with osteoporosis, with the benefits of increased bone density. Its osteo-anabolic action has led to the investigation of the use of teriparatide for the improvement of bone quality. Apart from the enhancement of fracture union, teriparatide has been extensively studied in the promotion of fusion rate after spinal fusion. This study summarizes the preclinical and clinical results of the off-label use of teriparatide in the spine, and specifically its intermittent administration after instrumented spinal arthrodesis along with its impact on the spinal bone quality and spinal bone mineral density.

We present the case of a patient who presented with worsening chest pain and tachycardia. We were able to monitor her remotely through her pacemaker. She had been started on the injectable medication teriparatide (Forteo) and since then she had an increase in her symptoms. She was found to have intermittent atrial tachycardia with 1:1 conduction and occasional atrioventricular block transiently, coinciding with her injection of teriparatide. This specific-associated arrhythmia has yet to be described.

Teriparatide is a safe and effective anabolic treatment for osteoporosis. In postmenopausal women, it increases BMD and decreases vertebral fractures by about 70% and non-vertebral fractures by about 45% (although there is no evidence that it prevents hip fractures). The current evidence indicates that it should be administered for a single course of 24 months, and followed with an anti-resorptive agent to maintain the BMD gain. There is no clear benefit to repeated or cyclical treatment. Combination treatment, particularly with denosumab achieves greater BMD increase than either agent alone, but there are no available fracture data for combination treatment. There are some unknowns; most fundamentally why daily PTH administration is anabolic to bone when continuous high PTH is catabolic. Also, a better understanding of why the anabolic action declines with time and why there is a poor response to repeated treatment may help us to use teriparatide more effectively, and increase our understanding of bone biology and osteoporosis pathophysiology.

Teriparatide is a drug currently approved for treating patients with osteoporosis who are at high risk for future fracture. In the treatment of osteoporosis, teriparatide works as an anabolic agent stimulating bone formation throughout the skeleton by principally enhancing osteoblast-derived bone formation relative to osteoclast-derived bone resorption. The net effect is increased bone mass. For patients with a fracture, a similar process of increased bone formation is required transiently at the fracture site for repair. Teriparatide has been investigated in animal models and in patients as a potential agent to enhance fracture repair. In addition, evidence that teriparatide enhances chondrogenesis has generated interest in using the agent for articular cartilage repair. Research is currently underway to understand the effects teriparatide may have on mesenchymal stem cells, and on other effects that have been reported anecdotally in patients using the drug for osteoporosis care, including the healing of fracture nonunions and a decreased incidence of back pain. We review the current animal and human reports available on the uses of teriparatide in musculoskeletal diseases beyond osteoporosis.

The efficacy, safety, and cost of teriparatide in the treatment of osteoporosis are reviewed.

Traditionally, the management of osteoporosis in men and women has included the use of antiresorptive agents in combination with calcium and vitamin D supplementation. The mechanism of action of teriparatide is unique in that it possesses anabolic properties and therefore builds bone. Since the approval of teriparatide in the United States in 2002, a great deal of interest regarding its use in osteoporosis has developed.

To review the pharmacology, toxicology, pharmacokinetics, pharmacodynamics, efficacy, safety, therapeutic controversies, administration, patient counseling, and formulary recommendations for teriparatide (rDNA origin).