Review of Current Real-World Experience with Teriparatide as Treatment of Osteoporosis in Different Patient Groups

Hauser, Barbara; Alonso, Nerea; Riches, Philip

doi:10.3390/jcm10071403

Cited by 16 publications

(16 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Zoledronic acid, denosumab, and teriparatide are recommended by ACR as second-line treatment if oral bisphosphonates are not effective or not tolerated ( 72 ). However, there is increasing clinical trial and observational evidence that teriparatide is superior to oral bisphosphonates in preventing vertebral fractures in GC-naïve and GIOP patients with severe spinal osteoporosis ( 44 , 76 , 77 ). Additionally, considering the pathophysiology of GIOP is driven by effects on osteoblasts, teriparatide is a particularly attractive treatment option as it stimulates bone formation ( 77 ).…”

Section: Starting Treatment To Prevent Giopmentioning

confidence: 99%

“…However, there is increasing clinical trial and observational evidence that teriparatide is superior to oral bisphosphonates in preventing vertebral fractures in GC-naïve and GIOP patients with severe spinal osteoporosis ( 44 , 76 , 77 ). Additionally, considering the pathophysiology of GIOP is driven by effects on osteoblasts, teriparatide is a particularly attractive treatment option as it stimulates bone formation ( 77 ). We therefore suggest that teriparatide may be considered as first-line therapy in patients at high risk of vertebral fractures (e.g., with a recent vertebral fracture or very low vertebral BMD).…”

Section: Starting Treatment To Prevent Giopmentioning

confidence: 99%

See 1 more Smart Citation

When to Start and Stop Bone-Protecting Medication for Preventing Glucocorticoid-Induced Osteoporosis

et al. 2021

Self Cite

View full text Add to dashboard Cite

Glucocorticoid-induced osteoporosis (GIOP) leads to fractures in up to 40% of patients with chronic glucocorticoid (GC) therapy when left untreated. GCs rapidly increase fracture risk, and thus many patients with anticipated chronic GC exposures should start anti-osteoporosis pharmacotherapy to prevent fractures. In addition to low awareness of the need for anti-osteoporosis therapy among clinicians treating patients with GCs, a major barrier to prevention of fractures from GIOP is a lack of clear guideline recommendations on when to start and stop anti-osteoporosis treatment in patients with GC use. The aim of this narrative review is to summarize current evidence and provide considerations for the duration of anti-osteoporosis treatment in patients taking GCs based on pre-clinical, clinical, epidemiologic, and pharmacologic evidence. We review the pathophysiology of GIOP, outline current guideline recommendations on initiating and stopping anti-osteoporosis therapy for GIOP, and present considerations for the duration of anti-osteoporosis treatment based on existing evidence. In each section, we illustrate major points through a patient case example. Finally, we conclude with proposed areas for future research and emerging areas of interest related to GIOP clinical management.

show abstract

Section: Starting Treatment To Prevent Giopmentioning

confidence: 99%

Section: Starting Treatment To Prevent Giopmentioning

confidence: 99%

When to Start and Stop Bone-Protecting Medication for Preventing Glucocorticoid-Induced Osteoporosis

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…The intermittent systemic administration of PTH has been previously reported to have a beneficial effect on skeletal bone mass of patients with osteoporosis 38 . Due to its anabolic effect, the systemic application of PTH has been extensively studied in pre‐clinical and clinical models with promising results not only for the treatment of osteoporotic patients, 39 but also to promote fracture healing, 40 to treat/prevent medication‐related osteonecrosis 41–43 and to improve bone formation in critical defects 44 and around implanted devices in challenging bone‐healing scenarios 45 . However, PTH systemic administration drawbacks include the need for daily/weekly self‐injections, the exposure of not‐target areas, and mild side‐effects 46 …”

Section: Discussionmentioning

confidence: 99%

Effects of local single dose administration of parathormone on the early stages of osseointegration: A pre‐clinical study

et al. 2022

View full text Add to dashboard Cite

The present study aimed to evaluate the effect of parathormone (PTH) administered directly to the implant's surface prior to insertion, using a large translational animal model. Sixty titanium implants were divided into four groups: (i) Collagen, control group, where implants were coated with Type‐I Bovine‐collagen, and three experimental groups, where implants received varying doses of PTH: (ii) 12.5, (iii) 25, and (iv) 50 μg, prior to placement. Fifteen female sheep (~2 years old, weighing ~65 kg) received four implants in an interpolated fashion in C3, C4 or C5 vertebral bodies. After 3‐, 6‐ and 12‐weeks, samples were harvested, histologically processed, qualitatively and quantitatively assessed for bone‐to‐implant contact (BIC) and bone area fraction occupancy (BAFO). BIC yielded lower values at 6‐weeks for 50 μg relative to the control group, with no significant differences, when compared to the 12.5‐ and 25‐μg. No significant differences were detected at 6‐weeks between collagen, 12.5‐ and 25‐μg groups. At 3‐ and 12‐weeks, no differences were detected for BIC among PTH groups. With respect to BAFO, no significant differences were observed between the control and experimental groups independent of PTH concentration and time in vivo. Qualitative observations at 3‐weeks indicated the presence of a more mature bone near the implant's surface with the application of PTH, however, no significant differences in new bone formation or healing patterns were observed at 6‐ and 12‐weeks. Single local application of different concentrations of PTH on titanium implant's surface did not influence the osseointegration at any time‐point evaluation in low‐density bone.

show abstract

“…It has direct actions on osteoblast activity, with biochemical and histomorphometric evidence of de novo bone formation within a week or two in response to teriparatide. [7] Abaloparatide is a synthetic analogue of human PTHrP, which has significant homology to PTH and also binds the PTH Type 1 receptor. Abaloparatide and teriparatide exert different binding affinities to the two different receptor conformations, R 0 and RG.…”

Section: Treatmentmentioning

confidence: 99%

“…Teriparatide is also approved for the treatment of glucocorticoid-induced osteoporosis. [1,7] Pharmacological treatments are the mainstream of fracture prevention. Local osteo-enhancement procedure (LOEP) is an emerging surgical procedure that has been shown to effectively reduce the risk of refracture.…”

Section: Treatmentmentioning

confidence: 99%

Osteoporosis

Mitra

2022

VJIM

View full text Add to dashboard Cite

Bone is a dynamic tissue that is remodelled constantly throughout life. The arrangement of compact and cancellous bone provides strength and density suitable for both mobility and protection. Osteoporosis is defined as a reduction in the strength of bone that leads to an increased risk of fractures. The World Health Organisation operationally defined osteoporosis as a bone density also referred to as a T-score of <–2.5 and is associated with increased risk of fractures. Bone remodelling is regulated by multiple hormones, including oestrogens (in both genders), androgens, Vitamin D and parathyroid hormone (PTH), as well as locally produced growth factors, such as IGF-I, transforming growth factor β, PTH-related peptide (PTHrP), interleukins, prostaglandins and members of the tumour necrosis factor superfamily. The risk of fracture can be predicted by the Fracture Risk Assessment score. Several non-invasive techniques are available for estimating skeletal mass or bone mineral density including single energy X-ray absorptiometry, dual-energy X-ray absorptiometry, quantitative computed tomography and ultra-sound. Total daily calcium intakes <400 mg are detrimental to the skeleton. The recommended daily required intake of 1000–1200 mg for adults accommodates population heterogeneity in controlling calcium balance. For optimal skeletal health, serum 25(OH)D should be >75 nmol/L (30 ng/mL). Bisphosphonates have become the mainstay of osteoporosis treatment. Calcitonin preparations are approved by the FDA for osteoporosis in women >5 years past menopause. Denosumab was approved by the FDA in 2010. Parathormone analogues augment trabecular bone mineral density and reduce fracture occurrence. PTH (1–34) (teriparatide) produced substantial increments in bone mass. Abaloparatide is a synthetic analogue of human PTHrP, which has significant homology to PTH and also binds the PTH Type 1 receptor increasing the bone mass. Ageing is associated with progressive decline in overall muscle strength and bone loss. Resistance training increases bone strength and density, reducing the risk of fracture during a fall. Increased levels of endurance, strength and balance with exercises increase the threshold for disability and dependence as we age. Inactive and sedentary lifestyle should be discouraged. Treatment accessibility could be improved and treatment adherence should be encouraged.

show abstract

Review of Current Real-World Experience with Teriparatide as Treatment of Osteoporosis in Different Patient Groups

Cited by 16 publications

References 74 publications

When to Start and Stop Bone-Protecting Medication for Preventing Glucocorticoid-Induced Osteoporosis

When to Start and Stop Bone-Protecting Medication for Preventing Glucocorticoid-Induced Osteoporosis

Effects of local single dose administration of parathormone on the early stages of osseointegration: A pre‐clinical study

Osteoporosis

Contact Info

Product

Resources

About