Treating osteoporosis
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Osteoporotic fractures are common resulting in increased morbidity and mortality.Exercise can help prevent osteoporosis.It can also benefit patients with osteoporosis, but the exercises must be tailored to the patient.Most Australians should be able to obtain adequate calcium in their diet and vitamin D from the sun.Supplements may be needed in some patients and they are recommended for use with other drugs for osteoporosis.Bisphosphonates, and in some patients denosumab, are first-line drugs for osteoporosis.Raloxifene and strontium ranelate can be considered in patients who cannot take bisphosphonates or denosumab.Teriparatide is reserved for patients with severe osteoporosis and the use of strontium ranelate is declining because of cardiovascular safety concerns.to higher peak bone mass in adulthood. 7,8Impact exercises are also beneficial for middle-aged and older adults for increasing or preventing age-related bone loss.Although the gains in bone mass are promising, there is insufficient evidence to suggest exercise might reduce fractures.The frequency and severity of falls may be reduced by exercises that maintain muscle strength, muscle mass, flexibility, mobility, balance and ease of movement.For people with established osteoporosis, any exercise that promotes these characteristics is recommended.The Box lists exercises according to their 'osteogenic' profile and more detailed information is available at www.osteoporosis.org.au/exercise.9][10][11] Any recommendation for exercise must be tailored to the individual.For example, in patients who have already sustained osteoporotic fractures, moderateto high-impact activities may be unsuitable.Keywords:
Strontium ranelate
Teriparatide
Denosumab
Raloxifene
Denosumab
Teriparatide
Bone remodeling
Bone Formation
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Atypical femoral fractures (AFFs) are a rare association of anti-resorptive therapy for osteoporosis. Limited evidence-based management guidelines on their optimal treatment exist, with observational studies suggesting a role for teriparatide (TPTD) in AFF healing. We report a case of a 65-year-old woman with postmenopausal osteoporosis who sustained an AFF following long-term bisphosphonate therapy, and who subsequently developed a new contralateral AFF after completion of TPTD therapy and initiation of strontium ranelate (SR) treatment. The sequence of events in this case report showed that TPTD and SR did not prevent the development of a new AFF, and questions the optimal treatment of these stress fractures.
Teriparatide
Strontium ranelate
Postmenopausal osteoporosis
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In postmenopausal osteoporotic women, denosumab fully inhibits teriparatide-induced bone resorption at approved doses. This property of denosumab is distinct from that of alendronate and likely contributes to the efficacy of combination denosumab and teriparatide therapy. Whether denosumab fully inhibits bone resorption when challenged by a higher dose of teriparatide is unknown.We aimed to define the comparative ability of denosumab and alendronate to block the acute proresorptive effects of high-dose teriparatide.In this randomized controlled trial, bone resorption (serum C-telopeptide [CTX]) was measured in 25 postmenopausal women prior to and 4 hours after a single 40-μg sc teriparatide injection. Subjects then received either a single injection of denosumab 60 mg or oral alendronate 70 mg weekly for 8 weeks. After 8 weeks, serum CTX was again measured before and 4 hours after a teriparatide a 40-μg injection.The primary outcome was the between-group difference in the teriparatide-induced change in CTX from baseline to week 8.At baseline, 40 μg of teriparatide induced similar 4-hour increases in mean CTX in both groups (alendronate 47% ± 14%, denosumab 46% ± 16%). After 8 weeks, teriparatide was still able to stimulate bone resorption in women treated with alendronate (mean CTX increase of 43% ± 29%) but not in women treated with denosumab (-7% ± 11%; P < .001 for between group comparison).Denosumab, but not alendronate, fully inhibits the ability of high-dose teriparatide to increase bone resorption acutely. These results suggest that combining denosumab with a more potent anabolic stimulus may result in greater separation between bone resorption and formation and hence greater increases in bone mass.
Teriparatide
Denosumab
N-terminal telopeptide
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Teriparatide
Denosumab
Bone remodeling
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Teriparatide
Raloxifene
Postmenopausal osteoporosis
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To evaluate the responses of serum beta-CTX and osteocalcin in patients who were undergoing treatment with teriparatide or strontium ranelate (SR).We analyzed 14 patients (12 women and 2 men; mean age of 71 years) taking teriparatide, and 13 female patients (mean age of 70 years) taking SR; all the patients having previously been on bisphosphonates. Serum beta-CTX and osteocalcin levels were determined before and after the first and third months of teriparatide treatment and up to the fourth month of treatment with SR.We observed an initial significant increase in osteocalcin levels during the first month (165%, p = 0.01) followed by a peak of beta-CTX (180%, p = 0.02) after the third month of treatment with teriparatide. An increase in these markers was also observed with SR: 49% in osteocalcin (p = 0.002) and 80% in beta-CTX (p = 0.008).SR had a predominantly short-term bone-forming effect in postmenopausal women with osteoporosis previously treated with bisphosphonates in a lesser degree than with teriparatide.
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Strontium ranelate
Bone remodeling
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To the Editor: We would like to comment on the article "Comparative Effects of Teriparatide and Strontium Ranelate on Bone Biopsies and Biochemical Markers of Bone Turnover in Postmenopausal Women With Osteoporosis" by Recker et al., which has recently been published in the JBMR.1 This study set out to show the superiority of teriparatide over strontium ranelate on bone histomorphometric parameters. However, there are several important limitations in this paper that need to be considered. First, there is a clear imbalance in the baseline characteristics of the 79 patients randomized, to the disadvantage of the strontium ranelate group. Indeed, this group had a lower vitamin D status than the teriparatide group (serum 25-hydroxyvitamin D, 68.5 ± 33.0 versus 79.8 ± 53.7 nM, respectively). In addition, there were more patients with previous treatment with hormone replacement therapy (HRT) or calcitonin in the strontium ranelate group than in the teriparatide group (12.5% versus 2.6%, respectively). These important differences are not discussed by the authors despite the fact that they could have had a dramatic impact on bone status and bone remodeling in the strontium ranelate group. In addition, the authors failed to give information on compliance with strontium ranelate, notably in terms of blood strontium content, which is an indirect assessment of compliance for this agent. Second, the authors report that there was no difference in osteoblast surface (Ob.S) between the teriparatide and strontium ranelate groups. Additionally, there was no significant difference in parameters related to bone structure between the two treatment groups, with the exception of cortical porosity, which was significantly increased in the teriparatide group (p = 0.037). Increased cortical porosity is a potential issue for bone quality and needs to be taken very seriously. Surprisingly, the authors interpreted these data as evidence of a limited anabolic effect of strontium ranelate in these patients. Furthermore, the authors made positive statements on the basis of nonsignificant results. For instance, the authors presented differences in histomorphometric parameters in a favorable way for teriparatide, even though the differences between strontium ranelate and teriparatide were not statistically significant. A typical example is "Although not statistically significant, the majority of the bone formation parameters in the teriparatide group were numerically greater than in the SrR group." Such an interpretation lacks scientific basis and may be misleading for the reader. Given the lack of significant difference in the histomorphometric parameters between the two treatments, a more consistent interpretation of these data are that teriparatide and strontium ranelate have similar anabolic effects on bone microarchitecture. These data support previous studies in postmenopausal osteoporosis2 and in appropriately designed preclinical studies in animals3, 4 showing that strontium ranelate improves bone mass and microarchitecture in vivo, as revealed by histomorphometric analyses. This, however, does not preclude that teriparatide and strontium ranelate may have different amplitudes of effect and distinct mechanisms of action on bone-forming cells.
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Teriparatide
Bone remodeling
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Denosumab
Teriparatide
Bone remodeling
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Abstract Background Continuous use of glucocorticoids (GCs) has become the primary cause of secondary osteoporosis. Bisphosphonate drugs were given priority over denosumab and teriparatide in the 2017 American College of Rheumatology (ACR) guidelines but have a series of shortcomings. This study aims to explore the efficacy and safety of teriparatide and denosumab compared with those of oral bisphosphonate drugs. Methods We systematically searched studies included in the PubMed, Web of Science, Embase, and Cochrane library databases and included randomized controlled trials that compared denosumab or teriparatide with oral bisphosphonates. Risk estimates were pooled using both fixed and random effects models. Results We included 10 studies involving 2923 patients who received GCs for meta-analysis, including two drug base analyses and four sensitivity analyses. Teriparatide and denosumab were superior to bisphosphonates in increasing the bone mineral density (BMD) of the lumbar vertebrae [teriparatide: mean difference [MD] 3.98%, 95% confidence interval [CI] 3.61–4.175%, P = 0.00001; denosumab: MD 2.07%, 95% CI 0.97–3.17%, P = 0.0002]. Teriparatide was superior to bisphosphonates in preventing vertebral fractures and increasing hip BMD [MD 2.39%, 95% CI 1.47–3.32, P < 0.00001]. There was no statistically significant difference between serious adverse events, adverse events, and nonvertebral fracture prevention drugs. Conclusions Teriparatide and denosumab exhibited similar or even superior characteristics to bisphosphonates in our study, and we believe that they have the potential to become first-line GC-induced osteoporosis treatments, especially for patients who have previously received other anti-osteoporotic drugs with poor efficacy.
Teriparatide
Denosumab
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Objectives In our previous 24-month study, we observed that teriparatide had some advantages over denosumab for bone mineral density (BMD) in glucocorticoid-induced osteoporosis (GIO) patients with prior bisphosphonate treatment. We conducted this extension study to investigate whether the advantage of teriparatide obtained in the first 2 years would be maintained after the switch to denosumab. Materials and Methods We switched patients who had completed 24-month daily teriparatide treatment to denosumab (switch group, n=18) and compared their BMD every 6 months up to 48 months with the group who continued to receive denosumab (denosumab group, n=16). Results At 48 months, the lumbar spine BMD was significantly increased from baseline in both groups (denosumab: 10.4 ± 8.7%, p<0.001; switch: 14.2 ± 6.8%, p<0.001). However, a significant increase in femoral neck BMD from baseline occurred only in the switch group (11.2 ± 14.6%, p<0.05); denosumab (4.1 ± 10.8%). The total hip BMD increased significantly from baseline in both groups (denosumab: 4.60 ± 7.4%, p<0.05; switch: 7.2 ± 6.9%, p<0.01). Femoral neck BMD was significantly increased in the switch versus the denosumab group (p<0.05). Conclusion In GIO patients with prior bisphosphonate treatment, the advantage of teriparatide may be maintained after the treatment period. A continuous increase in BMD can be expected with teriparatide followed by denosumab.
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Denosumab
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