Risedronate for the Prevention of Fractures in Postmenopausal Osteoporosis

2002 ◽  
Vol 36 (4) ◽  
pp. 664-670 ◽  
Author(s):  
Jennifer M Sickels ◽  
Chi-Sing Nip
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Bone Fragility ◽  
Mineral Density ◽  
Osteoporosis Therapy ◽  
Treatment Of Osteoporosis ◽  
Medline Search ◽  
Secondary Sources ◽  
Nonvertebral Fractures ◽  
Search Terms ◽  
Increased Risk

OBJECTIVE: To evaluate current scientific literature regarding the efficacy of risedronate in the prevention of vertebral and nonvertebral fractures in women with postmenopausal osteoporosis. DATA SOURCES: Primary research articles were identified by MEDLINE search (1966–May 2001) and through secondary sources. Key search terms were risedronate, postmenopausal osteoporosis, and fractures. DATA SYNTHESIS: Osteoporosis results in a reduction of bone mineral density, increased bone fragility, and increased risk of fractures. The goal of osteoporosis therapy is not only to increase bone mass, but also to reduce the rate of fractures. Risedronate is the newest bisphosphonate to be approved for the prevention and treatment of osteoporosis. An evaluation of clinical trials using risedronate in the treatment of postmenopausal osteoporosis was performed to determine its efficacy at decreasing fracture rates. CONCLUSIONS: Risedronate is an effective and safe option for the treatment of postmenopausal osteoporosis. Risedronate significantly decreases the risk of vertebral and nonvertebral fractures in women who have had ≥1 fractures in the past. More studies are warranted to evaluate the efficacy of risedronate in women without preexisting vertebral fractures.

scholarly journals Diabetes mellitus and osteoporosis: pathogenetic relationship and current principles of treatment

2021 ◽  
pp. 96-107
Author(s):  
T. Y. Demidova ◽  
V. M. Plakhotnyaya
Keyword(s):  
Diabetes Mellitus ◽  
Bone Matrix ◽  
Wnt Signaling Pathway ◽  
Bone Fragility ◽  
Current Data ◽  
Mineral Density ◽  
Increased Risk ◽  
Dm Type 2

Diabetes mellitus (DM) is a well known risk factor for osteoporosis and an increased risk of fractures. A lot of data has been published about the relationship between diabetes and bone health. DM type 1 and DM type 2 have different effects on bone mineral density (BMD). The central link in pathogenesis of bone fragility in patients with DM type 1 is a violation of the activity and gifferentiation of osteoblasts. On the contrary, hyperinsulinemia in DM type 2 activates the division and gifferentiation of osteoblasts and contributes to an increase in BMD. However, Higher BMD values in patients with DM type 2 are combined with slowdown in bone metabolism. As the result, high-quality bone remodeling does not occur. And bone strength decreases despite the high BMD. Despite the differences, DM type 1 and DM type 2 have common pathogenic pathways, that lead to increased bone fragility. For example, non-enzymatic glycation of bone matrix collagen and increase in concentration of sclerostin, which blocks the Wnt signaling pathway. In this review, we will analyze current data about epidemiology and pathogenesis of osteoporosis in DM and discuss the practical issues of the clinic, diagnosis, stratification of fracture risk and treatment. Special attention will be paid to the effects of glucose-lowering and anti-osteoporotic drugs on bone tissue.

scholarly journals Effects of anti-osteoporosis therapy on plasma aldosterone and renin

2020 ◽  
Vol 21 (2) ◽  
pp. 147032032092887
Author(s):  
Qingfen Hu ◽  
Kangla Liao ◽  
Longwei Zhang ◽  
Xiaoyu Shu ◽  
Zhixin Xu ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Femoral Neck ◽  
Postmenopausal Osteoporosis ◽  
Plasma Renin ◽  
Osteoporosis Treatment ◽  
Plasma Aldosterone ◽  
Mineral Density ◽  
Osteoporosis Therapy ◽  
Plasma Aldosterone Concentration ◽  
T Score

Objective: This study aimed to investigate the effect of anti-osteoporosis therapy on plasma aldosterone concentration (PAC), plasma renin concentration (PRC) and the aldosterone/renin ratio (ARR) in patients with postmenopausal osteoporosis. Methods: In 60 patients with postmenopausal osteoporosis, bone mineral density (BMD), PAC and PRC were measured before and after treatment with alendronate (70 mg/week, n=22) or recombinant human parathyroid hormone (20 μg/day, n=35) for 48 weeks. Results: PAC was negatively correlated with the T-score of lumbar spine BMD and femoral neck BMD (lumbar r=−0.386, p<0.01; femoral neck r=−0.262, p<0.05). With the improvement in lumbar BMD after anti-osteoporosis treatment (T-score −3.4±0.5 vs. –3.1 ±0.4, p<0.0001), PAC decreased from 182.8±53.2 to 143.7±68.6 pg/mL ( p<0.0001), PRC increased from 7.8±11.6 to 39.2±50.0 μIU/mL ( p<0.0001) and the ARR decreased from 74.8±75.2 to 13.1±17.1 pg/μIU ( p<0.0001). At baseline, 58% (35/60) of the patients had an ARR >37 pg/μIU, and the proportion decreased to 8% (5/57) after treatment. Conclusion: Treatment with alendronate or parathyroid hormone causes decreased PAC and increased PRC, resulting in a decreased ARR in postmenopausal women with osteoporosis.

scholarly journals Osteoblasts in osteoporosis: past, emerging, and future anabolic targets

2011 ◽  
Vol 165 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Pierre J Marie ◽  
Moustapha Kassem
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Matrix ◽  
Bone Fragility ◽  
Osteoblastic Cell ◽  
Medline Search ◽  
Cell Functions ◽  
Age Related ◽  
Increased Risk

ObjectiveAge-related bone loss is associated with significant changes in bone remodeling characterized by decreased trabecular and periosteal bone formation relative to bone resorption, resulting in bone fragility and increased risk of fractures. Prevention or reversal of age-related decrease in bone mass and increase in bone fragility has been based on inhibition of bone resorption using anticatabolic drugs. The current challenge is to promote osteoblastogenesis and bone formation to prevent age-related bone deterioration.MethodsA limited number of approved therapeutic molecules are available to activate bone formation. Therefore, there is a need for anabolic drugs that promote bone matrix apposition at the endosteal, endocortical, and periosteal envelopes by increasing the number of osteoblast precursor cells and/or the function of mature osteoblasts. In this study, we review current therapeutics promoting bone formation and anabolic molecules targeting signaling pathways involved in osteoblastogenesis, based on selected full-text articles searched on Medline search from 1990 to 2010.Results and discussionWe present current therapeutic approaches focused on intermittent parathyroid hormone and Wnt signaling agonists/antagonists. We also discuss novel approaches for prevention and treatment of defective bone formation and bone loss associated with aging and osteoporosis. These strategies targeting osteoblastic cell functions may prove to be useful in promoting bone formation and improving bone strength in the aging population.

Teriparatide: Its Use in the Treatment of Osteoporosis

2011 ◽  
Vol 3 ◽  
pp. CMT.S2358 ◽  
Author(s):  
Charles A. Inderjeeth ◽  
Kien Chan ◽  
Paul Glendenning
Keyword(s):  
Bone Formation ◽  
Bone Mass ◽  
Animal Studies ◽  
Safety Data ◽  
Ageing Population ◽  
Mineral Density ◽  
Duration Of Treatment ◽  
Treatment Of Osteoporosis ◽  
Teriparatide Treatment ◽  
Increased Risk

The prevalence of osteoporosis is likely to rise with the increase in life expectancy of an ageing population. Current first line therapies for the treatment of osteoporosis are predominantly anti-resorptive. Teriparatide is a first in class, anabolic agent with a unique mechanism that results in increased bone formation. Daily subcutaneous injection for 6–24 months was effective in reducing vertebral and non-vertebral fracture rates, in improving bone mineral density (BMD) and in increasing bone formation rates in postmenopausal osteoporosis, with effects persisting following treatment cessation. Similar benefits on bone mass and bone formation were seen in men with osteoporosis and glucocorticoid induced osteoporosis. Beneficial effects on bone mass have been demonstrated in treatment naive subjects treated with teriparatide alone, sequentially with anti-resorptive therapy and concomitantly with some, but not all, anti-resorptive treatments due to an early blunting of the anabolic effect. Teriparatide is generally well tolerated. However, the high treatment cost and inconvenient mode of administration has limited it's use to patients with osteoporosis who have experienced an unsatisfactory response, who are intolerant to other osteoporosis therapies, or to patients at very high risk of fracture. Teriparatide treatment is currently restricted to a total lifetime treatment dose of 18 months of daily subcutaneous therapy due to concerns from animal studies suggesting an increased risk of osteosarcoma. More safety data may permit a longer duration of treatment in the future but will necessitate prolonged human studies. Teriparatide may serve a more prominent role in the treatment of older patients who continue to fracture despite low bone turnover or sustain side effects with anti-resorptive therapy.

scholarly journals Biologicals and bone loss

2012 ◽  
Vol 4 (4) ◽  
pp. 245-247 ◽  
Author(s):  
Charlotte L.M. Krieckaert ◽  
Willem F. Lems
Keyword(s):  
Bone Loss ◽  
Active Rheumatoid Arthritis ◽  
Osteoporotic Fractures ◽  
Fracture Rate ◽  
Healthy Controls ◽  
Mineral Density ◽  
Common Pathway ◽  
Inflammatory Joint Diseases ◽  
Nonvertebral Fractures ◽  
Increased Risk

Inflammatory joint diseases are associated with extra-articular side effects including bone involvement.There is an increased risk of osteoporotic fractures. The pathogeneses of local and generalized bone loss share a common pathway. Early and active rheumatoid arthritis is associated with longitudinal observed bone loss and fracture rate is of vertebral and nonvertebral fractures is doubled compared with matched healthy controls. Lowering disease activity with TNF inhibitors or is associated with stabilisation of bone mineral density by counteracting elevated bone resorption.

scholarly journals Current Challenges in Osteoporosis Treatment Discontinuation

2021 ◽  
Vol 47 (3) ◽  
pp. 17-18
Author(s):  
Tang Ching Lau
Keyword(s):  
Fracture Risk ◽  
Osteoporotic Fractures ◽  
Osteoporosis Treatment ◽  
Bisphosphonate Therapy ◽  
Treat To Target ◽  
Mineral Density ◽  
High Fracture ◽  
Osteoporosis Therapy ◽  
Increased Risk ◽  
Rebound Increase

Osteoporosis is a chronic disease that may require lifelong therapy. Therefore, evidence-based approach regarding the efficacy and safety of long‐term osteoporosis therapy and therapy discontinuation is important. The most important goals for osteoporosis and fragility fracture patients are the recovery of pre-fracture functional level and reduction of fracture risk. There has been increasing consensus that a treat-to-target (T2T) strategy is applicable to osteoporosis and that bone mineral density (BMD) is currently the most clinically appropriate target. However, there is no clear consensus with regard to the definition of a specific BMD treatment target and timeframes applicable to T2T in osteoporosis, and these would need to be individually determined. Treatment with bisphosphonates may be interrupted after 3-5 years, only in patients in whom fracture risk is low or lowered because of the treatment itself. It is recommended never to discontinue treatment in patients with one or more prevalent osteoporotic fractures or in whom the BMD values are still below -2.5 (T score). Recent reports imply that denosumab discontinuation may lead to an increased risk of multiple vertebral fractures. Patients considered at high fracture risk should either continue denosumab therapy for up to ten years or be switched to an alternative treatment. For patients at low-risk, a decision to discontinue denosumab could be made after five years, but bisphosphonate therapy should be considered to reduce or prevent the rebound increase in bone turnover.

Sign in / Sign up

Export Citation Format

Share Document