scholarly journals Management of osteoporosis in women with breast cancer

2020 ◽  
Vol 9 (2) ◽  
pp. BMT40
Author(s):  
Charles L Shapiro

The screening, prevention and treatment of osteoporosis are similar in women with or without breast cancer. Breast cancer treatments, such as aromatase inhibitors, chemotherapy-induced ovarian failure and gonadotropin-releasing hormone antagonists all decrease estrogen levels, which in turn causes net bone resorption and bone loss. Bone loss over time will be of sufficient magnitude to cause some women to experience fractures. Thus, osteoporosis is an equation; the peak bone mass achieved by age 30 years minus the age-related and menopausal bone loss. Women should have their bone density measured by dual x-ray absorptiometry scans every 2 years. As clinically indicated, women should receive anti-osteoporosis drugs such as zoledronic acid, denosumab or oral bisphosphonates.

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3094
Author(s):  
Charles L. Shapiro

Osteoporosis is both a long-term effect (occurs during treatment and extends after treatment) and a late-effect (occurs after treatment ends) of breast cancer treatments. The worldwide prevalence of osteoporosis is estimated to be some 200 million patients. About one in three postmenopausal women will experience an osteoporotic (or fragility) fracture of the hip, spine, or wrist. breast cancer treatments, including gonadotropin-releasing hormone (GnRH) agonists, chemotherapy-induced ovarian failure (CIOF), and aromatase inhibitors (AIs), cause bone loss and increase the risks of osteoporosis. Also, breast cancer is a disease of aging, and most of the “one in eight” lifetime risks of breast cancer are in women in their sixth, seventh, and eighth decades. The majority of women diagnosed with breast cancers today will be long-term survivors and experience personal cures. It is the coalescence of osteoporosis with breast cancer, two common and age-related conditions that make osteoporosis relevant in women with breast cancer throughout the continuum from diagnosis, treatment, and survivorship. It is critical to remember that women (and men) will lose bone after age thirty years. However, only certain women will lose bone of sufficient magnitude to merit treatment with anti-osteoporosis drugs. The narrative review is intended for medical, surgical, radiation oncologists, and other mid-level providers, and provides an overview of bone loss and the prevention and treatment of osteoporosis.


1990 ◽  
Vol 10 (3) ◽  
pp. S298 ◽  
Author(s):  
Sarah Henzell ◽  
Carole Hickling ◽  
Joan Brayshaw ◽  
Donald Gutteridge ◽  
Richard Prince ◽  
...  

Bone ◽  
2009 ◽  
Vol 44 ◽  
pp. S165
Author(s):  
X. Chen ◽  
L.S. Fong ◽  
X. Yang ◽  
P. Maruthappan ◽  
T. Lee

1999 ◽  
Vol 10 (4) ◽  
pp. 295-302 ◽  
Author(s):  
H. Sievänen ◽  
K. Uusi-Rasi ◽  
A. Heinonen ◽  
P. Oja ◽  
I. Vuori

2016 ◽  
Vol 8 (6) ◽  
pp. 225-235 ◽  
Author(s):  
Bente Langdahl ◽  
Serge Ferrari ◽  
David W. Dempster

The adult skeleton is renewed by remodeling throughout life. Bone remodeling is a process where osteoclasts and osteoblasts work sequentially in the same bone remodeling unit. After the attainment of peak bone mass, bone remodeling is balanced and bone mass is stable for one or two decades until age-related bone loss begins. Age-related bone loss is caused by increases in resorptive activity and reduced bone formation. The relative importance of cortical remodeling increases with age as cancellous bone is lost and remodeling activity in both compartments increases. Bone modeling describes the process whereby bones are shaped or reshaped by the independent action of osteoblast and osteoclasts. The activities of osteoblasts and osteoclasts are not necessarily coupled anatomically or temporally. Bone modeling defines skeletal development and growth but continues throughout life. Modeling-based bone formation contributes to the periosteal expansion, just as remodeling-based resorption is responsible for the medullary expansion seen at the long bones with aging. Existing and upcoming treatments affect remodeling as well as modeling. Teriparatide stimulates bone formation, 70% of which is remodeling based and 20–30% is modeling based. The vast majority of modeling represents overflow from remodeling units rather than de novo modeling. Denosumab inhibits bone remodeling but is permissive for modeling at cortex. Odanacatib inhibits bone resorption by inhibiting cathepsin K activity, whereas modeling-based bone formation is stimulated at periosteal surfaces. Inhibition of sclerostin stimulates bone formation and histomorphometric analysis demonstrated that bone formation is predominantly modeling based. The bone-mass response to some osteoporosis treatments in humans certainly suggests that nonremodeling mechanisms contribute to this response and bone modeling may be such a mechanism. To date, this has only been demonstrated for teriparatide, however, it is clear that rediscovering a phenomenon that was first observed more half a century ago will have an important impact on our understanding of how new antifracture treatments work.


2020 ◽  
Vol 05 (03) ◽  
pp. 1-1
Author(s):  
Jacqueline Lamond ◽  
◽  
Charles L. Shapiro ◽  

Breast cancer and osteoporosis are both diseases of aging. The "one in eight" lifetime risks of breast cancer occur primarily in the sixth, seventh, eighth, and ninth decades of life. One-third of postmenopausal women will experience an osteoporotic fracture. It is the coalescence of osteoporosis, breast cancer, and breast cancer treatments that, in some cases, increases the risks of osteoporotic fracture. That makes it imperative to assess risk factors, screen, and prevent or treat osteoporosis in postmenopausal women with breast cancer. Osteoporosis is primarily a genetic disease with a few modifiable risk factors. These risk factors include greater than two to three alcoholic drinks per day, current smoking, and decreased physical activity. The standard screening tool for osteoporosis is dual-energy x-ray absorptiometry (DXA) that gives a readout of T-scores of the lumbar spine, total hip, and femoral neck. The T-score is the number of standard deviations (SD) above or below the mean bone mineral density (BMD) of an average young adult of the same sex. For every SD below the mean BMD, the fracture risks double. Osteoporosis prevention and treatment do not differ in women with or without breast cancer. The difference is in breast cancer treatments, such as aromatase inhibitors (AI), which cause two to three-fold higher bone loss than average postmenopausal bone loss. Two classes of drugs for osteoporosis are oral and intravenous (iv) bisphosphonates and the receptor activator of nuclear factor kappa B ligand (RANKL) ligand inhibitor, subcutaneous (sc) denosumab. All three prevent bone loss and reduce the likelihood of fragility fractures. The treatment choice depends upon patient and provider preferences, specific contraindications (e.g., renal insufficiency), compliance, and costs. Despite guidelines and algorithms for AI-induced bone loss, the screening and treatment of osteoporosis remain suboptimal in postmenopausal women with breast cancer.


2019 ◽  
Vol 9 (2) ◽  
pp. 3898-3906

Breast cancer is the most common malignancy in the worldwide. It is noteworthy, that several drugs are used for cancer breast; nevertheless, some these drugs can produce secondary effects such as changes in blood pressure, bone loss and others. The objective of this investigation was synthesizing three steroid derivatives (compounds 4, 5 and 6) to evaluate their theoretical activity against both aromatase (2W3D) and 17β-Hydroxysteroid dehydrogenase Type 1 (3BH4) enzymes using fisetin and exemestane as control in a docking model. The data found indicate that compound 5 could exert a greater interaction with the 2WD4 and 3BH4 proteins in comparison with fisetin, exemestane and compounds 4 or 6. In conclusion, this compound could be a good candidate as both aromatase and 17β-hydroxysteroid dehydrogenase enzymes inhibitor.


2020 ◽  
Vol 05 (02) ◽  
pp. 1-1
Author(s):  
Jacqueline Lamond ◽  
◽  
Charles L. Shapiro ◽  

Breast cancer and osteoporosis are both diseases of aging. The "one in eight" lifetime risks of breast cancer occur primarily in the sixth, seventh, eighth, and ninth decades of life. One-third of postmenopausal women will experience an osteoporotic fracture. It is the coalescence of osteoporosis, breast cancer, and breast cancer treatments that, in some cases, increases the risks of osteoporotic fracture. That makes it imperative to assess risk factors, screen, and prevent or treat osteoporosis in postmenopausal women with breast cancer. Osteoporosis is primarily a genetic disease with a few modifiable risk factors. These risk factors include greater than two to three alcoholic drinks per day, current smoking, and decreased physical activity. The standard screening tool for osteoporosis is dual-energy x-ray absorptiometry (DXA) that gives a readout of T-scores of the lumbar spine, total hip, and femoral neck. The T-score is the number of standard deviations (SD) above or below the mean bone mineral density (BMD) of an average young adult of the same sex. For every SD below the mean BMD, the fracture risks double. Osteoporosis prevention and treatment do not differ in women with or without breast cancer. The difference is in breast cancer treatments, such as aromatase inhibitors (AI), which cause two to three-fold higher bone loss than average postmenopausal bone loss. Two classes of drugs for osteoporosis are oral and intravenous (iv) bisphosphonates and the receptor activator of nuclear factor kappa B ligand (RANKL) ligand inhibitor, subcutaneous (sc) denosumab. All three prevent bone loss and reduce the likelihood of fragility fractures. The treatment choice depends upon patient and provider preferences, specific contraindications (e.g., renal insufficiency), compliance, and costs. Despite guidelines and algorithms for AI-induced bone loss, the screening and treatment of osteoporosis remain suboptimal in postmenopausal women with breast cancer.


2012 ◽  
Vol 15 (2) ◽  
pp. 135-145 ◽  
Author(s):  
Max-Ludwig Schäfer ◽  
Joachim Böttcher ◽  
Alexander Pfeil ◽  
Andreas Hansch ◽  
Ansgar Malich ◽  
...  
Keyword(s):  
X Ray ◽  

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