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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Bone Remodeling01:40

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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Hormones and Bone Tissue01:17

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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Role of Vitamins in Maintaining Bone Health01:25

Role of Vitamins in Maintaining Bone Health

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The growth and maintenance of bone are regulated by a combination of nutritional factors, including vitamins, such as vitamin A, B12, C, D, and K.
Vitamin A
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Menopause01:28

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Menopause, a natural biological process marking the end of a woman's fertility, typically occurs between the fifth and sixth decade of life. This phase is characterized by the exhaustion of the ovarian follicle pool, leading to less responsive ovaries despite the high levels of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). The consequential decrease in estrogen production results in symptoms like hot flashes, heavy sweating, headaches, hair loss, muscle pains, vaginal...
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Estrogen-Like Effect of Bazi Bushen Capsule in Ovariectomized Rats
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Androgen-deprivation-associated bone disease.

Ted A Skolarus1, Megan V Caram, Vahakn B Shahinian

  • 1aDivision of Urologic Oncology, Department of Urology, Dow Division of Health Services Research, University of Michigan bVA HSR&D Center for Clinical Management Research, VA Ann Arbor Healthcare System cDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.

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Androgen deprivation therapy (ADT) for prostate cancer can cause bone disease. While some treatments preserve bone density, none definitively reduce fracture risk, highlighting the need for judicious ADT use.

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Area of Science:

  • Oncology
  • Endocrinology
  • Bone Metabolism

Background:

  • Androgen deprivation therapy (ADT) is a common prostate cancer treatment, often used even when efficacy is uncertain.
  • ADT is associated with significant adverse effects, particularly bone disease, including osteoporosis and fractures.
  • Management of ADT-associated bone disease is a growing concern in prostate cancer care.

Purpose of the Study:

  • To review recently published literature on the effects of ADT on bone health.
  • To evaluate current management strategies for ADT-associated bone disease.
  • To assess the efficacy of interventions in preventing fractures.

Main Methods:

  • Review of recently published articles focusing on ADT and bone disease.
  • Analysis of available management strategies, including pharmacologic and complementary approaches.
  • Evaluation of outcome measures, particularly bone mineral density and fracture risk.

Main Results:

  • Antiresorptive agents like denosumab and bisphosphonates preserve bone mineral density.
  • Complementary approaches (calcium, vitamin D, exercise) show modest to no benefits.
  • Bone mineral density is an inadequate surrogate for fracture risk assessment.

Conclusions:

  • Antiresorptive agents effectively maintain bone mineral density in men receiving ADT.
  • No current intervention definitively reduces clinically relevant fracture outcomes.
  • ADT should be restricted to settings with clearly established benefits to minimize complications.