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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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Adrenal Gland Disorders01:27

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Adrenal gland disorders manifest when the production of adrenal hormones deviates from the norm, resulting in either excessive or insufficient concentrations.
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The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
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Hormones of the Adrenal Glands01:31

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Adrenal hormones play a pivotal role in maintaining the body's electrolyte balance and orchestrating responses to stress, showcasing the intricate functions of the adrenal cortex and medulla.
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Disorders of the Skeletal Muscle01:28

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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
Musculoskeletal disorders
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Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
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Author Spotlight: Developing a Rat Model for Weight-Bearing Intervention to Investigate Osteonecrosis of the Femoral Head
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Skeletal Fragility in Endogenous Hypercortisolism.

Gherardo Mazziotti, Adriano Delgado, Filippo Maffezzoni

    Frontiers of Hormone Research
    |May 24, 2016
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    Summary
    This summary is machine-generated.

    Endogenous hypercortisolism frequently causes skeletal fragility and fractures, particularly vertebral fractures. Some patients retain a high fracture risk even after treatment, necessitating further research into bone-specific therapies.

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    Area of Science:

    • Endocrinology
    • Bone Metabolism
    • Skeletal Diseases

    Background:

    • Endogenous hypercortisolism is a significant cause of skeletal fragility and fractures.
    • Vertebral fractures are common, occurring in 30-50% of patients with glucocorticoid excess.
    • Fracture risk may persist despite resolution of hypercortisolism, indicating a need for long-term management.

    Purpose of the Study:

    • To review the impact of endogenous hypercortisolism on skeletal health.
    • To discuss the challenges in managing persistent fracture risk after hypercortisolism treatment.
    • To highlight the scarcity of data on bone-active drug efficacy and safety in this context.

    Main Methods:

    • Literature review of studies on bone mineral density and fractures in endogenous hypercortisolism.
    • Analysis of existing data on fracture incidence and persistence post-treatment.
    • Evaluation of the current understanding of skeletal-specific treatment approaches.

    Main Results:

    • Skeletal fragility and vertebral fractures are early and frequent complications of hypercortisolism.
    • Bone mineral density may improve after hypercortisolism resolution, but fracture risk can persist.
    • Data on the effectiveness and safety of bone-modifying agents in this population are limited.

    Conclusions:

    • A skeletal-specific approach is warranted for patients with endogenous hypercortisolism, especially those with early vertebral fractures.
    • Further research is crucial to determine the cost-effectiveness of bone-active drugs for managing persistent fracture risk.
    • Long-term management strategies are needed for patients with prolonged or persistent hypercortisolism and associated skeletal fragility.