Bone resorption
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| Bone resorption | |
|---|---|
| Synonyms | |
| Pronounce | N/A |
| Specialty | N/A |
| Symptoms | Bone pain, fractures, osteoporosis |
| Complications | Hypercalcemia, osteopenia |
| Onset | |
| Duration | |
| Types | |
| Causes | Osteoclast activity, hormonal imbalance |
| Risks | Age, menopause, immobility, calcium deficiency |
| Diagnosis | Bone density test, X-ray, blood test |
| Differential diagnosis | Osteomalacia, Paget's disease of bone |
| Prevention | Calcium and vitamin D supplementation, weight-bearing exercise |
| Treatment | Bisphosphonates, hormone replacement therapy, calcitonin |
| Medication | Bisphosphonates, denosumab |
| Prognosis | |
| Frequency | Common in older adults |
| Deaths | |
Overview of bone resorption process
Bone Resorption
Bone resorption is a critical physiological process in which bone tissue is broken down and the minerals, such as calcium, are released into the bloodstream. This process is essential for the maintenance, repair, and remodeling of bones throughout life. It is primarily carried out by specialized cells known as osteoclasts.
Osteoclasts
Osteoclasts are large, multinucleated cells that originate from the monocyte-macrophage lineage. They are responsible for the degradation of bone matrix and the release of stored minerals. Osteoclasts attach to the bone surface and create a sealed environment where they secrete acids and proteolytic enzymes to dissolve the mineralized matrix and collagen fibers.
Mechanism of Bone Resorption
The process of bone resorption involves several steps:
- Osteoclast Activation: Osteoclasts are activated by signals from osteoblasts and other cells. Key signaling molecules include RANKL (Receptor Activator of Nuclear Factor Kappa-_ Ligand) and M-CSF (Macrophage Colony-Stimulating Factor).
- Sealing Zone Formation: Osteoclasts form a tight seal with the bone surface, creating a specialized compartment known as the resorption lacuna.
- Acidification: The osteoclasts secrete hydrogen ions into the resorption lacuna, lowering the pH and dissolving the inorganic components of the bone.
- Enzymatic Degradation: Proteolytic enzymes, such as cathepsin K, are secreted to degrade the organic matrix, primarily collagen.
- Endocytosis and Transcytosis: The degraded bone matrix is endocytosed by osteoclasts and transported across the cell to be released into the extracellular space.
Regulation of Bone Resorption
Bone resorption is tightly regulated by various hormones and cytokines to maintain calcium homeostasis and bone integrity. Key regulators include:
- Parathyroid hormone (PTH): Increases bone resorption to raise blood calcium levels.
- Calcitonin: Inhibits osteoclast activity, reducing bone resorption.
- Vitamin D: Enhances the resorptive activity of osteoclasts by increasing calcium absorption.
- Estrogen: Inhibits bone resorption, and its deficiency (as in menopause) can lead to increased resorption and osteoporosis.
Clinical Significance
Abnormal bone resorption can lead to various bone disorders. Excessive resorption can result in conditions such as osteoporosis, where bones become weak and prone to fractures. Conversely, insufficient resorption can lead to osteopetrosis, a condition characterized by overly dense but brittle bones.
See also
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Contributors: Prab R. Tumpati, MD