Bone Remodeling and Healing

Bone, while seemingly inert, is an active, growing, and changing part of the human body, in addition to being the body’s primary calcium reservoir. In the correct homeostatic conditions, bone can remodel in response to damage, stress, or hormonal signaling (parathyroid hormone and calcitonin). Osteocytes located deep in the bone sense damage and signal bone-lining cells that will begin the process of remodeling. This process is vital not only for damage repair but also to adapt to a new environment and conditions.

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Bone Remodeling

  • Total bone mass remains constant in adults; however, bones are not static:
    • Bone deposition and resorption are constantly occurring.
    • Deposition and resorption occur at the surfaces of both periosteum and endosteum.
  • Bone deposition:
    • Done by osteoblasts
    • Osteoid seam: unmineralized band of matrix deposited by osteoblasts
    • Calcification front: abrupt separation between old bone and osteoid seam
  • Bone resorption:
    • Done by osteoclasts: lysosomal enzymes and protons (H+) to break down bony matrix
    • Once resorption is complete, osteoclasts undergo apoptosis.
  • Initial signal:
    • Microdamage is sensed by osteocytes.
    • Damaged osteocytes undergo apoptosis, releasing intracellular components → bone-lining cells sense apoptosis and send chemoattractants
  • Control of remodeling:
    • Calcium levels control parathyroid hormone (PTH) levels, which in turn control osteoclast activity.
    • Response to mechanical stress (Wolff’s law): A bone remodels in response to the force applied to it.
      • Curved bones are thicker where they can bend.
      • Trabeculae align along lines of compression.
      • Bones on the dominant hand are thicker.
      • Large bony projections appear where muscle pull is greater.
Bone anatomy

Bone anatomy:
Bones are covered in a layer called the periosteum, composed of fibrous and cellular layers. Below the periosteum is the endosteum, a complex architecture constructed on a mineral scaffold (the bony matrix) and composed of osteocytes, osteoclasts, and osteoblasts.

Image: “607 Periosteum and Endosteum” by OpenStax College. License: CC BY 3.0

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Bone Repair

  • After a fracture occurs, healing and repair take around 6–8 weeks.
  • Steps of repair:
    • Hematoma formation/bone tissue death
    • Fibrocartilaginous callus formation:
      • Soft granulation tissue (blood vessels grow into the hematoma, phagocytic cells start clearing the tissue remnants)
      • Fibroblasts, chondroblasts, and osteogenic cells invade the area.
      • Fibroblasts produce collagen that reunites the 2 separated bone ends.
      • Chondroblasts form cartilaginous matrix.
      • Osteoblasts start forming spongy bone.
    • Bony callus formation:
      • After a week, trabeculae form in the callus.
      • After a few months, the callus becomes bone.
    • Bone remodeling:
      • Excess material on the diaphysis is removed.
      • Compact bone will form the shaft.

Hormonal Control of Bone Remodeling

Parathyroid hormone (PTH)

  • Secreted by parathyroid glands
  • Raises blood calcium levels by releasing it from bone: 
    • Indirect activation of osteoclasts 
    • Also acts on kidneys and intestine to regulate calcium secretion/absorption

Calcitonin

  • Released by thyroid C cells
  • Down-regulates bone resorption by inhibiting osteoclasts
  • Often supplemented to treat osteoporosis

Growth hormone

  • Secreted by pituitary gland
  • Stimulates release of insulin-like growth factor (IGF)
  • Causes both osteoblast and osteoclast release, but net effect is bone growth

Estrogen

  • Secreted by ovaries in females and testes in males
  • Blocks osteoclast proliferation/activity 
  • Absence leads to decrease bone mass.

Clinical Relevance

  • Bone fractures: break in a bone that results from accidental trauma, falls, or sports injuries. Fractures may even arise spontaneously in weakened bones, such as bones of low density and osteoporotic bones, or during overuse and stress. Fractures are classified into 4 categories: comminuted, impacted, greenstick, and oblique. Bone remodeling is activated in response to fractures and leads to repair.
  • Osteomalacia and rickets: caused by insufficient dietary calcium or by vitamin D deficiency. In these conditions, the bones are poorly mineralized. Rickets affects the cartilage of the epiphyseal growth plates in children, while osteomalacia affects the sites of bone turnover in children and adults. As an end result, the patient’s bones are poorly mineralized. The osteoid scaffold is assembled, but calcium salts do not fill this matrix sufficiently resulting in brittle bones that deform easily. Usually, taking vitamin D restores the homeostasis of bone formation and calcium deposition.
  • Osteoporosis: disease process in which bone resorption is greater than bone deposition. Etiologies may vary, but estrogen deficiency after menopause is a common cause. The composition of the matrix remains normal but bone mass declines, and the bones become porous and light. People with osteoporosis become prone to fractures with even slight trauma. Treatment/prevention can be done with exercise, hormone replacement therapy, bisphosphonates, and statins. 

References

  1. Gallagher, J.C. (2018). Advances in osteoporosis from 1970 to 2018. Menopause 25:1403–1417 https://pubmed.ncbi.nlm.nih.gov/30489459/ 
  2. Kenkre, J.S., Bassett, J. (2018). The bone remodelling cycle. Ann Clin Biochem 55:308–327. https://pubmed.ncbi.nlm.nih.gov/29368538/ 
  3. Bakr, M.M., et al. (2019). Single injection of PTH improves osteoclastic parameters of remodeling at a stress fracture site in rats. J Orthop Res 37:1172–1182. https://pubmed.ncbi.nlm.nih.gov/30816593/ 
  4. Parfitt, A.M. (1994). Osteonal and hemi-osteonal remodeling: the spatial and temporal framework for signal traffic in adult human bone. J Cell Biochem 55:273–286. https://pubmed.ncbi.nlm.nih.gov/7962158/ 

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