Bone Tissue — In-Depth Study Guide Chp7

What are the primary differences between compact (cortical) and spongy

• Compact bone is dense and organized into osteons (Haversian systems); it provides strength and forms the outer layer of bones.

• Spongy bone has a porous structure made of trabeculae; it’s lighter, found at the ends of long bones and inside flat bones, and helps absorb shock and reduce bone weight.

• Compact bone resists bending; spongy bone resists compression from multiple directions.

How does the organization of osteons contribute to bone strength?

Osteons are cylindrical units with concentric lamellae around a central canal containing blood vessels. The alternating collagen fiber orientation in each lamella resists torsion (twisting) and bending forces, giving bone both flexibility and high tensile strength.

What roles do collagen fibers and hydroxyapatite crystals play in bone strength?

• Collagen fibers give bone flexibility and tensile strength (resistance to stretching).

• Hydroxyapatite (calcium phosphate) provides hardness and compression resistance.
  Together, they form a composite material — strong yet slightly elastic.

How do the periosteum and endosteum contribute to bone growth and remodeling?

• The periosteum covers the outer bone surface and contains osteoblasts that form new bone during growth and repair.

• The endosteum lines the medullary cavity and houses osteogenic and osteoclast cells, which remodel the internal bone surface.

Why is bone considered a dynamic connective tissue rather than static?

Bone is constantly being broken down and rebuilt by osteoclasts and osteoblasts. This ongoing remodeling allows bone to adapt to stress, repair damage, and maintain mineral balance (especially calcium and phosphate).

How do the four main bone cell types interact to maintain homeostasis?

• Osteogenic cells differentiate into osteoblasts.

• Osteoblasts build bone matrix.

• Some osteoblasts become osteocytes, which monitor and communicate stress.

• Osteoclasts resorb bone by secreting acids and enzymes.
  These processes work in balance to regulate bone density and shape.

What triggers the transition from osteoblasts to osteocytes?

When osteoblasts become trapped in the matrix they secrete, they mature into osteocytes. These cells maintain the surrounding matrix and signal when remodeling is needed.

How do osteocytes communicate through canaliculi?

Osteocytes extend cellular projections through tiny channels called canaliculi, which allow nutrient and waste exchange via gap junctions. This network enables coordination of bone maintenance and repair.

How do osteoclasts differ from other multinucleated cells?

Osteoclasts form by the fusion of monocytes (macrophage lineage), not by mitosis. They secrete acid (H+) and lysosomal enzymes to dissolve bone mineral and collagen. Their ruffled border increases surface area for resorption

What is the difference between intramembranous and endochondral ossification?

• Intramembranous ossification: Bone develops directly from mesenchymal tissue (e.g., flat bones of the skull, clavicle).

• Endochondral ossification: Bone replaces a hyaline cartilage model (e.g., long bones).
  Endochondral ossification allows for growth in length during childhood.

How does mechanical stress influence bone density (Wolff’s Law)?

Bone grows stronger where mechanical stress is greatest. Weight-bearing exercise stimulates osteoblast activity, increasing bone mass and strength. Lack of stress (e.g., immobilization or spaceflight) leads to bone loss.

What hormones regulate bone remodeling?

• Parathyroid hormone (PTH): Increases blood calcium by stimulating osteoclasts.

• Calcitonin: Lowers blood calcium by inhibiting osteoclasts.

• Vitamin D: Enhances calcium absorption from the gut.

• Estrogen/testosterone: Promote osteoblast activity; their decline increases bone resorption.

How does the balance between resorption and deposition change with age?

In youth, deposition > resorption (growth phase).
In adulthood, they balance out.
With aging, especially after menopause, resorption > deposition, leading to bone loss and osteoporosis risk.

What triggers remodeling at microfracture sites?

Osteocytes detect mechanical stress or damage and release signaling molecules (e.g., prostaglandins, nitric oxide) that recruit osteoclasts to resorb old bone and osteoblasts to rebuild new bone.

How does bone act as a calcium reservoir?

Bone stores about 99% of the body’s calcium. When blood calcium drops, osteoclasts release calcium from bone. When levels rise, osteoblasts deposit it into bone matrix.

How do PTH and calcitonin regulate calcium levels?

• PTH (parathyroid hormone): Raises calcium by stimulating osteoclasts, increasing kidney reabsorption, and activating vitamin D.

• Calcitonin (thyroid): Lowers calcium by inhibiting osteoclast activity.
  They act as antagonistic hormones maintaining calcium balance.

What is the kidney and intestine’s role in calcium balance?

• Kidneys: Reabsorb or excrete calcium depending on PTH levels.

• Intestines: Absorb calcium under the influence of active vitamin D (calcitriol).
  Together, they regulate how much calcium enters and leaves the bloodstream.

What happens in osteoporosis?

Osteoclast activity outpaces osteoblast activity, reducing bone mass and weakening structure. Bones become brittle and fracture-prone. It’s common in postmenopausal women due to low estrogen.

. How do bone fractures heal?

1. Hematoma formation – blood clot stabilizes area.

2. Fibrocartilaginous callus – collagen and cartilage fill gap.

3. Bony callus – spongy bone replaces cartilage.

4. Remodeling – compact bone replaces spongy bone; bone returns to original shape

How do osteomalacia, rickets, and osteogenesis imperfecta differ?

• Osteomalacia (adults): Soft bones due to poor mineralization (vitamin D deficiency).

• Rickets (children): Growth deformities from weak, poorly mineralized bones.

• Osteogenesis imperfecta: Genetic collagen defect → brittle bones, frequent fractures.

How does space travel or immobility affect bone structure?

Without mechanical stress, osteoblast activity decreases and osteoclast activity increases, leading to rapid bone loss (similar to osteoporosis). Exercise and resistance training in microgravity reduce these effects.

How are modern imaging techniques used to study bone health?

• DEXA scans: Measure bone mineral density.

• Histomorphometry: Quantifies bone formation/resorption microscopically.

• Micro-CT: Provides 3D detail of trabecular structure.
  These reveal bone quality, not just density — important for fracture risk analysis.