Forms flat bones of skull during fetal development.

1) Sheet of connective tissue membrane forms

2) Mesenchymal cells differentiate into osteogenic cells which differentiate into osteoblasts. Osteoblasts begin secreting osteoid tissue and calcification begins.

3) This forms the trabeculae of spongy bone.

4) More calcium salts are deposited on the surface to make compact bone.

Forms most bones during fetal development.

1) A hyaline cartilage model forms in the area of the bone covered its perichondrium. The perichondrium makes chondrocytes and chondrocytes produce the rubbery cartilage matrix.

2) The perichondrium developes into the periosteum and produces osteoblasts.

3) Osteoblasts produce a thin collar of bone around the diaphysis.

4) Chondrocytes in the enlarge (hypertrophy), creating the primary ossification center in the diaphysis.  The enlarged chondrocytes eventually die, and their lacunae merge forming a single cavity.

5) Blood vessels and cells from the periosteum invade the space in the diaphysis. It fills with blood and cells and is further hollowed out. At this point it is known as the primary marrow cavity. Osteoblasts thicken the compact bone collar and produce spongy bone. Osteoclasts remove remaining cartilage.

6) A second ossification center forms in the epiphysis and becomes the secondary marrow cavity in a similar way as the primary. The secondary marrow cavity is usually formed at birth.

7) After birth, spongy bone fills secondary marrow cavity. Cartilage found only on articular surfaces and at epiphyseal plate between cavities.

8) During childhood/adolescence bones grow in length and width.

Longitudinal Growth: (interstitial growth) cartilage in epiphyseal plate continues to divide pushes the diaphysis and epiphysis apart cartilage is replaced with bone: older chondrocytes near edge of the plate enlarge, die, replaced by bone.

Latitudinal Growth:(appositional growth) osteoblasts in periosteum produce layers of matrix around outside of the bone osteoclasts widen the marrow cavity form the inside the bone

9) By early 20s, all the epiphyseal cartilage is ossified. Bones cannot grow in length, but may still grow in width. Bones are remodeled continuously though life.

Stimulates bone elongation and cartilage proliferation at the epiphyseal plate. Increases urinary excretion of calcium, but increases absorption in the intestines to even it out.

Too much GH: Gigantism (children) acromegaly (adults).

Too little GH: pituitary (proportional) dwarfism.

Stimulates division of chondrocytes in long bones.

Defective FGF receptor = achondroplasia.

Produced in the blood vessels. Increases bone growth by inhibiting osteoclasts. Delays conversion of cartilage to bone so cartilage grows longer.

CNP deficiency = dwarfism.

Stimulates osteoblasts for increased bone growth and to promote closing of the epiphyseal plate that stops growth.

Estrogen deficiency = tall stature, because epiphyseal plate doesn't close.

Testosterone has a weaker effect on bone deposition, so boys usually grow taller (epiphyseal plate stays open longer).

1) Bleeding from damaged blood vessels in bone. A blood clot forms = fracture hematoma. Many cells invade the clot: osteogenic cells, osteoclasts, macrophages, leukocytes, fibroblasts, chondroblasts = granulation tissue.

2) Fibroblasts secrete collagen and chondroblasts deposit fibrocartilage, forming the soft callus to hold the ends of the bone together.

3) Osteoblasts produce a collar of compact bone around the break that forms the hard callus. Takes 4-6 weeks.

4) Osteoblasts produce spongy bone and convert it to compact bone. Osteoclasts remove fragments and extra bone to restore original shape occurs over 3-4 months.

Hypocalcemia: Excessive excitability of nervous/muscle tissue. Leads to muscle tremors, spasms, or tetany.

Hypercalcemia: Nerve/muscle tissue less excitable. Can cause emotional disturbances, muscle weakness, sluggish reflexes, and cardiac arrest.