skeletal System 2

• Osteogenesis (ossification)—bone tissue formation
• Stages
• Bone formation—begins in the 2nd month of development
• Postnatal bone growth—until early adulthood
• Bone remodeling and repair—lifelong

• Membrane bone develops from fibrous membrane
• Forms flat bones, e.g. clavicles and cranial bones

• Cartilage (endochondral) bone forms by replacing hyaline cartilage
• Forms most of the rest of the skeleton

• 1. Ossification centers appear in the Fibrous Connective Tissue Membrane
• *Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center.
• 2. Bone matrix(osteoid) is secreted within the fibrous membrane and calcifies
• *Osteoblasts begin to secret osteoid, which is calcified within a few days.
• *trapped osteoblasts become osteocytes
• 3. Woven Bone and Periosteum From
• *Accumulating osteoid is laid down between embryotic blod vessels in a random manner. Resuting in network of trabeculae woven bone.
• *vascularized mesencyme condenses on the external face of the woven bone and becomes the periosteum.
• 4. Lamellar bone rplaces wovenBone, just deep to the Periosteum. Red Marrow Appears
• *Trabeculae just deep to the perioseum thincken and are later replaced with mature lamellar bone
• 5. End product is a flat done

1. Bone Collar forms around hyline cartilage model.

2. Cartilage in the center of the diaphysis calcifies and then develops cavities

3.The periosteal bud invades the internal cavities and the spongy bone begins to form

4. The diaphysis elongates and the medullary cavity forms.

5. The epiphyses ossidy. when completed hyline cartiglage remains only in the epiphysial plates and the articular cartilage.

• * From within
• * Grows in length of the bone

• * on the outer surface
• * thickness and remodeling of al bones by osteoblasts and osteoclasts on bone surfaces

Epiphyseal plate cartilage organizes into four important functional zones:

• Proliferation (multiplication of cells)
• Hypertrophic (growth of cells)
• Calcification (invasion of mineral salts)
• Ossification (osteoblasts lay down collagen which combines with mineral salts)

• *Occurs where bone is injured or added strength is needed
• *Requires a diet rich in protein; vitamins C, D, and A; calcium; phosphorus; magnesium; and manganese
• *Sites of new matrix deposit are revealedby the
• Osteoid seam
• Unmineralized band of matrix
• Calcification front
• The abrupt transition zone between the osteoid seam and the older mineralized bone

• Is stored in bones
• Calcium is necessary for
• *Transmission of nerve impulses
• *Muscle contraction
• *Blood coagulation
• *Secretion by glands and nerve cells
• *Cell division

• *Hormonal mechanisms that maintain calcium homeostasis in the blood
• *Mechanical and gravitational forces

• 1. Position of bone ends after fracture:
• Nondisplaced—ends retain normal position
• Displaced—ends out of normal alignment

• 2.Completeness of the break
• Complete—broken all the way through
• Incomplete—not broken all the way through
• 3. Orientation of the break to the long axis of the bone
• Linear—parallel to long axis of the bone
• Transverse—perpendicular to long axis of the bone
• 4.Whether or not the bone ends penetrate the skin:
• Compound (open)—bone ends penetrate the skin
• Simple (closed)—bone ends do not penetrate the skin

• 1. Hematoma Forms
• *Torn blood vessels hemorrhage
• *Clot (hematoma) forms
• *Site becomes swollen, painful, and inflamed
• 2.Fibrocartilaginous callus forms
• 3.Bony callu Forms
• 4. Bone remodeling occurs

• *Phagocytic cells clear debris
• *Osteoblasts begin forming spongy bone within 1 week
• *Fibroblasts secrete collagen fibers to connect bone ends
• *Mass of repair tissue now called fibrocartilaginous callus

• Osteomalacia and rickets
• Calcium salts not deposited
• Rickets (childhood disease) causes bowed legs and other bone deformities

Cause: vitamin D deficiency or insufficient dietary calcium

• *Loss of bone mass—bone resorption outpaces deposit
• *Spongy bone of spine and neck of femur become most susceptible to fracture

*Risk factorsLack of estrogen, calcium or vitamin D; petite body form; immobility; low levels of TSH; diabetes mellitus

Excessive and haphazard bone formation and breakdown, usually in spine, pelvis, femur, or skull

Pagetic bone has very high ratio of spongy to compact bone and reduced mineralization

Unknown cause (possibly viral)

Treatment includes calcitonin and biphosphonates