Chapter 6 - Bones And Bone Tissues

bone deposition exceeds bone resorption. osteoblasts are making bone faster than the osteoclasts can reabsorb it = stronger bones.

Osteoblasts

pressure. Where continuous pressure is placed, osteoclasts are stimulated and bone resorption occurs.

osteoblasts

diaphysis

Appositional growth (width)

- calcium ion intake - vitamin D - vitamin C - vitamin K - protein intake

Articular cartilage

Zone of proliferation

Canaliculi

1. Perichondrium is invaded by blood vessels. 2. Perichondrial cells differentiate into osteogenic cells then into osteoblasts. 3. Osteoblasts build the bone collar on the external surface of the bone. 4. Chondrocytes die. 5. In the primary ossification center, osteoblasts replace calcified cartilage with early spongy bone.

Calcitonin

appositional bone growth increases (width)

osteons

growth in width

epiphyseal plate

hematopoiesis

Osteoclast

osteoblasts

diaphysis

infants

Hyaline cartilage

Irregular bone have an irregular shape.

mineral storage and acid-base homeostasis

Sesamoid bones are generally small, relatively flat, and oval-shaped. They give the tendon a mechanical advantage, providing better leverage for muscles, and also reduce wear and tear on the tendon.

Hematopoiesis, or blood cell formation, happens inside red bone marrow.

internal layer of spongy bone in flat bones.

triglyceride storage.

true

Osteocytes

Osteoclasts

Trabeculae

page 191

The predominant protein fiber in osteoid is collagen.

Osteoblasts perform the process of bone deposition, during which they build up the bone ECM. An easy way to remember what they do is to remember the mnemonic "osteoBlasts Build Bone."

osteogenic cells.

Mesenchymal cells differentiate into osteoblasts

chondroblasts differentiate into osteoblasts

During intramembranous ossification, embryonic connective tissue called mesenchyme is replaced with bone.

by pushing the epiphysis away from the diaphysis.

A deficiency in growth hormone causes stunted or even halted growth. Children with this disorder are affected by dwarfism, grow slowly, and have puberty that may be delayed by several years or even indefinitely.

diaphysis

- growth hormone, length (longitudinal) - testosterone, width (appositional growth) - estrogen, width, promotes closure

sensor: parathyroid --> control center: parathyroid --> releases: parathyroid hormone when amt of Ca+ in the blood is too low, breaks bone down to release into blood stream by activating --> osteoclasts

sensor: thyroid --> control center: thyroid --> releases calcitonin --> effector/ response: osteoblasts. when Ca+ in the blood is too high, calcitonin is released to signal osteoblasts to start putting Ca+ back into bone (building new bone)

- Vitamin D (actually functions as a hormone!) - Parathyroid Hormone PTH (when Ca+ in blood low, osteoclasts) - Calcitonin (takes Ca+ from blood, adds to bone, osteoblasts)

ossification of the zone of proliferation

epiphyseal lines are matured epiphyseal/ growth plates and will no longer grow. OR The epiphyseal plates have ossified and further growth in length is not possible.

circumferential lamellae. page 191

- directly stimulates osteoblasts in the periosteum to promote appositional growth. - increases the rate of mitosis in the epiphyseal plate of growing bones. - increases the activity of osteogenic cells.

appositional bone growth increases. (width)

It stimulates the intestines to absorb calcium. This causes an increase in blood calcium to restore homeostasis.

Calcitonin causes a decrease in osteoclast activity and an increase in bone deposition, so excess calcium is removed from blood and deposited in bones.

parathyroid hormone (PTH)

increase bone deposition

low blood calcium ion levels

osteoclast