Childhood:

• Bone Modeling
• Formation > Resorption
• Osteoblasts > Osteoclasts

Adulthood

• Bone Remodeling
• Formation = Resorption
• Osteoblast = Osteoclasts

Senescence

• Bone Remodeling
• Resorption > Formation
• Osteoclasts > Osteoblasts

• Human RANK: A protein receptor expressed osteoclast precursors
• Human RANK-LIgand: The RANK/RANK-L interactaction in bones stimulate osteoclast activation and differentiation and inhibits osteoclast apoptosis, it promotes bone resorption.
• Osteoprotegrin (OPG):
• OPPOSES RANK/RANL-L
• A decoy receptor for RANK-L made by pre-osteoblasts
• The OPG-RANK interaction causes osteoclasts to undergo apoptosist to promote bone formation
• Sclerostin
• Produced by osteocytes and supresses bone formation

• A condition where there is excessive bone growth. Muscle progressively transforms into bone (pathological metamorphosis), creating a 2nd skeleton.
• Ribbons and sheets of bone fuse the jonts of the asiam and appendicular skeleton, entombing the patient in a skeleton of heterotopic (abnormal location) bone.

Fetal skeleton is initially made up of fibrous membranes and hyaline cartilage which begins to ossify at approximatley 7-9 weeks of gestation.

Bone developes from a fibrous membrane from center outwards = membrane bone

Ossification of flat bones, cortical bone, and diploe

1. Mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center in the fibrous conective tissue membrane.
2. The osteoblasts begin to secrete osteoid, which is calcified within a few days. Trapped osteoblasts become osteocytes.
3. Accumulating osteoid is laid down between embryonic blood vesssels in a random manner. The result is a network of trabeculla called woven bone. Vascularized mesenchyme condesnes on the external face of the woven bone and becomes the periosteum.
4. Trabeculae just deep to the periosteum thickens and are later replaced with mature lamellar bone, formign compact bone plates. Diploe persists internally and its vascular tissue beomes red marrow.

Soft spots on a baby's head which , during birth, enable the bony plates of the skull to flex, allowing the child's head to pass through the birth canal.

• If fontanels close too soon the chld will get craniosynotosis (premature cranial suture fusion). Often causes abnormall skull shape, blindness, and mental retardation.
• Noggin, a bone morphogenic protein antagonist, regulates cranial fusion. Found in open, but not fusing together, cranial sutures.

• Bone forms by replacing hyaline cartilage (echondrial bone)
• Begins in the second month of development.
• Uses hyaline cartilage as models for bone construction.
• Requires breakdown of hyaline cartilage prior to ossification.

1. Ossification center forms in the center of the bone and a bone collar forms around hyaline cartilage model.
2. A cavity forms at the ossification center of the cartilage model.
3. internal cavities invade from a periosteal bud and spongy bone forms.
4. Mediullar cavity orms; Secondary ossification centers form at epiphyseaes.
5. Epiphyses ossify. When completeed hyaline cartilage remain only in the epiphyseal plates and articular cartilage.