Intramembranous bone formation:
Flat Bones
Primary ossification center
o Vascular zone that stimulates mesenchymal cells to differentiate into osteoblasts and begin secreting
osteoid
Calcification takes place
o Osteoblast get trapped in their own matrix and become osteocytes
Calcification forms columns of bones the fuse with each other to form trabeculae
Blood vessels invade the area as the other undifferentiated mesenchymal cells give rise to bone marrow
Periosteum and endosteum develop from portions of mesenchyme layer that do not undergo ossification
Mesenchymal cells give rise to osteoprogenitor cells that form more osteoprogenitor cells or differentiate into
osteoblasts within the inner layer of developing periosteum
Endochondral bone formation:
Long bones
Starts with the embryonic skeleton at about 2 months AOG
Primary Ossification center at mid diaphysis of hyaline cartilage model
o Vascularization of perichondrium transform chondrogenic cells to osteoprogenitor cells, which differentiate
into osteoblasts- forms the periosteum
Osteoblast lay down osteoid deep to the periosteum
o Via intramembranous bone formation forms the subperiosteal bone collar
Chondrocytes within the core undergo hypertrophy and degenerate and their lacunae become confluent, forming
large cavities (eventual marrow spaces)
Osteoclast create perforations in the bone collar and permit the periosteal bud (blood vessels, osteoprogenitor cells
and mesenchymal cells) to enter the newly formed spaces in the cartilaginous model
o Cartilage wall of spaces become calcified
Subperiostal bone collar elongates towards the epiphyses
Osteoclast begin to resorb the calcified cartilage walls to enlarge the primitive marrow cavity
Bone formation spreads towards the epiphyses
Secondary Ossification center develop at the epiphyses
o Osteoprogenitor cells invade the epiphyses and become osteoblasts, which elaborate bone matrix to replace
the disintegrating cartilage
o Epiphyses are filled with bone tissue
o Cartilage remains in 2 areas- articular and epiphyseal plates
Epiphyseal plates continue to grow by adding new cartilage at the epiphyseal end while it is being replaced by bone
at the diaphyseal end (lengthening of the bone)
No osteoclast activity
Bone Remodelling: bone is constantly being remodeled as necessary for growth and to alter its structural makeup to
adapt to changing stresses in the environment throughout life
Role of Vitamins in bone formation:
Vitamin D: abosrpton of calcium from small intestine
o Rickets: in children Vit D deficiency that results in poorly calcified bones
Deformation of bone at the epiphyseal plates
Bones grow more slowly and are deformed by the stress of weight bearing
o Osteomalacia: rickets of adults
Results from calcium deficiency
Deficient calcification in newly formed bone and decalfication of already calcified bone
May be severe during pregnancy because calcium requirements of fetus may lead to calcium loss in
the mother
Vitamin A deficiency inhibits proper bone formation and growth
o Excess accelerates ossification on the epiphyseal plates
o Deficiency or excess results in small stature
Vitamin C: necessary for collagen formation
o Deficiency results in scurvy, poor bone growth and inadequate fracture repair
Role of Hormones in bone formation:
PTH: activates osteoblasts to secrete osteoclast-stimulating factor which activates osteoclast to resorb bone to
elevate blood calcium levels
o Hyperparathyroidism: renders bone more susceptible to fracture and subsequent deposition of calcium in
arterial wall and certain organs such as the kidney
Calcitonin: produced by parafollicular cells (C cells) of the thyroid gland
o Inhibits bone matrix resorption to prevent the release of calcium
Pituitary growth hormone (somatotropin) stimulates overall growth, especially at the epiphyseal plates
o Influences bone growth via insulin like growth factors (somatomedin), especially stimulating the growth of
epiphyseal plates
o Deficiency- dwarfism
o Excess- pituitary gigantism and acromegaly
