Endochondral ossification goes through a cartilage model on its way to being bone, Membranous ossification does not
However one can not tell in the end whether was formed one way or the other on appearance alone
Endochondral ossification
(cartilage model replaced by bone) is involved in: embryonic bone formation, growth in length of long bones, and fracture healing
Intramembranous ossification
– forms FLAT BONES (skull, sternum, mandible, and clavicle). Multipotent mesenchymal cells differentiate directly into osteoblasts and bone is formed. Growth and modeling occur by bone formation on the convex surface and bone resorption on the concave surface.
Appositional growth
: adding layers outside, like rings on a tree. Interstitial growth: growth from within.
The formation of LONG BONES takes place via Endochondral ossification as well as Intramembranous ossification. Both appositional (
Ý bone width) and Interstitial(Ý bone length) growth take place in each
The formation of long bones begins (~8wks gestation) with the proliferation and aggregation of mesenchymal cells at the site of future bone. These cells differentiate into chondroblasts and produce cartilage. The cartilage (mainly type II and proteoglycans) assumes the shape of the future bone. The area surrounding the cartilage in the diaphysis (the perichondrium) starts to give rise to bone forming cells (osteoblasts) and this layer is now known as the periosteum. As a result a thin layer of bone is formed around the cartilage model. The chondrocytes within the center of the model become hypertrophic and begin to synthesize alkaline phosphatase. Subsequently the matrix surrounding undergoes calcification. The calcified matrix inhibits the diffusion of nutrients causing the death to the chondrocytes. This leaves large holes where blood vessels can grow in to once they have pierced the thin layer of bone on the diaphysis. Cells from the periosteum enter with the invading blood vessels and become osteoprogenitor cells in the cavity left by the dying chondrocytes. When the invading osteoblasts come in contact with chondrocytes in the cavity they begin to lay down osteoid (bone that lacks minerals) on the remaining calcified cartilagenous spicules. Additional bone is formed via appositional growth.
Initially the perichondrium becomes the periosteum and starts laying down bone on the diaphysis. Then after vessel invasion, the growth plate forms at the primary ossification center. Later when vessels invade the proximal end of the bone, a secondary center is formed
The secondary ossification center expands until it fills the epiphysis except for the articular cartilage on the joint surface and the physis itself
The physis (growth plate), with the articular cartilage, is the site of endochondral ossification. It is covered peripherally with perichondrium. It grows transversely by appositional growth, longitudinally by interstitial growth. It shrivels ~14yrs due to estrogen
Zones of the physis
As the diaphysial marrow cavity enlarges a zonation occurs in the cartilage at the ends of the cavity.
zone of reserve cartilage
: (resting zone) no cellular proliferation or active matrix production
zone of proliferation
: cartilage cells undergo division and organize into distinct columns. Start matrix production
zone of maturation
: matrix production (type II collagen and proteoglycans)
zone of hypertrophy
: massive increase in size, mechanical integrity is provided by the matrix
zone of provisional calcification
: enlarged cells begin to degenerate, the matrix becomes calcified
zone of vascular invasion
: 2/3rds of the mineralized chondrocytes are removed by chodroclasts
zone of ossification
: woven bone is formed on the 1/3rd of mineralized cartilage left = primary trabeculae
On the sides of the growth plate (physis) the Ossification groove of Ranvier provides cells for growth in width. The Fibrous Ring of La Croix lies outside the physis and keeps the cells from oozing out under axial loading
Metaphysis
primary trabeculae are remodeled to secondary trabeculae. Modeling occurs peripherally.
Funnelization
: the process of keeping the diaphysis tapered and the metaphysis flared, is a result of resorption under the periosteum (cutback zone) with concurrent bone formation on the endosteal surface. In Osteopatrosis the osteoclasts do not work well and an Erlenmyer flask deformity is the result of inadequate resorption during funnelization.
Osteoclasts
break down, Osteoblastsmake bone, coupled together they form a bone remodeling unit.
Wolfe’s law
: "Bony structures orient themselves in form and mass to best resist external loads". In bony remodeling, compression signals osteoblasts to deposit bone, whereas tensile stress signals osteoclasts to resorb bone.
Pathologic bone remodeling
occurs with age; endosteal bone is resorbed but no new bone is added.
Material properties of bone: Type I collagen
Þ tensile strength. Mineral deposition Þ compressive strength
Structural properties: Cortical: strong, tough, axially loaded. Cancellous: slightly compressible, loaded in many planes