Development of Organs
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Development of Bone (Synovial Joint)
How to link synovial joint with bone? Essay plan.
Endochondral ossification and how it assists with the growth in length of long bones.
When long bones meet, they form a structure called the synovial joint.
Briefly mention development of joint structures and their functions.
Developmental abnormality- Achondroplasia.
There are 6 types of synovial joints: pivot, plane, hinge, saddle, condyloid, ball-and socket.
Such joints are formed where bones come together to allow for movement and prevent friction between ends of bones. A typical synovial joint forms between ends of long bones.
Articular/hyaline cartilage is avascular and aneural. They line the articular surfaces, withstand compression and reduce friction.
The 6 features of a synovial joint are hyaline/articular cartilage, fibrous capsule, synovial cavity, synovial membrane, synovial fluid and periosteum.
Articular cartilage degenerates with age. If the bony surfaces are exposed, it will cause severe pain when the ends come together.
Ligaments which connect bone to bone also blend with periosteum to reinforce the joint capsule, increase stability of the joint and prevents injury from excessive movement.
Articular surface is the only component of the synovial joint that’s not surrounded by the periosteum.
Synovial fluid is secreted by the synovial membrane as a lubricant. However, the fluid can accumulate when the membrane is irritated which causes joint swelling.
During development, cavitation appears along planes of the future articular surfaces of synovial joints.
All the features of the synovial joints are mesoderm derived.
Bone is a type of dense connective tissue derived from mesoderm.
Made up of mineralised ground substance and collagen fibre reinforcement.
Axial skeleton is derived from paraxial mesoderm which forms the sclerotome.
Appendicular skeleton is derived from lateral plate mesoderm.
There are other parts of the skeleton which are derived form neural crest cells to form bones of the cranium and the face. For example, cranial neural crest cells migrate into the branchial arches and form the craniofacial bones and cartilages.
There are two types of ossification- intramembranous and endochondral.
Intramembranous ossification commences at around 6.5 weeks and occurs within condensation of mesenchymal tissue.
It is responsible for both the growth of short bones and the thickening of long bones.
This mesenchymal (connective tissue) is replaced by bone.
More precisely, bone is formed by differentiation of mesenchymal cells into osteobalsts.
Osteoblasts begin to secrete osteoid (new bone matrix) which are uncalcified bone.
The osteoblasts are trapped within the osteoid and become osteocytes.
At the same time, islands of developing bones known as spicules appear in an ossification centre.
A separate group of mesenchymal cells differentiate into osteoblasts which lineup on the surface of spicules to secrete more osteoid. This increases the sir of the spicules.
The spicules eventually fuse to become bony trabeculae.
As trabeculae grows in size, they become interconnected and woven bone is formed.
Connective tissue between the spicules contain blood vessels and haemangioblasts which make the bone vascularised.
Periosteum around the bone is formed by differentiating mesenchymal cells. Bone deposition occurs under the periosteum, in the area between the periosteum and the endosteum. This allows for growth in width and bone collar is formed.
Bone is resorbed on the inner aspect of the compact bone by osteoclasts.
Endochondral ossification takes place in a piece of hyaline cartilage and it is responsible for the growth in length of long bones.
2 ossifications centres appear: primary ossification centre first appears in the middle of the diaphysis; secondary ossification centre appears at the epiphyses.
Primary ossification centre appear at around 8 weeks of gestation. It first appears in the centre of the diaphysis of a long bone. This process occurs when the entire bone is still covered by uncalcified cartilage.
Here, the resting chondrocytes begin to undergo hypertrophy and apoptosis. The space between the cartilage matrix allows for blood vessel invasion from the bone marrow which brings osteoprogenitors and bone marrow precursors to the area.
Slowly, osteoprogenitors differentiate into osteoblasts that congregate on irregular spicules of the uncalcified cartilage matrix and begin to deposit bone matrix.
Secondary ossification centre first appears during the first few years of postnatal life, on the upper and lower end of the epiphyses.
Similar to primary ossification, resting chondrocytes in the epiphyseal growth plate under goes proliferation, hypertrophy and apoptosis, vascular tissue invades the spaces left by dead chondrocyte and bring in osteoblasts, osteoprogenitors and bone marrow precursors. Those cells perform the same roles as during primary ossification. Upper and lower epiphyseal growth plates are now evident at the border of epiphysis and diaphysis.
The growth plates disappear at the end of puberty and hyaline cartilage are now only present at articular end of the bones.
Abnormality: Achondroplasia
Decrease in endochondral ossification in the proliferative zone.
Normal periosteal and intramembraneous ossification.
Caused by a mutation in fibroblast growth factor receptor 3 (FGFR3).
Disproportionate