Intramembranous Bone Formation Discussion
The connective tissue of the non-differentiated embryonic connective tissue cells turns into bone and bone matrix cells.
Bone formation center and bone matrix or osteoid formation occur in the membrane fibrosa.
Osteoblasts form osteoid by differentiation from the ectomesenchyme condensation center to produce the matrix. Then, osteoid gets mineralized and trapped as osteocytes.
Osteoid accumulation occurs between the embryonic vascular system that forms a trabeculated bone tissue network.
Mesenchyme with increased blood supply thickens on the outer side of the woven bone to become periosteum.
Osteoid calcification: Bone matrix mineralization causes nutritional substances impermeability. The entangled vascular system provides nutrients to osteocytes and removes metabolic wastes. The essential membrane of bone outside the bone is known as the bone endosteum that is essential for bone survival.
Mineralization is the process in which minerals get deposited on the bone matrix. The enzyme alkaline phosphatase accelerates the mineralization process, and this process needs adequate calcium and phosphate in the extracellular fluid.
The completely mineralized bone surrounds the osteoblast. As a result, the synthetic activity of osteoblasts gets slowly reduced, and the cells get converted into osteocytes.
The tissue that becomes bone first forms from cartilage endochondral ossification, which occurs only in short bones, but both perichondrium and endochondral play an important function in forming long bones.
The stromal stem cells gather to form a structural model of the succeeding bone, and they differentiate into cartilage cells. Overgrowth of cartilage cells and formation of the matrix calcification occur.
The blood vessel supplying nutrients to the perichondrium is responsible for stimulating the osteoprogenitor cells to form osteoblasts that convert the perichondrium into the periosteum.
The periosteum develops, and chondrocytes division continues to increase matrix production. The perichondrial cells at the central cartilage split to activate calcification.
At the second or third month of the fetal stage, ossification increases and forms a primary ossification center. The chondrocytes and cartilage continuously grow at the succeeding epiphysis.
After complete fetal skeleton formation, the cartilage stays at the joint surface and epiphyseal plate. The bone increases in length due to the formation of a new bone from the epiphyseal plate. During puberty, the epiphysis fuses with the shaft, and the bone growth stops.
At birth, the sequence of bone formation happens in the epiphyseal plate.
During the bone formation process, immature bones are formed. They undergo the process of bone remodeling, which involves bone resorption and deposition to become mature bone.
Clinical Significance
Vitamin D and calcium deficiency affect the normal bone formation process and cause various diseases. Rickets is one of the major disorders of bones that occur in children. It is caused by the lack of calcium and vitamin D in the body. It causes the weakening of bones and the affected children face muscle cramps, stunted growth, and bone fractures. This disease can be prevented by the exposure of the skin to sunlight. Sunlight exposure stimulates vitamin D synthesis which is essential for calcium absorption and bone deposition. The condition of rickets in adults is known as osteomalacia and results in various disorders due to the reduced mineralization of the bones. Malnutrition is a major cause of osteomalacia. Due to the less deposition of calcium ions (lack of calcification), the bones become soft and weak. This condition mainly occurs in women after more pregnancies due to the deficiency of vitamin D and calcium. The main symptom of osteomalacia is the pain and discomfort after carrying weight on the affected bone.
