What is the difference between intramembranous ossification and endochondral

Press ESC to cancel. Skip to content Home Social studies What is the difference between Intramembranous ossification and endochondral ossification? Social studies. Ben Davis November 30, What is the difference between Intramembranous ossification and endochondral ossification? What is the difference between Intramembranous bones and endochondral bones?

Which of these is developed by Intramembranous ossification? Which of the following is involved in endochondral bone formation? What are the 6 steps of endochondral ossification? What happens during Intramembranous ossification? What are the steps in Intramembranous ossification? What is meant by ossification? What is an example of Intramembranous bone? What is the role of vitamin D in bone development? What is the difference between primary and secondary ossification centers? Endochondral ossification refers to a type of ossification that takes place from the centers arising in the cartilage and involving the deposition of lime salts in the cartilage matrix followed by secondary absorption and replacement by the true bony tissue.

The intramembranous ossification refers to the development of osseous tissue within the mesenchymal tissue without prior cartilage formation. In endochondral ossification, a cartilage forms first and the bone is laid down on it while in intramembranous ossification, the bone directly forms on mesenchyme. Endochondral ossification proceeds through intermediate cartilage while the intramembranous ossification does not form intermediate cartilage.

Endochondral ossification is important in the formation of long bones while intramembranous ossification is important in the formation of flat bones. Endochondral ossification takes a longer time to form a bone while intramembranous ossification takes less time to form a bone. Most of the chondrocytes in the zone of calcified matrix , the zone closest to the diaphysis, are dead because the matrix around them has calcified. Capillaries and osteoblasts from the diaphysis penetrate this zone, and the osteoblasts secrete bone tissue on the remaining calcified cartilage.

Thus, the zone of calcified matrix connects the epiphyseal plate to the diaphysis. A bone grows in length when osseous tissue is added to the diaphysis. Bones continue to grow in length until early adulthood. The rate of growth is controlled by hormones, which will be discussed later. When the chondrocytes in the epiphyseal plate cease their proliferation and bone replaces the cartilage, longitudinal growth stops. All that remains of the epiphyseal plate is the epiphyseal line [link].

How Bones Grow in Diameter While bones are increasing in length, they are also increasing in diameter; growth in diameter can continue even after longitudinal growth ceases.

This is called appositional growth. Osteoclasts resorb old bone that lines the medullary cavity, while osteoblasts, via intramembranous ossification, produce new bone tissue beneath the periosteum.

The erosion of old bone along the medullary cavity and the deposition of new bone beneath the periosteum not only increase the diameter of the diaphysis but also increase the diameter of the medullary cavity. This process is called modeling. The process in which matrix is resorbed on one surface of a bone and deposited on another is known as bone modeling.

However, in adult life, bone undergoes remodeling , in which resorption of old or damaged bone takes place on the same surface where osteoblasts lay new bone to replace that which is resorbed. Injury, exercise, and other activities lead to remodeling.

Those influences are discussed later in the chapter, but even without injury or exercise, about 5 to 10 percent of the skeleton is remodeled annually just by destroying old bone and renewing it with fresh bone. Skeletal System Osteogenesis imperfecta OI is a genetic disease in which bones do not form properly and therefore are fragile and break easily. It is also called brittle bone disease. The disease is present from birth and affects a person throughout life. The severity of the disease can range from mild to severe.

Those with the most severe forms of the disease sustain many more fractures than those with a mild form. Frequent and multiple fractures typically lead to bone deformities and short stature.

Bowing of the long bones and curvature of the spine are also common in people afflicted with OI. Curvature of the spine makes breathing difficult because the lungs are compressed.

Because collagen is such an important structural protein in many parts of the body, people with OI may also experience fragile skin, weak muscles, loose joints, easy bruising, frequent nosebleeds, brittle teeth, blue sclera, and hearing loss.

There is no known cure for OI. Treatment focuses on helping the person retain as much independence as possible while minimizing fractures and maximizing mobility. Toward that end, safe exercises, like swimming, in which the body is less likely to experience collisions or compressive forces, are recommended. Braces to support legs, ankles, knees, and wrists are used as needed. Canes, walkers, or wheelchairs can also help compensate for weaknesses.

When bones do break, casts, splints, or wraps are used. In some cases, metal rods may be surgically implanted into the long bones of the arms and legs. Research is currently being conducted on using bisphosphonates to treat OI. Smoking and being overweight are especially risky in people with OI, since smoking is known to weaken bones, and extra body weight puts additional stress on the bones. All bone formation is a replacement process. Connective tissue in the matrix differentiates into red bone marrow in the fetus.

The spongy bone is remodeled into a thin layer of compact bone on the surface of the spongy bone. Endochondral ossification is the process of bone development from hyaline cartilage. All of the bones of the body, except for the flat bones of the skull, mandible, and clavicles, are formed through endochondral ossification.

In long bones, chondrocytes form a template of the hyaline cartilage diaphysis. Responding to complex developmental signals, the matrix begins to calcify. This calcification prevents diffusion of nutrients into the matrix, resulting in chondrocytes dying and the opening up of cavities in the diaphysis cartilage.

Blood vessels invade the cavities, and osteoblasts and osteoclasts modify the calcified cartilage matrix into spongy bone. Osteoclasts then break down some of the spongy bone to create a marrow, or medullary, cavity in the center of the diaphysis. Dense, irregular connective tissue forms a sheath periosteum around the bones. The periosteum assists in attaching the bone to surrounding tissues, tendons, and ligaments.

The bone continues to grow and elongate as the cartilage cells at the epiphyses divide. In the last stage of prenatal bone development, the centers of the epiphyses begin to calcify.

Secondary ossification centers form in the epiphyses as blood vessels and osteoblasts enter these areas and convert hyaline cartilage into spongy bone.

Until adolescence, hyaline cartilage persists at the epiphyseal plate growth plate , which is the region between the diaphysis and epiphysis that is responsible for the lengthwise growth of long bones Figure 1. Figure 1. The periosteum is the connective tissue on the outside of bone that acts as the interface between bone, blood vessels, tendons, and ligaments. Long bones continue to lengthen, potentially until adolescence, through the addition of bone tissue at the epiphyseal plate.

They also increase in width through appositional growth. Chondrocytes on the epiphyseal side of the epiphyseal plate divide; one cell remains undifferentiated near the epiphysis, and one cell moves toward the diaphysis.