It’s a Blast!
Unlike the enamel of teeth, bone is living tissue, containing cells that can remodel the bone for normal growth and to repair any damage that may occur.
Bone Growth
During embryonic and fetal development, bones form in one of two ways, through intramembranous osteogenesis or endochondral osteogenesis.
The process of intramembranous osteogenesis forms the flat bones of the skull, clavicle, and sternum, among others. During embryonic development, connective tissue cells derived from the embryonic membranes start to gather and divide in the future sites of the bones. These cells form early bone cells called osteoblasts, which begin forming the calcium phosphate–rich bone matrix. This process continues until the bone cells completely surround themselves with bone matrix, at which time they become osteocytes and reside inside cavities in the bone called lacunae.
Since bone matrix is too dense for the diffusion of gases and nutrients, osteocytes are interconnected via cytoplasmic extensions that extend through small tunnels in the bone matrix and form a network of canals (canaliculi). Bone cells pass materials along the chain of interconnected cells much like a bucket brigade passes buckets of water to the fire. Each cell along the way uses the materials it requires to survive and passes the remainder along the chain to the next cell.
Thus, these bones resemble a cream-filled cookie with two outer layers of highly compacted bone called the tables with a region of more spongy bone (diploe) and a marrow cavity in between. The process of endochondral osteogenesis forms the long bones, such as the humerus and femur. They begin as small cartilaginous templates that exhibit the rudimentary shape of the adult bone. As the fetus grows, the cartilaginous templates also grow until blood vessels penetrate the middle of the long shaft (diaphysis). These vessels bring and deposit bone stem cells into the region of cartilage.
First, a collar of bone grows around the middle of the shaft. Since cartilage is fed by diffusion, this collar of dense bone suffocates and kills the cartilage cells, leaving room for the newly deposited bone cells. This primary ossification (bone forming) center begins the restructuring of the shaft of cartilage into bone. The outer portion of the shaft is composed of layers of compact bone with just enough room for the passage of blood vessels and nerves along the length of the bone.
In the center, the bone forms into shards called trabeculae, leaving much space and making the area appear spongy. This is the location of the marrow cavity, which fills with fat (yellow marrow) or blood stem cells (red marrow).
Vessels also enter the bulbous heads of the bones (the epiphyses), repeating the process of bringing bone cells to the site, killing the cartilage cells and forming a secondary ossification center. With bone forming from the middle of the shaft toward the ends and the secondary centers forming bone from the ends toward the middle, the only cartilage that remains is what is caught in between these two ossification centers at the junction between the epiphysis (the end part of a bone) and diaphysis (the midsection of the bone). These plates of cartilage persist until the individual is in his or her early to mid-twenties, at which time all cartilage will have been replaced with bone.
Bone Repair
Most people will experience a broken bone at some point in their life. In most cases, bone can repair itself because bone has a blood supply and is rich in living cells.
When a bone breaks, blood vessels within the bone are severed, and bleeding and blood clotting occur at the injured site. Shortly afterward, connective tissue cells that surround the bone in the layer called the periosteum begin to divide, migrate into the injured site, and lay down connective tissue materials, which are equivalent to the granulation tissue seen in wound healing of the skin. This material bridges the gap between the broken ends and stimulates changes that occur at both edges of the broken bone.
Within a few weeks, some of these connective tissue cells will change and first become cartilage cells. In the long bones, this is similar to how the bone first forms during embryonic development. This time, the cartilage provides structural material to fill in the gap between the broken ends where bone will be deposited. Osteoblasts then produce bone, which grows into the newly formed cartilage and completes the repair process. These new layers of bone are modified slowly over time, just as all bone is modified and reshaped as the body ages.
Bone Growth Diseases
As mentioned before, bones are rich in calcium, which is a key ion in many physiological activities in the body. Calcium can be deposited into bone as storage and also recruited from the bone to be used elsewhere. Over time, the balance between give and take of calcium from the bones can become unbalanced and result in weakening of the bone. Additionally, if certain key minerals and vitamins aren’t a part of the diet, the process of normal bone growth can become unbalanced and lead to bone growing irregularly. The following are two such problems related to bone growth.
Osteoporosis
This degenerative bone disease occurs primarily in women of postmenopausal age and leads to a weakening of the bones in the body, sometimes resulting in bone fractures. Because the bone is losing mass or becoming more porous, the disease was named after this histological appearance. After menopause, hormone levels, especially those of estrogen, fall below what is needed to maintain the balance between bone absorption and bone deposition. Thus, cells called osteoclasts, which remove bone matrix and free calcium for return to the blood stream, become more active than the osteoblasts (bone-depositing cells).
Additionally, the hormones that control calcium reabsorption and storage also appear to change in favor of calcium restoration into the blood stream, which accelerates the loss of bone mass with age.
Treatment of osteoporosis
Hormone replacement therapy (HRT) is a clinical option for these patients; however, certain hormones have been shown to increase the risk of breast cancer, and HRT must be done under the close supervision of a physician.
Rickets
Bones in individuals with rickets are typically seen as bowing in the long bones of the legs or otherwise misshaped bones within the arms or legs. The underlying cause of this disease is inadequate calcium deposition into bones, resulting in thinner and weaker bones (which bow under the weight of the body). While calcium may be present in the diet, what is missing is vitamin D. This is essential for proper absorption of calcium across the wall of the intestinal tract and transport into the blood stream where it can be utilized by the body. Likewise, calcium deficiency may also lead to rickets; however, this typically only occurs in areas where people, especially children, are living in conditions of famine and starvation.