Anatomy and Physiology: The More Things Change …
The More Things Change …
Bones can be very surprising. The simple fact that bones can repair themselves seems almost miraculous! Imagine, if you can, being able to pay a little more for a car that actually fixes itself! Simply put, bones are not the dried up sticks you thought they were, but rather complex and dynamic structures.
Bone development is a multistep process from hyaline cartilage to compact and spongy bone. The process is a bit like the opposite of certain hard candies, for bone starts out soft, with the hard part starting in the center:
- Bone starts as hyaline cartilage. Chondrocytes in the diaphysis enlarge and then die, leaving cavities in their wake.
- Perichondral cells (around the cartilage) turn into osteoblasts and begin to form a bony outer layer, and blood vessels start to grow around the edge of the developing bone.
- Blood vessels start to grow in the central region of the bone, and fibroblasts become osteoblasts in the same region and start to build spongy bone in a region called the primary ossification center. This process spreads toward the epiphyseal regions.
- The spongy bone in the center is broken down by osteoclasts, forming the marrow cavity. The bone grows longer and wider.
- Osteoblasts and capillaries begin to infiltrate the epiphyses, producing secondary ossification centers.
- The cartilage in the epiphyses is replaced by spongy bone, and the epiphyseal plate forms in the metaphysis. Eventually compact bone forms around the perimeter of the bone, leaving the epiphyseal plate as the area for bone growth.
Making and Breaking
One of the coolest things about our fetal development is what happens to our tail! As you will see in The Joints, we do indeed have a tail! Our tail, known as the coccyx, is extremely short (between three to five fused vertebrae). When we are an embryo we grow a longer tail, only to destroy it during development! Why waste all that time and energy? The answer? Evolution! Our evolutionary ancestors had tails, and some of our development contains vestiges (vestigial structures) from our evolutionary past!
The histology of bone is cool because people think of growth as a constructive process. Growth makes perfect sense because bones get longer, but what about the width? The width of a bone increases, but at the same time something has to happen to the medullary (marrow) cavity. If the medullary cavity walls all grew inward, the cavity would fill up during childhood. In order to have a medullary cavity the same relative size as the bone grows, the width of the cavity must increase. The only way to do that is to literally destroy the cells that line the walls of the cavity.
All of these changes require different cell types. Since bone is basically connective tissue, we should talk a little about the matrix that separates the cells. The matrix in bone is about 1/2 mineral salts, 1/4 protein fibers, and 1/4 water. Water? Yes! Bone cells are alive, and to stay alive they need to have contact with the cardiovascular system. Each cell is bathed in interstitial fluid, which flows throughout the haversian system in all the canaliculi described previously.
The Big Picture
Two hormones are responsible for calcium homeostasis: parathyroid hormone (PTH) from the parathyroid glands increases blood calcium levels, and calcitonin from the thyroid decreases blood calcium levels. PTH stimulates osteoclasts to break down the matrix, thus releasing calcium. Calcitonin, on the other hand, inhibits osteoclasts. This leaves the osteoblasts free to deposit the calcium in bone. As such, which hormone would you expect to be prescribed to patients with osteoporosis? That's right, calcitonin!
There are four types of bone cells. First of all, connective tissues all derive from an undifferentiated form called mesenchyme. From this mesenchyme there is an undifferentiated bone cell called an osteoprogenitor cell. These cells are found in both the periosteum and the endosteum, as well as the various canals that carry blood throughout bone.
Osteoprogenitor cells divide (through mitosis) and can develop into bone building cells called osteoblasts. Although they cannot divide, they can secrete collagen necessary for bone building. As they build bone and become surrounded by the matrix, they eventually stop making collagen and become the main cells in bone: osteocytes (osteo = bone and cyte = cell).
The last type of bone cell is thought to come from a type of white blood cell called a monocyte. These cells migrate all over the body, eventually becoming macrophages. Some of these end up in bone, and become somewhat iconoclastic bone-breaking cells called osteoclasts. It is the osteoclasts in the endosteum that destroy the matrix of the bone lining the medullary cavity, thus making it wider as the bone grows larger.
Bones respond to stress by increasing osteoblast activity. A highly active person will have more pronounced bone landmarks, particularly where muscles attach, due to the increased stresses there. One unusual thing about the bone matrix crystals is that they produce a tiny electrical field when stressed, and osteoblasts are attracted to the field, and once there they start to produce bone. Doctors have used this to their advantage by stimulating bone growth electrically in particularly bad fractures.
Out with the Old …
Osteoblasts and osteoclasts are busy little critters. Due to the need for a certain level of calcium in the body, especially in terms of muscle contraction (see The Structure of the Muscles and Muscle Cells), the matrix in bone needs to be continually broken down (to release calcium) and rebuilt (to deposit calcium). This continual activity is called remodeling.
Remodeling usually occurs at a balanced rate, which means for every osteon broken down, another is rebuilt. The rate of turnover varies according to the location of the bone, as well as the part of the bone, but about 20 percent of the bone tissue in a young adult is remodeled in a year. Areas of bone that receive a lot of stress, such as the spongy bone in the head of the femur can be replaced in anywhere from 4 to 6 months, but the compact bone in the diaphysis, which receives far less stress, is hardly changed at all.
Given the increase in bone density in response to stress, an active person can build stronger bone. Young women who are very active can actually reduce their risk of developing osteoporosis (the thinning of bone matrix, most commonly in older women) in their later years. One cause of osteoporosis is not having enough dietary calcium during pregnancy; the baby's need to build bone will cause the mother to draw calcium from her own bones, causing them to become more porous—osteoporosis means porous bone.
Another far less common way to reduce bone density is to become an astronaut! In order to mimic the effect of gravity on bone, an astronaut would have to exercise for about eight hours a day to prevent bone loss; as that is not possible, a typical astronaut is asked to exercise only two hours a day! For this very reason, physical therapy for women with osteoporosis involves a great deal of weight-bearing exercises; the greater the stress, the busier the osteoblasts!
Excerpted from The Complete Idiot's Guide to Anatomy and Physiology © 2004 by Michael J. Vieira Lazaroff. All rights reserved including the right of reproduction in whole or in part in any form. Used by arrangement with Alpha Books, a member of Penguin Group (USA) Inc.
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