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02.03 Development of Bones

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  1. Intramembranous → cranium & splanchnocranium
    1. Begins with flat sheets of CT (“Mesenchyme”)
    2. Primary ossification center forms (POC)
      1. Fibroblasts → osteoblasts
      2. Osteoblasts → trabecular bone
      3. Blood vessels grow into POC
      4. Marrow precursors enter
        1. Will become red bone marrow in spaces of trabecular bone
      5. Surface membrane → periosteum
      6. Produces thin layer of compact bone over POC
      7. Steps of ossification expand to edges of the membrane model
    3. 6 Fontanels @ birth
      1. Membrane spaces between fetal cranial bones
      2. Ossify this way
      3. At birth, cranial bones overlap one another to allow the skull to adapt to the birth canal
      4. See Peds 01.04 for timing of closures
  2. Intracartilaginous → long, short, irregular
    1. Ossification of long bone diaphysis
      1. All begin as hyaline cartilage
      2. Perichondrium → periosteum @ POC
      3. Periosteum → osteoblasts → thin compact bone
      4. “Bony collar” formed @ POC
      5. Cartilage inside bony collar grows and expands → compressing the matrix into flat plates
      6. Blood vessels grow in and bring calcium
        1. Cartilage becomes calcified
        2. Cartilage cells begin to die
      7. Osteoblasts and bone marrow precursors enter
        1. Osteoblasts → trabecular bone
        2. Precursors produce Red Marrow
      8. Process extends to ends to complete diaphysis
      9. Periosteum produces more compact bone at edges
      10. Osteoclasts from Red Bone Marrow break down spongy bone to create the Bone Marrow cavity of long bones
    2. Ossification of long bone epiphyses
      1. Secondary ossification center (SOC) forms in epiphyses
      2. Same steps as for diaphysis
      3. No bone marrow cavity
      4. Condition of epiphysis
        1. Articular cartilage
        2. Thin compact bone surrounds epiphyses underneath articular cartilage
        3. Central spongy bone containing red bone marrow
        4. Epiphyseal plate (disc)(growth plate)
          1. Hyaline cartilage
          2. Between epiphysis and diaphysis

Nursing Points


  1. Growth of bone through adolescence
    1. Length
      1. Intracartilaginous
      2. Site: epiphyseal plate
      3. Cartilage cells divide and grow next to epiphysis
      4. Old cartilage cells die → spongy bone
      5. Osteoclasts expand BM cavity to new areas
      6. Occurs simultaneously at both ends
    2. Circumference
      1. Intramembranous
      2. Site: Periosteum
        1. Osteoblasts →  compact bone at out surface of bone
      3. Endosteum
        1. Osteoclasts → expand BM cavity
  2. Factors affecting growth
    1. Thyroxine (thyroid gland)
      1. Metabolism of cartilage cells in epiphyseal plate
      2. Lack of thyroxine after birth
        1. Long bones shorter than normal
        2. Dwarfism
    2. Somatotropic hormone (anterior pituitary gland)
      1. Growth hormone → to liver
      2. Hypersecretion before closure = gigantism (8’ tall)
      3. Hyposecretion before closure = dwarfism (3’-3’6”)
    3. Estrogens and testosterone
      1. Affect closure
      2. Epiphyseal plate disappears, forming the epiphyseal line
        1. Stops growth in length of long bones
      3. Females→ 17-19
      4. Males → 19-21
      5. Everyone → by age 25
    4. Vitamin A Deficiency
      1. Reduces rate of cartilage cycle in epiphyseal plate
        1. Length = short
        2. Diameter = not affected
        3. Short and stubby
  3. Calcification = addition of calcium and phosphate to organic matrix (i.e. making the bone harder)
    1. Hormonal control
      1. Calcitonin (thyroid gland)
        1. Inhibits osteoclasts
        2. Favors production of new bone
      2. Parathormone (parathyroid gland)
        1. Stimulates osteoclasts
        2. Favors breakdown of bone
        3. Destroys inorganic matrix of bone
          1. Removes calcium and phosphate
    2. Vitamins
      1. Vit. A
        1. Excess → ↑ osteoclastic activity
        2. Bone breaks down and becomes brittle
      2. Vit. C
        1. Deficiency = abnormal proteoglycans in organic matrix
        2. Lack calcium and phosphate therefore bones are soft
      3. Vit. D
        1. Stimulates uptake of calcium and phosphate  from small intestine
        2. Deficiency = low calcium and phosphate
        3. Less calcification
        4. Soft bones
          1. Rickets in young
          2. Osteomalacia in aged

Betts, J.G., et al. (2017). Anatomy and physiology. Houston, TX: OpenStax, Rice University. Retrieved from

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Video Transcript

In this lesson we’re going to take a look at the development of bones.

In bone development we have two ways that it happens. The first one is called intramembranous bone development and the second one is called intracartilaginous bone development.

Intramembranous bone development is responsible for the flat bones so these are things like skull bones, clavicle, and the ribs. These are all flat bones and and they’re develop differently than things like long bones. So before we get into the intracartilaginous bone development let’s first look at the intramembranous bone development.

In utero you have these group of cells called mesenchymal stem cells and they all come together and they form something called the primary ossification center. These mesenchymal stem cells are turned into osteoblasts and osteoblasts begin to lay down new layers of bone tissue around the primary ossification center. These layers will eventually spread to the edges of whatever bone they’re forming but a couple of things happen during this process. First off any osteoblast to get trapped inside of the osteoid or the central location are turn into osteocytes. The other thing that happens is that blood vessels are formed into the primary ossification center. As this expansion occurs this osteoid forms this network called woven bone which is eventually turned into trabecular bone or spongy bone. And as it gets to the edge it begins to lay down the periosteum and underneath the periosteum will eventually be a layer of thin compact bone. And this process happens in sheets so you’ll have one layer that is going and you’ll have another layer that’s going at the same time until the entire bone is formed, and then it’s hardened over time.

Now that we’ve looked at intramembranous bone development let’s take a look at intracartilaginous bone development.

Alright so this process is really complicated so stick with me. In long bone, you have the diaphysis. It’s the shaft of the bone, and this is where all of this begins. You initially start with something call the hyaline cartilage and in the middle is the primary ossification center. At the primary ossification center the periosteum begins to form and it creates this thing around the bone called the bony collar. The cartilage inside the bony collar grows and expands, and it compresses all of the cells into these flat plates and it begins to harden. But it can’t do it without blood vessels. So the blood vessels grow in and they bring in the calcium and that’s when the ossification occurs. The osteoblasts begin to work on building the hard bone and the osteoclast begin to carve out in the middle of the bone known as the medullary cavity. That’s really how it works along the middle of the bone, so let’s check out what it looks like on the ends of the bone.

Intracartilaginous bone development in the epiphyses are not very different from the diaphysis. Instead of having a primary ossification center, you have something known as a secondary ossification center and it’s at the end of each bone. It’s the essential same concept as the diaphysis. However no bone marrow cavities are formed in each epiphysis.

But here’s some really interesting characteristics of the epiphysis that happened as a result of the bone development. First off there covered in articular cartilage. Then underneath it is a thin layer of compact bone than most of that after that is comprised primarily of central spongy bone. However a really unique characteristic of bone development is that the epiphysis has to meet the diaphysis. And this happens it’s something called the epiphyseal plate, or something we commonly known as a growth plate. And now we’ll look at how bone growth actually occurs.

Okay so let’s take a look at bone growth especially through adolescence. What we’re talking about right now is a length of the bone.

So you have the diaphysis and you have the epiphysis and then you have the epiphyseal plate here.

As cartilage cells come in they lie next to the epiphyseal plate and the bone gets longer. These cartilage cells did generate, and are converted into spongy bone. As the bone lengthens the osteoclasts will come in and break down areas Within the bone to lengthen the diaphysis.

So this is what it would look like in terms of length. You have your epiphysis which grows new cartilage and then you have your medullary cavity. As a bone gets longer do you have more layers of cartilage that is converted into spongy bone. Well your medullary cavity needs to increase so the osteoclasts come in and cave out more medullary cavity.

When we talk about circumference, especially in flat bone, this happens underneath the periosteum. The osteoblasts put down new bone cells at the outer surface of the bone. Inside the bone, the endosteum expands the bone marrow cavity when osteoclasts break down bone tissue to allow for bone marrow cavity formation as the bone grows larger.
So now let’s take a look at different types of factors that will affect the growth of the bone.

Thyroxine is the thyroid hormone, and what we’re looking at is that when you have decreased thyroxine you’re going to have decreased bone growth.

The somatotropic hormone is produced in the anterior pituitary gland and if you have an overproduction of the somatotropic, and you’re going to have increased bone growth and if you have a decreased secretion you’re going to have decreased bone growth.

Estrogen and testosterone also affect bone growth. They affect closure of the epiphyseal plates are the growth plates, and this is related to puberty. Because of this bone development stops around 17 to 19 in females, and males around the ages of 19 to 21.

Vitamin A deficiency also affect bone growth. Reduced vitamin A intake causes a reduced rate of the cartilage cycle, and the length of the overall bones are shortened.

Now what kind of things affect calcification of the bone?

Well calcitonin which is produced in the thyroid gland that inhibits osteoclasts. And that in turn favors production of new bone.

Parathormone or the parathyroid hormone is produced in the parathyroid gland. It stimulates osteoclasts and that favors the breakdown a bone. What happens is it destroys the inorganic Matrix of the bone and removes calcium and phosphate from the bone. This is important in the regulation of calcium in the blood, but problems with the parathyroid gland can actually cause changes in overall calcium levels in can lend itself to conditions like osteoporosis.

Let’s take a look at how vitamin intake effects bone production.

Vitamin A is really important for bone development. However excess vitamin A actually increases osteoclast activity meaning that you’re going to have an excess breakdown on that bone. So too much vitamin A causes bones to break down and become brittle.

Vitamin C is important because vitamin C deficiencies cause an abnormal matrix and that and causes decreases in the calcium and phosphate.

And then there’s vitamin D. Vitamin D is responsible for stimulating the uptake of calcium from the small intestine. So if you don’t have enough vitamin D, you can’t stimulate that process and calcium is not deposited into bones.

Okay so let’s recap.

Intramembranous bone development is formed in sheets and it starts from one primary ossification center and moves outward until the entire bone is formed.

Intracartilaginous bone development starts centrally and grows outward but it also text in the process of making that medullary cavity. There’s also the secondary ossification centers in the epiphyses which are important for those ends of the bone growth.

When we are talking about bone growth, especially through adolescence, this growth happens along the epiphyseal plate, then the medullary cavity expands.

Calcification of bone is influenced by both calcitonin and parathormone. Calcitonin impedes osteoclasts, and parathormone promotes osteoclasts.

Vitamin intake is vitally important for bone growth. Vitamin A, C and D all impact how bones develop.

That’s it for our lesson on bone development. Make sure you check out all the resources attached to this lesson. Now go out and be your best I was today, and as always happy nursing.