How are bones growing, if bones are not connected to the brain?

How are bones growing, if bones are not connected to the brain?

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If the bones are not connected to the brain, how is their growth controlled?

This question is not a duplicate of the question Mechanisms of bone growth, as this question deals with how bone growth is controlled, and not which bone structures or bone tissues are involved.

The developmental growth of bone tissue is hormonally controlled. It is, as far as I know, not under direct neuronal control. Before reaching adolescence, the long bones (mainly in the arms and legs) grow in the epiphyseal plate, the area of the bone where cartilage is formed and ossified on the diaphyseal side, thereby lengthening the bone. The longitudinal growth of long bones continues until early adulthood at which time the chondrocytes in the epiphyseal plate stop proliferating and the epiphyseal plate transforms into the epiphyseal line as bone replaces the cartilage (boundless website). The growth and stop of growth in adulthood is hormonally controlled. Bone tissue growth is controlled by various hormones including parathyroid hormone and growth hormone.

Growth hormone (GH) is secreted by the pituitary, in turn controlled by the hypothalamus in the brain. So although the brain is involved, it is not directly involved, in that it regulates growth, and cessation of it through hormone release. Growth hormone is probably the most important hormone and is released by the pituitary, but parathyroid hormone released by the thyroid, among other hormones, may play a role as well.

Edit: Your question implies bone growth, which at first seemed to point toward developmental growth to me. However, there is also the more dynamic control of bone mass due to the forces that act on them in everyday life, referred to as bone mass accrual. This process is controlled by the sympathetic and parasympathetic system (Bajayo et al., 2012):

This system acts through direct neural innervation of bone tissue and stimulates bone formation when needed (after imposed strain on the skeletal system), but by default stimulates the breakdown (resorption) of bones to salvage its components for other uses (use it or loose it principle). So yes, the skeletal system is directly connected to the brain (with credits to @anongoodnurse).

  • The epiphyseal plate, the area of growth composed of four zones, is where cartilage is formed on the epiphyseal side while cartilage is ossified on the diaphyseal side, thereby lengthening the bone.
  • Each of the four zones has a role in the proliferation, maturation, and calcification of bone cells that are added to the diaphysis.
  • The longitudinal growth of long bones continues until early adulthood at which time the chondrocytes in the epiphyseal plate stop proliferating and the epiphyseal plate transforms into the epiphyseal line as bone replaces the cartilage.
  • Bones can increase in diameter even after longitudinal growth has stopped.
  • Appositional growth is the process by which old bone that lines the medullary cavity is reabsorbed and new bone tissue is grown beneath the periosteum, increasing bone diameter.
  • metaphysis: the part of a long bone that grows during development
  • periosteum: a membrane surrounding a bone
  • ossification: the normal process by which bone is formed
  • chondrocyte: a cell that makes up the tissue of cartilage
  • hypertrophy: to increase in size
  • diaphysis: the central shaft of any long bone
  • epiphysis: the rounded end of any long bone
  • medullary: pertaining to, consisting of, or resembling, marrow or medulla

Heterotopic ossification occurs when the body gets signals mixed up, and bone cells begin to create new bone outside of the normal skeleton. The body constantly makes new bone to replace bone within the skeleton. When fractures occur in the bone, new bone is formed to heal the damaged bone. In people with heterotopic bone formation, a similar process takes place, but often for an unknown reason.  

The process of new bone formation is called skeletogenesis. When this process occurs outside of where normal bone should exist, the result is called heterotopic ossification. The consequences can range from inconsequential to severe. In some cases, heterotopic bone will only be noticed because an x-ray was done for an unrelated concern. In others, the results can limit an individual's ability to perform even simple activities, such as walking.

There are several causes of heterotopic bone formation. These include:

  • Genetic conditions (such as fibrodysplasia ossificans progressiva and progressive osseous heteroplasia)  
  • Surgical procedures (including total hip replacement, elbow fracture, and forearm fracture surgery)
  • Brain or spinal cord injury (traumatic brain injury and spinal cord injury)
  • Sports injuries (myositis ossificans)

Bone Development

Intramembranous ossification stems from fibrous membranes in flat bones, while endochondral ossification stems from long bone cartilage.

Learning Objectives

Distinguish between intramembranous and endochondral ossification

Key Takeaways

Key Points

  • The ossification of the flat bones of the skull, the mandible, and the clavicles begins with mesenchymal cells, which then differentiate into calcium-secreting and bone matrix-secreting osteoblasts.
  • Osteoids form spongy bone around blood vessels, which is later remodeled into a thin layer of compact bone.
  • During enchondral ossification, the cartilage template in long bones is calcified dying chondrocytes provide space for the development of spongy bone and the bone marrow cavity in the interior of the long bones.
  • The periosteum, an irregular connective tissue around bones, aids in the attachment of tissues, tendons, and ligaments to the bone.
  • Until adolescence, lengthwise long bone growth occurs in secondary ossification centers at the epiphyseal plates (growth plates) near the ends of the bones.

Key Terms

  • osteoid: an organic matrix of protein and polysaccharides, secreted by osteoblasts, that becomes bone after mineralization
  • endochondral: within cartilage
  • chondrocyte: a cell that makes up the tissue of cartilage
  • diaphysis: the central shaft of any long bone

Development of Bone

Ossification, or osteogenesis, is the process of bone formation by osteoblasts. Ossification is distinct from the process of calcification whereas calcification takes place during the ossification of bones, it can also occur in other tissues. Ossification begins approximately six weeks after fertilization in an embryo. Before this time, the embryonic skeleton consists entirely of fibrous membranes and hyaline cartilage. The development of bone from fibrous membranes is called intramembranous ossification development from hyaline cartilage is called endochondral ossification. Bone growth continues until approximately age 25. Bones can grow in thickness throughout life, but after age 25, ossification functions primarily in bone remodeling and repair.

Intramembranous Ossification

Intramembranous ossification is the process of bone development from fibrous membranes. It is involved in the formation of the flat bones of the skull, the mandible, and the clavicles. Ossification begins as mesenchymal cells form a template of the future bone. They then differentiate into osteoblasts at the ossification center. Osteoblasts secrete the extracellular matrix and deposit calcium, which hardens the matrix. The non-mineralized portion of the bone or osteoid continues to form around blood vessels, forming spongy bone. 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

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.

Process of endochondral ossification: Endochondral ossification is the process of bone development from hyaline cartilage. The periosteum is the connective tissue on the outside of bone that acts as the interface between bone, blood vessels, tendons, and ligaments.

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, while 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.

How Bones Change Throughout Life

Throughout life, bones change in size, shape, and position. Two processes guide these changes—modeling and remodeling. When a bone is formed at one site and broken down in a different site its shape and position is changed. This is called modeling (Figure 2-2). However, much of the cellular activity in a bone consists of removal and replacement at the same site, a process called remodeling. The remainder of this section explains why and how these processes occur.

Figure 2-2

Modeling and Remodeling. Note: In modeling, osteoblast and osteoclast action are not linked and rapid changes can occur in the amount, shape, and position of bone. In remodeling, osteoblast action is coupled to prior osteoclast action. Net changes in (more. )

Why We Need Modeling and Remodeling

During childhood and adolescence bones are sculpted by modeling, which allows for the formation of new bone at one site and the removal of old bone from another site within the same bone (Seeman 2003) (Figure 2-2). This process allows individual bones to grow in size and to shift in space. During childhood bones grow because resorption occurs inside the bone while formation of new bone occurs on its outer (periosteal) surface. At puberty the bones get thicker because formation can occur on both the outer and inner (endosteal) surfaces. As people get older, resorption occurs on inner surfaces while formation occurs on outer surfaces, which can partially compensate for the loss of strength due to the thinning of the cortex. The size and shape of the skeleton follows a genetic program, but can be greatly affected by the loading or impact that occurs with physical activity. Ultimately bones achieve a shape and size that fits best to their function. In other words, 𠇏orm follows function.”

The remodeling process occurs throughout life and becomes the dominant process by the time that bone reaches its peak mass (typically by the early 20s). In remodeling, a small amount of bone on the surface of trabeculae or in the interior of the cortex is removed and then replaced at the same site (Figure 2-2). The remodeling process does not change the shape of the bone, but it is nevertheless vital for bone health, for a variety of reasons. First, remodeling repairs the damage to the skeleton that can result from repeated stresses by replacing small cracks or deformities in areas of cell damage. Remodeling also prevents the accumulation of too much old bone, which can lose its resilience and become brittle. Remodeling is also important for the function of the skeleton as the bank for calcium and phosphorus. Resorption (the process of breaking down bone), particularly on the surface of trabecular bone, can supply needed calcium and phosphorus when there is a deficiency in the diet or for the needs of the fetus during pregnancy or an infant during lactation. When calcium and phosphorus supplies are ample the formation phase of remodeling can take up these minerals and replenish the bank.

Modeling and remodeling continue throughout life so that most of the adult skeleton is replaced about every 10 years. While remodeling predominates by early adulthood, modeling can still occur particularly in response to weakening of the bone. Thus with aging, if excessive amounts of bone are removed from the inside, some new bone can be laid down on the outside, thus preserving the mechanical strength of the bone despite the loss of bone mass.

How Modeling and Remodeling Occur

The process of building the skeleton and continuously reshaping it to respond to internal and external signals is carried out by specialized cells that can be activated to form or break down bone. Both modeling and remodeling involve the cells that form bone called osteoblasts and the cells that break down bone, called osteoclasts (Figure 2-3). In remodeling there is an important local interaction between osteoblasts or their precursors (the cells that will develop into osteoblasts by acquiring more specialized functions𠅊 process called differentiation) and osteoclasts or their precursors. Since remodeling is the main way that bone changes in adults and abnormalities in remodeling are the primary cause of bone disease, it is critically important to understand this process. In addition, recent research has provided exciting information about these cell interactions.

Figure 2-3

Bone Remodeling. Note: The sequence of activation, resorption, reversal, and formation is illustrated here. The activation step depends on cells of the osteoblast lineage, either on the surface of the bone or in the marrow, acting on blood cell precursors (more. )

Osteoblasts are derived from precursor cells that can also be stimulated to become muscle, fat or cartilage however, under the right conditions these cells change (or differentiate) to form new bone, producing the collagen that forms the scaffolding or bone matrix. This calcium- and phosphate-rich mineral is added to the matrix to form the hard, yet resilient, tissue that is healthy bone. Osteoblasts lay down bone in orderly layers that add strength to the matrix. Some of the osteoblasts are buried in the matrix as it is being produced and these are now called osteocytes. Others remain as thin cells that cover the surface and are called lining cells. Osteocytes are the most numerous cells in bone and are extensively connected to each other and to the surface of osteoblasts by a network of small thin extensions. This network is critical for the ability of bone to respond to mechanical forces and injury. When the skeleton is subjected to impact there is fluid movement around the osteocytes and the long-cell extensions that provides signals to the bone cells on the surface to alter their activity, either in terms of changes in bone resorption or formation. Failure of the osteoblasts to make a normal matrix occurs in a congenital disorder of the collagen molecule called osteogenesis imperfecta. Inadequate bone matrix formation also occurs in osteoporosis, particularly in the form of osteoporosis produced by an excess of the adrenal hormones called glucocorticoid-induced osteoporosis. This form of osteoporosis differs from primary osteoporosis and most other forms of secondary osteoporosis because with glucocorticoid-induced osteoporosis inhibition of bone formation is the dominant mechanism for weakening of the skeleton.

The osteoclasts remove bone by dissolving the mineral and breaking down the matrix in a process that is called bone resorption. The osteoclasts come from the same precursor cells in the bone marrow that produce white blood cells. These precursor cells can also circulate in the blood and be available at different sites in need of bone breakdown. Osteoclasts are formed by fusion of small precursor cells into large, highly active cells with many nuclei. These large cells can fasten onto the bone, seal off an area on the surface, and develop a region of intense activity in which the cell surface is highly irregular, called a ruffled border. This ruffled border contains transport molecules that transfer hydrogen ions from the cells to the bone surface where they can dissolve the mineral. In addition, packets of enzymes are secreted from the ruffled border that can break down the matrix. Excessive bone breakdown by osteoclasts is an important cause of bone fragility not only in osteoporosis, but also in other bone diseases such as hyperparathyroidism, Paget’s disease, and fibrous dysplasia (see Chapter 3). Inhibitors of osteoclastic bone breakdown have been developed to treat these disorders (see Chapter 9).

Removal and replacement of bone in the remodeling cycle occurs in a carefully orchestrated sequence that involves communication between cells of the osteoblast and osteoclast lineages (Hauge, Qvesel et al. 2001 Parfitt 2001). It is controlled by local and systemic factors that regulate bone remodeling to fulfill both its structural and metabolic functions. The activation of this process involves an interaction between cells of the osteoblastic lineage and the precursors that will become osteoclasts. What stops this process is not known, but the osteoclasts machinery clearly slows down and the osteoclasts die by a process that is called programmed cell death. Thus the amount of bone removed can be controlled by altering the rate of production of new osteoclasts, blocking their activity, or altering their life span. Most current treatments for osteoporosis work by slowing down osteoclastic bone breakdown through use of antiresorptive agents.

The activation and resorption phases are followed by a brief reversal phase (Everts, Delaisse et al. 2002). During the reversal phase the resorbed surface is prepared for the subsequent formation phase, in part by producing a thin layer of protein, rich in sugars, which is called the cement line and helps form a strong bond between the old bone and the newly formed bone.

These three phases are relatively rapid, probably lasting only 2 to 3 weeks in humans. The final phase of bone formation takes much longer, lasting up to 3 or 4 months. Thus active remodeling at many sites can weaken the bone for a considerable period of time (even if formation catches up eventually), as many defects form in the bony structure that have not yet been filled. Formation is carried out by large active osteoblasts that lay down successive layers of matrix in an orderly manner that provides added strength. The addition of minerals to the collagenous matrix completes the process of making strong bone. Any error in this complex process can lead to bone disease.

Since remodeling serves both the structural and metabolic functions of the skeleton, it can be stimulated both by the hormones that regulate mineral metabolism and by mechanical loads and local damage acting through local factors. Repair of local damage is an important function of remodeling. Over time repeated small stresses on the skeleton can produce areas of defective bone, termed micro-damage. Replacement of that damaged bone by remodeling restores bone strength. Signals for these responses are probably developed by the network of osteocytes and osteoblasts, which, through their multiple connections, can detect changes in the stress placed upon bone and in the health of the small areas of micro-damage. Factors that affect the formation, activity, and life span of osteoclasts and osteoblasts as they develop from precursor cells can affect the remodeling cycle. Drugs have been developed that act in these ways, with the goal of reducing bone loss or increasing bone formation and maintaining skeletal health.


Fractures to the zygomatic bone are diagnosed through an X-ray. Patients are instructed not to blow their nose or perform any large facial movements which may cause pain or further disturb the fracture. Depending on the severity of the fracture, the zygomatic bone may be monitored through home health and treated with antibiotics to prevent or treat infection.

More serious zygomatic fractures may result in inward displacement of the eyeball, persistent double vision, or cosmetic changes. These instances require surgery to apply fixators to the bones and minimize complications.

The absence of cosmetic changes following a facial injury in children can result in a delayed diagnosis. White-eyed blowouts are orbital fractures which occur in children and result in a presentation similar to that of a concussion. This may include nausea, vomiting, and cognitive changes. Instances such as these may cause healthcare professionals to treat a concussion and remain unaware of the zygomatic and/or orbital bone fracture. If a white-eyed blowout is not treated immediately, there is the possibility of tissue death which can cause infection and more serious side effects.

Why the Procedure is Performed

A baby's head, or skull, is made up of eight different bones. The connections between these bones are called sutures. When a baby is born, it is normal for these sutures to be open a little. As long as the sutures are open, the baby's skull and brain can grow.

Craniosynostosis is a condition that causes one or more of the baby's sutures to close too early. This can cause the shape of your baby's head to be different than normal. It can sometimes limit how much the brain can grow.

An x-ray or computed tomography (CT) scan can be used to diagnose craniosynostosis. Surgery is usually needed to correct it.

Surgery frees the sutures that are fused. It also reshapes the brow, eye sockets, and skull as needed. The goals of surgery are:

Cerebrospinal Fluid Flow

CSF flow is like the life-blood of the brain. As we have seen, the pressure from breathing pushes CSF up the spinal column.

During exhalation, increased pressure in the chest causes a shift of CSF up to the sphenoid ventricle system. The sphenoid bone receives the CSF and pushes it through the ventricle system. The ventricles house these most precious outputs of the brain, and sphenoid bone deformities are known to produce CSF leaks.

At the front, the sphenoid serves as a bony encasing for the pituitary gland. At the back is the pineal gland, which is uniquely bathed in CSF with its own blood-pineal barrier. In the daytime, the pituitary releases a cascade of functioning hormones, and at night the pineal sends melatonin to calm and sleep.

As the foundation for these glands, the sphenoid bone could not be more critical.

Patient Guide to Bone Growth Stimulation

Bone growth stimulation (BGS) is a therapy your surgeon may prescribe following a spinal fusion procedure. A bone growth stimulator is a supplemental device worn following cervical (neck) or lumbar (low back) spine surgery. BGS may be utilized to help spinal bone fuse after a fusion procedure or as a treatment for failed fusion. Naturally, you have questions about this technology.
Bone growth stimulation may be utilized to help spinal bone fuse after a fusion procedure or as a treatment for failed fusion. Photo Credit:

The information provided in this patient guide can help you learn:

  • How bone heals
  • Risk factors for a poor or failed fusion
  • Role of bone growth stimulation in spine fusion aftercare
  • Questions to ask your spine surgeon

Orthopaedic spine surgeon, explains BGS

Gerard J. Girasole, MD, explained, “Bone growth stimulation for use in both the cervical and lumbar spine has shown to significantly benefit fusion results. Having been a study center for this technology, I have used bone growth stimulation in the majority of my post-operative cervical and lumbar patient cases. Not every patient is a candidate for bone growth stimulation. The patient evaluation criteria I use includes:

  • Patients who smoke
  • Multi-level fusions more than 1 level of the spine is fused
  • Co-morbidities (risk factors) that could hinder bone healing and growth

About Spinal Fusion

Spinal fusion is performed to stop movement of the spine and help prevent neurologic deficit. During the procedure, 2 or more vertebral bodies are joined together using instrumentation and bone graft. Spinal instrumentation includes rods, screws, plates, and/or interbody devices (implants). Bone graft may include your own bone (autograft), donor bone (allograft), or other types of graft.

Bone graft helps stimulate new bone to grow through 3 stages:

  1. Inflammatory stage: Cells begin to form new tissue
  2. Repair stage: Small blood vessel ingrowth starts
  3. Remodeling stage: Bone structure becomes strong

Post-operative image of a neck (cervical) surgery using spinal instrumentation. Spinal instrumentation creates an internal cast, which allows the inflammatory process to stimulate bone healing. With time, new bone grows into and around the implanted instrumentation healing into a solid construct.

Some patients are at-risk for spinal fusion to not heal properly or fail. A failed fusion is also called pseudarthrosis or non-union. Pseudarthrosis and non-union are medical terms your surgeon may use to define a fusion problem.

Common spinal problems treated surgically with fusion include:

Cervical (neck) / Lumbar (low back)

How Can a Bone Growth Stimulator Help Spinal Fusion?

A BGS sends low level electrical signals to the fusion site. The electrical signals activate the body's natural bone healing process, which may be impaired in at-risk patients.

Bone Growth Stimulation Has Been Used for Decades to Help Bone Heal

Over 50 years ago, scientists discovered that low-level electrical fields stimulate the body's bone-healing process. Other advances that include finding different types of energy that stimulate bone growth, electromagnetic coil technology and simply better devices— supported by scientific and clinical research—have improved bone healing in patients who undergo spinal fusion.

Different Types of Bone Growth Stimulators

All bone growth stimulators are different. Certain types are designed to be surgically implanted (internal BGS) and other stimulators are worn outside the body (external BGS). Other differences include the type of electrical current or magnetic field generated by the device and how stimulation is transmitted to the spine.

The types of bone growth stimulation devices approved by the U.S. Food and Drug Administration (FDA) use direct current 1 , capacitive coupling 2 , combined magnetic fields 3 , or pulsed electromagnetic fields. 4-6 Overall, it has been proven that fusion success can be increased in a patient treated with BGS compared to surgery without the use of BGS.

1. Kane WJ. Direct current electrical bone growth stimulation for spinal fusion. Spine. 1988 Mar13(3):363-5.

2. Goodwin CB, Brighton CT, Guyer RD, et al. A double-blind study of capacitively coupled electrical stimulation as an adjunct to lumbar spinal fusions. Spine. 1999 Jul 124(13):1349-57.

3. Linovitz RJ, Pathria M, Bernhardt M, et al. Combined Magnetic Fields Accelerate and Increase Spine Fusion. A double-blind, randomized, placebo-controlled study. Spine. 2002 Jul 127(13):1383-9.

4. Foley KT, Mroz TE, Arnold PM, et al. Randomized, prospective, and controlled clinical trial of pulsed electromagnetic field stimulation for cervical fusion. The Spine Journal. 2008 May-Jun8(3):436-42.

5. Simmons JW Jr, Mooney V. Thacker I. Pseudarthrosis after lumbar spine fusion: non-operative salvage with pulsed electromagnetic fields. American Journal of Orthopedics. 2004 Jan33(1): 27-30.

6. Mooney V. A Randomized Double-blind Prospective Study of the Efficacy of Pulsed Electromagnetic Fields of Interbody Lumbar Fusions. Spine. 1990 July15(7):708-12.

People don't directly control their bones.

One of the staples of Halloween costumes and horror movies is the walking skeleton. Of course, such a creature is pure fiction because it has no brain or nervous system to control its movements. But even if it did have these vital components, the undead monster would still be unable to walk around.

When people move their arms, legs or any other part of their bodies, it's not because they tell their bones to move &mdash it's because they tell their muscles, which are attached to their bones, to move.

Watch the video: How to grow a bone - Nina Tandon (October 2022).