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How does cartilage become bone?

How does cartilage become bone?


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It's a famous fact that bones begin as cartilage and later become bone, but I never was clear how exactly this changeover occurs. Could someone please explain this to me?


The process is called endochondral ossification.

It is important to point out that not all bone is derived from cartilage. For example, when a bone is fractured and is healing, the new bone does not always come from cartilage, rather intramembranous ossification occurs. There are therefore multiple mechanisms at a microscopic level by which bone may form. Additionally, bone formation in the long bones is different to that in, for example, the flat bones of the skull.


5.2: Bone Formation and Development

In the early stages of embryonic development, the embryo&rsquos skeleton consists of fibrous membranes and hyaline cartilage. By the sixth or seventh week of embryonic life, the actual process of bone development, ossification (osteogenesis), begins. There are two osteogenic pathways&mdashintramembranous ossification and endochondral ossification&mdashbut bone is the same regardless of the pathway that produces it.

Cartilage Templates

Bone is a replacement tissue that is, it uses a model tissue on which to lay down its mineral matrix. For skeletal development, the most common template is cartilage. During fetal development, a framework is laid down that determines where bones will form. This framework is a flexible, semi-solid matrix produced by chondroblasts and consists of hyaluronic acid, chondroitin sulfate, collagen fibers, and water. As the matrix surrounds and isolates chondroblasts, they are called chondrocytes. Unlike most connective tissues, cartilage is avascular, meaning that it has no blood vessels supplying nutrients and removing metabolic wastes. All of these functions are carried on by diffusion through the matrix. This is why damaged cartilage does not repair itself as readily as most tissues do.

Throughout fetal development and into childhood growth and development, bone forms on the cartilaginous matrix. By the time a fetus is born, most of the cartilage has been replaced with bone. Some additional cartilage will be replaced throughout childhood, and some cartilage remains in the adult skeleton.

Intramembranous Ossification

During intramembranous ossification, compact and spongy bone develops directly from sheets of mesenchymal (undifferentiated) connective tissue. The flat bones of the face, most of the cranial bones, and the clavicles (collarbones) are formed via intramembranous ossification.

The process begins when mesenchymal cells in the embryonic skeleton gather together and begin to differentiate into specialized cells (Figure 6.16a). Some of these cells will differentiate into capillaries, while others will become osteogenic cells and then osteoblasts. Although they will ultimately be spread out by the formation of bone tissue, early osteoblasts appear in a cluster called an ossification center.

The osteoblasts secrete osteoid, uncalcified matrix, which calcifies (hardens) within a few days as mineral salts are deposited on it, thereby entrapping the osteoblasts within. Once entrapped, the osteoblasts become osteocytes (Figure 6.16b). As osteoblasts transform into osteocytes, osteogenic cells in the surrounding connective tissue differentiate into new osteoblasts.

Osteoid (unmineralized bone matrix) secreted around the capillaries results in a trabecular matrix, while osteoblasts on the surface of the spongy bone become the periosteum (Figure 6.16c). The periosteum then creates a protective layer of compact bone superficial to the trabecular bone. The trabecular bone crowds nearby blood vessels, which eventually condense into red marrow (Figure 6.16d).

Intramembranous ossification begins in utero during fetal development and continues on into adolescence. At birth, the skull and clavicles are not fully ossified nor are the sutures of the skull closed. This allows the skull and shoulders to deform during passage through the birth canal. The last bones to ossify via intramembranous ossification are the flat bones of the face, which reach their adult size at the end of the adolescent growth spurt.

Endochondral Ossification

In endochondral ossification, bone develops by replacing hyaline cartilage. Cartilage does not become bone. Instead, cartilage serves as a template to be completely replaced by new bone. Endochondral ossification takes much longer than intramembranous ossification. Bones at the base of the skull and long bones form via endochondral ossification.

In a long bone, for example, at about 6 to 8 weeks after conception, some of the mesenchymal cells differentiate into chondrocytes (cartilage cells) that form the cartilaginous skeletal precursor of the bones (Figure 6.17a). Soon after, the perichondrium, a membrane that covers the cartilage, appears Figure 6.17b).

As more matrix is produced, the chondrocytes in the center of the cartilaginous model grow in size. As the matrix calcifies, nutrients can no longer reach the chondrocytes. This results in their death and the disintegration of the surrounding cartilage. Blood vessels invade the resulting spaces, not only enlarging the cavities but also carrying osteogenic cells with them, many of which will become osteoblasts. These enlarging spaces eventually combine to become the medullary cavity.

As the cartilage grows, capillaries penetrate it. This penetration initiates the transformation of the perichondrium into the bone-producing periosteum. Here, the osteoblasts form a periosteal collar of compact bone around the cartilage of the diaphysis. By the second or third month of fetal life, bone cell development and ossification ramps up and creates the primary ossification center, a region deep in the periosteal collar where ossification begins (Figure 6.17c).

While these deep changes are occurring, chondrocytes and cartilage continue to grow at the ends of the bone (the future epiphyses), which increases the bone&rsquos length at the same time bone is replacing cartilage in the diaphyses. By the time the fetal skeleton is fully formed, cartilage only remains at the joint surface as articular cartilage and between the diaphysis and epiphysis as the epiphyseal plate, the latter of which is responsible for the longitudinal growth of bones. After birth, this same sequence of events (matrix mineralization, death of chondrocytes, invasion of blood vessels from the periosteum, and seeding with osteogenic cells that become osteoblasts) occurs in the epiphyseal regions, and each of these centers of activity is referred to as a secondary ossification center (Figure 6.17e).

How Bones Grow in Length

The epiphyseal plate is the area of growth in a long bone. It is a layer of hyaline cartilage where ossification occurs in immature bones. On the epiphyseal side of the epiphyseal plate, cartilage is formed. On the diaphyseal side, cartilage is ossified, and the diaphysis grows in length. The epiphyseal plate is composed of four zones of cells and activity (Figure 6.18). The reserve zone is the region closest to the epiphyseal end of the plate and contains small chondrocytes within the matrix. These chondrocytes do not participate in bone growth but secure the epiphyseal plate to the osseous tissue of the epiphysis.

The proliferative zone is the next layer toward the diaphysis and contains stacks of slightly larger chondrocytes. It makes new chondrocytes (via mitosis) to replace those that die at the diaphyseal end of the plate. Chondrocytes in the next layer, the zone of maturation and hypertrophy, are older and larger than those in the proliferative zone. The more mature cells are situated closer to the diaphyseal end of the plate. The longitudinal growth of bone is a result of cellular division in the proliferative zone and the maturation of cells in the zone of maturation and hypertrophy.

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 (Figure 6.19).


Bone or cartilage? Presence of fatty acids determines skeletal stem cell development

A histologic section of a mouse bone fracture. Safranin O has been used to colour the cartilage cells red (specifically the proteins produced by cartilage cells) all other tissues are blue. Credit: Nick van Gastel.

In the event of a bone fracture, fatty acids in the blood signal to stem cells that they have to develop into bone-forming cells. If there are no blood vessels nearby, the stem cells end up forming cartilage. The finding that specific nutrients directly influence the development of stem cells opens new avenues for stem cell research. Biomedical scientists from KU Leuven and Harvard University published these results in Nature.

Bone fractures heal through the action of skeletal progenitor cells: stem cells that have evolved further but can still develop into different types of cells. Bone healing occurs in one of two ways: The progenitor cells evolve into bone-forming cells when the fracture is small, and into cartilage cells when the fracture is bigger. This cartilage is later replaced by bone. Until now, scientists did not know how progenitor cells decide whether to become bone or cartilage cells.

"Our hypothesis was that the presence of blood vessels plays a role," explains first author Nick van Gastel. "Despite what many people think, our bones are full of blood vessels, while cartilage does not have any." This new study on mice confirmed the team's assumption: when blood vessels surrounding a fracture were blocked, cartilage was formed. When they were not, new bone was created immediately.

In a second phase of the study, the researchers tried to find out which signal the blood vessels actually send to the progenitor cells to make them evolve into either a bone or a cartilage cell. "Our previous research had already shown that nutrients play a role in the biology of progenitor cells," explains Professor Geert Carmeliet from the Clinical and Experimental Endocrinology Unit at KU Leuven, who led the study. For the current study, the team tested how the presence of different nutrients influences progenitor cell fate. Their results show that the fatty acids present in blood cause progenitor cells to grow into bone-forming cells.

If there are no fatty acids nearby, progenitor cells activate the SOX9 gene, which plays an important role in skeletal development. This is the signal for the cell to become a cartilage cell. Cartilage cells do not need fatty acids to survive and form cartilage.

"This study is useful for researchers in regenerative medicine, since we still know little about cartilage formation," says Professor Carmeliet. "Research into cartilage disorders such as osteoarthritis may also benefit from these findings. There are indications that cartilage cells receive more fatty acid signals and don't produce enough of the SOX9 gene in patients with such disorders, which can have adverse effects on the joints. Finally, our study shows for the first time that specific nutrients can inform stem cells which type of cell they should become. That is an important step forward in stem cell research." Eventually, the researchers hope to map out the effects of different nutrients on different types of progenitor cells.


Bone vs Cartilage (Similarities and Differences between Bone and Cartilage)

Bone and cartilage are connective tissues which form the skeletal system in the body. Bones are hard and tough which gives the structural framework of the skeleton in the body. Cartilages are soft and flexible components present in ear, nose and joints. Cartilage acts as shock absorbers between two bones and they prevent the rubbing between them the bones. Even though the bones and cartilages are connective tissues and they are the components of the skeletal framework, both show considerable differences in their formation, organization and functions.

The present post discusses about the Similarities and Differences between Bone and Cartilage with a Comparison Table.

Similarities between Bone and Cartilage

Ø Both bone and cartilage are connective tissues.

Ø Both are the components of the skeletal system.

Ø Both provide shape to body parts.

Ø Both provide protection to vital organs.

Ø Both are mesodermal in origin.

Ø Both composed of specialized cells embedded in the matrix of fibrous proteins.

Difference between Bone and Cartilage

Sl. No.BoneCartilage
1Bone is tough and hardCartilage is soft and flexible
2Bones cannot bendCartilages can bend
3Function: protection against mechanical damage, movement of body parts, provides shape produce blood cells, storehouse of mineralsFunctions: Reduce friction at joints, support the respiratory tract, acts as shock absorbers, and provides shape and flexibility of fleshy appendages such as ear and nose
4Bone matrix composed of ossein *Cartilage matrix composed of chondrin *
5Ossein is tough and inflexibleChondrin is firm but flexible
6Bone matrix is organic and inorganicCartilage matrix is completely organic
7Bone matrix made up of proteins, calcium and phosphorousCartilage matrix made of proteins and sugars
8Bone matrix is always impregnated with calcium saltsCartilage matrix is free or impregnated with calcium salts
9Matrix is lamellate and occurs in concentric mannerMatrix occurs as homogenous mass
10Osteocytes * are irregularChondroblasts * are oval shaped
11Osteoblasts * present: Osteoblasts are the layer of bone forming cells. They present as outer and inner layersNo special cartilage forming cells. Cartilage grows by the division of all chondroblasts
12Only one cell per bone lacunaeEach cartilage lacunae with a single or group of two or four cells
13Osteocytes give off branching processes in the developing boneProcesses are absent in chondroblasts
14Lacunae give off canaliculi *Lacunae do not have canaliculi
15Bone is vascularCartilage is non-vascular
16Bone is porousCartilage is non-porous
17Nerve supply presentNerve supply absent
18Bone usually has bone marrow at the centerNo such tissue present in cartilage
19Two types of bones: Compact bone and spongy boneThree types of cartilages: hyaline-cartilage, fibro-cartilage and elastic-cartilage
20Bones possess Haversian system * and Volkman’s canals *Cartilage does not have Haversian system and Volkman’s canals
21The growth pattern of bone is bidirectional.Growth pattern of Cartilage is unidirectional
22The covering of bone is called periosteumThe covering of cartilage is called perichondrium
23Bones never change to cartilageCartilage sometimes becomes bony due to calcification
24Metabolic activity of bone is highMetabolic activity of cartilage is low
25Oxygen demand high in bonesOxygen demand low in cartilage
26Bones possess extensive repair capabilitiesCartilages have very limited range of repair capabilities

Ossein: The main protein component of bone also known as the collagen of bones.

Chondrin: A complex protein-carbohydrate mixture, the major component of cartilage.

Osteocytes: A type of bone cell, formed when an osteoblast becomes embedded in the material it has secreted.

Osteoblasts: main bone producing cell in the bone.

Chondroblasts: major cell component of cartilage, produces the chondrin which forms the matrix of cartilage.

Bone canaliculi: minute canals between the lacunae of ossified bones.

Haversian system: A structural unit of bone consisting of a Haversian canal and corresponding lamellae of compact bone.

Volkman’s canal: Channels in the bone that transmit blood vessels from the periosteum into the bone and that communicate with the haversian canals.

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Bone Formation

1. Intramembranous Ossification: In this process, the formation of the compact and spongy bone takes place directly from the sheets made of the undifferentiated mesenchymal connective tissue. By this process the bones that are located in the face such as flat bones, the collar bones or clavicle, and cranial bones.

There are 4 Stages of Bone Formation and Growth in Intramembranous ossification:

When the mesenchymal cells that are present in the embryonic skeleton gather together then the process begins in order to differentiate into specialized cells. Some of these cells become osteogenic cells and some of them differentiate as capillaries. The osteogenic cells are further converted into osteoblasts. The early osteoblasts in a cluster of cells called the ossification centre.

The osteoblasts secrete osteoid, it is an uncalcified matrix that consists of collagen precursors and other types of organic molecules. Within a few days, mineral salts are deposited on the matrix and it gets hardened by entrapping the osteoblasts. When these are entrapped the osteoblasts get converted into osteocytes. The osteogenic cells that are present in the surrounding of the connective tissue get differentiated to form new osteoblasts at the edge of the growing bone tissue.

Osteoid clusters get united around the capillaries in order to form a trabecular matrix whereas the osteoblasts that are present on the surface of the newly formed spongy bone that becomes the cellular layer of the periosteum.

This periosteum then secretes the superficial of the compact bone to spongy bone. Nearby the blood vessels the spongy bone crowds that eventually condenses to form new red bone marrow. Under the action of osteoclasts, the new bone gets remodeled.

[Image will be uploaded soon]

Formation of the ossification centre

Trabecular matrix and periosteum form

Development of compact bone

2. Endochondral Ossification: In this process, bone develops by replacing cartilage. Cartilage does not become bone. Instead, cartilage serves as a template to be completely replaced by new bone. Endochondral ossification takes much longer than intramembranous ossification. Bones that are present at the base of the skull and long bones form through the process of endochondral ossification.

In a long bone, a number of the mesenchymal cells differentiate into chondroblasts or cartilage cells at about 6 to eight weeks after conception, which forms the hyaline cartilaginous skeletal precursor of the bones. This cartilage is a flexible, semi-solid matrix that is produced by cartilage cells and consists of chondroitin sulfate, collagen fibres, hyaluronic acid, and water. They're also called chondrocytes as the matrix surrounds and isolates the chondroblasts. Unlike most connective tissues, cartilage is avascular which means that it has no blood vessels that are supplying the nutrients and removes the metabolic wastes. All of those functions are carried on by the process of diffusion through the matrix from vessels within the surrounding perichondrium, a membrane that covers the cartilage.

As more and more matrix is produced, the cartilaginous model grows in size. Blood vessels that are present in the perichondrium bring the osteoblasts to the edges of the structure and these arriving osteoblasts deposit bone in a ring around the diaphysis this process is called a bone collar. The bony edges of the developing structure prevent the nutrients from diffusing into the middle of the cartilage. This leads to the death of chondrocytes and disintegration within the centre of the structure.

Without cartilage inhibiting vessel invasion, blood vessels penetrate the resulting spaces, not only enlarging the cavities but also carrying osteogenic cells with them, many of which can become osteoblasts. These enlarging spaces eventually combine to become the medullary cavity. Bone is then deposited within the structure that is creating the first ossification centre.

While these deep changes are occurring, chondrocytes and cartilage still grow at the ends of the structure, which increases the structure’s length at an equivalent time bone is replacing cartilage in the diaphyses. This continued growth is the reason for the remodeling inside the medullary cavity and the overall lengthening of the structure. Cartilage remains at the epiphyses and the joint surface as articular cartilage when the fetal skeleton is formed completely.

After birth, this same sequence of events occurs within the epiphyseal regions, and each of these centres of activity is referred to as a secondary ossification centre. Throughout childhood and adolescence, there remains a skinny plate of cartilage between the diaphysis and epiphysis referred to as the expansion or epiphyseal plate. Eventually, these cartilages are going to be removed and replaced by bone to become the epiphyseal line.

[Image will be uploaded soon]

Bone Development

While bones are increasing long, they are also capable of increasing in diameter, whereas growth in diameter can continue even after the cease of the longitudinal growth. This growth by adding to the free surface of the bone is also known as appositional growth. This appositional growth is found at the endosteum or periosteum where the osteoclasts resorb old bone that is present as a lining to the medullary cavity, whereas the osteoblasts produce to form new bone tissue. The erosion of old bone along the medullary cavity and hence the deposition of the latest bone takes place under the periosteum.

This not only increases the diameter of the diaphysis but also increases the diameter of the medullary cavity. This remodeling of bone primarily takes place during the process of bone growth. However, in adult life, bone undergoes constant remodeling, during which resorption of old or damaged bone takes place on an equivalent surface where osteoblasts lay new bone to exchange 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 five to ten percent of the skeleton is remodeled annually just by destroying old bone and renewing it with fresh bone.

Conclusion

All bone formation processes are replacement processes. During bone development, by the ossification process tissues are replaced by bone. In the intramembranous type of ossification, the bone develops directly from sheets that are made of mesenchymal animal tissue. In the endochondral type of ossification, the bone develops directly by replacing the cartilage. Activity within the epiphyseal plate enables bones to grow long. Appositional growth allows bones to grow in diameter. The remodeling process occurs as bone is resorbed and replaced.


ELI5: During ossification, how does cartilage turn into bone, and where does marrow come from?

How does the bone collar come about? I know that osteoblasts form bone within the cartilage structure, but how are these osteoblasts introduced and what exactly happens to the cartilage?

And how does the final structure result in a bone longer than the original cartilage structure?

The bone collar derives from the perichondrium of the hyaline cartilage template which presumably includes osteoprogemitor cells (from original basic mesenchymal cells) that become osteoblasts. In the centre of the cartilage differentiated chondrocytes form the primary ossification centre, releasing vascular endothelial growth factor (VEGF) which promotes blood vessel formation. As these grow into the centre of the cartilage they bring ostoprogenitor cells and vascular structures that become the bone marrow. The length of the bone is added by secondary ossification centres which form the epiphysial plates.


Footnotes

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Endochondral ossification: how cartilage is converted into bone in the developing skeleton

Endochondral ossification is the process by which the embryonic cartilaginous model of most bones contributes to longitudinal growth and is gradually replaced by bone. During endochondral ossification, chondrocytes proliferate, undergo hypertrophy and die the cartilage extracellular matrix they construct is then invaded by blood vessels, osteoclasts, bone marrow cells and osteoblasts, the last of which deposit bone on remnants of cartilage matrix. The sequential changes in chondrocyte behaviour are tightly regulated by both systemic factors and locally secreted factors, which act on receptors to effect intracellular signalling and activation of chondrocyte-selective transcription factors. Systemic factors that regulate the behaviour of chondrocytes in growth cartilage include growth hormone and thyroid hormone, and the local secreted factors include Indian hedgehog, parathyroid hormone-related peptide, fibroblast growth factors and components of the cartilage extracellular matrix. Transcription factors that play critical roles in regulation of chondrocyte gene expression under the control of these extracellular factors include Runx2, Sox9 and MEF2C. The invasion of cartilage matrix by the ossification front is dependent on its resorption by members of the matrix metalloproteinase family, as well as the presence of blood vessels and bone-resorbing osteoclasts. This review, which places an emphasis on recent advances and current areas of debate, discusses the complex interactions between cell types and signalling pathways that govern endochondral ossification.


Finding the fossil

Finding a very rare fossil in the field gives one a kind of euphoric rush and I recall it well the day I found the Gogo shark, at 11am on July 7, 2005. I was searching for fossils on Gogo Station in the Kimberley, near Fitzroy Crossing, about a four-hour drive inland from Broome.

I had just split a limestone nodule with my hammer and saw a vague outline of a pair of jaws staring at me. Examining the specimen with my hand lens revealed the teeth had multiple cusps fixed onto a broad bony base – a feature unique to sharks at this time. I was overjoyed at finding the first fossil shark in more than 60 years of collecting from the site.

This photo of me holding the Gogo shark was snapped minutes after the discovery on July 7, 2005. Lindsay Hatcher , Author provided

So why the big deal about finding a shark at Gogo? The Gogo Formation is undoubtedly one of the world’s best sites for studying the early evolution of fishes as it yields superb three-dimensional specimens that lived 380 million years ago, a very important time in fish evolution.

Gogo has a diverse fauna of many kinds of ancient armoured placoderm fishes as well as early bony fishes (osteichthyans), but no sharks.

Finding a shark at Gogo has been a bit of a holy grail for fish palaeontologists as we all expected a shark from this site would have extraordinarily good preservation. It should reveal something new about early shark evolution, as nearly all other sharks of this age were flattened and poorly preserved.

Back in the lab, I prepared the specimen in dilute acetic acid, which slowly dissolved away the limestone rock surrounding the fossil. I was surprised to find the cartilaginous elements of the shark easily came out of the rock. This suggested that the skeleton was made of a special kind of highly mineralised cartilage.

Although mostly incomplete, the specimen comprised the complete lower jaws, shoulder girdles which support the pectoral fins, some isolated gill-arch elements and many small teeth and scales.

Top, the Gogo shark specimen in rock as it was found. Below, after three weeks of dilute acetic acid preparation the large lower jaw cartilages are seen emerging in perfect 3D form. John Long , Author provided

The teeth were highly unusual, with many small cusps surrounding the larger fangs. From the distinctive teeth we knew we had a new species of shark, as every living shark on the planet has its characteristic teeth that can identify the species from teeth alone.

Gogoselachus was clearly a fast-swimming predator that hunted other fishes using its jagged teeth to snare prey. Gogoselachus lived on an ancient reef that teemed with many kinds of large predatory placoderm fishes, so had to hold its own in this piscine rat race.

Teeth of Gogoselachus are distinctive with many small cusps. The image far right is a CT-scanned tooth showing internal structure. John Long, Flinders University, and Tim Senden, ANU , Author provided


Hyoid Bone and Sleep Apnea

Obstructive sleep apnea syndrome (OSAS) is a chronic breathing disorder that occurs during sleep when the pharynx collapses.

As the tongue bone is an attachment point for the suprahyoid and infrahyoid muscle groups, and as it is these muscles together with muscles of the oropharynx that keep the airway open, it is easy to understand why this bone plays a role. When we sleep, many neurological stimuli fall away – this is particularly noticeable in our muscles. People who suffer from sleep paralysis will know exactly how unresponsive the muscles become.

In OSAS, relaxed muscles and pressure from fatty tissue (OSAS is usually associated with people who are overweight), cause the upper airway to close.

Hyoid position is a contributing factor to obstructive sleep apnea. When the two hyoid muscle groups are not working in sync, they contribute to pharyngeal collapse.

While OSAS is commonly treated with continuous positive airway pressure – the blowing of air into the airway under pressure – this chronic disorder can also be treated with surgery.

Surgical treatments typically involve the hyoid bone. Examples of sleep apnea surgery are hyoidothyroidopexy, hyoid suspension, and hyoid myotomy. The former stitches the hyoid to the upper portion of the thyroid cartilage. Hyoid suspension brings the bone forward by fixing it to the lower jaw (below). The latter surgery type (carried out with or without suspension) cuts into the muscles of the hyoid to create more room for air to pass through.


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