03 - Theories of Craniofacial Growth

Introduction

Introduction

Before viewing this program, you should have looked at the module entitled “The Nature of Craniofacial Growth,” which reviews the principles of skeletal growth and describes the sites and types of growth in the craniofacial skeleton.

This program focuses on the determinants of craniofacial growth, that is, why the bones of the cranium and face grow in the way they do. To take advantage of growth for clinical treatment and even manipulate it to our advantage, we must understand what controls or determines it.

Learning Objectives

The objective of this program is to review and put in perspective the three major theories of craniofacial growth:

• Theory 1 – Bone at sutures and surfaces is the primary determinant of its own growth

• Theory 2 – Cartilage is the primary determinant of skeletal growth, with bone and sutures reacting passively

• Theory 3 – The soft tissue matrix is the primary determinant of growth, while bone and cartilage both are secondary followers

After viewing the program and doing the reading (40-50 in the 5th ed or pages 47-58 in the 4th ed of Contemporary Orthodontics), be sure that you are able to:

• indicate the strengths and weaknesses of each theory
• describe the mechanism of growth for the cranium, cranial base, maxilla and mandible from a current perspective
• describe the growth of facial soft tissue

Definitions, Suture Theory

Definitions

Before we begin our review of growth theories and what they imply for growth control, some important terms must be defined:

Site of growth: Simply an area where growth is occurring

Center of growth: A site of growth that has the ability to grow on its own, independently of its surroundings—it contains the information to control growth

All centers of growth are also sites, but not all sites are centers. Growth at some sites occurs only in response to growth in other areas. Growth at centers is internally stimulated and controlled.

Definitions (cont.)

Mode of growth: The way it occurs. In the case of skeletal growth, there are two possible modes: replacement of cartilage (endochondral ossification) or direct apposition of bone (intramembraneous ossification)

Mechanism: How growth changes occur at a higher level, such as downward and forward movement of the jaws or expansion of the cranial vault

Determinant: The cause of the observed growth changes (and therefore what controls them)

Suture Theory: Harry Sicher

The suture theory of craniofacial growth was popularized by Harry Sicher, an Austrian anatomist who came to the United States prior to World War II.

Dr. Sicher observed that new bone was formed at the synchondroses of the cranial base, at the mandibular condyle, and at the sutures of the cranial and facial bones. He theorized that pressures created by formation of new bone at these sites literally pushed the bones apart.

The theory says, therefore, that in the absence of cartilage, the intramembranous bones are able to determine their own growth. For example, Sicher believed that growth at the sutures of the maxilla casued it to be translated downward and forward.

Suture Theory: Sites vs. Centers

Let’s characterize the suture theory using the terms we just defined. Sicher’s theory was that sutures are both sites and centers of skeletal growth; and in his view, so were synchondroses, condylar cartilage, and at least to some extent, periosteal surfaces.

To him, the mode of growth was somewhat irrelevant, since there was no difference in how the two modes were controlled. The mechanism of growth movements was that the bones were pushed to a new position by growth at their points of attachment (the sutures of the cranium and maxilla, the synchondroses of the cranial base, the condyle of the mandible). The determinant was genetic information that operated at those areas.

Suture Theory: Sites vs. Centers (cont.)

It is clear now that sutures and periosteal surfaces are not primary determinants of craniofacial growth and must be considered sites, but not centers, of growth. Growth at sutures does not push bones apart. Instead, when sutures are pulled apart, growth occurs to fill in the gaps.

Two lines of evidence lead to this conclusion. First, when sutures are transplanted to different locations, they fail to grow as centers would. Second, in both animal experiments and in humans with growth problems, it can be shown that sutures respond to outside influences. If the cranial or facial bones are pulled apart at the sutures, new bone will fill in and the bones end up bigger than they would have been otherwise. If the sutures are compressed, growth is inhibited. The sutures react rather than acting independently.

Why did Sicher, a highly intelligent and respected scientist, think as he did? At the time he proposed his theory (in the 1940s), the role of genetics in controlling growth was just becoming clearer, and it seemed obvious that direct genetic control was the explanation. The “sutural push” mechanism followed logically from that assumption.

Cartilage Theory

James H. Scott

The second major theory, popularized by the Irish anatomist James H. Scott in the 1950s, is that the determinant of craniofacial growth, even in areas distant from the cartilage locations, is the growth of cartilages. Cartilage growth would push the bones to new positions; in response, bone would fill in at sutures and surface remodeling would occur.

The fact that in many areas cartilage does the growing while bone merely replaces it makes this theory attractive.

Mandibular Growth

Scott accepted the evidence that sutures reacted rather than acted on their own, and so did not push bones apart by growing independently. He agreed with Sicher about “cartilage push” by the cartilages of the cranial base and the mandible as a major mechanism for cranial and facial growth, and he offered a clearer explanation of how growth at the mandibular condyle would control the growth of the mandible.

One way to visualize the mandible is by considering it as analgous to the diaphysis of a long bone, bent into a horseshoe and with the epiphyses removed. Then the condylar cartilage represents “half an epiphyseal plate” on each end of the bone. If this represents the true situation, then indeed the cartilage at the condyle should be a growth center, exactly analogous to epiphyseal cartilage except that there was bone only on one side.

Maxillary Growth

Growth of the maxilla, however, would be much harder to explain as determined by cartilage. How could cartilage determine maxillary growth when there is no endochondral replacement involved in the growth of this bone?

There is cartilage in the nasal septum, however, and in the 1950s Scott hypothesized that the cartilaginous nasal septum serves as a “pacemaker” for other aspects of maxillary growth.

This diagram from Scott’s work shows the septal cartilage (yellow) at a fetal stage. Note that it is located so that its growth could pull the maxilla downward and forward. If the sutures on the maxilla served as reactive areas, they would respond by forming new bone as they were pulled apart by the forces created by the growing cartilage. Although the amount of cartilage in the septum decreases as growth continues, enough remains even into adult life to make the pacemaker role potentially possible.

Experimental Support

Two types of experiments have been used to clarify whether specific cartilages are true growth centers: (1) transplanting it to see if it still grows and removing it to see whether that area then fails to grow, and (2) removing it surgically to see what the effect on growth would be.

If transplanted cartilage continues to grow, it must have innate growth potential and can be considered an independent growth center. If doesn’t grow in its new location, it probably doesn’t have innate growth potential and can’t be an independent growth center.

Similarly, if a cartilage is removed surgically and that area no longer grows, it may be a growth center (but damage from the surgery could be another explanation). But if the area grows just as well without the cartilage, it definitely wasn’t a growth center.

Experimental Support (cont.)

When cartilage from an epiphyseal plate is transplanted, it grows very nicely—so the epiphyseal plates meet the criteria for a growth center.

Cartilage from cranial base synchondroses is difficult to get at in order to transplant it, and transplantation experiments have not given a clear picture. This cartilage, like the cartilage of the epiphyseal plates, is a remnant of the original skeletal cartilage. It seems reasonable then to consider it a growth center, especially in light of what happens in patients with a genetic mutation that prevents its growth (discussed later).

Transplanting cartilage from the nasal septum gives equivocal results. Sometimes it grows reasonably well, sometimes it doesn’t.

When mandibular condyles are transplanted, they hardly grow at all.

Based on this evidence, we have to doubt that the mandibular condylar cartilage could possibly act as a growth center, and we would have some doubts about the nasal septum.

Surgical Removal of the Nasal Septum

Removing the presumed growth center for a craniofacial structure ought to seriously affect growth of that structure.

The impact of removing a segment of the cartilagenous nasal septum from a rabbit is shown here. The lower rabbit (image 2) had a piece of the septum removed at an early age, while his brother, shown above (image 1), did not.

Obviously, losing that little piece of cartilage cost a great deal of growth in the midface. It can be argued that the surgery itself, not the loss of the cartilage, caused the deficient growth, but removing the cartilage decreases growth so much that it looks to most observers as if growth potential was lost along with it.

Image 1, rabbit with the nasal septum in tact: Note the normal projection of the midface.	Image 2, rabbit after the nasal septum has been experimentally removed: Note the severely decreased distance from the eye to nose as a result of deficient growth.

Loss of Nasal Cartilage after Trauma

When this man sought treatment for his midface deficiency, we were intrigued to learn that following an accident at age 7, all of his nasal cartilage was removed. He certainly looks like a human analog of the experimental rabbit, doesn’t he?

Remember that the lack of growth in the area could be due to the original injury or the surgery rather than to the loss of the cartilage growth center, but in humans also there is decreased forward growth of the maxilla when the nasal cartilage is removed.

Is the nasal septum a growth center, and if so, does it determine maxillary growth? At least in part, perhaps it does.

Maxillary Growth and Achondroplasia

The maxilla is affected by cartilage growth in another way: because it is attached to the cranial base, the maxilla is pushed forward as lengthening of the cranial base occurs. Is this evidence of “cartilage push” from growth at the synchondroses? An interesting “experiment of nature” sheds some light on this.

This girl has moderately severe achondroplasia, a condition in which the primary growth cartilages fail to grow because of a genetic mutation. She has short arms and legs because of lack of growth at the epiphyseal plates. Note the midface deficiency. The maxilla has not been pushed forward because of lack of growth at the synchondroses of the cranial base, which are affected in the same way as the epiphyseal plates. It looks as if the cranial base lengthening is due to, or at least greatly affected by, a push from growth at the synchondroses.

That kind of push is important in midface development, and Scott cited it in support of the cartilage theory, but the push doesn’t open space at the sutures of the maxilla. Some kind of pull is necessary for that, and Scott’s theory was that growth of the septal cartilage pulled the maxilla forward and opened space at the sutures.

Mandibular Growth and Achondroplasia

Take a good look at the mandible in this achondroplasia patient. You can see that the midface wasn’t pushed forward by lack of growth at the synchondroses and the nose is small and underdeveloped—but the mandible seems to have grown almost normally.

What does that imply about the condyle as a growth center, with its growth determined by its internal genetic information? It doesn’t look as if the condyle was affected by the genetic mutation in the same way as the other cartilaginous growth centers.

Remember what you learned earlier about the origin of the cartilage of the mandibular condyles. It isn’t part of the chondocranium, the primary cartilage that is the origin of the cranial base. When does the cartilage that becomes the condylar cartilage first appear? That’s right, weeks after the primary cartilage. Where does it arise? Yes, in mesenchyme rather far away from the primary cartilage. So a mutation affecting primary cartilage might well not affect it.

Condylar Fracture

The effect of removing the mandibular condyle can be observed in inadvertent human experiments, because the condyle, cartilage and all, gets removed rather frequently in growing children through trauma. The neck of the condyle is a fragile area, and when the jaw is struck sharply on one side, the condylar process on the other side often fractures. Usually when this happens, the condyle fragment is retracted well away from its previous location by the pull of the lateral pterygoid muscle, and it resorbs over a period of time.

The condyle literally has been removed when this happens, and the cartilage is gone. If this occurred at an early age and the cartilage was an important growth center, severe growth impairment would occur. As recently as the 1960s, standard texts stated that early fracture of the mandibular condyle was a devastating injury because of the growth problems that would follow.

Condylar Fracture (cont.)

Two studies in Scandinavia in the 1960s disproved the idea that early condylar fracture always produced a growth problem. The studies showed that after fracture of the condylar process in children, there was about a 75% chance that the condyle would regenerate and the mandible would grow normally.

In experimental animals, the condyle resorbs after a fracture, but a new one regenerates directly from the periosteum at the fracture site, complete with a new layer of cartilage. Presumably the same thing happens in human children. The human observations of lost condyles lend no support to the idea that the condyle is a growth center. We’ll come back to the 25% of children with a later growth problem shortly.

Functional Matrix Theory

Melvin Moss

If neither bone nor cartilage is the determinant for skeletal growth, what does determine it? The “functional matrix” theory was offered as an alternative in the 1960s by Melvin Moss, a dentist-anatomist at Columbia University. It became the subject of much debate in orthodontics in the 1970s because its implications changed clinical practice.

In its simplest form, Moss’s theory says that growth in the cranium and face occurs as a response to functional needs and is mediated by the soft tissue adjacent to the skeletal units. In this conceptual view, the external soft tissues grow, and both bone and cartilage merely react.

Natural Experiments

Growth of the cranial vault illustrates this view of skeletal growth very well. There can be little question that under normal circumstances the brain case grows in direct response to the growth of the brain. The pressure exerted by the growing brain separates the bones at the sutures, and new bone passively fills in so that the brain case fits (and protects) the brain.

Two “experiments of nature” illustrate this very well. First, when the brain is very small or does not grow, the cranial vault also is very small, and the condition of microcephaly (small head) results. In this case, the size of the head is an accurate representation of the size of the brain.

Natural Experiments (cont.)

The second natural experiment is the condition called hydrocephaly. When reabsorption of cerebrospinal fluid is impeded, the fluid accumulates and intra-cranial pressure builds up. The increased pressure impedes development of the brain, so the hydrocephalic person may have a small brain and be mentally retarded, but it also leads to enormous growth of the cranial vault.

Uncontrolled hydrocephaly may result in a cranium the size of a basketball due to pressure separating the sutures where bone then fills in.

Another example is that an enlarged or small eye will cause a corresponding change in the size of the orbit by the same mechanism: pressure from within the orbital cavity shapes the bone around it.

No Cartilage Growth Centers?

Professor Moss theorized that the determinant of growth of the nasal and oral structures is similar to that of the cranial vault, and that they grow because of functional demands from the nasal and oral cavities.

The theory does not make it clear how functional needs are transmitted to the tissues of the mouth and nose, but it does say that the cartilages of the cranial base, nasal septum and mandibular condyles are unimportant as determinants of growth and are not growth centers. To Moss, the cartilages of the cranium and face merely react to outside influences, just as sutures react. He argued strongly that the synchondroses of the cranial base respond to the growth of the brain and behave like sutures, and that when the nasal cartilage is removed, any growth deficit is just due to the surgery.

The cartilage of the mandibular condyle was viewed in the same way, as reacting to growth of the mandible rather than controlling it. The functional matrix theory predicts that if proper function could be maintained, loss of the condylar cartilage in a child would have no effect on growth of the mandible.

Loss of Condylar Cartilage

We have already seen that in 75% of the children who suffer a condylar fracture, there is no problem with subsequent mandibular growth. What about the other 25%? Could some interference with function be the cause of their growth problem?

The answer is yes. It has been known for many years that mandibular growth is greatly impeded by ankylosis of the mandible. Ankylosis of a joint is defined as fusion across it (by scar tissue in most cases) so that motion is prevented or extremely limited. Don’t confuse this with what happens with an ankylosed tooth. The tooth is fused to the alveolar bone and can’t move at all; the ankylosed joint can’t move normally but often does have some degree of motion.

This boy’s pediatrician noticed that his facial asymmetry appeared to be increasing and referred him for further evaluation. From the history and routine x-ray examination it did not appear that there was anything unusual about the left mandibular condyle.

Image 1, ¾ view: Note the mandibular asymmetry.	Image 2, frontal view: Note the mandibular asymmetry.
Image 3, smiling view: Note the mandibular asymmetry.	Image 4, profile view: Note the mandibular deficiency.

Loss of Condylar Cartilage: Radiographic View

When special laminagraphic x-rays were made, an old fracture of the left condylar neck was observed. In this instance, the condyle was not retracted by the muscles, but instead was bent over and partially locked in the joint area. Although the boy could open his mouth, translation of the condyle down to articular eminence was limited and the affected side did not grow normally.

Loss of Condylar Cartilage: Surgical Repair

In this case the damaged condyle was removed surgically, and a section of rib taken at the costo-chondral junction (image 1) was used as a graft to replace it. It can be seen wired in place in image 2.

The piece of rib was chosen because when it was grafted in place, there would be cartilage covering the joint between the graft and the tempormandibular fossa. Why the cartilage on the new “condylar process”? Not because it would be necessary for future growth, but because if raw bone were placed into the joint, the bone of the graft probably would unite with the bone of the fossa, producing an even worse ankylosis. Some material to separate the bony areas is needed. The surgeon could have used a sheet of Teflon or other inert material, but Mother Nature uses cartilage, and in this case the surgeon did too.

Image 1, costo-chondral graft: Material from the rib is used because is includes cartilage to prevent bony union with the temporal bone, not because cartilage is necessary for growth.	Image 2, intra-operative view of costo-chondral graft: An extra-oral approach is necessary to graft bone from the rib to the ramus.

Loss of Condylar Cartilage: Post-Repair Growth

The facial asymmetry was greatly improved, and the mandibular ramus continued to grow after the damaged condyle had been removed and replaced with the rib graft. In the profile view (image 4) you can detect the scar from the extra-oral surgical approach, but already it’s hardly visible.

Both the growth deficit when motion was limited following the fracture, and the excellent growth after the ankylosis was released by removing the condyle, support the functional matrix view that the soft tissue environment, not the cartilage of the condyle, is the determinant of mandibular growth.

Image 1, ¾ view: Note the improved symmetry.	Image 2, frontal view: Note the improved symmetry.
Image 3, smiling view: Note the improved symmetry.	Image 4, profile view: Note the scar from the surgical approach and improved a-p mandibular growth.

”Functional Matrix”

The term “functional matrix” can be misunderstood easily, because in order to grow normally, the mandible really doesn’t have to be doing anything except opening a reasonable amount.

Remember that when opening, the mandible first rotates in a hinge motion and then translates down the articular eminence. In order to grow normally, it’s not enough to be able to open just on a hinge. The condyle has to be able to translate. Scarring of the capsule around the condyle can impede translation, and it’s the extent of the soft tissue injury that accompanies a condylar fracture, not the extent of injury to the bone, that determines how well it will grow later.

Why did normal growth occur after a condylar fracture in 75% of the children, and growth problems develop in 25%? In the fortunate 75%, the soft tissues around the TM joint were uninjured or minimally injured, and no scarring to restrict translation occurred. The unfortunate 25% had more extensive soft tissue injury and subsequent scarring.

”Functional Matrix” (cont.)

So what was the functional matrix that controlled mandibular growth? It was the soft tissues that surround the bone. What determines the growth of the soft tissues? At this point we have to say that it’s largely genetically determined.

This leads to another term that you must understand: epigenetic, which means genetic control at a distance. The bone of the mandible (and the condylar cartilage) reacts to the soft tissue growth around it, and the ultimate determinant appears to be the genetically-controlled soft tissue itself.

But the soft tissues can be affected by environmental influences, trauma being an excellent example. We have seen how scarring of soft tissues can impede mandibular growth. What would happen to growth of the maxilla if the facial soft tissues over it were scarred by trauma, as in this boy injured in an automobile accident? You should be thinking that the maxilla would not grow downward and forward as it normally would because the growth of the soft tissue surrounding it would be affected.

Absence of Nasal Cartilage

As you think about the importance of soft tissue in craniofacial growth, keep in mind that like bone and cartilage not all soft tissues are created equal with regard to their ability to grow independently.

This girl was born with cebocephaly, characterized by total absence of all the nasal structures and the areas of the brain to which they project. Almost all such children die at birth, but this one survived for several years and it was possible to study her facial growth.

With the absence of the nasal structures, including the cartilage, there was an obvious severe deficiency in midface growth, more severe than just the absence of the nose.

This is another experiment of nature that suggests a role for the nasal cartilage in determining maxillary growth.

Achondroplasia

Look again at achondroplasia. In this condition that we considered previously, the primary growth cartilages (those formed first in embryonic life) do not grow normally. Such individuals are characterized by extremely short arms and legs, as you would expect—and also by severe midface deficiency.

This occurs because the cranial base does not lengthen as it should (although growth of the brain is normal) and so the maxilla is not pushed forward. This is, of course, evidence that the cartilage of the cranial base is an important determinant of growth in that area. In achondroplasia, however, the mandible is not affected at all—note its normal size. The nose is small, but it’s hard to tell whether the midface deficiency also relates to diminished activity of the nasal septal cartilage.

Summary

Growth of the Cranial Vault

Let’s summarize. What determines growth of the cranial and facial units? Consider first the cranial vault, in the context of our descriptive terms:

Sites of growth: primarily sutures, some remodeling of surfaces

Centers of growth: none

Mode: intramembraneous ossification

Mechanism: separation of sutures → growth to fill in the gaps

Determinant: growth of brain → pressure to separate the sutures

Growth of the Cranial Vault (cont.)

What’s the best evidence? The experiments of nature with decreased growth of the brain (microcephaly) and increased intracranial pressure (hydrocephaly).

Image 1, the cranial vault and brain within: When the brain fails to grow, so does the cranial vault, and microcephaly results.	Image 2, skull of a person with hydrocephaly: As intra-cranial pressure builds, the cranial vault reacts by growing larger.

Growth of the Cranial Base

For the cranial base:

Sites of growth: primarily synchondroses, some apposition at sutures and remodeling of surfaces away from the midline

Centers of growth: synchondroses

Mode: primarily endochondral ossification

Mechanism: interstitial growth of cartilage → pressure to separate the bones

Determinant: expression of genetic information at the synchondroses

Growth of the Cranial Base (cont.)

What’s the best evidence? The natural experiment of achondroplasia, in which failure of growth at the synchondroses occurs, as it also does at the epiphyseal plates of the long bones.

Growth of the Naso-Maxillary Complex

For the naso-maxillary complex:

Sites of growth: primarily sutures and cartilage of nasal septum, but major remodeling of surfaces and apposition of bone at tuberosity

Centers of growth: cartilage of nasal septum (?)

Mode: primarily intramembraneous ossification

Mechanism: push from behind by lengthening of cranial base pull from in front → separation of sutures

Determinant: push: growth at synchondroses pull: facial soft tissues (epigenetic) growth of nasal cartilage (internal genetic control?)

Growth of the Naso-Maxillary Complex (cont.)

What’s the best evidence for mechanism and determinant?

push: maxillary deficiency in achondroplasia, because the maxilla isn’t pushed forward by growth at the synchondroses

pull: mid-face deficiency after loss or absence of nasal cartilage (?) maxillary deficiency after facial trauma and soft tissue scarring

Image 1, a girl with achondroplasia: Her midface deficiency is the result of inadequate growth at the synchondroses of the cranial base.	Image 2, a boy with an injury to the soft tissue of the midface: As a result of impeded soft tissue growth, the maxilla has not grown down and forward.

Growth of the Mandible

For the mandible:

Sites of growth: surfaces of bone, especially remodeling of ramus; condylar cartilage

Centers of growth: none

Mode: primarily intramembraneous ossification; endochondral ossification at condyle

Mechanism: soft tissue pull → reactive growth at condyle and surfaces

Determinant: epigenetic at soft tissues

Growth of the Mandible (cont.)

What’s the best evidence for mechanism and determinant?

Growth (or growth distortion) after condylar fracture. Remember, 75% of children who had a condylar fracture grew normally afterward, while 25% had a growth problem—because of more severe soft tissue injury near the condyle.

Image 1, ¾ view: Note the mandibular asymmetry.	Image 2, frontal view: Note the mandibular asymmetry.
Image 3, smiling view: Note the mandibular asymmetry.	Image 4, profile view: Note the mandibular deficiency.
Image 5, radiographic view of fractured condyle: The condyle remained in the joint area and inhibited movement.

Theories of Craniofacial Growth

Sometimes students think learning about theories is a waste of time. It’s hard to realize that even the questions one asks are based on some level of theoretical understanding. For many years nobody tried to modify facial growth—because they “knew” that the sites of growth were genetically controlled and therefore growth could not be modified. The new understanding of how and why jaws grow has led quite directly to clinical advances in treating growth problems.

You should not be surprised, either, if current understanding proves to be inadequate long before you finish a clinical career. You’ll have to understand the theories of the early 21st century to keep up with early 21st century practice. But to follow the further development of concepts, you have to know something of the background—so what you have learned at this point will stand you in good stead even if new theories are developed.

Now, be sure that you have read pages 40-50 in the 5th ed or 47-58 in the 4th ed of Contemporary Orthodontics, then take the self-test in the following section to consolidate what you have learned and to be sure that you have understood the material.

Self-Test

Question 1

Which of the following is not the focus of a major theory of craniofacial growth?

1. nervous system ✓
2. bone
3. cartilage
4. soft tissue matrix

Correct

That is correct. There have been no serious efforts to explain craniofacial growth as determined by the nervous system, but major theories have been build around bone as the primary determinant of its own growth, cartilage as the primary determinant with bone as a follower, and the soft tissue matrix as the primary determinant with cartilage and bone as secondary followers.

Incorrect

That’s wrong. There have been no serious efforts to explain craniofacial growth as determined by the nervous system, but major theories have been built around bone as the primary determinant of its own growth, cartilage as the primary determinant with bone as a follower, and the soft tissue matrix as the primary determinant with cartilage and bone as secondary followers.

Question 2

Which of the following can be considered evidence that the sutures between craniofacial bones are sites but not centers of growth?

1. failure of suture growth on transplantation
2. increased growth when sutures are mechanically pulled apart
3. decreased growth when sutures are mechanically compressed.
4. 1 only
5. 1 and 2
6. 1, 2 and 3 ✓
7. none of the above

Correct

That’s right, all three are correct. Both the failure of sutures to grow when they are transplanted and their response to outside influences suggest that sutures react to other influences and are not the primary determinant of their own growth.

Incorrect

No, that’s wrong. All three are correct. Both the failure of sutures to grow when they are transplanted and their response to outside influences suggest that sutures react to other influences and are not the primary determinant of their own growth.

Question 3

(A) The epiphyseal plates of long bones and the synchondroses of the cranial base can be considered centers of growth because (B) these areas are capable of growing independently of local environment influences.

1. A true, B true, A and B related ✓
2. A true, B true, A and B not related
3. A true, B false
4. A false, B true
5. A and B false

Correct

That’s right. The epiphyseal plates certainly, and the synchondroses almost certainly, can grow independently. That’s the definition of a growth center. The independence of growth distinguishes a growth center from a growth site.

Incorrect

No, that’s wrong. The statements are both true and are related. The epiphyseal plates certainly, and the synchondroses almost certainly, can grow independently. That’s the definition of a growth center. The independence of growth distinguishes a growth center from a growth site.

Question 4

Cartilage whose growth could potentially pull the maxilla away from the cranium and cranial base, putting tension on sutures, is found in the:

1. maxillary tuberosity
2. synchondroses of the cranial base
3. mandibular condyle
4. nasal septum ✓
5. all of the above

Correct

That’s right. The cartilage of the nasal septum is located so that its growth could pull the maxilla forward, separating the sutures and leading to growth at those sites.

Incorrect

No, that’s wrong. The cartilage of the nasal septum is located so that its growth could pull the maxilla forward, separating the sutures and leading to growth at those sites. There is no cartilage in the tuberosity. Cartilage growth in the cranial base pushes the maxilla forward but doesn’t put tension on the sutures, and growth of the mandible by any mechanism has little effect on the maxilla because they’re so loosely connected.

Question 5

What happens when the cartilage of the nasal septum is surgically removed at an early age?

1. the prominence of the midface is greatly reduced ✓
2. the prominence of the midface is slightly reduced
3. there is essentially no effect on the prominence of the midface
4. the midface isn’t affected but mandibular growth is stimulated

Correct

That’s right, surgical removal of the septum at an early age greatly reduces the prominence of the midface. That isn’t controversial, but why it happens is. Proponents of the cartilage theory say it’s just what you’d expect if a growth center were removed. Functional matrix proponents say it’s just the effect of the surgery and collapse of structures afterward, and the loss of the cartilage wasn’t what made the difference. It’s hard to be absolutely certain, but the septal cartilage seems to behave as if it had at least some characteristics of a growth center.

Incorrect

No, that’s incorrect. Surgical removal of the septum at an early age greatly reduces the prominence of the midface. That isn’t controversial, but why it happens is. Proponents of the cartilage theory say it’s just what you’d expect if a growth center were removed. Functional matrix proponents say it’s just the effect of the surgery and collapse of structures afterward, and the loss of the cartilage wasn’t what made the difference. It’s hard to be absolutely certain, but the septal cartilage seems to behave as if it had at least some characteristics of a growth center.

Question 6

What happens when the mandibular condyle is transplanted to a different location?

1. grows exuberantly, more than normal
2. grows normally
3. grows noticeably but perhaps less than normal
4. grows poorly, almost not at all ✓

Correct

That’s correct, condylar cartilage grows very poorly when transplanted, almost not at all. This is evidence that it is different from the primary growth cartilages and lacks the potential to grow independently.

Incorrect

That’s wrong. Condylar cartilage grows very poorly when transplanted, almost not at all. This is evidence that it is different from the primary growth cartilages and lacks the potential to grow.

Question 7

(A) Fracture of the condylar process of the mandible in a growing child is a devastating injury because (B) the fractured condyle is displaced, resorbs and is lost.

1. A true, B true, A and B related
2. A true, B true, A and B not related
3. A true, B false
4. A false, B true ✓
5. A and B false

Correct

That’s right, the first statement is false even thought the second is true. Early condylar fracture usually does not lead to long term growth problems. The fractured condyle is displaced, resorbs and is lost, but a new condylar process (complete with a cartilage cap) usually regenerates and often normal growth occurs.

Incorrect

No, that’s wrong. The first statement is false even though the second is true. Early condylar fracture usually does not lead to long term growth problems. The fractured condyle is displaced, resorbs and is lost, but a new condylar process (complete with a cartilage cap) usually regenerates and often normal growth occurs.

Question 8

What is the chance in humans that essentially normal growth will be observed after the mandibular condyle, and its presumed growth center, are lost?

1. less than 15%
2. 15 – 40%
3. 40 – 75%
4. 65 – 85% ✓
5. greater than 85%

Correct

That’s right. The chance of essentially normal growth is about 75% after a condylar fracture that leads to resorption of the original condyle and regeneration of a new one. But keep in mind that although most of the children do well, about 1 in 4, at least of those who were diagnosed, has a growth problem long-term.

Incorrect

No, you’re wrong. The chance of essentially normal growth is about 75% after a condylar fracture that leads to resorption of the original condyle and regeneration of a new one. But keep in mind that although most of the children do well, about 1 in 4, at least of those who were diagnosed, has a growth problem long-term.

Question 9

What is the usual determinant of growth of the cranial vault (brain case)?

1. mechanical pressure from growth of the brain ✓
2. neurotrophic growth factors released by the growing brain
3. higher pressure in the cerebrospinal fluid as life stresses increase with age
4. cartilage proliferation at the synchondroses of the cranial base

Correct

That’s right, under normal conditions the size of the cranial vault reflects the size of the brain beneath it because mechanical pressure form the growing brain separates the sutures. Neurotrophic growth factors and cranial base growth have little or nothing to do with the bone growth in the cranial vault, and cerebrospinal fluid pressure doesn’t increase during normal growth (although if it does increase, as in hydrocephaly, brain growth is inhibited while the cranial vault expands).

Incorrect

No, that’s wrong. Under normal conditions the size of the cranial vault reflects the size of the brain beneath it because mechanical pressure from the growing brain separates the sutures. Neurotrophic growth factors and cranial base growth have little or nothing to do with the bone growth in the cranial vault, and cerebrospinal fluid pressure doesn’t increase under normal conditions (although if it does increase, as in hydrocephaly, brain growth is inhibited while the cranial vault expands).

Question 10

(A) Ankylosis of the mandible leads to growth failure because (B) displacement of the mandible away from the skull as its soft tissue matrix grows is the normal determinant of mandibular growth.

1. A true, B true, A and B related ✓
2. A true, B true, A and B not related
3. A true, B false
4. A false, B true
5. A and B false

Correct

That’s right, both statements are true and very much related. Ankylosis that prevents mandibular displacement impedes growth because the mandible has to be displaced from the skull in order to grow. That doesn’t mean there are no limits on the mandible’s growth, just that the limits are in the soft tissue, not in the bone itself.

Incorrect

That’s wrong! Both statements are true and very much related. Ankylosis that prevents mandibular displacement impedes growth because the mandible has to be displaced from the skull in order to grow. That doesn’t mean there are no limits on the mandible’s growth, just that the limits are in the soft tissue, not in the bone itself.

Question 11

Lengthening of the cranial base occurs primarily because of:

1. pressure created by the growing brain above it
2. cartilage growth at the synchondroses ✓
3. bony remodeling at the anterior and posterior sutures
4. forward displacement of the anterior cranial base due to jaw function

Correct

That’s right. The cranial base lengthens primarily as a result of growth at the synchondroses, which seems rather independent of the growth of the brain above it (though some influence cannot be totally ruled out). Remodeling at the sutures and jaw function are not determinants of this growth.

Incorrect

No, that’s wrong. The cranial base lengthens primarily as a result of growth at the synchondroses, which seems rather independent of the growth of the brain above it (though some influence cannot be totally ruled out). Remodeling at the sutures and jaw function are not determinants of this growth.

Question 12

The maxilla grows forward because it is:

1. wedged forward by growth at the sutures
2. pulled from in front by the soft tissues and nasal septum
3. pushed from behind by the lengthening cranial base
4. 1 only
5. 2 only
6. 3 only
7. 1 and 2
8. 2 and 3 ✓

Correct

That’s right, the maxilla grows forward for two reasons. It’s both pushed forward by the cranial base, and pulled forward by the soft tissue matrix in which it’s embedded. But growth at the sutures is a reaction to the pull of the soft tissues, not a reason for the growth.

Incorrect

No, that’s wrong. The maxilla grows forward for two reasons. It’s both pushed forward by the cranial base, and pulled forward by the soft tissue matrix in which it’s embedded. But growth at the sutures is a reaction to the pull of the soft tissues, not a reason for the growth.

Question 13

The mandible grows forward because it is:

1. pushed forward by growth at the condyles
2. pulled forward by growth of the soft tissues in which it is embedded
3. pushed from behind by the lengthening cranial base
4. 1 only
5. 2 only ✓
6. 3 only
7. 1 and 2
8. 2 and 3
9. all the above

Correct

That’s right. The mandible grows because it is pulled forward by the soft tissue matrix. Condylar growth is reactive, and the cranial base growth is largely irrelevant to forward movement of the mandible.

Incorrect

That’s wrong. The mandible grows because it is pulled forward by the soft tissue matrix. Condylar growth is reactive, and the cranial base growth is largely irrelevant to forward movement of the mandible.

Question 14

How does the body of the mandible become longer during growth?

1. cartilage growth and endochondral ossification at the anterior growth center
2. remodeling of the ramus
3. addition of bone at the chin
4. 1 only
5. 2 only ✓
6. 1 and 2
7. 2 and 3
8. 1 and 3
9. all the above

Correct

That’s correct. The body of the mandible gets longer as the ramus is remodeled, with bone added to the posterior surface and removed from the anterior surface. The remodeling is part of the response to growth of the soft tissue matrix around the mandible.

Incorrect

No, that’s wrong. The body of the mandible gets longer as the ramus is remodeled, with bone added to the posterior surface and removed from the anterior surface. There is no growth center in the mandibular body, and there’s little or no addition of bone at the chin. The remodeling is part of the response to growth of the soft tissue matrix around the mandible.