Frontal Bone A vertical portion, which corresponds to the forehead, and an horizontal portion which is part of the skull base, forming the roofs of the orbital and nasal cavities. Parietal Bone The two parietal bones form the sides and roof of the cranium. Occipital Bone The occipital bone forms the postero-lateral and posterior part of the cranial vault, more than the floor of the posterior skull base.
It contains a central large oval opening, the foramen magnum. Temporal Bone The temporal bone has a petrous portion part of the skull base , a lateral squama forming the lateral cranial vault and a mastoid portion. Sphenoid Bone Unpaired bone, of which the two lateral greater wings contribute to the formation of the anterior lateral cranial vault. The most typical mechanism of cranial vault fractures are high velocity impact traumas. Cranial vault fractures are the result of a force that causes the skull to bend inward.
The primary consideration in depressed closed or open skull fractures is the involvement of the brain and the meninges. The involvement of the meninges can lead to CSF leaks. If associated with frontal sinus fractures, typically a rhinorrhea is present. Cranial vault fractures can also cause entrance of air into the intracranial cavity pneumocephalus. These conditions may require emergency surgery.
The clinician should examine for contracoup lesions for example frontal trauma with a occipital contralateral lesion as they frequently occur with skull fractures.
Although frontal bone fractures can be seen on plane x-rays, the gold standard for the radiographic detection of skull fractures is computer tomography CT. Calvarium Calvaria Skull vault Skullcap.
URL of Article. On this page:. Journal of Korean Neurosurgical Society. Frederic N. Silverman, Jerald P. Caffey's pediatric X-ray diagnosis. ISBN: Related articles: Anatomy: Head and neck.
Promoted articles advertising. Skull and facial bones illustrations Skull and facial bones illustrations. Loading more images Close Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Loading Stack - 0 images remaining. By System:. Patient Cases. This is an important aspect of our model, which may model suture formation. Change of region of high concentration of osteoblast over time. The regions originally marked by the differentiation of osteoblasts expand from the primary centers of ossification over time.
Because these osteoblasts differentiate into osteocytes and eventually become trapped within mineralized bone, it can be said to show pattern of bone growth. The results agree well with experimental observation showing two frontal bones, two parietal bones, and one interparietal bone. Sutures form between bones as bones grow according to repulsive effect between bones in our model.
The number and locations of ossification centers found in the simulation results Figure 10 agree well with experimental data showing five ossification centers representing the two frontal, the two parietal, and the single interparietal bones of the cranial vault Figures 2 and 7 B. The results of simulation of bone growth Figure 11 show that the region of osteoblasts expands from the ossification centers. Our bone growth model explains this process as differentiation of adjacent undifferentiated mesenchymal cells near primary centers of ossification into osteoblasts by the action of a morphogen that is expressed from pre-existing osteoblasts and diffused in space with time.
This is in agreement with previous research that demonstrates that the cells that add to the primary ossification centers by differentiating into osteoblasts come from the condensations rather than being recruited from other mesenchymal populations surrounding the brain Yoshida et al. Once differentiated, osteoblasts function to produce osteoid along collagen bundles and then mineralize that matrix eventually becoming trapped within mineralized lacunae and differentiating into osteocytes.
Here, we have not modeled the entrapment of osteocytes into a mineralized matrix, but the expansion of regions of high concentration of osteoblasts is considered as bone growth. Results shown at E The simulation result shows smaller volume of bones compared to experimental data Figure 2 , which means a slower growth rate. In addition, the relative size and shapes of the individual bones are somewhat different from experimental observations. These differences can be overcome by subtle adjustment of model parameters and, importantly, the adjustments may add to our knowledge of the processes involved in the formation of ossification centers and their growth.
The effects of different model parameters on the simulation are presented in Supplementary Material. Our hypothesis that morphogens from one bone element inhibits the growth of contiguous bones [equation 6 ], may not be true, but can be tested experimentally.
That our results show suture formation similar to what is observed experimentally suggests that suture formation involves some kind of mechanism of repulsive factors between bones, and this does not counter a hypothesis of boundary formation between cellular compartments that serve as signaling interfaces as suggested by others Merrill et al.
Here, we suggest that the factors driving the formation of sutures may include chemical substances or mechanical stimuli by the growing brain or by opposing bones as the gaps between them narrow.
Since the processes that control normal suture development and the mechanisms underlying abnormal premature suture closure are not well understood, further research into the effects of mechanical stress on bone growth is warranted.
Although the simulation captures many features of the developmental process, it has some limitations as well.
Key molecules play important roles in cell differentiation and their identity, as well as the real values of these parameters remain to be determined. We expect this to be achieved in a follow-up study that will elucidate the cellular-level changes that occur in cranial development providing the basis for joining molecular cues and cell behavior with 3D shape changes that occur during ontogeny.
The number of cells in initial ossification centers, rate of OLC differentiation and proliferation, intracranial pressure gradients from growth induced skull-soft tissue interaction, and rate of suture closure can be parameterized and modified in the model. The results can be continually quantitatively compared to our extensive image archive of developing cranial soft and hard tissues.
In this study, the computational domain is fixed in both size and shape while in biological systems the surface on which bone development occurs expands and changes shape as the underlying brain grows. Indeed, the size and shape of the domain does affect the number and location of ossification centers because diffusion is strongly related with geometry of the domain.
This would offer a more realistic model, but we realize that our diffusional parameters will need to change over time as well. Some parts of our model are based on the experimental observation rather than clear mechanical mechanisms of how sutures form, why ossification does not occur at the top of the domain and how subtle, complicated shape of each bone forms.
We expect that mechanical stimuli such as pressure and stress may affect these phenomena and they will be a focus of a future study. In a forthcoming study, our proposed framework will be improved by including effects of brain growth and mechanical stimuli e. Growth of the cranial vault is coordinated through tissue—tissue interactions between the brain, the developing meninges, the bone primordia, and the cranial sutures Han et al. Here, the processes associated with formation of primary centers of ossification and bone growth were mathematically modeled and solved using the finite volume method.
The results show that five primary ossification centers form at positions like those identified in experimental data Figure Our results reveal bone growing from the primary ossification centers forming sutures between bones Figure Our study shows that the development of the cranial vault can be numerically simulated using the established computational framework.
We expect that changes in model parameters, when examined in parallel with laboratory experimentation, will help clarify some of the key players and mechanisms of skull development, both normal and pathological. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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