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Cranial growth centers: The foramen cecum i s located in the midline of the terminal sulcus. Development of cartilage and bones of the facial skeleton. The filtration rate of the glomeruli of the. These cells originate from somitomeres and the most cranial somites. Starvation alters the composition of the body. It is thought that the growth hormone, although not essential for fetal growth, is essential to growth from birth onward.
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Orthodontic centers of america 0. E line invisible orthodontics. Math Music Textbook clip art. Paper Sheets. Lord clip art. Vector Brochure Template with Love Heart. The following describes the derivatives of each component of the pharyngeal arches. This information is summarized in Table Nerve Components A specific cranial nerve grows from the brain and invades each arch Figure All structures, including muscles, dermis, and mucosa, arising from that arch are innervated by the associated cranial nerve.
Arch I: The trigeminal nerve cranial nerve V is the nerve for the first arch. The trigeminal nerve is the main sensory nerve of the head and neck, and it innervates the face, teeth, and mucosa of the oral cavity and anterior two thirds of the tongue. It also innervates the muscles of mastication. The mandibular division V1 grows into the main portion of arch 1, which is the mandibular process. The maxillary division V2 supplies the maxillary process of arch I.
Arch The facial nerve cranial nerve VII is the second arch nerve. Arch III: The glossopharyngeal nerve cranial nerve IX is the nerve for arch Arches IV and VI: The vagus nerve cranial nerve X is the nerve for the fused fourth and sixth arches. The superior laryngeal branch of the vagus nerve innervates arch IV structures, and the recurrent laryngeal branch of the vagus supplies arch VI. Figure Lateral view of the embryo illustrating the cranial nerves to the pharyngeal arches.
A specific cranial nerve is associated with each arch and innervates structures such as cartilages and muscles arising from that arch. Cartilage Components Arch I, called the mandibular arch, is a major contributor to development of the face. This pair of arches has distinct maxillary and mandibular processes, or prominences Figure The processes form mainly from the migration of neural crest cells into the arches during the fourth week. Neural crest mesenchyme in the maxillary process undergoes intramembranous ossification to give rise to the zygomatic bone, the maxilla, and the squamous portion of the temporal bone.
The cartilage of the first arch is Meckel's cartilage see Figure and Figure The dorsal end of Meckel's cartilage becomes ossified to form two of the middle ear ossicles-the malleus and incus. The middle portion of Meckel's cartilage regresses, but its perichondrium forms the sphenomandibular ligament. The ventral part of Meckel's cartilage forms a. The mesenchymal tissue lateral to the cartilage undergoes intramembranous ossification to produce the mandible as the original Meckel's cartilage disappears.
The cartilage of arch II is known as Reichert's cartilage see Figure Its dorsal end becomes ossified to produce the other middle ear ossicle, the stapes, and the styloid process of the temporal bone see Figure A portion of the perichondrium of Reichert's cartilage forms the stylohyoid ligament. Pharyngeal arch II is called the hyoid arch because of its contribution to development of the hyoid bone, specifically, the lesser horn and the superior portion of the body.
The cartilage of the third arch gives rise to the greater horn and the inferior part of the body of the hyoid bone see Figure Figure Lateral view of the embryo illustrating the cartil age components of the pharyngeal arches. Meckel's cartilage is associated with arch I and Reichert's cartilage with arch II.
Figure Cartilaginous and skeletal derivatives of the pharyngeal arches. This schematic drawing summarizes the arch of origin of some head and neck structures. The cartilages of the fourth and sixth arches fuse to form the laryngeal cartilages, including the thyroid, cricoid, and arytenoid cartilages, but not the epiglottis see Figure Muscle Components Skeletal muscles of the head and neck are derived from cells that migrate into this region from somitomeres and the most cranial somites see Figure These muscles include the important muscles of mastication: Other muscular derivatives are the anterior belly of the digastric, mylohyoid, tensor veli palatini, and tensor tympani.
Arch II: The muscles of facial expression arise from the second arch. The facial muscles are characteristically thin, have their origin and insertion in the skin, and are found throughout the face and neck. Examples include the frontalis, orbicularis oris, orbicularis oculi, zygomaticus,. Nonfacial muscles from the second arch include the stapedius, stylohyoid muscle, and posterior belly of the digastric muscle. These muscles gives rise to the stylopharyngeus muscle. These muscles form the muscles of the pharynx and larynx.
Arch IV gives rise to the cricothyroid muscle, and arch VI produces the rest of the intrinsic muscles of the larynx. Arterial Components The pharyngeal arch arteries are called the aortic arches. The arteries from arches I and II are significantly smaller than those from the remaining arches.
Arch I contributes to part of the maxillary artery. Arch II gives rise to the hyoid and stapedial arteries. Arch III contributes to part of the carotid system. The left side of arch IV contributes to the arch of the aorta and the right side to the right subclavian artery. Arch VI is associated with the pulmonary arteries. Figure Skeletal muscle derivatives of the pharyngeal arches. This drawing summarizes some of the head and neck muscles and their pharyngeal arch of origin.
Figure Derivatives of pharyngeal pouches, grooves, and membranes shown in anteroposterior longitudinal section. Note that pouch 5 and all grooves and membranes except the first regress.
Derivatives of Pharyngeal Pouches Pharyngeal pouches represent extensions of the developing pharynx interposed between the inner surface of adjacent pairs of arches. The first pair of pouches is located between arches I and II Figure Pouch 1 gives rise to the tympanic cavity, the pharyngotympanic tube auditory or eustachian tube , and the mastoid antrum.
Pouch 2 endoderm forms the lining of the crypts of the palatine tonsils. The lymphoid tissue of the tonsils forms from mesenchyme surrounding the crypts rather than from pouch endoderm.
Pouch 3 has a dorsal part that gives rise to the infe-. The early parathyroid glands and thymus lose their connection with the pharynx and migrate into the neck. Pouch 4 also has dorsal and ventral portions. The dorsal part gives rise to the superior parathyroid glands, whereas the ventral part produces an ultimcbranchial body.
The ultimobranchial body fuses with the thyroid gland, and its cells become diffusely scattered throughout the thyroid and differentiate into parafollicular cells C cells , which produce calcitonin.
Pouch 5 typically regresses. Derivatives of Pharyngeal Grooves Clefts The external surface of the head and neck region of an embryo displays four pairs of pharyngeal grooves, or clefts, located between the arches see Figure Groove 1 is located between arches I and II, and it is the only groove to give rise to structures in the adult, namely the external auditory meatus. Mesenchymal tissue of arches 11 and III proliferates and covers the remaining grooves, forming a temporary, fluid-filled cavity called the cervical sinus.
Normally the cervical sinus and grooves 2 to 4 are obliterated during development of the neck. The cervical sinus rarely persists after birth.
It may have a pathologic connection with the pharynx, called a pharyngeal sinus, or to both the pharynx and the outside of the neck, called a pharyngeal fistula. Derivatives of Pharyngeal Membranes A pharyngeal membrane consists of endoderm lining a pharyngeal pouch, ectoderm lining a pharyngeal groove, and a layer of mesenchyme in between.
The first pharyngeal membrane forms the tympanic membrane, whereas the remaining membranes regress. Derivatives of pharyngeal pouches, grooves, and membranes are summarized in Box Development of the Face Development of the face occurs primarily between weeks 4 and 8, so that by the end of the eighth week the face has taken on a human appearance.
Facial development after week 8 occurs slowly and involves changes in facial proportions and relative positions of facial components.
The discussion of facial and palatal development in this chapter concentrates on weeks 4 through Facial development results mainly from enlargement and movement of the frontonasal prominence and four prominences from pharyngeal arch I, the. These structures surround the stomodeum. The maxillary and mandibular prominences develop as a result of neural crest cells migrating and proliferating into pharyngeal arch I.
One of the first events in formation of facial structures is fusion of the medial ends of the mandibular prominences in the midline to form the chin and lower lip. In the inferior and lateral portion of the frontonasal prominence, bilateral localized areas of surface ectoderm thicken to form nasal placodes Figure , A.
The mesenchyme along the periphery of the nasal placodes proliferates and forms horseshoeshaped ridges called the medial nasal prominences and lateral nasal prominences Figure , B. The center of the placode becomes thinner, eventually leading to loss of ectoderm and formation of nasal pits. The nasal pits are the precursors of the nostrils and nasal cavities. Mesenchymal connective tissue in the maxillary prominences proliferates.
The result is that the maxillary prominences become larger and move medially toward each other and toward the medial nasal prominences Figure , C.
The medial nasal prominences move toward each other, fuse in the midline, and form the intermaxillary segment Figure , D.
The intermaxillary segment is of special importance because it gives rise to the philtrum middle portion of the upper lip Figure , E , four incisor teeth, alveolar bone and gingiva surrounding them, and primary palate.
A number of facial prominences fuse between weeks 7 and The maxillary prominences fuse laterally with the mandibular prominences. The medial nasal prominences fuse with the maxillary prominences and lateral nasal prominences see Figure , C. The nasolacrimal ducts originally called the nasolacrimal grooves are bilateral epithelial structures that form at the line of fusion between lateral nasal.
Figure Development of the face. Thickening of surface ectoderm forms the nasal placodes. B, Approximately 6 weeks. Proliferation of mesenchyme forms the medial and lateral nasal prominences. The nasal pits develop in the center of the nasal placodes. C, Approximately 7 weeks.
The maxillary prominences enlarge and push the medial nasal prominences toward each other. Fusion between the maxillary prominences and the medial nasal prominences occurs.
The nasolacrimal groove develops at the line of fusion between the lateral nasal prominences and the maxillary prominences. D, Intermaxillary segment occlusal view. The medial nasal prominences move toward each other, fuse in the midline, and form the intermaxillary segment. The intermaxillary segment is the origin of the philtrum of the upper lip, the four maxillary incisor teeth with their surrounding alveolar process, and the primary palate. E, Approximately 10 weeks.
The entire upper lip is derived from the fused medial nasal prominences and maxilla ry prominences. The midline of the nose comes from the medial nasal prominence, whereas the ala of the nose is derived from the lateral nasal prominence. Each nasolacrimal duct eventually connects the lacrimal sac to the nasal cavity.
It should be noted that fusion, or merging, of prominences involves first a breakdown of the surface epithelium at the area of contact. This allows the underlying mesenchymal cells in the two prominences to mingle with one another. Development of the Palate The palate begins to develop early in week 6, but the process is not completed until week The most critical period during palatal development is the end of the sixth week to the beginning of the ninth week.
The primary palate is the triangular-shaped part of the palate anterior to the incisive foramen. The origin of the primary palate is the deep portion of the intermaxillary segment, which arises from the fusion of the two medial nasal prominences Figure , B.
The secondary palate gives rise to the hard and soft palate posterior to the incisive foramen. The secondary palate arises from paired lateral palatine shelves of the maxilla see Figure , B. These shelves are comprised initially of mesenchymal connective tissue and are oriented in a superior-inferior plane with the tongue interposed Figure , C. Later, the lateral palatine shelves become elongated and the tongue becomes relatively smaller and moves inferiorly.
This allows the shelves to become oriented horizontally, to. The median palatine raphe is a clinical remnant of fusion between the palatine shelves, and the incisive foramen is present at the junction of the primary palate and the lateral palatine shelves. The lateral palatine shelves also fuse with the primary palate and the nasal septum. Fusion between the nasal septum and palatine processes proceeds in an anteroposterior direction beginning in the ninth week.
Pathogenesis of Cleft Lip and Cleft Palate Cleft lip and palate occur when mesenchymal connective tissues from different embryologic structures fail to meet and merge with each other. The common form of cleft lip is a result of failure of fusion of the medial nasal process with the maxillary process.
Cleft lip may be unilateral or bilateral and may extend into the alveolar process see Chapter 2. Cleft palate is the result of failure of the lateral palatine shelves to fuse with each other, with the nasal septum, or with the primary palate. Cleft lip and cleft palate are distinct and separate congenital abnormalities, but they often occur concomitantly. Development of the Tongue The tongue develops from several different sources.
The mucosa of the body of the tongue or anterior two thirds of the tongue develops from the first pharyngeal arch, whereas the mucosa of the base of the tongue or posterior third develops from arch III. The skeletal muscle of the tongue develops from myoblasts that migrate into the tongue from occipital somites. Figure A, The postnatal primary and secondary palates occlusal view. The primary palate is the triangular por-.
The secondary palate gives rise to the hard and soft palates posterior to the incisive foramen. B, Development of the palate occlusal view. The primary palate develops from the deep portion of the intermaxillary segment. The secondary palate arises from paired lateral palatine shelves of the maxilla.
C, Development of the palate frontal view at 6 to 7 weeks. The lateral palatine shelves are initially oriented in a superior-inferior plane with the tongue interposed. D, Development of the palate frontal view at 7 to 8 weeks. Later the tongue moves inferiorly and the lateral palatine shelves elongate, become oriented horizontally, and fuse in the midline. E, Occlusal view of the palate after fusion of the primary palate with lateral palatine processes.
The incisive foramen is located at the junction of the primary and secondary palates. Fusion occurs progressively in the direction of the arrows.
Development of the tongue. A, Anteroposterior longitudinal section at approximately 5 weeks. The mucosa of the anterior two thirds of the tongue body develops from the first pharyngeal arch. Two lateral lingual swellings overgrow a midline structure called the tuberculum impar The mucosa of the posterior third base develops from the hypobranchial eminence, which is derived from the third pharyngeal arch.
The hypobranchial eminence overgrows the second arch and fuses with the lateral lingual swellings and tubercul um impar. The skeletal muscles of the tongue arise from myoblasts that migrate into the tongue from the occipital somites. B, Dorsal view at approximately 5 months. The terminal sulcus is the line of demarcation between the body and base of the tongue.
The foramen cecum i s located in the midline of the terminal sulcus. The innervation of the mucosa of the tongue can be explained by its embryologic development.
Cranial nerve V from the first arch innervates the body, and cranial nerve IX from the third arch innervates the base. The tongue begins its development near the end of the fourth week as a midline enlargement in the floor of the primitive pharynx cranial to the foramen cecum. The enlargement is called the tuberculum impar Figure , A. Two lateral lingual swellings form adjacent to the tuberculum impar. All three structures form as a result of proliferation of first arch mesenchyme.
The lateral lingual swellings rapidly enlarge, fuse with one another, and overgrow the tuberculum impar. These three structures give rise to the body of the tongue Figure , B. The posterior third, or base, of the tongue develops from the hypobranchial eminence, which is a midline swelling caudal to the foramen cecum see Figure , A.
The hypobranchial eminence is comprised primarily of mesenchyme from arch III. The copula is a midline enlargement derived from arch II. The hypobranchial eminence overgrows the copula and fuses with the tuberculum impar and lateral lingual swellings.
The copula disappears without contributing. Thus the base of the tongue is derived from the third pharyngeal arch. The line of demarcation between the body and base is called the terminal sulcus, and the foramen cecum is found in the midline of this structure see Figure , B. Sensory innervation to the mucosa of the body of the tongue is almost entirely from the nerve of the first arch, the trigeminal nerve cranial nerve V. Sensory innervation to the mucosa of the base of the tongue comes mainly from the nerve of the third arch, the glossopharyngeal nerve cranial nerve IX.
The skeletal muscles of the tongue bring their nerve supply with them in the form of the hypoglossal nerve cranial nerve XII. Development of the Thyroid Gland The thyroid gland begins its development as a thickening of endoderm in the midline of the floor of the. Figure A, Development of the thyroid gland.
A sagittal view at approximately 5 weeks. The thyroid gland develops close to the foramen cecum as an endodermal thickening and then as a pouch called the thyroid diverticulum.
The diverticulum migrates ventrally but remains connected with the developing tongue by the thyroglossal duct. B, Development of the thyroid gland sagittal view at approximately 6 weeks. The thyroid gland reaches its final location in the neck by about the seventh week. The thyroglossal duct degenerates, but the foramen cecum persists on the dorsal surface of the tongue. The endodermal thickening forms a pouch called the thyroid diverticulum, which migrates ventrally in the neck.
The thyroglossal duct connects the developing and migrating thyroid gland with the developing tongue.
By week 7 the thyroid gland has reached its final site in the neck Figure , B. The thymus, parathyroid glands, and ultimobranchial bodies also migrate to this region. The ultimobranchial bodies become an intrinsic part of the thyroid gland and give rise to parafollicular cells, which produce calcitonin. The thyroglossal duct degenerates, but its proximal opening persists on the dorsum of the tongue as the foramen cecum. Remnants of the thyroglossal duct may persist after birth and give rise to thyroglossal duct cysts, most commonly in the neck.
All or part of the developing thyroid may remain in the region of the foramen cecum, enlarge, differentiate, and produce a lingual thyroid. Development of the Skull The skull forms from mesenchymal connective tissue around the developing brain. The development of the skull is considered in two components. One is the development of the neurocranium, which is the calvaria and base of the skull.
It is derived mainly from occipital somites and somitomeres. The other is the development of the viscerocranium, which includes the skeleton of the face and associated structures.
Each component has some structures that form by endochondral ossification cartilaginous component and other structures that form by intramembranous ossification membranous component Figure , A and B. The cartilage junctions between two bones are called synchondroses. New cartilage cells continually form in the center of the synchondrosis, move peripherally, and then undergo endochondral ossification along the lateral margins.
The occipital bone is formed first, followed by the body of the sphenoid bone and then the ethmoid bone. Other structures formed by the chondrocranium include the vomer bone of the nasal septum and the petrous and mastoid parts of the temporal bone.
Sutures and fontanelles are present during fetal and early neonatal life. Sutures, also called syndesmoses, are fibrous joints comprised of sheets of dense connective tissue that separate the bones of the calvaria. The sutures help the calvaria to change shape during birth, a process called molding. Fontanelles are regions of dense connective tissue where sutures come together. Sutures and fontanelles ossify at variable times after birth.
Figure Development of the skull. A, A lateral view at approximately 12 weeks. The developing skull has two components. The neurocranium includes the calvaria and the base of the skull, and the viscerocranium includes the facial skeleton and associated structures. Each component has some structures that develop by endochondral ossification cartilaginous and others that develop by intramembranous ossification membranous component.
B, A lateral view at approximately 20 weeks. The viscerocranium, which includes the facial skeleton, arises from the pharyngeal arches. The earlier discussion in this chapter on cartilage components of the pharyngeal arches includes information about skeletal derivatives of the pharyngeal arches.
The cartilaginous viscerocranium includes the middle ear ossicles, the styloid process of the temporal bone, the hyoid bone, and the laryngeal cartilages. The membranous viscerocranium includes the maxilla, zygomatic bones, the squamous temporal bones, and the mandible. These bones form by intramembranous ossification except for the mandibular condyle and the midline of the chin. The squamous temporal bones later become part of the neurocranium. Sadler TW: Ten Cate AR ed: Oral histology: Thesleff 1: Homeobox genes and growth factors in regulation of craniofacial and tooth morphogenesis, Acta Odontol Scand Sandra A, Coons WJ: Avery JK: Development of cartilage and bones of the facial skeleton.
In Avery JK ed: Oral development and histology, ed 2, New York, , Thieme Medical. Figure A series of infants and children showing variability of clefting along lines of expected embryologic fusion between the median nasal and maxillary processes and between the right and left palatal shelves.
In addition to the cleft defect there is also a change in the orientation of the various arch segments. A, Infant with unilateral cleft of the li p and an intact dental alveolus and palate. The nose is symmetric compared with some of the subsequent examples. A small notch at the crest of the alveolar ridge is at the site of fusion of the right maxillary and median nasal processes.
B, Infant with an isolated cleft of the lip and palate. The anterior portions of the palate and dental alveolus are intact. Some deviation of the arch is evident in three dimensions. C and D, Infant with bilateral cleft of the lip and palate but with portions of the anterior palate intact. The arch has a relatively normal configuration.
Dental Defects in the Lines of Clefting Children with clefting of the dental alveolus frequently have various dental anomalies, but it is i mportant to realize that anomalies also occur along the lines of potential clefting i. Thus the lessons from facial development can be used to better understand dental development.
The suggested diagnostic approach adds perspective and awareness in anticipating patient needs. Anomalies in Number of Teeth The developmental process of tooth initiation is affected by the embryologic defect of clefting. The position of the lateral incisor is also unpredictable i.
Caution must be taken by the clinician in deciding on the fate of supernumerary teeth, particularly in cases with lateral incisors in both the premaxillary and maxillary segments. The decision may be to keep one or both teeth or to extract them. Tooth shape is also affected in the area of an alveolar cleft. Thus the morphodifferentiation of the tooth could be affected by this embryologic failure. The most common example is the peg-shaped, or malformed, maxillary lateral incisor.
As stated previously, the area of the maxillary lateral incisor could also be a site for developmental anomalies in children without clefts. The notion has been advanced that anomalies in the lateral incisor.
Figure , cont'd E, Infant with unilateral cleft of the lip and palate. In addition to the cleft, the arch is deviated in three dimensions, leaving the buccal segments in a rotated appearance. The nose is asymmetric as a result of the cleft. The nares-the site of fusion of the median nasal and maxillary processes-are affected by the cleft.
F, Infant with complete bilateral cleft of the lip and palate. In addition to the marked clefting, the buccal segments appear rotated, the premaxilla is rotated upward, and the nasal septum is deviated. The nose is distorted by the presence of the cleft. The orbicularis oris muscle and its movements are limited to respective segments and cannot function coherently. G, Incomplete formation and fusion of the horizontal shelves of the hard palate result in a submucous cleft.
The condition was detected onlywhen speech difficulties were assessed. Deficiency in the hard palate apparently led to inadequate muscle movement for speech.
The frequency of the occurrence of peg-shaped lateral incisors and other anomalies must be viewed in the context of the major embryologic events in the area. The cleft is larger beneath the mucosa than at the oral surface.
This tear drop shape of the defect may not allow the tooth to erupt in its normal position and emerge with its roots upright.
Therefore the embryologic defect has an effect on the eruptive phase of tooth development many years later. Moving the roots into. Therefore it is important to coordinate the timing of alveolar bone grafting of the cleft defect with orthodontic tooth movement. Figure illustrates radiographs of different clefts and root alignment without bone grafting and orthodontic treatment. Emergence of the permanent canine is often at risk in children with alveolar clefting because of its mesial inclination.
The canine crown is usually oriented mesially when the tooth begins its eruptive path i. Therefore before orthodontic alignment of the canine is initiated, it is important to plan and perform the bone grafting of the alveolar defect to ensure proper tooth eruption. Figure A series of radiographs from children with cleft lip and palate showing the vulnerability of teeth in their formation and eruption.
The shape of the cleft influences the orientation of the teeth. Eruption and enamel integrity are often compromised. Bone grafting can facilitate the eruption of teeth adjacent to a cleft.
Restoration by recontouring the tooth with dental composites can camouflage the tooth defects. A, Radiograph showing orientation of teeth to conform to the shape of the cleft. Such an orientation can divert the eruption path of the tooth in any of the three dimensions. Also note the defective enamel on the mesial surface of the lateral incisor adjacent to the cleft arrow.
It is also noteworthy that the lateral incisor is in the maxillary segment and not in the premaxillary segment. B, Radiograph showing a bilateral cleft of the dental alveolus and palate. Normal alignment of teeth would not be possible in this case without a bone graft. Attempts to align the teeth would result in the roots positioned into the cleft. C, Radiograph showing a bilateral cleft of the dental alveolus and palate. Lateral incisor teeth are missing and enamel is distorted.
D, Radiograph from a child with a unilateral cleft of the lip, dental alveolus, and palate. The erupti on path of the maxillary canine is medial to its normal course.
Defective enamel hypoplasia and opacities is common in the teeth adjacent to the cleft site. Enamel defects occur in persons with untreated clefts of the lip and alveolus but increase in frequency following surgical intervention. Because there is a higher occurrence of caries in teeth with enamel defects, the issue of prevention is of great importance in cleft children.
There are many lessons to be learned from nature's variability of expression. Some of these lessons help. For example, the formation of lateral incisors on either side of the cleft supports the migratory idea for tooth-forming cells.
Other lessons sharpen the dentist's observations such as the higher frequency of anomalies in the maxillary lateral incisor area. Although the time for cleft occurrence is in the first few weeks of life, its impact on the subsequent stages of facial and dental development continues for the life of the individual. The child with a cleft often faces considerable social challenges and deserves the most empathetic care from the dentist.
Figure A sample of malformations resulting from failure of embryologic components to fuse or to form. A, Infant with midline cleft. The cleft is at the site of the midline groove. Midline clefts are less common than clefts from failed fusion of the maxillary and median nasal process. Midline clefts are commonly associated with neurologic deficits as was the case with this infant. B, Child with a bilateral horizontal facial cleft. The cleft is along the line of expected fusion between the first branchial mandibular arch and the maxilla.
C, Child with agenesis of the premaxilla.
D, Child with unilateral cleft of the lip, palate, and lip pits. The presence of lip pits increases the chance of clefting in offspring. In all the cases discussed, the clinician can learn much from these children and adults who happen to have a variation from the average physical presentation.
Mishima K et al: Three-dimensional comparison between the palatal forms in complete unilateral cleft lip and palate with and without Hotz plate from cheiloplasty to palatoplasty, Cleft Palate Craniofac J 33 4: Mortier PB et al: Evaluation of the results of cleft lip and palate surgical treatment: Honda Y et al: Primary repair of the unilateral cleft lip nose: Enamark H et al: Lip and nose morphology in patients with unilateral cleft lip and palate from four Scandinavian centres, Scand j Plast Reconstr Hand Surg 27 1: Frequency of dental trait anomalies in cleft, sibling, and noncleft groups, J Dent Res 54 4: Mazaheri M et al: Evaluation of maxillary dental arch form in unilateral clefts of lip, alveolus, and palate from one month to four years, Cleft Palate Craniofac J 30 1: Ranta R: Dental anomalies in the deciduous and permanent dentitions of individuals with cleft lip and palate, J Dent Res Tsai T -Z et al: Distribution patterns of primary and permanent dentition in children with unilateral complete cleft lip and palate, Cleft Palate Craniofac 2: Anomalies associated with hypodontia of the permanent lateral incisor and second premolar, J Clin Pediatr Dent 17 2: Neville BW et al: Abnormalities of the teeth.
In Neville BW et al eds: Oral and maxillofacial pathology, Philadelphia, , WB Saunders. Tooth eruption in patients with cleft lip and palate, Acta Chir Plast Johnsen DC, Dixon M: Dental caries of primary incisors in children with cleft lip and palate, Cleft Palate Craniofac J 21 2: Pope AW: Points of risk and opportunity for parents of children with craniofacial conditions, Cleft Palate Craniofac J 36 1: Thomas PT et al: Satisfaction with appearance among subjects affected by a cleft, Cleft Palate Craniofac J 34 3: These are general guidelines and do not include the extremes of variation, which may occur in postnatal growth.
Growth Study Types Growth studies are of three basic types: Health professionals need to compare the rate or velocity of growth of a patient with standards for velocity at the patient's age. Standards for velocity can only be derived from a longitudinal study. Cross-Sectional Studies in cross-sectional studies a large number of individuals of different ages are examined on one occasion to develop information on growth attained at a particular age.
The method has the advantage of accumulating much information about growth at many ages in a short period of time. The majority of information about growth has been obtained using cross-sectional methods. Cross-sectional studies provide the best data for establishing national standards for growth and for comparing growth in different populations. A random or representative sample of boys and girls at each age is needed for construction of national standards.
The number of children measured at each age should be proportional to the rate of growth. In the first year, samples should be taken at three intervals, the second year at two intervals, and during adolescence at two intervals each year. Although a mean rate of growth for a population can be estimated from cross-sectional data, nothing.
Longitudinal Studies Longitudinal studies involve the examination of a group of children repeatedly over a long period during active growth. This method produces the most valuable data for the study of growth rates and the variability of individual growth.
However, the drawbacks of this kind of study include small sample size, difficulties in keeping subjects in the study, and long-term data collection.
Analysis of the data must follow the period of data collection. Mixed Longitudinal Studies Mixed longitudinal studies are a combination of the cross-sectional and longitudinal types.
Subjects at different age levels are seen longitudinally for shorter periods e. In a 6-year span, growth can be studied between birth and 6 years for one group, between 5 and 11 years for another group, between 10 and 16 years for another group, and between 15 and 21 years in another group so that growth from birth to 21 years can be studied in 6 years.
Figure Height curves for distance, A , and velocity, B , and weight curves for distance, C , and velocity, D , for English boys and girls. Arch Dis Child Graphic Interpretation of Growth Data Growth data are presented in a graphic format, which reveals the substance of growth study findings in an easily grasped illustration. The two basic curves of growth are as follows: The distance curve, or cumulative curve, indicates the distance a child has traversed along the growth path Figure , A and C.
The velocity curve or incremental curve indicates the rate of growth of a child over a period see Figure , B and D. Data are derived from longitudinal studies.
Assessment of Normal Growth Knowledge of normal human growth is essential to the recognition of abnormal or pathologic growth. Clinicians need norms or standards for height, weight,. Growth studies of a representative sample of a population provide the data from which standards are developed. For example, the growth of North American white people should be assessed by standards derived from a representative sample from this population. Normal height growth is commonly and arbitrarily referred to as the measurements that fall one standard deviation around the mean Figure Patients who fall outside the normal range are unusual, but not necessarily abnormal.
Standard deviations usefully describe data that fall into a normal distribution such as height and age at menarche. Data for body weight and skinfold thickness do not fall into a normal distributions Those. Normal distribution curve divided into percentiles and standard deviations.
Clinically normal measurements are arbitrarily defined as those falling in the interval between one standard deviation above and below the mean Height and weight data are usually represented in charts based on percentiles.
The normal range of one standard deviation about the mean for a normal distribution falls between the 16th and 84th percentiles see Figure Variation in Systemic Growth Richard Scammon6,7 reduced the growth curves of the tissues of the body to four basic curves. For each year, each curve has a certain percentage of its adult value.
He proposed four curves from top to bottom: The lymphoid curve includes the thymus, pharyngeal and tonsillar adenoids, lymph nodes, and intestinal lymphatic masses. The neural curve includes the brain, spinal cord, optic apparatus, and related bony parts of the skull, upper face, and vertebral column. The curve rises strongly during childhood. Growth in size is accompanied by growth in internal structure, enabling the 8-year-old child to function mentally at nearly the same level as an adult.
Figure Scammon's basic growth curves. Redrawn from Scammon RE: The measurement of the body in childhood.
In Harris JA et al [eds]: Figure Growth curves for height of boys and girls. The general curve includes external dimensions of the body, respiratory and digestive organs, kidneys, aorta and pulmonary trunks, spleen, musculature, skeleton, and blood volume.
This curve rises steadily from birth to 5 years of age and then reaches a plateau from 5 to 10 years, followed by another upsweep during adolescence and finally a slowdown in adulthood. The genital curve includes the primary sex apparatus and all secondary sex traits. The curve has a small upturn in the first year of life and then is quiescent until after 10 years of age, at which time growth of these tissues increases during the time of puberty.
Growth in Height When a chart showing height for age is constructed from data taken from a large number of children, a wide spread of measurements is seen for each age.
The curve shown is a distance curve. Curves of males and females differ and are used separately in clinical applications. A child who falls beyond the average measurements for his or her age is not necessarily abnormal. Parental heights are important factors in determining the potential for height growth because.
When the distance curves of boys and girls are compared, the girls' curve crosses the boys' curve at about 10 years of age, the beginning of the pubertal growth spurt, which occurs earlier in girls.
From 10 to 13 years of age the girls are, on average, taller than the boys. At age 14 the boys overtake the girls in height see Figure , A.
This is known as the adolescent spurt, the prepubertal acceleration, or the circumpubertal acceleration. The earlier onset of the spurt in females is illustrated in Figure , B.
During the spurt boys grow about 8 inches in height, whereas girls grow about 6 inches. In girls, menarche always follows the peak velocity of the adolescent spurt in height.
One reason the females are shorter on average than males is that they grow for a shorter period of time than males during postnatal growth. When longitudinal measurements taken from several children are combined on the same velocity graph and averaged, the adolescent spurt is smoothed out and less dramatic. This happens because the spurt occurs at different ages in the children. When the peak velocity for each child is superimposed on the peak velocities of other children, the spectacular nature of the spurt and the variability in spurt onset, magnitude, duration, and cessation can be usefully described.
Although growth in height stops at about 18 years in females and 20 years in males, there is evidence that height may slightly increase up to 30 years of age because of growth of the vertebral column. Loss of height begins at middle age and is caused by degeneration of intervertebral disks and to thinning of joint cartilages in the lower limbs.
On the basis of longitudinal data, it is possible to obtain a reasonably accurate prediction of adult height. Figure Growth curves for weight of boys and girls. From age 3 years to the adolescent spurt, the predictions are most reliable. In comparison to height, there is much more variation in weight measurements Figure However, with weight, every tissue in the body is involved.
The distance curves for height and weight illustrate this difference see Figures and Weight at birth is more variable than length. At birth, full-term females are on the average about 5 oz lighter than full-term males.
Small mothers have small babies. Later children in a family are usually heavier than the first born. Weight gain is rapid during the first 2 years of postnatal growth.
This is followed by a. At ages 11 to 13 years of age, girls are, on average, heavier than boys. Following their adolescent spurt, boys become heavier see Figure , C. The average age for the adolescent weight spurt in girls is 12 years and in boys is 14 years. The spurt is of less magnitude in girls compared with boys see Figure , D.
The adolescent first becomes taller and then begins to fill out in weight. Similarly, body weight does not reach its adult value until after adult height has been attained. I ndices of Maturity Several methods are used to assess the level of maturity attained by a child during postnatal growth.
The dental age maturity indicator based on tooth crown and root calcification has an advantage over the maturity indicator based on eruption age because it is useful throughout the development of the teeth, not just during the narrow period covered by eruption.
Body Build and Proportions A continual change in body proportions is seen during postnatal growth. Figure shows some of the major changes that include shrinking proportions for the head and increasing proportions for the lower limbs.
These changes in proportions are related to the varying rates and duration of growth of the component parts of the body. The center of gravity is higher in children than in adults, which makes children top heavy.
At all ages the head is in advance of the trunk and the trunk is in advance of the limbs regarding maturity. The more peripheral parts of the limbs are in advance of the more. Figure Developmental stages of permanent teeth. Human Biol There is a transient stage during adolescence when the hands and feet are large and ungainly relative to the rest of the body.
The foot stops growing early, before most other parts of the skeleton. In the later stages of adolescence, laterality overtakes linearity in growth. In adolescence, male shoulders grow more than the pelvis, and the reverse occurs in females.
Deposition of fat in the female body produces considerable alterations in body shape. In general, male and female differences are exaggerated in adolescence. Systolic pressure is about 80 mm Hg at age 5 and rises to the adult value of mm Hg. Girls show a pubertal spurt in systolic blood pressure, which occurs earlier than the corresponding spurt in the male.
Heat production decreases during postnatal growth, with females experiencing a greater decrease in heat production than males. Differences are seen between the sexes in the increase in muscle strength during adolescence.
From Krogman WM: Sexual Development Body Composition In a breakdown that may be overly simple, it is possible to say that there are five major structural components of the human body: Changes in the proportional amounts of these five components occur during postnatal growth Table At adolescence, a number of changes occur in the development of the primary and secondary sex apparatus.
The earliest sign of male puberty is the growth of the testicles. In response to hormone production of the testes, the other parts of the sex apparatus begin their adolescent development. In the females, growth of the ovaries precedes growth of the rest of the sex apparatus. Menarche occurs after the peak velocity in height growth. The potential for growth is genetic. The actual outcome of growth depends on the interaction between the genetic potential and environmental influences. Studies of twins have shown that body size, body shape, deposition of fat, and patterns of growth are all more under genetic control than under environmental control.
Heredity controls both the end result and rate of progress toward the end result. The handwrist, dental, sexual, and other biologic ages of identical twins are similar, whereas the maturity indicators for nonidentical twins may differ considerably.
Genetic factors most likely play a leading role in male-female growth differences. The marked advancement of girls over boys in the rate of maturation is attributed to the delaying action of the Y chromosome in males. By delaying growth, the Y chromosome allows males to grow over a longer period of time than females, therefore making possible greater overall growth. Individuals with the chromosome pattern XXY Klinefelter's syndrome are long legged and have a growth pattern similar to males even with the presence of two X chromosomes.
Individuals with Turner's syndrome, having only one X chromosome, develop with a female pattern of growth. Physiologic Changes Many physiologic changes occur during postnatal growth, many of which show male-female differences. This agrees with the general biologic rule that the heart rate is inversely related to body size. Resting mouth temperature falls in females a degree or more from infancy to maturity, whereas in males the drop continues another half degree. Some physiologic functions mature much earlier than others.
The filtration rate of the glomeruli of the. Individuals with an XYY chromosome constitution are very tall 6 feet or more , which lends support to the hypothesis that the Y chromosome has a delaying effect on growth. Neural Control It is thought that a growth center exists in the region of the hypothalamus, which keeps children on their genetically determined growth curves.
Although the correlation between birth size and adult size is low, by the age of 2 the correlation becomes reasonably high. The interpretation of this fact is that during the first 2 years of postnatal growth, the neural control system has got the child on its predetermined genetic curve.
At birth, body size is limited to accommodate the birth process. After birth, those children destined to become large experience a burst of growth activity, which levels off during the first 2 years.
Not all children experience this burst of early growth, thus some mechanism is obviously operating to make these early changes. The hypothalamus is located above the pituitary gland, and it is thought that the hypothalamus sends messages to the pituitary gland through an elaborate feedback system. There is also evidence that the peripheral nervous system plays a part in growth control.
If a somatic muscle is denervated, it atrophies. It is suggested that peripheral nerve fibers exert a nutritive or trophic effect on the structures they innervate. Hormonal Control Probably all of the endocrine glands influence growth. The anterior lobe of the pituitary gland produces a protein called growth hormone, or somatotropin.
This can be detected at the end of the second fetal month, soon after the pituitary has formed. It is thought that the growth hormone, although not essential for fetal growth, is essential to growth from birth onward. Growth hormone maintains the normal rate of protein synthesis and appears to inhibit the synthesis of fat and the oxidation of carbohydrate. It is necessary for the proliferation of cartilage cells thus it has a great effect on bone growth and, consequently, height growth.
Its growth functions become ineffective when the epiphyses close, but it probably maintains its effects on protein synthesis throughout life. Production of growth hormone is thought to be controlled by the hypothalamus.
An excess of growth hormone produces a pituitary giant, and a deficiency of the hormone produces a pituitary dwarf. Human growth hormone is used in the treatment of pituitary dwarfism. A complicated interaction exists between growth hormone and insulin.
Insulin is important in protein synthesis, and growth hormone is incapable of causing the formation of normal amounts of ribonucleic acid without the help of insulin. Other evidence suggests that, in diabetes, excess production of growth hormone may depress insulin production.
There may be an antagonism between the production of growth hormone and production of cortisone by the cortex of the suprarenal glands.
Growth hormone is produced in a daily rhythmic secretion, the amount varying inversely with cortisone secretion. The peak of daily secretion of growth hormone is in the early stages of sleep. The anterior lobe of the pituitary gland also secretes thyrotrophic hormone, which affects growth by stimulating the thyroid gland to secrete. The hormones of the thyroid gland, thyroxine and triiodothyronine, both stimulate general metabolism and are important in growth of the bones, teeth, and brain.
Iodine deficiency reduces the production of these hormones. Deficiency in childhood of the thyroid hormones produces a mentally retarded dwarf.