Category Archives: Management of Patients with Orafacial Clefts

Speech Difficulties

Speech Difficulties

Four speech problems are usually created by cleft lip and palate deformity. Retardation of consonant sounds u is the most common finding. Because consonant sounds are necessary for the development of early
vocabulary  much language activity is omitted. As a result, good sound discrimination is lacking by the time the palate is.closed. Hypernasality is usual in the patient with a deft of the soft palate and may remain after surgical correction. Dental malformation, ‘malocclusion, and abnormal
tongue placement may develop before the palate is closed and thus produce an articulation problem. Hearing problems contribute significantly to the many speech disorders common in patients with oral clefts. In the normal individual, speech is created by the following scheme. Air is allowed to escape from the lungs, pass through the vocal cords, and enter the oral cavity.  The position of the tongue, lips, lower jaw, and soft palate working together In a highly ‘coordinated fashion results in the sounds of speech being produced. If the vocal cords are set hlto ‘vibration while the airstream is passing . between, then voice is superimposed on the speech sounds that result from the relationships of the oral structures

FIG, 27-7 Upward and backward movement of soft palate during normal speech, Its contact with posterior pharyngeal wall is shown.'

FIG, 27-7 Upward and backward movement of soft palate during
normal speech, Its contact with posterior pharyngeal wall is shown.’

The soft palate is raised during speech production, preventing air from escaping through the nose. . For clear speech it is necessary for the individual to have complete control of the passage of air from  he oropharynx to the nasopharynx. The hard palate provides he partition between the nasal and oral cavities. The soft palate functions as an important valve to control the distribution bf escaping air between the oropharynx and nasopharynx (Fig. 27-7). This is called the velopharyngeal mechanism (velo means soft palate). As the name Implles, its two main components are (1) the soft palate  and (2) the. pharyngeal walls. When passive the soft palate hangs downward toward the tongue, but during
.. speech the muscles of the soft palate elevate it and draw it toward the posterior pharyngeal wall, Which is what happens to the normal individual’s soft palate when he or she is asked to say IIah.” In normal speech this action
takes place rapidly and with an unbelievable complexity, so that the valvlng mechanism can allow large amounts of air to escape into the nasopharynx or can limit the escape to none. . In individuals whose soft palate is cleft, the velopharyngeal mechanism cannot function because of the discontinuity
of the musculature from one side to the other, The soft palate thus cannot elevate to make contact with the pharyngeal wall. The result of this constant escape of air into the nasal cavity is hypemasal speech. Individuals with cleft palate develop compensatory velopharyngeal, tongue.rand nasal mechanisms in an , .attempt to produce intelligible speech. The posterior and lateral pharyngeal walls obtain .great mobility and attempt to narrow the .passageway between the oropharynx and nasopharynx during speech. A muscular bulge of the pharyngealwall actually develops during attempts at closure of the passagewayin some individuals with cleft palate and is known as Passavant’s ridge or bar. Individuals with cleft palates develop compensatory tongue postures and positions during speech to help valve their coming from the larynx into the pharyngeal areas. Simllarly,
the superficial muscles around the nose involved in facial expression are recruited to help limit the amount of air escaping from the nasal cavity. In this instance the valving is .at the other end of the nasal cavity from the
velopharyngeal  mechanism. However, in an uncorrectedcleft of the soft palate, it is literally impossible for compensatory mechanisms to produce a satisfactory velopharyngeal mechanism. Unfortunately in surgically corrected soft palates, velopharyngeal competence is not always achieved with one operation, and secondary procedures are frequently necessary.
Speech pathologists are well versed in assisting children with cleft deformities to develop normal articulation skills. The earlierIn life speech training is started in patients with cleft deformities, the better the eventual
outcome. The patient may need to undergo speech counseling for several years to produce acceptable speech. When hearing problems are also present, the speech problems are compounded. Hearing loss at an early age is especially detrimental to the development of normal speech skills. The child who is unable to hear is unable to imitate normal speech. Thus the parents must be cognizant of their child’s development and ensure that regular  visits to the pediatrician are undertaken.

 

 

 

Ear Problems

Ear Problems

Children afflicted with a cleft of the soft palate are predisposed to middle ear infections. The reason for this becomes clear on review of the anatomy of the soft palate musculature. The elevator veli palatini and tensor veli palatini,
which are normally inserted into the same muscles on the opposite side, are left unattached when the soft palate is cleft. These muscles have their origins either directly on or near the auditory tube. These muscles allow opening of the ostium of this tube into the nasopharynx.This action is demonstrated when middle ear pressures are equalized by swallowing during changes in atmospnerte pressure, as when ascending or descending in an airplane, when this function is disrupted, them  ear is essentially a closed space, without a drainage mechanism. Serous fluid may then  ccumulate and result in serous. otitis media. Should bacteria find their way from the  nasopharynx into the middle ear, an infection can develop (i.e., suppurative otitis media). To make matters worse the auditory tube in infants is at an angle that does not promote dependent· drainage. With age this angulation changes and allows more dependent drainage of (he middle
ear.  Children afflicted ~ith cleft palate will frequently needto have their middle ear “vented.” The otorhinolaryngologist, who creates a hole through the inferior aspect of the tympanic membrane and inserts a small plastic tube, performs  this procedure, which drains the ear to the outsideInstead of the nasopharynx (myringotomy). Chronic serous otitis media is common among children with cleft palate, and multiple myringotomies are
frequently nece ssary. Chronic serous otitis media presentsa serious threat to hearing. Because of the chronic inflammation in the iniddle ear, hearing impalements are common in patients with cleft palate. The type of hearing loss experienced by the patient with cleft palateis conductive, meaning that theneural pathway to the brain continues •to function normally. The defect in these instances is simply that sound cannot reach the· auditory sensory organ as efficierrtly as it should because of the chronic inflammatory
changes  in the middle ear. However, if the problem isnot corrected, permanent damage to the auditory sensory nerves (i.e., sensory neural loss) can also result. This type of damage is irreparable. The range of hearing impairment found in individuals with cleft palates is vast. The loss can be great enough so that normal-sounding speech is heard at less than one half of expected volume. In addition, certain sounds of speech (called phonemes), such as the 5, sh, and t sounds, may be heard poorly. Audio grams are useful tools and are performed repeatedly on patients with palates, to monttorhearlng ability and performance

Feeding

Feeding

Babies with cleft palates can swallow normally once the material being fed reaches the hypopharynx but have extreme difficulty producing the necessary negative pressure in their mouth to allow sucking either breast or milk. When a nipple is placed in the baby’s mouth, he or she starts to suck just like any other newborn, becaese the

FIG. 27-6 A, Facial profile of typical cleft patient. Note pseudoproqnathic appearance of mandible. B, Occlusal relationship of patient showing Angle's Cass III relationshlp with anterior crossbite. C, Lateral ceph.alogram showing maxillary skeletal sagittal deficiency contributing to Cass III occlusal .relationship.

FIG. 27-6 A, Facial profile of typical cleft patient. Note pseudoproqnathic appearance of mandible.
B, Occlusal relationship of patient showing Angle’s Cass III relationshlp with anterior crossbite.
C, Lateral ceph.alogram showing maxillary skeletal sagittal deficiency contributing to Cass III occlusal
.relationship.

sucking and swallowing reflexes are normal. However, the musculature is undeveloped or not properly oriented to allow the sucking to be effective. This problem is easily overcome through the use of specially designed nipples that are elongated and extend further into the baby’s mouth. The .9pening should be enlarged, because the suck will not be as effective as in a normal baby. Other satisfactory methods are the use of eyedroppers or large syringes with rubber extension tubes connected to them. The tube
-is placed in the baby’s mouth, and a small amount of solution is .mjected. These methods of feeding, while adequate for .sustenanc.e, require more time and care. Because the child will swallow a considerable amount of air when these feed methods are used, the child is not usually fed while
recumbent, and more frequent burping is necessary.

 

 

 

Nasal Deformity

Nasal Deformity

Deformity of normal nasal architecture is commonly seen in individuals with cleft lips (see Fig. 27-2). If the cleft extends into the floor of the nose, the alar cartilage on that side is flared and the columella of the nose is  ulled toward’the noncleft side. A lack of underlying bony support to the base of the “nose compounds the problem. Surgical correction of nasal deformities should usually  be deferred until all clefts and associated problems have been corrected, because correction of the alveolar cleft defect and the maxillary skeletal retrusion wrll after the osseous foundation of the nose. Improved changes in the  nasal form will therefore result from these osseous procedures.
Thus nasal revision may be the last corrective surgical procedure the cleft-afflicted individual will undergo.

Malocclusion

Malocclusion

Individuals affected with cleft deformities, especially those of the palate, show skeletal discrepancies between the size, shape, and position of their jaws. Class III malocclusion. seen in most cases, is caused by many factors.
A common finding is mandibular prognathism, which is frequently relative and is caused mo\e by the retrusion of the maxilla than by protrusion of the mandible (i.e., pseudoprognathism) (Fig. 27-6). Missing or extra teeth
may partially contribute to the malocclusion. However, retardation of maxillary growth is the factor most responsible for the malocclusion. Generally the operative trauma of the cleft closure and the resultant fibrosis (i.e., scar contracture) severely limit the amount of maxillary growth and development that can take place. The maxilla may be deficient in all three planes of space, with retrusion, constriction, and vertical underdevelopment common. Unilateral palatal clefts show collapse of the cleft  side of the maxilla (i.e., the lesser segment) to the center of the palate, which produces a narrow place arch. Bilateral palatal clefts show collapse of all  omention or may have constriction of the posterior segments and protrusion of the anterior segment.

FIG. 27-5 Occlusal radiographs from individuals with various types of cleft deformities. A, Bilateral complete cleft of alveolus and palate. Note absence of permanent lateral incisors. B, Bilateral complete .deft of alveolus and palate. Note absence of permanent lateral incisor on patient's left side. C, Unilateral complete ~Ieft of alveolus and palate. Note supernumerary teeth.

FIG. 27-5 Occlusal radiographs from individuals with various types of cleft deformities. A, Bilateral
complete cleft of alveolus and palate. Note absence of permanent lateral incisors. B, Bilateral complete
.deft of alveolus and palate. Note absence of permanent lateral incisor on patient’s left side. C, Unilateral
complete ~Ieft of alveolus and palate. Note supernumerary teeth.

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Orthodontic treatment may be necessary throughout the individual’s childhood and adolescent years. Space maintenance and control is instituted during childhood. Appliances to maintain or increase the width of the dental arch are frequently used. This treatment is usually begun with the eruption of the first’ maxillary permanent molars. Comprehensive orthodontic care is. deferred until later, when most of the permanent teeth have erupted. Consideration for orthognathic surgical intervention for
correction of skeletal discrepancies and occlusal disharmonies is frequently necessary at this time.

 

 

 

 

 

 

PROBLEMS OF CLEFT-AFFLICTED INDIVIDUALS

Dental Problems

A cleft of the alveolus can often affect the development of the primary and permanent teeth, and the jaw Itself.” The most common problems may be related to congenital absence of teeth and, ironically, supernumerary teeth
(Fig. 27-5). The cleft usually extends between the lateral . incisor and canine area. These teeth, because of their proximity to the cleft, may be absent; when present, they may be severely displaced so that eruption into the cleft margin is common. These teeth may also be morphologically
deformed or hypomineralized. Supernumerary teeth occur frequently, especially around the cleft margins. These t,ee!p usually must be removed at some point during the child’s development. However, they may be
retained if they can furnish any useful function in the patient’s overall dental rehabilitation. Frequently, supernumerary teeth of the permanent dentition are left until 2 to 3 months before alveolar cleft bone grafting, because these teeth, although nonfunctional, maintain the surrounding
alveolar  one. If extracted earlier, this bone may resorb, making the alveolar cleft larger.

CAUSATIVE FACTORS

CAUSATIVE FACTORS

The causes of facial elefting have been extensively investigated. The exact cause of elefting is unknown in most cases. Fdr most cleft conditions, no single factor can be identified as the cause. However, it is important to distinguish between isolated clefts (in which the patient has no other related health problem) and clefts associated with other birth disorders or syndromes. A syndrome is a set of physical, developmental, and sometimes behavioral traits that occur together. Clefts have been identified as a fear
ture ill over 300 syndromes, most of which are-rare.’ Syndromes account for approximately 15% of the total number of cases of cleft lip and cleft palate but nearly 50% of cases of isolated cleft palate. Medical geneticists are usually asked to consult with the family of children born with syndromes to identify the specific syndrome and to provide information to the parents about the likelihood of another child being affected. For nonsyndromic clefts, it was initially thought that heredity played a significant role in the causation. However, studies have been able to-implicate genetics Inonly 20% to 30% of cleft lip or palate patients. Even in those individuals whose genetic backgrounds may verify familial tendencies
for facial clefting, the mode of inheritance is not completely understood. It is not a simple case of mendelian dominant or recessive inheritance but is multigenetic. The majority of nonsyndromic clefts appear to be caused by’ an interaction between the individual’s genes (i.e., genetic predisposition) ant! certain factors in the environment that mayor may not be specifically identified. Environmental factors seem to playa contributory role at the critical time of embryologic development when the lip and palatal halves are fusing. A host of environmental factors have been shown in experimental animals to result in clefting. Tutritional deflciencies, radiation, several drugs, hypoxia, viruses, and vitamin excesses or deficiencies can produce clefting in certain situations. The risk for having another child with a cleft is based upon a number of factors that are often unique in a particular family. These include the number of family members
with clefts, how closely they are related, the race and sex of the affected individuals, and the type of cleft each person has. After a syndrome or complex disorder is excluded, recurrence ri~ counseling for a cleft can be
offered to families. No genetic test can determine a person’s individual chance of having a child with a cleft. Every parent has approximately a 1 in 700 risk of having a child with a cleft.’ Once parents have a child with
a cleft, the risk that the next child (and each succeeding child) will be affected is 2(Yt, to Sf){ (i.e.. 2 to 5 chances in lOO).1 If more than one person in the immediate family  has a cleft, the risk rises to 10% to ] 291) (i.e., roughly 1 chance in 10). i\. parent who has a cleft has a 2% to So/u chance that his or her child will have a cleft. If the parent with a cleft also has a close relative with a cleft, the risk increases to lorVi) to 12°1<) for their child being born with a cleft. The unaffected siblings of a child with a cleft
have an Increa ed risk of having a child with a cleft (1% or 1 in 100, compared with 1 in 700 when no history of cleft exists). If a syndrome is involved, the risk for recurrence within a family can be as high as 50%.1 Genetic counselors may be consulted for parents of children with
clefts or for people with clefts who would like to obtain more information on the relative risks for their offspring. In summary, orofacial elefts are produced by incompletely understood mechanisms, both genetic and environmental. With lack of complete knowledge of the causes, effective preventive measures, other than good prenatal practices (e.g., avoiding medications that are not absolutely necessary), are not available to prevent this deformity from developing.

EMBRYOLOGY

EMBRYOLOGY

To understand the causes. of oral clefts, a review of nose, lip and palate embryology is necessary. The entire process takes place between the fifth and tenth weeks of fetal lifer’ During the fifth week, two fast-growing ridges, the atemand media! nasa/ swellings, surround the nasal- vestige (Fig. 27,-3). The lateral swellings will form the alae of the nose; the medial swellings will give rise to four areas: (1) the middle portion of the nose, (2) the middle portion
of the upper lip, (3 ) the middle portion of the maxilla,and (4) the entire primary palate. Sim

FtG. ~7-3 Frontal aspect.of face. A, Five-week-old embryo. B, Six-week-old embryo. Nasal swellings are gradually separated from maxillary swelling by deep furrows. At no time during normal development does this tissue break down. C, Seven-week-old embryo. 0, Ten-week-old embryo. Maxillary swellings gradually merge with nasal folds, and furrows are filled with mesenchyme. (From Langman J: Medical embryology, ed 3, Baltimore, 1975, Williams & Wilkins.)

FtG. ~7-3 Frontal aspect.of face. A, Five-week-old embryo. B, Six-week-old embryo. Nasal swellings
are gradually separated from maxillary swelling by deep furrows. At no time during normal development
does this tissue break down. C, Seven-week-old embryo. 0, Ten-week-old embryo. Maxillary
swellings gradually merge with nasal folds, and furrows are filled with mesenchyme. (From Langman J:
Medical embryology, ed 3, Baltimore, 1975, Williams & Wilkins.)

.During. the next 2 weeks, the appearance of the face .changes considerably. The maxillary swellings continue to grow in a medial direction and  ompress themedial nasal swellings toward the midline. ‘Subsequently these swellings simultaneously merge with each other and with the maxillary swellings laterally. Hence the upper lip is, formed by the two medial. nasal swellings and the two maxillary swellings. The two medial swellingsmerge not only at the surface but also at the deeper level. The structures formed by the two merged swellingsare known together as the intermaxilar  segmellt (Fig.27-4), which is comprised of three components: (1) a labial component, which forms the philtrum of the upper lip; (2) an upper jaw component, which carries the four incisor teeth; and (3) a palatal component, which forms the triangular primary palate. Above, the intermaxillary segment is continuous with the nasal septum, which is formed by the frontal prominence. Twoshelflike outgrowths from the maxillary swellings form the.secondary palate. These palatine shelves appearin the sixth week of development and are directed obliquely downward on either side of the tongue. In the seventh week, however, the palatine shelves ascend to
attain a horizontal position above the’ tongue and fuse with each other, thereby forming the secondary palute.Anteriorly the shelves fuse with the triangular primary palate, and the incisive foramen is formed at this junction. At the same time, the nasal septum grows down and’ joins the superior surface of the newly formed palate. The palatine shelves fuse with each other and with the primary palate between the seventh and tenth weeks of development Clefts of the primary palate result from a failure of
mesoderm to penetrate into the grooves’ between the – medial nasal’ and maxillary processes, which prohibits their merging with one another. Clefts of the secondary palate are caused by a failure of the palatine shelves to
fuse with one another. The causes for this are speculative ‘and include failure of the tongue to descend int.g the  oral cavity

FIG. 27-4 A, Frontal section through head of 61/2-week-old·embryo. Palatine shelves are located in. vertical position on each side of tongue. B, Ventral view of same. Note clefts between primary triangular palate and palatine shelves, which are still in vertical position. C, Frontal section through head of . 71/2-week-old embryo. Ton~ue has moved downward, and palatine shelves have reached horizontal position.D, Ventral view of same. Shelves are in horizontal position. E, ~rontal section through head of 10-week-old embryo. Two palatine shelves have fused with each 'other and with nasal septum. F,Ventral view of same. (From Lang.'Tlan J: Medical embryology, ed 3, Baltimore, 1915, WiII!ams & Wilkins.)

FIG. 27-4 A, Frontal section through head of 61/2-week-old·embryo. Palatine shelves are located in.
vertical position on each side of tongue. B, Ventral view of same. Note clefts between primary triangular
palate and palatine shelves, which are still in vertical position. C, Frontal section through head of .
71/2-week-old embryo. Ton~ue has moved downward, and palatine shelves have reached horizontal
position.D, Ventral view of same. Shelves are in horizontal position. E, ~rontal section through head of
10-week-old embryo. Two palatine shelves have fused with each ‘other and with nasal septum.
F,Ventral view of same. (From Lang.’Tlan J: Medical embryology, ed 3, Baltimore, 1915, WiII!ams & Wilkins.)

 

 

 

 

 

 

 

 

 

 

 

 

 

Management of Patients with Orafacial Clefts

CHAPTER OUTLINE

EMBRYOLOGY ,
tAUSATIVE fACTORS
PROBLEMS OF CLEFT-AFFLICTED INDIVIDUALS
Dental Problems
Malocclusion
Nasal Deformity
Feeding
Ear Problems
Speech Difficulties
Assoclated Anomalies
TREATMENT OF CLEFT LIP AND PALATE
Timing of Surgical Repair
Cheilorrhaphy
Objectives’
Surgical Techniques
Palatorrhaphy
Objectives
Surgical Techniques
Hard Palate Closure
Soft Palate Closure
Alveolar Cleft Grafts
Timing of Graft’ Procedure
Surgical Procedure
Correction of .Maxillomandibular Disharmonies
Secondary Surgical Procedures
DENTAL NEEDS OF CLEFT-AFFLICTED INDIVIDUALS
. Prosthetic Speech Aid Appliances

 Acleft is a congenital abnormal space or gap in , the upper lip, alveolus, or palate, The colloquial’ term for this condition is harelip. The use of this
term should be discouraged, because it carries demeaning connotations of lnferlority, The more appropriate terms are cleft lip, cleft palate, or cleft ‘lip and palate. ‘ Clefts of the lip and palate are the most common serious
congenital anomalies to affect the orofacial region. Their initial appearance may be grotesque. Because they are deformities that can be seen, felt, and heard, they constitute a serious affliction to those who have them. Because of their location, they’ are deformities that involve the dental specialties throughout their protracted course of treatment. The general dentist will become involved in managing these patients’ special ‘dental needs, because they may’ have partial anodontia and supernumerary teeth. Malocclusion is usually present orthodontic therapy with or without corrective jaw
surgery is freque ntly indicated.The occurrence of a cleft deformity is a source of  slderable ,shock to the parents of an afflicted ‘baby, and the, most appropriate approach to the parents is one of  informed explanation and reassurance. They should be told that the defects are correctable and need not adversely affect the child’s future. However, they shouldbe pre-‘ . pared for a protracted course of therapy to correct the deft deformities and to allow the individual to function with them.

FIG. 27-' Ventral view of palate,.Iip, and nose showing variability of cleft lip and palate deformity. A, Normal. B, Unilateral cleft lip extending into nose. C, Unilateral cleft involving lip and alveolus, extending to incisive foramen. 0, Bilateral cleft involving lip and alveolus. E, Isolated cleft palate. F, Cleft palate combined with unilateral cleft of alveolus and lip. G, Bilateral complete cleft of lip and palate. (From Langman J: Medical embryology, ed 3, Baltimore, 1975, Williams & Wilkins.)FIG. 27-' Ventral view of palate,.Iip, and nose showing variability of cleft lip and palate deformity. A, Normal. B, Unilateral cleft lip extending into nose. C, Unilateral cleft involving lip and alveolus, extending to incisive foramen. 0, Bilateral cleft involving lip and alveolus. E, Isolated cleft palate. F, Cleft palate combined with unilateral cleft of alveolus and lip. G, Bilateral complete cleft of lip and palate. (From Langman J: Medical embryology, ed 3, Baltimore, 1975, Williams & Wilkins.)

FIG. 27-‘ Ventral view of palate,.Iip, and nose showing variability of cleft lip and palate deformity.
A, Normal. B, Unilateral cleft lip extending into nose. C, Unilateral cleft involving lip and alveolus,
extending to incisive foramen. 0, Bilateral cleft involving lip and alveolus. E, Isolated cleft palate.
F, Cleft palate combined with unilateral cleft of alveolus and lip. G, Bilateral complete cleft of lip and
palate. (From Langman J: Medical embryology, ed 3, Baltimore, 1975, Williams & Wilkins.)

The problems encountered in rehabilitation of patients – with cleft deformities are unique. Treatment must address patient appearance, speech, hearing, mastication, and deglutition. A team manages most children currently affected with orofacial clefts. Cleft teams are found in most cities of at least moderate size. These teams commonly comprise a general or pediatric dentist, ‘an orthodontist, a prosthodontist, an oral and maxillofacial surgeon or a plastic surgeon, an audiologist, .an otorhinolaryngologist, a pediatrician, a speech pathologist, a psychologist or psychiatrist, and a social worker. The number of specialists required reflects the number and “complexity of the problems faced by individu als with orofacial clefts.The occurrence of oral clefts in the United States has been estimated as 1 in 700 births. I Clefts exhibit interesting racial predilections, occurring less frequently in bl-acks but more so in Asians. Boys are affected by orofacia I clefts more often than girls, by a ratio of 3:2. Cleft lip and palate (together) occurs about twice as often in boys as in girls, whereas isolated clefts of the palate (without cleft lip) occur slightly more often in girls. Oral clefts commonly affect the lip, alveolar ridge) and . hard and soft palates. Three fourths are unilateral defermities; one fourth are bilateral. The left side is involved more frequently than the right when the defect is unilateral. The cleft may be incomplete, that is, it may not extend the entire distance from lip to soft palate. Cleft lip may occur without clefting of the palate, and isolated cleft palate may occur without clefttngof the lip (Fig. 27 -1). A useful classification divides the anatomy into primary
and secondary palates. The primary palate involves

FIG. 27-2 Photographs of various types of cleft deformities. Nasal deformities are also apparent. A, Unilateral complete cleft of lip and palate. B, Bilateral complete cleft lip and palate. C, Palatal view of bilateral complete cleft lip and palate. The nasal septum is unattached to either palatal shelf. 0, Isolated cleft of soft palate.

FIG. 27-2 Photographs of various types of cleft deformities. Nasal deformities are also apparent.
A, Unilateral complete cleft of lip and palate. B, Bilateral complete cleft lip and palate. C, Palatal view
of bilateral complete cleft lip and palate. The nasal septum is unattached to either palatal shelf. 0, Isolated
cleft of soft palate.

those structures anterior to the incisive foramen-the lip and alveolus; the secondary palate consists of those structures posterior to the incisive foramen-the hard and soft yalates 2 Thus an individual may have clefting of the primary palate, the secondary palate, or both (Fig. 27-2). Clefts of the lip may range from a minute notch on the edge ‘of the vermilion border to a wide cleft that extends into the nasal cavity and thus divides the nasal floor. Clefts of the soft palate may also show wide-variations from a bifid uvula to a wide inoperable cleft. The bifid uvula is. the most minor form of ‘cleft palate, in which only the uvula is clefted. Submucosal clefts of the soft palate are occasionally seen. These clefts are also called occult clefts, because they arc not readily seen on cursory examination. The defect ill such a cleft is a lack of continuity in the musculature of the soft palate. However,  the nasal and oral mucosa is continuous and coversthe muscular defect. To diagnose such a defect, the dentinspects the soft palate while the patient says This ~on lifts the soft palate, and in individuals  it submucosal palatal clefts, a furrow in the midline is seen can also palpate the posterior aspect of the hard palate to detect the absence’of the posterior nasal spine, which is characteristically absent in submucosal clefts. If a patient shows hypernasal speech without an obvious soft palatal cleft, the dentist should suspect a submucosal cleft of the soft-palate.