File Name: types of cleft lip and palate .zip
Cleft lip with or without cleft palate CP is one of the most common congenital malformations. Ultrasonographers involved in the routine wk ultrasound screening could encounter these malformations. The face and palate develop in a very characteristic way.
- Cleft Lip and Palate Patients: Diagnosis and Treatment
- Cleft Lip and Palate
- Cleft Lip and Palate
- Cleft Lip and Palate
Cleft Lip and Palate Patients: Diagnosis and Treatment
Cleft lip with or without cleft palate CP is one of the most common congenital malformations. Ultrasonographers involved in the routine wk ultrasound screening could encounter these malformations. The face and palate develop in a very characteristic way. For ultrasonographers involved in screening these patients it is crucial to have a thorough understanding of the embryology of the face.
This could help them to make a more accurate diagnosis and save time during the ultrasound. Subsequently, the current postnatal classification will be discussed to facilitate the communication with the CP teams. Currently a thorough ultrasound examination during the wk ultrasound is performed to exclude an oral cleft of the face. This study provides important embryological information to facilitate the ultrasonographer in making an accurate diagnosis and safe time during the ultrasound.
Subsequently, the current postnatal classification will be discussed to facilitate the communication with the cleft palate teams. Orofacial clefts OFCs are common craniofacial malformations. However, isolated cleft palate CP is more common in females and an equal incidence of 0. Clefts occur in a ratio of unilateral left, unilateral right, and bilateral [ 2 ].
The etiology of OFCs is complex and believed to be multifactorial, representing an interaction between genetics and environment during a critical stage of development [ 3 ].
Recently several genes causing CL and palate have been discovered. The nature and function of these genes vary widely, illustrating high complexity within the craniofacial developmental pathways [ 4 - 6 ]. The interested reader is referred to comprehensive studies that focus specifically on these genes.
In different countries routine ultrasound screening in pregnancy does not consistently include screening for facial clefts. However, the increased use of transabdominal ultrasound 3D certainly leads to an increased frequency of oral clefts being diagnosed antenatally [ 7 ]. There are few articles that focus on different ultrasound approaches to visualize the palate and lips both 2D and 3D [ 8 - 10 ].
As oral clefts typically occur in facial areas where the normal embryological fusion of structures did not occur, knowledge of the embryological background could aid the ultrasonographer to understand and more accurately diagnose these clefts. The aim of this review is to familiarize the ultrasonographer with the embryology of the face, which will subsequently aid in more accurate diagnosis of the extent of the facial cleft.
For a more extensive overview the reader is referred to textbooks [ 11 - 13 ]. The different classifications systems of clefts are also summarized. This might facilitate communication between the ultrasonographer and the CP team after birth. The basic morphology of the face is established between the 4 th and 10 th week after conception. Upper lip formation commences at 24 d postconception and is completed by 37 d [ 11 - 13 ].
Special neural crest cells of ectodermal origin differentiate to form a special ectomesenchyme. The ectomesenchyme migrates over and around the head and participates in the formation of five facial prominences that surround the primitive oral cavity: The frontonasal prominence, the paired maxillary prominences and the paired mandibular prominences.
The frontonasal prominence develops in the midline over the brain. During the 5 th week of embryogenesis the nasal component of the frontonasal prominence forms bilateral two ectodermal thickenings, the nasal placodes Figure 1 [ 13 ].
Each nasal placode invaginates to form an oval nasal pit and divides the frontonasal prominence into a medial and lateral nasal process. During the 6 th week, the two medial nasal processes fuse and gives rise to the midline of the nose, medial part of the upper lip, philtrum, incisor teeth and the primary palate. The primary palate is the part of the palate that is located ventrally to the foramen incisivum, while the secondary palate is the part located dorsally to the foramen incisivum.
The lateral nasal process subsequently forms the nasal alae and alar base. During the 6 th week the maxillary processes on each side of the mouth grow forward and merge with the medial nasal processes that lead to the formation of the lateral upper lip, the majority of the maxilla and the secondary palate. The mandibular prominences give rise to the mandible and lower lip. The fusion of the facial swellings occurs between the 4 th -6 th weeks postconception. Failure of fusion between any of the facial swellings results in facial clefts and can occur either unilaterally or bilaterally and typically happens at the junction of the lateral incisor and the first premolar teeth.
In patients with mild CL defects the cleft could be limited to a notch in the vermillion border of the lip that probably represents a failure of localized growth of the medial nasal process. In more severe defects, the cleft runs through all the lip structures and completely separates the lateral lip from the philtrum and nasal cavity. These clefts are caused by failure of fusion between the medial nasal process and the maxillary prominence. The depth of the cleft may vary from the soft tissue of the lip to a complete cleft of the maxillary bone.
The normal palate fusion process starts at the foramen incisivum and subsequently closes in a posterior direction. The actual lip fusion starts cranially and subsequently closes in a caudal direction. Oblique OFCs can also involve the side of the face and even involve the orbit. Midline clefting syndromes can be divided into two groups: The premaxilla agenesis-holoproencephaly syndrome and frontonasal-median cleft syndrome [ 15 ]. Midline clefts arise due to incomplete merging of the median nasal prominences that form the inter-maxillary segment.
The premaxilla agenesis-holoproencephaly syndrome Demyer sequence has a frontonasal deformity associated with hypotelorism, holoprosencephaly and facial deformity ranging from cyclopia to midline facial cleft with pre-maxillary ageneses. The median cleft face syndrome is often associated with a nasal deformity and hypertelorism usually either with no or little brain deformity corpus callosum agenesis. In these cases surgical reconstruction is feasible due to the probability of normal life expectancy.
Palatogenesis begins at the end of the 5 th week and the development of the palate is not completed until the 12 th week postconception [ 11 - 13 ]. The palate develops from two primordia: The primary and the secondary palate. The most important cell types in palate development are the neural crest-derived palatal mesenchyme, ectoderm-derived epithelial lining and the most apical layer composed of periderm cells [ 16 ].
The soft palate also includes the cranial paraxial mesoderm derived myogenic cells. The primary palate is formed by merging of the medial nasal prominences during the 6 th week and gives rise to the four central incisors and extends to the foramen incisivum. The secondary palate that separates the nasal cavity from the oral cavity is the primordium of the hard and the soft palate and is formed by the fusion of neural crest mesenchyme that lies within the maxillary primordia.
The development of the secondary palate starts with the outgrowth of two palatine shelves from the maxillary process that extend vertically on either side of the tongue. The palatal shelves subsequently rotate to a horizontal position dorsal to the tongue and then undergo intramembranous ossification to form the palatine process of the maxilla and the palatine bone. The transition from vertical to horizontal position happens in the eight week postconception and is completed, incredibly, in only some hours.
There is considerable sex difference in the timing of palatal closure. Shelf elevation and fusion begin a few days earlier in males than in females [ 13 ]. Just as the formation of the lip, the subsequent fusion process is an incredibly complex process.
Before fusion the palatal shelves are two cell layers thick. The outer layer is sloughed off by apoptosis , leaving only a basal epithelial layer which composes the medial edge of each palatal shelf. The shelves grow towards each other in the midline and approximate to form the midline epithelial seam.
The seam subsequently degenerates, leading to mesenchymal confluence between the two palatal shelves. At the same time fusion with the nasal septum and the primary palate occurs. Gradually, bone extends from the palatine process of the maxilla and the palatine bone into the palatal shelves to form the hard palate. The posterior parts do not become ossified and extend posteriorly and fuse to form the soft palate, including the uvula [ 13 ].
If the fusion process of the palate which occurs between the 9 th and 12 th week of gestation, is disrupted by either genetic, mechanical or teratogenic factors, a cleft of secondary palate results. Because the secondary palate closes from the foramen incisivum in a posterior dorsal direction, it is not possible for the palate to be open just posterior to the foramen incisivum in the hard palate and then subsequently fuse again in the soft palate part.
If the initial process of fusion is defect the rest of the fusion process will not take place. This means that an intact soft palate implies the presence of an intact hard palate. These cases have been attributed to trauma and not due to a defective fusion process. Especially the submucous cleft could be vulnerable [ 17 ]. However, some mouse models do suggest that initial contact is made in the middle-anterior region with fusion proceeding in both anterior and posterior directions [ 17 ].
Abnormality of the mandible appears to have a related cause with CP. Hypoplasia of the mandible micrognathia interferes with descent of the tongue and positions the tongue superiorly between the two palatal shelves. This causes mechanical disruption of palatal closure and could result in a CP. Micrognathia could be associated with Robin sequence. This sequence or phenomenon consisting of a triad of micrognathia, glossoptosis and breathing problems often involves an associated CP [ 18 ].
This condition could be associated with life threatening breathing problems postnatal and is often associated with other anomalies such as heart defects [ 19 ]. Fusion between the two maxillary processes differs on a molecular level from the fusion between the medial nasal process and the maxillary process. Postnatal the prevalence of associated anomalies is lowest in CL and ranges from 7. Data from postnatal studies show that concerning CLP the frequency is higher and ranges from CP is the category most frequent associated with additional congenital anomalies and the prevalence of associated malformations with CP ranges from Antenatally isolated CP is usually not diagnosed and associated abnormalities are reported in It is becoming more frequent to use the transabdominal ultrasound screening during the second trimester of pregnancy to evaluate the face.
The very low detection rate of CP demonstrates that there are no satisfactory sonographic indicators of an isolated CP that might be one of the reasons why the palate is often not visualized during the ultrasound screening. Yet, the ultrasonographer should be aware that micrognathia could be associated with a CP.
Subsequently, when the ultrasonographer encounters other malformations such as heart defects with the micrognathia, evaluation of the palate is mandatory. Some forms of CL only have a small indentation in the vermillion. When CL is seen on 2D or 3D ultrasound, the position of the alar base nostrils can help to determine whether the alveolar ridge or palate is involved as well. An isolated incomplete CL without a maxillary or palatal defect will appear as a linear defect running from the lip towards the nasal floor Figure 3A.
In complete CL the lip defect could be well visualized, although the nose distortion is likely to be minimal Figure 3B. In complete bilateral CL the maxilla is intact there is no maxillary protrusion and the alar bases or nostrils are symmetrical. Recently we have demonstrated that with a normal maxilla-nasion-maxilla angle, it was unlikely to find a cleft that included the alveolus [ 22 ]. A complete CL with alveolar ridge involvement but without involvement of the primary palate is called an incomplete CL.
Incomplete involvement of the alveolar ridge usually does not substantially change the position of the alar base.
Cleft Lip and Palate
Cleft lip or palate is one of the most common types of craniomaxillofacial birth anomalies. Midface deficiency is a common feature of cleft lip and palate patients due to scar tissue of the lip and palate closure. Cleft lip and palate patients should be carefully evaluated by the craniofacial team in order to detect potentially serious deformities. Craniofacial team is involved with diagnosis of facial morphology, feeding problems, guidance of the growth and development of the face, occlusion, dentition, hearing and speech problems, and psychosocial issues and jaw discrepancy of the patients with cleft lip and palate or craniofacial syndromes. Treatment for cleft children requires a multidisciplinary approach including facial surgery in the first months of life, preventive and interceptive treatment in primary dentition, speech therapy, orthodontics in the mixed dentition phase, oromaxillofacial surgery, and implant and prosthetics in adults. Treatment plan from orthodontic perspective can be divided into the following stages based on the dentition stages: 1 presurgical orthopedics, 2 primary dentition, 3 mixed dentition, and 4 permanent dentition.
Cleft Lip and Palate
A unique feature of the book is that it largely consists of longitudinal facial and palatal growth studies of dental casts, photographs, panorexes, and cephalographs from birth to adolescence. Throughout the discussion of growth and treatment concepts, the importance of differential diagnosis in treatment planning is underscored. The underlying argument is that all of the treatment goals — good speech, facial aesthetics, dental occlusion, and psychological development — may be realized without the need to sacrifice one for another. In this third edition, further successful physiological treatment protocols are considered and the occurrence and prevention of relapses after some surgical treatments are discussed; again, all solutions are backed up by follow-up records. Additional topics not previously covered include strategies for coping with psychological effects on patients and intra-team conflict, the excellent clinical work being undertaken in Asia, and future multicenter palatal growth studies.
They occur in approximately one in births. This causes a gap or defect to occur in the affected area, involving skin, muscle and the lining of the mouth. There is often an associated deformity of the nose on the affected side. Similarly, a cleft palate may occur in isolation, without a corresponding deformity of the upper lip. Various family and environmental factors may contribute to a child's cleft.
A cleft lip is an opening or split in the upper lip that occurs when developing facial structures in an unborn baby don't close completely. Cleft lip may be unilateral or bilateral. A baby with a cleft lip may also experience a cleft in the roof of the mouth cleft palate.
Cleft Lip and Palate
Our understanding of cleft palates has come a long way over the last few decades. A better understanding of the long-term consequences of a cleft palate and its effect on speech development challenges surgeons to not only effectively repair the cleft, but to also restore function of the palate for adequate speech. Coordination with speech pathologists is integral for effective management of cleft palate patients, particularly as children begin to develop language. In this article, the authors review and summarize the various challenges and goals of cleft palate management. Cleft lip and palate are the most common congenital craniofacial anomalies evaluated by a plastic surgeon. These anomalies are being detected earlier, often with fetal ultrasound and magnetic resonance imaging MRI , thus preparing parents with a prenatal diagnosis.
Сзади послышался возглас: - Двухминутное предупреждение. Джабба в отчаянии бросил взгляд на ВР. Последний щит начал рушиться. Техники сновали по комнате. Что-то подсказывало Сьюзан, что они близки к разгадке.
- Стратмор внимательно посмотрел не. - Я должен найти его партнера, прежде чем он узнает о смерти Танкадо. Вот почему я тебя вызвал.
Водитель отказался его впустить. Машина была оплачена человеком в очках в тонкой металлической оправе, и он должен был его дождаться. Беккер оглянулся и, увидев, как Халохот бежит по залу аэропорта с пистолетом в руке, бросил взгляд на свою стоящую на тротуаре веспу. Я погиб.
Так вот какова месть Танкадо. Уничтожение ТРАНСТЕКСТА. Уже несколько лет Танкадо пытался рассказать миру о ТРАНСТЕКСТЕ, но ему никто не хотел верить. Поэтому он решил уничтожить это чудовище в одиночку. Он до самой смерти боролся за то, во что верил, - за право личности на неприкосновенность частной жизни.
И сразу же услышала треск.
Беккер мрачно кивнул невидимому голосу. Замечательно. Он опустил шторку иллюминатора и попытался вздремнуть. Но мысли о Сьюзан не выходили из головы. ГЛАВА 3 Вольво Сьюзан замер в тени высоченного четырехметрового забора с протянутой поверху колючей проволокой.
Она там, потому что я ее туда запустил. Сквозь строй не позволял мне загрузить этот файл, поэтому я обошел фильтры. - Глаза коммандера, сузившись, пристально смотрели на Чатрукьяна. - Ну, что еще - до того как вы отправитесь домой. В одно мгновение Сьюзан все стало ясно.
Люди на подиуме не отрываясь смотрели на экран. Агент Смит начал доклад. - По вашему приказу, директор, - говорил он, - мы провели в Севилье два дня, выслеживая мистера Энсея Танкадо. - Расскажите, как он погиб, - нетерпеливо сказал Фонтейн. Смит сообщил: - Мы вели наблюдение из мини-автобуса с расстояния метров в пятьдесят.
Этот человек сломал запястье, у него травма головы. Он был принят сегодня утром. Его карточка должна лежать где-то сверху.
Беккер изумился. - Un punqui. - Si. Punqui.
Пользователь вводил информацию с помощью крошечных контактов, закрепленных на пальцах. Контакты соединялись в определенной последовательности, которую компьютер затем расшифровывал и переводил на нормальный английский. Киллер щелкнул миниатюрным тумблером, и очки превратились в дисплей. Опустив руки, он незаметными быстрыми движениями соединял кончики пальцев. Перед его глазами появилось сообщение, которое он должен был отправить.
- Мы нашли Северную Дакоту. Вызовите службу безопасности. И давайте выбираться отсюда.
Стратмора это не поколебало. - Я готов рискнуть.