Anatomy Palate

The palate consists of the hard palate in the anterior part and the soft palate in the posterior part. The anterior part of the mucosa hard palate has irregular layer covered by rugae while the posterior part of the hard palate and soft palate is covered by a smooth mucosal layer. ^1,2,4

Incisive papillae located on posterior from alveolar ridge And track The median column extends from the incisive papillae to the uvula. The tonsillar pillars are located on the posterolateral walls on each side of the oral cavity. The palatoglossus muscle forms the anterior pillar and the palatopharyngeus muscle forms the posterior pillar. Passavant ridge horizontal can seen on wall posterior pharynx. Passavant ridge formed by muscular constrictor pharynx superior or fiber horizontal from the palatopharyngeal muscle. ^1.4

Palate hard consists of from epithelium squamous layered And keratinized. The soft palate is composed of nonkeratinized stratified squamous epithelium on the oral surface and of pseudostratified ciliated columnar epithelium on the nasal surface. The anterior part of the hard palate is formed by the palatine processes of the maxilla and the posterior part of the hard palate is formed by the horizontal plates of the palatine bones. The palatine foramen is composed of neurovascular tissue located at the posterolateral bone.Vomer attached on part posterior bone palatine. The sphenoid is located posterior to the palatine bone and has two vertical processes, namely pterygoid medial And pterygoid lateral. Pterygoid hamulus expand from inferior part medial pterygoid and functions as a pulley for the tensor muscle the great palatines. Bone temporal located posterolateral from bone sphenoid And form part bone from tube Eustachian. Part cartilage expand from part bone to the inferior, medial, And front from pharynx. Opening from tube Eustachian located above the hard palate on the lateral wall of the pharynx. The torus tubarius appears as a protrusion from the posterior wall of the pharynx at the opening of the tube. ^1,4

The muscles in the velopharyngeal area have an important role in the chewing process, production voice, And function tube auditory. Muscle extrinsic from palatum are the levator veli palatini, tensor veli palatini, palatoglossus, palatopharyngeus, salpingopharyngeus, and superior constrictor which have their bases or insertions on the palate. The only intrinsic muscle is the uvula muscle. The levator veli palatine is muscle cylindrical Which to form hanger Which holds the soft palate from the skull base . This muscle originates posteromedially from the Eustachian tube on meeting from cartilage And bone. Muscle the descending from each side anteriorly and medially towards the soft palate between the muscles constrictor superior And skull base . Muscle the enter palate molle with spread and located between the two ends of the palatopharynx. The muscle fibers spread until three quarter part posterior palate molle. Muscle levator is located in the medial 50% of the length of the soft palate. The muscle fibers cross the line middle For join with fiber muscle lifter side next to it. Levator muscle attached in front with edge posterior from aponeurosis muscular tensor veli palatini. ^1.4

Muscle lifter veli palatine tend thin And hypoplastic on palatoschisis patients. The posterior bundle runs posterolaterally towards the palatopharynx and the bundle medial spread until to edge gap. File front attached on tendon area triangular on edge posterior palate or in a way direct relate with the tendon of the tensor veli palatini muscle. The function of the levator muscle is to elevate the soft palate and to place the soft palate backwards on the while talking and swallow. Lever veli palatini causes upward, medial, and posterior displacement of the medial tubal cartilage with isotonic muscle contraction with superior and posterior displacement of the levator sling , causing opening of the lumen of the Eustachian tube. This also causes dilation of the membranous portion of the Eustachian tube. Serous otitis media in patients with palatoschisis due to Because dysfunction from muscles tube, especially levator veli palatini. The ability of the levator veli palatini to dilate the Eustachian tube is reduced in palatoschisis. Repositioning of the levator veli palatini during intervelar veloplasty And Furlow double opposing Z-plasty expected can repair This helps dilate the Eustachian tube. ¹

Tensors veli palatine originate from fossa scaphoid from greater wing of sphenoid between the superior tip of the medial pterygoid and the spine of the sphenoid and the adjacent superolateral aspect of the cartilaginous and bony portions along the Eustachian tube. The muscle is triangular in shape, forming a 30–40 degree angle with the Eustachian tube. The tendon of the tensor veli palatini forms a hook on the anterior aspect of the hamulus and enters the soft palate at a 90 degree angle. The tendon spreads out into a horizontal aponeurosis-like bundle covering the anterior quarter of the soft palate. The tensor veli palatini is thinner on patient palatoschisis. A number of file muscle attached on hamulus. The front from file muscle the expand throughout aponeurosis palatine rudimentary to nasal spine part posterior or move to lateral going to edge posterior to the palatine bone. The main tendon curves back to the edge of the fissure and ends in two different ways. First, the tendon is sometimes partially spread And part triangle enter to file front from lever. Second, the tendon is not spread out and inserts anteriorly into the levator veli palatini to form a thick muscle tendon bundle. The tensor veli palatini dilates the Eustachian tube. with interesting to direction inferior, lateral, And anterior. Together with levator veli palatini, the tensor will increase the opening of the tube. Complete fracture of the hamulus can decrease the effectiveness of the tensor veli palatini tube dilation. palatini. The uvula muscle is a pair of muscles that run longitudinally in the midline of the nose and soft palate. The uvula is attached anteriorly to the aponeurosis and posteriorly to the base of the uvula. The uvula has no muscle fibers. ^1,4

salpingopharyngeal muscle is located in the salpingopharyngeal fold, extending from the posteroinferior end of the medial border of the Eustachian tube posteriorly towards the palatopharynx at the junction of the soft palate and the lateral wall of the pharynx. start from palate molle part superior to larynx inferior And posterior pharyngeal wall . The palatopharyngeal muscle occupies 50% of the length of the soft palate. Muscle palatopharynx own two end Which located on part nasal and part oral from lever. End palatal more develop compared to the nasal tip. Fiber from palatopharynx more thin And join with lifter on paramedian area. Two end from palatopharynx join For to form file the broader levator lateral muscle. Most of these fibers run posteriorly to form pillar posterior And to inferior join with superior constrictor . Muscle palatopharynx to form muscle on gap throughout fiber levator and inserts along the posterior edge of the hard palate. The palatopharyngeal muscle together with action antagonist from lifter modulate position palate molle, size, and shape to optimize velopharyngeal closure. Together with the superior constrictor, they cause medial placement of the posterior pharyngeal wall. ^1,4

The palatoglossus muscle is a thin muscle originating from the transverse muscle fibers of the tongue that passes through the superior part of the anterior faucial pillar and enters muscle on palate molle. On palatoschisis, palatoglossus enter to edge of the gap on edge posterior palate hard. Constrictor superior is muscle square shaped originate from limit posterior pterygoid medial around palate hard to tip of the hamulus. It then continues downward and forward turning into the pterygomandibular ligament and extending along the pharynx to form the lateral and posterior walls. The muscle inserts posteriorly into the pharyngeal ligament. Constrictor superior cause movement to medial from wall lateral pharynx by sphincter mechanism palatopharynx. Matter This cause movement to front from the posterior wall of the pharynx by fibers that meet at the posterior midline, is an important component of the Passavant ridge . ^1,4

The palatine artery is a terminal branch of the internal maxillary artery which has several branches to the tonsil and soft palate. It passes through the posterior palatine foramen, just above the periosteum and continues forward near the edge of the alveolar on each side as artery palatine major to incisive fossa . The terminal branches of the palatine artery pass through the incisive foramen and anastomose with the terminal branches of the sphenopalatine artery. The sphenopalatine artery is a branch of the internal maxillary artery. One of its branches descends into the incisive canal and anastomoses with the terminal branches of the posterior palatine artery to supply the palate. The posterior septal arteries arise from the sphenopalatine artery. on roof cavity nose And down vomer to incisive foramen . Artery palatine major give vascularization surface oral on palate hard and has several fine branches to the horizontal plate of maxilla to vascularize the nasal mucosa. The lesser palatine artery vascularizes the anterior half of the oral surface of the soft palate. The ascending palatine artery , a branch of the facial artery, is the largest of the vessels Which enter palate molle. Artery the walk go on to side lateral from muscular constrictor superior to direction lower And front going to palate molle between the tensor and levator palatini. There are two terminal branches, namely the anterior branch And branch posterior. Vascularization palate molle No too threatened by surgery. In bilateral complete labiopalatoschisis, the fusion of the superior labial arteries is still lacking. There is no anastomosis between the posterior septal artery and the greater palatine artery. Therefore, the premaxilla and philtrum receive vascularization from artery septal posterior And lateral And branch terminal of the anterior ethmoidal artery which passes through the columella. The palatal vessels enter the bone And No like part other body Which through periosteum. Therefore it is possible to peel the periosteum from its attachments. with bone without bother vessels blood. Palate The durum and its mucoperiosteal membrane are vascularized by the nasopalatine vessels and by the descending palatine artery . The palatal bone hasseparate blood vessels that protect the palatal bone from necrosis in conventional palatal surgery. ^1,4

The sensory branches of the palate arise from the maxillary branch of the trigeminal nerve. The facial nerve supplies sympathetic fibers to the maxillary portion via the sphenopalatine ganglion. The greater palatine artery descends through the greater palatine canal, emerges through the greater palatine foramen, and courses anteriorly to supply the palatine bone and the mucous membrane of the hard palate. Branches of the sphenopalatine appear from incisive foramen to front palate hard. Palatine fibers minor down through foramen palatine minor, give vascularization on the uvula, palate molle, And tonsils. Supply motor on tensor veli palatine different from muscle velopharynx Which other. Tensors veli palatine innervated by nerve internal pterygoid , a branch of the third mandibular nerve (V3) of the trigeminal nerve. Glossopharyngeal nerve, a pharyngeal branch of the vagus nerve and accessory nerve innervates the motor fibers of the muscles of the pharynx and soft palate except the tensor muscle. veli palatine. Uvula And muscular constrictor superior innervated by facial nerve and pharyngeal plexus. ^1,4

Embryology

Embryological development of the nose and upper lip begins in the fourth week of gestation. The bilaminar prechordal plate is composed of ectodermal elements. And endoderm Also start formed. Structure the will develops into a stomodeum or primitive mouth with five facial prominences including: frontonasal prominences, a pair of maxillary prominences, and a pair of mandibular prominences. These five structures also undergo development. ^1,2

Development lips part on And nose controlled through a number of developmental pathways , including sonic hedgehog (SHH), wingless type (Wnt), bone morphogenic protein (BMP), and fibroblast growth factor (FGF). Fusion of the frontonasal and maxillary processes on the anterior face begins to occur at approximately 32 days of gestation, when the ventrolateral aspect of the frontonasal prominence experience proliferation cellular For to form nasal placodes , Which will to form process nasal medial And lateral. ⁵

Process maxilla Also experience development mesenchymal with rapidly. At 38 days of gestation, fusion begins between these processes and the lateral and medial nasal prominences, around the distal ends of the medial and lateral nasal processes which will eventually lead to further fusion. Development more carry on on lips part on And nose will to be continued with development of the maxillary process causing the nasal pit to move to an anteromedial position, which then leads to maturation of the nasal duct . Complete development of the upper lip occurs at 48 days of gestation, shortly after element epithelial experience apoptosis And element mesenchymal Which remaining will be experience merger end with prominence nasal part medial and the maxillary prominence, ^which is followed by the anteroposterior formation of the primary and secondary palates.5,6

The anatomy of the palate is divided into the primary and secondary palate, with the primary palate primary formed by prominence frontonasal And palate secondary formed by a pair of lateral maxillary prominences. The tongue begins to retract from its position between the lateral maxillary prominences and begins to change from a vertical to a horizontal orientation, eventually undergoing fusion in the normal fetus. Some mechanism Which different Also contribute on migration vertical, including improvement proliferation mesenchymal, improvement component fluid on the network, And various track signaling , including platelets derived growth factor , FGF 10, SHH, and TGFβ3. As the palatal parts meet at the midline, the line of union will to form point middle on palate hard, Then will experience anterior and posterior development from that point. ⁷

Epidemiology

The incidence of palatoschisis in America is reported to be 0.1 – 1.1 cases per 1000 population. While the incidence of labiopalatoschisis is 0.2 – 2.3 cases per 1000 population. Labiopalatoschisis is the most common congenital anomaly in North America. The prevalence of labiopalatoschisis varies quite a bit. between various group ethnicity, including: 3.6 : 1000 on American population original, 2.1 : 1000 on resident Asia, 1 : 1000 on resident Caucasians, and 0.41:1000 in African-Americans. While the incidence of palatoschisis is relatively stable in various ethnicities. In palatoschisis there is a ratio based on sex where Woman more often than man with ratio men to women is 1:2. ^2.9

Etiology And Factor Risk

Development of palatoschisis and/or labioschisis is a process the complex And multifactorial Which involving factor risk Which diverse, such as: mutation genetics, history family, history maternal, And deficiency nutrition. Family history with labiopalatoschisis is factor risk Which strong And first studied in 1942, where Fogh-Anderson first performed a statistical analysis about pattern history family on labiopalatoschisis. Studies genetics in humans And mouse identify TGFβ3 ( transforming growth factor beta 3 ) and MSX1 ( MSH homeobox 1 ) as genes that play an important role in the occurrence of labiopalatoschisis. ²

Most cases of labiopalatoschisis are not a syndrome, although there are various syndrome genetics Which relate with labioschisis and/or palatoschisis. The most common syndrome associated with labioschisis and/or palatoschisis is Van der Woude syndrome, an autosomal dominant syndrome. The most common syndrome associated with palatoschisis is an autosomal dominant syndrome caused by a microdeletion or disruption of chromosome 22q11.2. Other syndromes associated with labiopalatoschisis include: DiGeorge syndrome, Stickler syndrome, popliteal pterygium syndrome and many more. ²

Environmental factors are also believed to play an important role in labiopalatoschisis. These factors are grouped into several categories, namely: maternal health, teratogenic substances, and nutritional factors. Association between defect on moment born And disturbance on mother like diabetes mellitus And diabetes gestational studied in a way deep. Improvement The incidence of congenital malformations is stated to be found in diabetes mellitus. Maternal obesity has also been studied as a risk factor for labiopalatoschisis, where women with a BMI of more than 29 kg/m2 ^have a 1.3 times greater risk of having a child with labiopalatoschisis. Teratogenic treatments that can cause labiopalatoschisis covering sour valproate, phenytoin, retinoic acid, And thalidomide. History smoke on mother Also own implications in the occurrence labiopalatoschisis with risk 1.2 time more greater than the normal population without risk factors. Although alcohol consumption during pregnancy is known to increase the risk of congenital malformations, specific relationship between the occurrence of labiopalatoschisis and history of consumption alcohol on mother Still Not yet known in a way Certain. A Animal studies have found that folic acid supplementation is considered to have a protective effect on the occurrence of labiopalatoschisis. However, a case-control study in the United States found that folic acid supplementation was not associated with a decrease in the incidence of labiopalatoschisis. ^9,10

Diagnosis Prenatal And Screening

Prenatal diagnosis of labiopalatoschisis, along with developmental anomalies more frequently with the increasing use of prenatal screening with ultrasonography. Approximately 50% of children with labiopalatoschisis also have other congenital anomalies. In larger studies, labiopalatoschisis deformities can be identified by ultrasonography in 30-55% of cases at 24 weeks' gestation. The high variability in detection rates is believed to be due to differences in ultrasound protocols at each health center. The ability to identify labiopalatoschisis with USG relatively low around 1.4%. Number detection with Newer modalities, such as 3D ultrasound and MRI have not been further described. ¹ Purpose  detection  defect  orofacial  on  time  prenatal  is  For

prepare parents to obtain appropriate genetic counseling, support emotional, And planning therapy. On counseling person old it would be better too to discuss about possibility risk birth child second/next with orofacial defects. A population study found that there was a risk of children who born furthermore Also can born with labiopalatoschisis. When first degree family with labiopalatoschisis without syndromic then the possible risk of having a child with labiopalatoschisis is 3% to 4%. ¹¹

Operation

Therapy main on palatoschisis is with done surgery or operation reconstruction of the cleft palate. The right time to do palatoplasty A little different on various center service. According to Dao, palatoplasty surgery should be done before age 18 month, that is between age 10 – 12 months to avoid delays in the development of speech skills. ¹³ According to Agrawal,age optimal done palatoplasty is age 6 – 12 month and at the latest at the age of 10-12 months. ¹² Speech development is also a consideration.

The operation is performed under general anesthesia, the patient is in the supine position with the neck extended with a pillow under the shoulders. A RAE ( right angle endotracheal ) endotracheal tube with packing in the throat is used. In reconstruction palate, packing throat more small than that used on reconstruction labioschisis. Dingman mouth gag Also used on operation. Dingman mouth gag can cause edema of the tongue if used for more than 2 hours. Lidocaine 0.5% And epinephrine 1:200,000 infiltrated on palate with maximum dose of 1 ml/kg. The operation begins after 7 – 10 minutes after injection. ¹

Cleft palate surgery is performed with the surgeon standing at the patient's head. Marking and draping are performed with a bipolar cautery and a coblator, if available, for hemostasis. The incisions on each side are made with the contralateral hand. The greater palatine neurovascular fibers appear through foramen palatine major on aspect posterolateral palate hard. Liberation circular on adhesion in around pedicle And the stretch that gentle on pedicle important For give closing Which free pressure

Furlow double opposing Z- plasty

Furlow described the double opposing Z-plasty technique for cleft palate reconstruction in 1980. A Dingman retractor is placed to hold the mouth open and retract the tongue. A lateral relaxing incision is made in the crease where the buccal wall and soft palate meet laterally, extending along the posteromedial aspect of the maxillary tuberosity to the surface of the tongue at hard palate. Palpation is performed the perfect Which located on part posterior from maxillary tuberosity . Marking is done at the junction of the soft palate/hard palate and the base of the uvula. The medial aspect of the cleft edge is also marked, extending from the junction of the soft palate/hard palate to the base of the uvula, over the oral surface with a thickness of 1 mm to allow sufficient mucosa to cover the nasal passage. Musculomucosal ridge on base posterior marked on part left patient, from hamulus to the meeting palate molle And palate hard. Jabir mucosa oral on the basis anterior part right marked from base uvula until hamulus. Care is taken to maintain an adequate mucosal bridge between the incisions to maintain vascularization of the flap. ^1,2,12,13

Furthermore, done infiltration on palate molle with epinephrine which is disbursed, And dissection was performed with scissors on uvula. Jabir The musculomucosa of the left posterior floor is incised along the marked line. Deeper dissection separates the musculature of the soft palate from the underlying nasal mucosa. Maintenance Which Good must done For ensure three abnormal attachments of the levator are released, namely: the posterior edge of the hard palate, the tensor aponeurosis, and the superior pharyngeal constrictor muscle. This maneuver will allow jabir musculomucosa posterior side left transformed from the anteroposterior orientation transverse to the posterior orientation. ^1,2,8,12,13

Jabir mucosa oral base front side right Then incised throughout edge of the gap And base uvula to hamulus. Network soft Which underlying withdrawn so that it can be divided with dissecting scissors until the palatopharyngeal and palatoglossal aponeuroses are identified and preserved. Submucosal dissection is continued laterally while still paying attention to the subcutaneous layer and mucous glands which are important to help the vascularization of the mucous membrane. Abnormal relationships between the muscles lifter And edge posterior from palate hard identified And separated 2–3 mm posteriorly, to preserve the nasal mucosa along the posterior edge of the hard palate for nasal reconstruction. Dissection is performed posterolaterally from the point where the levator exits the skull base beneath the superior constrictor muscle. ^1,2

The mucoperiosteal ridge of the hard palate is incised and mobilized with a Blair elevator, identification and preservation of the neurovascular pedicle is performed upon exit. from posterolateral foramen palatine. Withdrawal Which gentle on periosteum around pedicle often times required to be able to move the jabir hard palate properly. The nasal mucosa is dissected from the undersurface of the maxillary prominence throughout edge bone from gap with elevator Woodson. If If necessary, the vomer mucoperiosteal flap is used to close the nasal portion of the hard palate. 1,2,12,13

Jabir nasal from palate molle made. Jabir mucosa nasal base front The left side is designed and incised from the base of the uvula to the base of the levator veli palatini part. posterolateral Which go out from skull base. Jabir musculomucosa nasal posterior base side right incised on point posterior from meeting palate hard and the soft palate, extending posterolaterally from the base of the levator veli palatini which emerges from the skull base, leaving a cuff of nasal lining along the posterior edge palate hard For repair layer nose. Jabir layer the nose will transposed And inserted on technique Z-plasty . On a number of case where closure of the nasal lining is difficult, a thin acellular dermal matrix can be used to assist. Careful handling is required to avoid suturing the graft and levator sling , ensuring that the sutures are done on layer nasal, aponeurosis tensors, And edge posterior from the palate molle. After reconstruction on layer nasal finished to be continued with reconstruction of the uvula. The oral mucosa was transposed using the Z-plasty technique , moving jabir musculomucosa base posterior side left to orientation transverse to complete the reconstruction of the soft palate. Mucoperiosteal flap of the hard palate inserted on line middle with sewing use thread which can be absorbed along the anterior edge of the lingual surface of the alveolar incision. 1,2,12,13

Straight line repair with intravelar veloplasty

Cleft palate reconstruction technique with straight line repair with intravelar veloplasty has Lots used by for doctor surgery. Principle from palate reconstruction with straight line with intravelar veloplasty similar with Furlow palatoplasty Where element important on technique the is muscle restoration procedure in the levator sling to a transverse orientation from an abnormal anteroposterior orientation. ²

A medial incision is made at the edge of the cleft from the base of the uvula extending anteriorly along the cleft. Sharp dissection is performed in the submucosa while taking into account the submucosal fat and mucous glands of the oral mucosal ridge. mucosa oral expanded until aspect lateral from palate molle with objective to gain adequate access on both sides of the levator muscle. Wide dissection was performed between muscle lifter And layer nasal, separate palate molle into three divided layers.

Muscle lifter veli palatine in a way Be careful released from its abnormal attachment to the posterior border of the hard palate, tensor aponeurosis, and constrictor muscle pharynx superior. Nasal layer throughout gap reconstructed using acellular dermal matrix to adhere the closure if there is an area closing Which loose or defect mucosa Which No can closed primary. When the nasal mucosal layer has been reconstructed, posterior transposition is performed from muscular lifter veli palatine to orientation transverse, Where muscle These are then subjected to the proper pressure to be sewn together at the center line. After closing on muscle the, done sewing with absorbable suture for oral mucosal closure. ²

Complications

Some complications of palatoplasty that can occur are the formation of fistulas, impaired speech function, and maxillary hypoplasia. Palate fistulas cause partial loss of nasal air and nasal regurgitation of fluid. Fistula often occur on gap palate Which wide And more often happen after surgery with two flap technique compared with Furlow Z-plasty . Early closure of cleft palate fistula after 3 months from the first operation is recommended especially with mucoperiosteal flap or von Langenbeck flap. Palate patch can help in fistula management if there is delay in operation. ¹

Normal speech ability is the main goal of palatoplasty . With operation early before age 1 year, operation reconstruction Which Good with intravelar veloplasty And maintenance operation Which Good can produced speaking ability Which Good. Reconstruction primary on palatoschisis should done at the age of 9 – 12 months. To get speech function development which is optimal then reconstruction palate Which done on age more from 15-18 months is not recommended unless considering the patient's comorbid or syndromic illnesses. The surgical results are also felt to be better in nonsyndromic patients compared to syndromic patients, patients with unilateral clefts compared to bilateral, and patients with narrower clefts. A study by Wu et al. found that that width gap on palatoschisis own connection positive with duration time operation, delay function talk, And the emergence hypernasal voice. ^1,2,14

Growth maxilla normal is objective secondary from palatoplasty .We must avoid raw area Which wide on palate hard For minimize the occurrence of scarring. Fistulas will require additional procedures for the healing process. closing Which will increase formation network scar And decreased maxillary growth. Maxillary hypoplasia often occurs in cleft palate with syndromic Which usually need procedure advanced on puberty. ¹

DISCUSSION

Cleft palate or palatoschisis is a condition where there is an abnormal gap in the roof of the oral cavity which occurs due to the failure of the fusion process. process facialist on time pregnancy. Gap palate can It stands alone or can be accompanied by a gap in the lip or labiopalatoschisis. Matter This can happen Because development embryology palate which also accompanies the development of the lips during pregnancy. ^1,2,3

The overall incidence of labiopalatoschisis is about 1.5 per 1000 births. life (around 220,000 case new per year) with variation Which wide across geographic regions, ethnic groups and the nature of the cleft itself. The highest incidence is in Asians (0.82 – 4.04 per 1000 live births), the intermediate incidence in Caucasian (0.9 – 2.69 per 1000 birth life) And low in Africa (0.18 – 1.67 per 1000 birth life). China show 1.76 per 1000 live births, while Japan reported 0.85-2.68 per 1000 live births of labiopalatoschisis. While the incidence of palatoschisis is relatively stable in various ethnicities. In palatoschisis there is a ratio based on sex where women are more frequent than men with a male to female ratio of 1:2. ^2,9,15

Development of palatoschisis and/or labioschisis is a complex process And multifactorial Which involving factor risk Which diverse, such as: mutation genetics, history family, history maternal, And deficiency nutrition. Family history with labiopalatoschisis is factor risk Which strong And first studied in 1942, where Fogh-Anderson first performed a statistical analysis about pattern history family on labiopalatoschisis. Studies genetics in humans And mouse identify TGFβ3 ( transforming growth factor beta 3 ) and MSX1 ( msh homeobox 1 ) as genes that play an important role in the occurrence of labiopalatoschisis. ² Environmental factors are also believed to have an important role in labiopalatoschisis.  Factors  the  grouped  become  a number of categories, namely: maternal health, teratogenic substances, and nutritional factors. Van Aalst et al. found that there was a role for environmental factors such as maternal health, smoking habits, alcohol consumption, and drug use during pregnancy. pregnancy as wrong One factor Which participate play a role to the occurrence of labiopalatoschisis. ^9,10

Prenatal diagnosis of labiopalatoschisis, along with other developmental anomalies, is becoming more common with the increasing use of prenatal screening with ultrasonography. Approximately 50% of children with labiopalatoschisis also have other congenital anomalies. Larger studies have shown that labiopalatoschisis deformities can be identified by Ultrasonography on 30-55% case on age gestation 24 Sunday. High variability in numbers trusted detection occurs due to differences in ultrasound protocols. each center health. Ability identification labiopalatoschisis with USG relatively low around 1.4%. Number detection with modality Recent studies, such as 3D USG and MRI have not been further described. ¹¹ Transabdominal ultrasonography (TA-US) performed in the second trimester of pregnancy is an option. First for screening orofacial cleft . TA-US widely performed because it is easy and does not cause radiation. ¹⁶ In addition, there is also 3-D US such as Ultrasonographic surface rendered oro-palatal (SROP) which is a 3D reconstruction image of the fetal perioral region. SROP can see the superior lip, alveolar ridge , and secondary palate in one scan. SROP is used for the management of cleft lip with or without cleft palate , uni or bilateral which has been diagnosed at 22-28 weeks of gestation. However, 3-D US is less commonly used because it takes longer. ¹⁷ In addition to ultrasound which is usually performed at 24-26 weeks of gestation, MRI can also be performed at 29-30 weeks of gestation if ultrasound examination is too difficult. The certainty of the diagnosis will be confirmed when a clinical examination is performed on the baby who has been born. ¹⁸

Therapy main on palatoschisis is with done surgery or reconstructive surgery on the cleft palate. The right time to do palatoplasty A little different on various center service. According to Dao, operation palatoplasty should done before age 18 month, that is between age 10 – 12 months to avoid delays in the development of speech skills. ¹³ According to Agrawal, age optimal done palatoplasty is age 6 – 12 month and at the latest at the age of 10-12 months. ¹² Speech development is also a consideration.

There is diverse technique operation For reconstruction gap palate. The choice of technique used is highly dependent on the patient's condition, the extent of the cleft palate, and the surgeon's expertise. However, the principles of palatoschisis surgery must remain a priority. The principles of palatoplasty are closing the gap, correcting the abnormal position of the muscles in the palate, reconstructing the muscle sling , retropositioning the soft palate as best as possible, minimizing the raw area , suturing with tension-free , and closing in layers of palatum. Surgical techniques and incisions in cases of palatoschisis continue to develop. Until now, several surgical techniques are known, namely: von Langenbeck repair, two flap palatoplasty, Furlow double opposing Z-plasty , and straight-line repair with intravelar veloplasty . ^1,12,13

The von Langenbeck operation technique has the advantage of requiring only minimal dissection and the technique tends to be simple, but this technique has the disadvantage of not increasing the length of the palate due to the limitations of proper closure and the additional gap. The two flap technique is most commonly used for closure in gap complete, there is no additional width that is usually done to close the gap in the alveolar but has a raw area that requires good care. The double Z-plasty technique is good for narrow gaps or if there is a submucosal gap. With this technique, it is able to increase the movement of the soft palate and improve closure velopharynx through reconstruction lifter sling so that expected phonation function will be better. The disadvantages of this technique are that it is difficult to perform on wide gaps and the difficulty of dissection and increased operating time compared to other techniques. ^1,2,12,13

CONCLUSION

Cleft palate or palatoschisis is a condition where there is an abnormal gap in the roof of the oral cavity which occurs due to the failure of the fusion process. process facialist on time pregnancy. Gap palate can It stands alone or can be accompanied by a gap in the lip or labiopalatoschisis. Matter This can happen Because development embryology the palate Also along with development lips on time pregnancy. The existence of gap in palate can cause a number of problem, that is: disturbance on speech function, swallowing function, hearing, malposition of teeth, respiratory function, development face, And disturbance psychological from patient And parents of the patient. Prenatal detection is expected to help the management of palatoschisis. The purpose of prenatal detection of orofacial defects is to prepare parents to obtain appropriate genetic counseling, emotional support, and therapy planning. Management of palatoschisis requires cooperation of a multidisciplinary team with surgery being the primary therapeutic option.

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