## 1 Introduction  
Cleft lip and palate (CLP) is the most common craniofacial malformation, affecting one in every 500 to 700 live births, thus accounting for about 220000 new cases each year worldwide with disparity across geographic areas, racial groups, and socioeconomic status [1]. No effective preventive measures exist. The ongoing manifestation of CLP as well as its broad implications on psychological well-being, speech, orofacial development, and therapeutic burden underline the need to identify and targeting the intrinsic causes [2; 3; 4]. The etiology of CLP is complex, which could occur as a result of multiple genetic and environmental factors or a combination of both [5; 6]. The clefting of the lip and/or palate may occur in a unilateral or bilateral fashion, and the embryological pattern of clefting results from a fusion failure during the development of maxilla and palate. The normal fusion of the medial frontonasal process with the maxillary process of the first pharyngeal arch takes place at 4-6 weeks of gestation forming a primary palate [7]. A complete fusion failure results in a cleft of the lip through the vermillion border that extends to the nasal sill and in a cleft of the alveolar process [7]. The cleft of the secondary palate occurs at 8-12 weeks of gestation due to fusion failure of the palatal shelves of the maxillary processes [8; 9] that results in a cleft in the palatal roof and soft palate that extends to the uvula. Affected children have a range of both functional and esthetic problems. They comprise feeding difficulties at birth due to incomplete oral seal, swallowing, nasal regurgitation, respiratory problems, hearing difficulties due to abnormalities in the palatal musculature, and speech impairments due to air escape and articulation problems [10]. Therefore, an ideal early and complete cleft treatment would allow the normalizing of food intake, speech development, growth and esthetics - while imposing minimal treatment burden to child and family. Several different surgical protocols have been advocated for managing children with CLP. The amount of palatal mucosa present and timing of the surgery play important roles in healing success after surgery. Clefting of the palate at birth structurally results in 16% less palatal mucosa compared with a normal child [11] and anatomically smaller palatal shelves on the cleft and noncleft sides [12; 13]. The intrinsic tissue deficiency in the palate has no spontaneous improvement trend. It persists until adulthood in both unilateral cleft lip and palate (UCLP) and bilateral cleft lip and palate (BCLP) [14]. A scientific basis was proposed in 2005 for determining the optimal conditions for palatal cleft closure in complete UCLP and BCLP [15]. This should be performed when the surface area of the cleft space does not exceed 10% of the surrounding palatal surface bounded by the alveolar ridges, because under these circumstances the facial growth is less affected, independent of the patient's age at surgery [15]. This recommendation may be applicable for clefts which are smaller in size, whereas in cases of wider clefts it is imperative for surgeons to mobilize the tissue adjoining the cleft more extensively which may lead to open wound areas that undergo secondary healing. This may lead to structural tissue deficiencies and pronounced interference with the normal growth and development of the midface [16]. The use of a palatal appliance for presurgical maxillary orthopedics is a widely accepted non-surgical therapeutic adjunct for addressing the problem of tissue deficiency in wider clefts. Such an appliance approximates the palatal shelves and thus reduces the alveolar and palatal cleft width prior to surgery [17]. The effect of those appliances on the growth is controversial. Some proponents of this technique have claimed that gradual adaptations of the appliance can stimulate palatal tissue growth [18; 19]. Others have shown that this approach resulted in retarded growth of the palatal tissue [20].