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An oral palatopharyngoplasty, was a surgical procedure developed in the 1980’s and first published in 1992. The purpose of the procedure was to reduce the incidence of palatal instability (PI) and subsequent dorsal displacement of the soft palate (DDSP). In the years following the first publication, the procedure underwent numerous modifications to improve the likelihood of obtaining useful increases in tension in the tissues supporting the palatine aponeurosis and at the same time reducing the incidence of wound breakdown. These changes have led to the present technique now referred to as a Modified Oral Palatopharyngoplasty or Modified Ahern Procedure.

Pathologic anatomy of the soft palate, part 2: The soft tissue lever arm, pathology, and reconstruction. In part two, we consider the soft tissue components of the soft palate: Epithelium, fascia, muscles, arterial supply, and innervation. These velar tissues constitute a functional “lever arm” for control of speech and swallowing. Fascia and peripheral nerves arise neural crest originating from rhombomeres 2–7. Muscles arise from paraxial mesoderm (PAM) of somitomeres 4, 6, and 7. Lateral plate mesoderm lying outside of PAM provides the building blocks of the circulatory system. Neurovascular analysis discloses the soft palate to have three developmental zones with distinct sources of neurovascular supply. Emphasis is placed on the anterior third of the palatine aponeurosis; this critical structure determines where the levator complex will insert. The basic field defect of soft palate clefts arises from insufficiency of the lesser palatine neurovascular pedicle affecting the posterior palatine shelf and anterior 1/3 of the palatine aponeurosis. This leads to forward displacement of the levator complex and pathologic insertion onto the bony margin of the cleft site. Soft-tissue disruption will then be presented in terms of the simple genetic loop between bone morphogenetic protein 4 (BMP-4) and Sonic hedgehog. The migration of soluble factors such as BMP-4 from their origin with developing bone to the free border of the epithelium permitting fusion of adjacent structures.

In human fetuses, the palatine process of the maxilla is attached to the inferior aspect of the horizontal plate of the palatine bone (HPPB). The fetal palatomaxillary suture is so long that it extends along the anteroposterior axis rather than along the transverse axis. The double layered bony palate disappears in childhood and the transverse suture is formed. To better understand the development of the double layered bone palate, we examined histological sections obtained from 25 fetuses of gestational age 9-11, 16-18 and 30 weeks. The double layered palate was seen in all of the specimens examined. Inferior angulation of the posterior end of the HPPB was evident at 9-11 weeks, but the initial palatine aponeurosis did not attach to the angulation but to a slightly anterior site. Both the maxilla and the HPPB were tightly attached to the vomer at 16-18 weeks. In both bones, bilateral plates met at the midline. The palatomaxillary suture was filled with short, randomly arranged collagen fibers. The nasal end of the suture was covered by a tight periosteum. Immunohistochemical examination of 3 fetuses at 16-18 weeks showed: 1) no expression of versican, tenascin-c or type II collagen in the suture; 2) few mitotic cells positive for proliferating cell nuclear antigen; 3) no or few CD34-positive developing vessels; and 4) no CD68-positive macrophages. These findings suggested that the fetal palatomaxillary suture was inactive for reconstruction and growth and that soft palate muscles likely did not contribute to the development of the double layered configuration.

The palatine aponeurosis is a thin, fibrous lamella comprising the extended tendons of the tensor veli palatini muscles, attached to the posterior border and inferior surface of the palatine bone. In dentistry, the relationship between the “vibrating line” and the border of the hard and soft palate has long been discussed. However, to our knowledge, there has been no discussion of the relationship between the palatine aponeurosis and the vibrating line(s). Twenty sides from ten fresh frozen White cadaveric heads (seven males and three females) whose mean age at death was 79 years) were used in this study. The thickness of the mucosa including the submucosal tissue was measured. The maximum length of the palatine aponeurosis on each side and the distance from the posterior nasal spine to the posterior border of the palatine aponeurosis in the midline were also measured. The relationship between the marked borderlines and the posterior border of the palatine bone was observed. The thickness of the mucosa and submucosal tissue on the posterior nasal spine and the maximum length of the palatine aponeurosis were 3.4 mm, and 12.2 mm on right side and 12.8 mm on left, respectively. The length of the palatine aponeurosis in the midline was 4.9 mm. In all specimens, the borderline between the compressible and incompressible parts corresponded to the posterior border of the palatine bone.

This biomechanical study aims to characterize the nasal mucosa during palatoplasty, thereby describing the soft tissue attachments at different zones and quantifying movement following their release.Palatal nasal mucosa was exposed and divided in the midline in 10 adult cadaver heads. Five consecutive maneuvers were performed: (1) elevation of nasal mucosa off the maxilla, (2) dissection of nasal mucosa from soft palate musculature, (3) separation of nasal mucosa from palatine aponeurosis, (4) release of mucosa at the pterygopalatine junction, and (5) mobilization of vomer flaps. The mucosal movements across the midline at the midpalate (MP) and posterior nasal spine (PNS) following each maneuver were measured.At the MP, maneuvers 1-4 cumulatively provided 3.8 mm (36.9%), 4.9 mm (47.6%), 6.1 mm (59.2%), and 10.3 mm, respectively. Vomer flap (10.5 mm) elevation led to mobility equivalent to that of maneuvers 1-4 (p = 0.72). At the PNS, cumulative measurements after maneuvers 1-4 were 1.3 mm (10%), 2.4 mm (18.6%), 5.7 mm (44.2%), and 12.9 mm. Here, vomer flaps (6.5 mm) provided less movement (p 0.001). Maneuver 4 yielded the greatest amount of movement of the lateral nasal mucosa at both MP (4.2 mm, 40.8%) and PNS (7.2 mm, 55.8%).At the MP, complete release of the lateral nasal mucosa achieves as much movement as the vomer flap. At the hard-soft palate junction, the maneuvers progressively add to the movement of the lateral nasal mucosa. The most powerful step is release of attachments along the posterior aspect of the medial pterygoid.

The purpose of this communication is to explore in detail the developmental anatomy of the soft palate, its pathologies, and strategies for management. Despite the voluminous literature regarding complete cleft palate in its usual presentation, little attention has been paid to the biology of the isolated soft palate cleft. It exists as a spectrum, ranging in severity from the submucous variant, with nothing notable save a groove and a palpable defect of the posterior spine, all the way to a complete disruption of the soft tissue envelope and the horizontal palatine shelves. All these presentations are but variations of common pathology. Much can be gained from a disciplined examination of these. Our discussion includes two parts. The first part is on the embryologic events that generate the mesenchymal building blocks from which the posterior palate is constructed: palatine bone, oral and nasal mucosa, palatine aponeurosis, and muscle slings. Palate structures develop from neural crest and mesoderm; these tissues originate at specific sites along the axis of the embryo and they can be mapped according to the developmental units of the central nervous system (CNS) from which they are innervated. These units, called neuromeres, are specific zones within the neural tube, the boundaries of which are established by the expression pattern of homeotic genes. The forebrain (prosencephalon) has telencephalon and 3 prosomeres, the midbrain (mesencephalon) has 1-2 mesomeres, and the hindbrain (rhombencephalon) has 12 rhombomeres. Each neuromere has a specific neuroanatomic content and is hardwired to specific tissues outside the brain. We next consider a model of the palate which is analogous to a pinball machine that consists of a platform (bone) and mobile “flippers” or lever arms (the velum). In this study, the osseous platform is discussed in detail with neural crest bones being coded by the sensory innervation of their surrounding soft-tissue envelope. Maxilla, palatine bone, and vomers are all derivatives of hindbrain neural crest arising from rhombomere 2 but distributed according to various neurovascular pedicles of the V2 stapedial system, the anatomy of which will be explained in detail. Next, the evolution of palate will be presented as a series of innovations favoring increased metabolic capacity. A final appendix presents a functional classification of cranial nerves which I have endeavored to make straightforward. This will prove useful when reading the second part of this manuscript having to do with the neuromuscular apparatus of the soft palate.

The tissue in the palatal region can be divided into the hard and the soft palates, each having a specialized function such as occlusion, speech, or swallowing. Therefore, an understanding of the mechanism of palatogenesis in relation to the function of each region is important. However, in comparison with the hard palate, there is still a lack of information about the mechanisms of soft palate development. In this study, the authors investigated the contribution of cranial neural crest (CNC) cells to development of both hard and soft palates. They also demonstrated a unique pattern of periostin expression during soft palate development, which was closely related to that of collagen type I (Col I) in palatine aponeurosis. Furthermore, organ culture analysis showed that exogenous transforming growth factor–β (TGF-β) induced the expression of both periostin and Col I. These novel patterns of expression in the extracellular matrix (ECM) induced by CNC cells suggest that these cells may help to determine the character of both the hard and soft palates through ECM induction. TGF-β signaling appears to be one of the mediators of Col I and periostin expression in the formation of functional structures during soft palate development.