Basic Embryology of Trunk
Knowledge of trunk embryology has significant clinical relevance. Many congenital deformities of the chest or abdomen are treated by reconstructive surgeons  ; thus, extensive knowledge of the normal embryologic processes and the aberrations in development of the trunk is of significant clinical relevance. [2, 3]
Much of the understanding of human embryology has been elucidated from extensive experimental manipulations of organisms such as Drosophila melanogaster, chick, and mouse. Human embryology, from conception through the embryonic and fetal periods and, finally, birth, has been characterized in detail.  The development of musculoskeletal structures associated with the trunk of the human body is a multistep process involving differential gene expression as well as cell interactions and cell signaling between precursor tissues. This process occurs during the fourth through eighth weeks of development. The purpose of this review is to provide the reader with an understanding of the development of the structural components of the trunk. The development of the individual organ systems within the trunk is beyond the scope of this review.
The musculoskeletal system associated with the trunk develops from paraxial and lateral plate (somatic layer) mesoderm.  The paraxial mesoderm in the trunk is transiently organized into approximately 40 segmental tissue blocks alongside the neural tube, known as somites, the cells of which segregate into 2 subpopulations. The dorsolateral subpopulation is called the dermomyotome, and the ventromedial subpopulation of cells is known as the sclerotome. Myoblasts differentiating within the dermomyotome eventually form the skeletal musculature of the trunk, while the sclerotome develops into the vertebrae and ribs. The sternum is derived from somatic mesoderm. See the image below.
The cells of the sclerotome shift their position during the fourth week of gestation to surround the spinal cord and the notochord. They organize into ventral and lateral subdivisions. Cells in the ventral subdivision of sclerotome form a sheath around the notochord and become organized into condensed and loosely arranged areas. The vertebral body forms in the loosely arranged areas, while the intervertebral discs form from the condensed areas.
Cells in the lateral subdivision of a sclerotome also organize into condensed and loosely arranged groups, but their position is somewhat offset from similar areas in the ventral subdivision. The vertebral arch is formed from the condensed areas of the lateral sclerotome. Because of the offsetting arrangement of condensed and loose portions of the lateral and ventral sclerotome tissue, the precartilaginous vertebral bodies are formed by tissue from 2 successive somite levels. A more classic view suggests that the caudal section of each sclerotome proliferates into the subjacent intersegmental tissue and, therefore, binds the caudal section of one sclerotome to the cephalic section of the subjacent sclerotome. In forming the intervertebral discs, the enclosed notochord becomes transformed into a nucleus pulposus with adjacent sclerotomic cells forming the annulus fibrosis.
The ribs are also derived from sclerotomic cells of the paraxial mesoderm. Although all vertebrae have a costal process, only those associated with the thoracic vertebrae extend ventrolaterally to form ribs. The sternum arises from paired longitudinal concentrations of the somatic mesoderm in the sixth week of development. The paired sternal bars fuse in the midline to form a cartilaginous sternal plate at around the 10th week. This fusion occurs in a cranial-to-caudal direction, and failure of this fusion leads to the congenital anomaly of cleft sternum. Ossification centers begin to appear at 60 days in a segmental arrangement. Several of these fuse to form the body of the sternum, but the manubrium remains separated from the body by a joint. The xiphoid process does not ossify until birth or later.
Cleft sternum, as well as several other chest wall deformities, is attributable to an error in the normal embryologic development of the chest wall structures. For example, pectus excavatum is the most common congenital chest wall deformity, characterized by excessive depression and, frequently, rotation of the sternum. Occurring in an estimated 1 in 300 live births, pectus excavatum shows a strong male predominance. Although the exact etiology is unknown, the overgrowth of costal cartilages that rotate and curve dorsally is believed to be the cause. Other examples of skeletal anomalies include pectus carinatum, bifid sternum, and thoracoabdominal ectopia cordis.
The dorsolateral subpopulation of somatic cells is called the dermomyotome. These cells maintain their segmental arrangement and give rise to a new layer of cells, the myotome, which provides the skeletal musculature for its own segment. The "rearrangement" or organization of sclerotomes into definitive vertebrae causes the myotomes to overbridge the intervertebral discs, allowing for movement of the spine. The remaining subset of cells, after migration of the myoblasts from the myotomes, is referred to as the dermatome, and forms the dermis on the dorsal side of the embryo.
A segmental nerve associates with the dermatome and the myotome. This early contact of the nerve and differentiating muscle not only provides motor innervation, but also provides sensory innervation, which develops to recognize pressure, touch, and temperature from the skin surfaces. This area of skin is supplied by branches of a specific single spinal nerve and, eventually, contributes to the dermis of the skin and is known as a dermatome. Although growth causes some changes in the original segmental size, these distinct dermatome patterns are maintained throughout life. The dermis on the ventrolateral side of the embryo is derived from the somatic mesoderm.
The cells of the myotomes subdivide into an epimere and hypomere. The epimeres give rise to the skeletal muscles of the back. The hypomeres differentiate into the skeletal muscles in the lateral and anterior regions of the thorax and abdomen. The hypomere splits into 3 layers, which, in the thorax, represent the external intercostals, the internal intercostals, and the innermost intercostals or transverse thoracic muscle. In addition, at appropriate axial levels, myoblasts from the hypaxial myotomes enter the developing limb buds, where they form the skeletal muscles of the limbs. The musculature of the anterior chest and abdominal wall is also derived from the myoblasts originating from hypomeres.
Poland syndrome consists of a variable constellation of anomalies that include congenital absence of the sternal head of the pectoralis major. Other muscle anomalies may exist, including deficiencies of the latissimus dorsi, serratus anterior, deltoid, supraspinatus, and infraspinatus muscles. Other associated conditions that may occur include aplasia or hypoplasia of ipsilateral breast, athelia (congenital absence of the nipple areolar complex), abnormalities of the ribs and costal cartilages, subclavian artery aplasia, axillary fat or hair absence, hand hypoplasia, and brachysyndactyly. In severe cases, acheiria, congenital absence of one or both hands, or an atrophic limb may occur.
In the abdominal region, myoblasts from the hypomeres migrate ventrally and laterally as the primordia of the right and left rectus abdominis muscles. Prior to the anterior fusion of rectus muscles, the developing mesoderm of the future anterolateral abdominal wall splits into 3 layers that ultimately give rise to the internal oblique, external oblique, and transversus abdominis muscles. Dorsally, the posterior serratus muscles develop from the superficial layer of the hypomere. 
As the anterior abdominal wall is developing, the intra-abdominal contents are also developing. Development of the primary intestinal loop is characterized by rapid growth and simultaneous expansion of the liver, which leads to a physiologic umbilical herniation. At approximately the end of the third month, the herniated intestinal loops begin to return, which, in some cases, may lead to a failure of the loops to completely return into the abdominal cavity. See the image below.
Mild umbilical hernias gradually close spontaneously in the postnatal period; however, more severe cases of failure of the abdominal wall to fuse completely can lead to an omphalocele or gastroschisis. Omphaloceles are differentiated by the presence of amnion or peritoneal covering, whereas gastroschisis are characterized by the complete absence of peritoneal covering and are thought to occur secondary to an abdominal wall weakness caused during the involution of the right umbilical vein early in development. Exstrophy of the urinary bladder may be present, as well as solid organ eventration with large omphalocele defects. In addition, associated congenital defects tend to be more severe with omphaloceles.
Several genetic and molecular techniques have been used to determine the source of myogenic progenitor cells and their developmental influences. Skeletal muscle differentiation requires a family of transcription factors known as myogenic regulatory factors. Most congenital muscle diseases and structural abnormalities have at least been mapped to chromosomal regions. Myogenic progenitor cells (MPC) of the somite originate from the dermomyotome and differentiate to form primary myofiber scaffolding. Continual muscle growth occurs through the addition of secondary myofibers from fetal myogenic progenitors. Secondary fibers acquire the characteristics of fast fibers, whereas the primary fibers tend to become slow fibers. By the end of the third month, cross-striations typical for skeletal muscle appear.
The limbs appear during the fourth week as buds covered by surface ectoderm with a core of somatic mesoderm.  During week 7, myoblasts from the dermomyotomes at appropriate axial levels migrate into the limb and organize as dorsal and ventral premuscle masses. At the distal edge of each limb bud is a thickened region of ectoderm, called the apical ectodermal ridge, which is an important signaling center for the outgrowth of a limb bud. Failure of this ectodermal ridge to develop leads to amelia, the absence of limb growth.
The myoblasts in the premuscle masses eventually form the skeletal muscles of the limb and are organized into flexor and extensor compartments. The upper limb bud appears first at axial levels C5-T1, followed shortly (in 1-2 days) by the appearance of the lower limb buds at axial levels L2-S3. Shortly after the limb buds are formed, neural tissue penetrates into the mesenchyme and innervates the dorsal and ventral premuscle masses.
A dermatome is a predictable area of skin in which afferent nerve fibers transmit impulses to a single posterior spinal root. The dermatomes of the developing limbs come primarily from the brachial plexus via the cervical nerve roots, while the dermatomes of the trunk arise primarily from the thoracic posterior spinal nerve roots with much smaller contributions from the lumbar and cervical spinal nerve roots. At around the sixth week of development, the limbs begin to rotate. The upper limbs rotate laterally, and the lower limbs rotate medially around the central axis of each limb. This explains the spiral dermatome distribution seen in the adult lower extremities.
The fingers and toes of the hands and feet, respectively, are the last structures of the limbs to be differentiated. Multiple limb and digit anomalies may occur such as duplication of digits (polydactyly) or fusion of digits (syndactyly).