The nerve associated with the second arch of the throat is the facial nerve (CN VII). It innervates all the muscle derivatives of the 2nd arch – the muscles of facial expression, stapedius, stylohyoid, platysma and the posterior abdomen of the digastrique. Each pharyngeal arch with its associated pouch and spine carries its own cranial nerve, which innervates the structures that develop from this arch. (Note: In older texts, throat slits/arches/pockets are called branch cracks/arcs/pockets) Failure of the fourth sac leads to impaired formation of the ultimobranchial body of the thyroid gland. These cells are responsible for secreting calcitonin in response to high serum calcium levels, downregulation of osteoclast function, and calcium reabsorption in the kidneys. Failure to develop parafollicular cells could lead to elevated serum calcium levels. Hypercalcemia affects the functioning of the brain, leading to lethargy, fatigue and confusion, causing gastrointestinal disorders and can induce cardiac arrhythmias. With ECG, hypercalcemia is observable by a shortened QT interval (<300ms). The second pharyngeal arch forms structures that are innervated by the facial nerve; Many of these structures help us make facial expressions.
There are also four pharyngeal membranes and, as mentioned above, these structures connect the opposite slits and pockets to each other. Below is a list describing the position of individual membranes and, if necessary, the structure of the adult: dorsal part of the sac 3: forms the lower parathyroid glands – the main (or main) and oxyphilic cells are derived from the endodermal mucosa of the ventral part of the sac of the sac 3: forms the thymus – reticular epithelial cells (including those, which include the thymus or hassall blood cells) are derived from the endodermal lining of the sac. Precursors of bone marrow T cells infiltrate the cortex to establish the definitive thymus. The fourth pharyngeal sac is responsible for the development of the upper region of the parathyroid gland and ultimobranchial body. Together, the third and fourth pharyngeal sacs play a crucial role in calcium and phosphate homeostasis via parathyroid gland function. Ultimobranchial cells grow in the C cells of the thyroid gland, which produce calcitonin in response to high serum calcium levels. The fifth and sixth pharyngeal sacs connect to the fourth pharyngeal pouch. The pathophysiology of pharyngeal pouch malformations covers a wide range of diagnoses due to the different derivatives of each bag.
Most of the recognizable abnormalities in the development of pharyngeal pouches that cause DiGeorge syndrome, branchio-oto-renal syndrome and congenital cysts are discussed below. Congenital cysts resulting from the development of the third and fourth arch of the throat can occur in newborns. Cysts tend to be large and filled with fluid and air, which displaces organs such as the trachea and anterior esophagus, as their location is in the anterior neck. In some cases, cysts attach to organs such as the thyroid gland, and in other cases, abscesses form, compressing the airways and causing shortness of breath. [21] Dorsal part of pouch 4: forms the upper parathyroid glands – the main (or main) and oxyphilic cells are derived from the endodermal mucosa of the sac The first pharyngeal arch is also part of the temporal bones as well as the bones of the cheekbone or cheekbones. As a reminder, you might think of Ziggy Stardust – who, we all agree, had prominent cheekbones! Pharyngeal sac derivatives produce the tissues necessary for hearing, calcium homeostasis and an adequate immune response. The first pharyngeal pouch develops in the cavity of the middle ear and the Eustachian tube, which connects the tympanic cavity to the nasopharynx. The inner surface of the Eustachian tube is covered with a mucous layer of hair cells, supporting cells, secretory cells and connective tissue. Hair cells in the Eustachian tube allow secretions from the middle ear cavity to enter and flow into the nasopharynx. The main function of the Eustachian tube is to balance the pressures between the ambient air pressure and the middle ear by allowing air to enter the middle ear cavity.
Failure of hair cells leads to pathologies such as otitis media with effusion, which lead to conductive hearing loss. The role of early innervation in tooth formation has been the subject of considerable interest (Christensen et al., 1993). Epithelial thickening to form the dental lamina begins about 6 weeks before innervation. When the epithelial buds develop, the nerve fibers grow towards them, with the tooth follicle receiving its first nerve fibers at the cap stage. After 15 weeks of CP, a dental nerve is connected to each developing tooth. Fibres are observed in the dental cell after 22 pc weeks, after the onset of dentinogenesis (Christensen et al., 1993). The development of the pharyngeal sac is hypothetically independent of the migration from the neural crest to the endoderm. [4] Neural kidney ablation experiments conducted showed that the endodermal pharyngeal pouch was not affected by the removal of the neural crescent. [5] [2] The expression of transcription factors in the endoderm results in the formation of pockets and pockets between each pharyngeal arch.
Ventral part of sachet 4: forms a diverticulum called ultimobranchial body, whose cells migrate into the thyroid gland and differentiate into parafollicular (C) cells of the thyroid gland. 1. Formation: The swelling of the bottom of the 3rd and 4th pharyngeal arches invades the 2nd arch and merges with the anterior 2/3 of the tongue. Thus, the posterior 1/3 of the tongue is derived from the 3rd and 4th arches and there is NO contribution of the 2nd pharyngeal arch in the adult language. Intrinsic musculature is also derived from occipital myoblasts. The fusion line of the anterior and 1/3 posterior 2/3 of the tongue is indicated by the terminal sulcus. The first pharyngeal arch consists of two parts: Below is a table summarizing the derivatives of branch sacs: The 2nd, 3rd and 4th columns form only temporary cervical cavities – which are then erased by the rapidly expanding 2nd pharyngeal arch. We remember it, because if we chew with structures formed by the first arc, we could end up biting the front part of the tongue! Proper development of the pharyngeal sac ensures adequate tissue formation in vital processes such as hearing, adequate immunity and regulation of calcium homeostasis.
The development of the pharyngeal sac also plays a crucial role in the correct formation of pharyngeal arcs. The inability to develop from one of the pharyngeal sacs has clinical consequences that contribute to syndromes such as DiGeorge syndrome and branchio-oto-renal syndrome, as well as other pathologies. The function of the third and fourth throat pocket is modulated by the roles of the Homeobox A3 (HOXA3), Glial cell missing 2 (GCM2), Forkhead box protein N1 (FOXN1), EYA1, TBX1 and Paired box 9 (PAX9) genes. HOXA3 genes organize the spatial identity of the developing embryo along the anterior-posterior axis. Mutations in this gene lead to partial parathyroid and thymusinesia. GCM 2 is the earliest marker of the parathyroid gland and a derivative of the third and fourth pharyngeal sacs. The FOXN1 gene is required for the differentiation of thymus epithelial cells into cortical and medullary epithelium. EYA1 also affects the development of the thymus and parathyroid glands. TBX1 and PAX9 are involved in the successful development of the thymus and parathyroid glands from the third and fourth pharyngeal sacs.
[2] Together, these genes work together to form derivatives of the third or fourth pharyngeal sac. The muscles that come from the first arch of the throat include the muscles that help us chew (the temporalis, masseter and pterygoid muscles); a muscle that prevents sounds from chewing (the tympani tensor) and some of the muscles that help us swallow (the tensor veli palatini, the mylohyoid muscle and the anterior abdomen of the digastrique).