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PubMed1996

Differential diagnosis of common causes of pediatric pharyngitis.

Pharyngitis or sore throat is a common result of illness in pediatric and adolescent populations. Sore throat can signal either nonsystemic or systemic disease processes. Clinicians in ambulatory settings are often faced with deriving a differential diagnosis based on this symptom. Prompt and appropriate treatment depends on identification of the underlying causative agent or illness. This article examines common causes of sore throat in the pediatric and adolescent populations. These diagnoses are: (1) group A beta-hemolytic streptococcal pharyngitis; (2) non-group A beta-hemolytic streptococcal bacterial pharyngitis; (3) viral pharyngitis; (4) infectious mononucleosis; and (5) chronic conditions. Less common causes are also considered. Differential diagnosis is dependent on complete and accurate history, distinct physical finding, and interpretation of adjunct diagnostic tests. The value of critical data sources is essential in arriving at a differential diagnosis of pharyngitis. Once a diagnosis is established, an appropriate treatment plan can be initiated.

Adolescent↗

PubMed1998

Reducing the burden of oral and pharyngeal cancers.

In the United States, oral and pharyngeal cancers continue to result in significant morbidity and mortality. Dental professionals play a pivotal role in all facets of controlling the burden of oral and pharyngeal cancer-from efforts to prevent its occurrence, to ensuring that oral cancers are detected at the earliest possible stage, to treating these cancers, and to ensuring maximum quality of life and function for oral and pharyngeal cancer survivors. Individually and by making linkages within the community and beyond, dentists can help patients modify their risk of these cancers and can take steps to screen for them, thereby potentially improving survival and function of those who develop oral cancer. Creative partnerships between community dentists and academic and other research centers will help move knowledge of the biological processes involved in carcinogenesis and innovations in treatment into clinical practice. Partnerships between dental and medical professionals may also help efforts to reduce the morbidity related to oral and pharyngeal cancers. Local, state and national multidisciplinary initiatives are emerging that focus more broadly on risk factor control or oral and pharyngeal cancer issues. These many forms of cooperative approaches offer excellent opportunities to make a significant impact on reducing the incidence of and in treating these debilitating and disfiguring malignancies.

Computer Communication Networks↗

PubMed2003

Development of the pharyngeal arches.

The oro-pharyngeal apparatus has its origin in a series of bulges that is found on the lateral surface of the embryonic head, the pharyngeal arches. The development of the pharyngeal arches is complex involving a number of disparate embryonic cell types: ectoderm, endoderm, neural crest and mesoderm, whose development must be co-ordinated to generate the functional adult apparatus. In the past, most studies have emphasised the role played by the neural crest, which generates the skeletal elements of the arches, in directing pharyngeal arch development, but it has also become apparent that the other tissues of the arches, most notably the endoderm, also plays a prominent role in directing arch development. Thus pharyngeal arch development is more complex, and more consensual, than was previously believed.

Animals↗

PubMed2006

Inferring parrotfish (Teleostei: Scaridae) pharyngeal mill function from dental morphology, wear, and microstructure.

Morphology, occlusal surface topography, macrowear, and microwear features of parrotfish pharyngeal teeth were investigated to relate microstructural characteristics to the function of the pharyngeal mill using scanning electron microscopy of whole and sectioned pharyngeal jaws and teeth. Pharyngeal tooth migration is anterior in the lower jaw (fifth ceratobranchial) and posterior in the upper jaw (paired third pharyngobranchials), making the interaction of occlusal surfaces and wear-generating forces complex. The extent of wear can be used to define three regions through which teeth migrate: a region containing newly erupted teeth showing little or no wear; a midregion in which the apical enameloid is swiftly worn; and a region containing teeth with only basal enameloid remaining, which shows low to moderate wear. The shape of the occlusal surface alters as the teeth progress along the pharyngeal jaw, generating conditions that appear suited to the reduction of coral particles. It is likely that the interaction between these particles and algal cells during the process of the rendering of the former is responsible for the rupture of the latter, with the consequent liberation of cell contents from which parrotfish obtain their nutrients.

Animals↗

PubMed1997

Chicken Nkx-2.8: a novel homeobox gene expressed in early heart progenitor cells and pharyngeal pouch-2 and -3 endoderm.

Members of the NK family of homeobox transcription factors regulate critical steps of organogenesis during vertebrate development. In the studies described in this report, we have isolated and functionally characterized the chicken Nkx-2.8 (cNkx-2.8) cDNA and protein and defined the temporal and spatial pattern of cNkx-2.8 gene expression during chicken development. cNkx-2.8 transcripts are first detectable at HH stage 7 in the splanchnopleura. At stage 10(+), the cNkx-2.8 gene is expressed in the linear heart tube and the dorsal half of the vitelline vein. However, after looping, HH stage 13, cNkx-2.8 is no longer expressed in the looped heart tube, but is expressed in the ventral pharyngeal endoderm. At stage 15, in addition to the pharyngeal expression pattern, cNkx-2.8 is expressed in the ectoderm of the pharyngeal arches and the aortic sac. By HH Stage 17, cNkx-2.8 expression is detectable in lateral endoderm of the second and third pharyngeal pouches, the posterior portion of the aortic sac, and the sinus venosus. cNkx-2.8 binds to previously characterized Nkx2-1 and Nkx2-5 DNA-binding sites and overexpression of cNkx-2.8 transactivates a minimal promoter which contains multimerized Nkx-2 DNA-binding sites. In addition, cNkx-2.8 and serum response factor can coactivate a minimal cardiac alpha-actin promoter. These data are consistent with a model in which cNkx-2.8 performs a unique temporally and spatially restricted function in the developing embryonic heart and pharyngeal region. Moreover, the coexpression of cNkx-2.5 and -2.8 raises the possibility that cNkx-2. 8 may have a redundant role with cNkx-2.5 in the coalescing heart tube and may play an important role in the transcriptional program(s) that underlies thymus formation. The existence of multiple NK-2 family members and their partially overlapping patterns of expression are discussed within the framework of a "Nkx code."

Amino Acid Sequence↗

PubMed1996

Influence of cold stimulation on the normal pharyngeal swallow response.

We examined the potential influence of cold stimulation of the anterior tonsillar pillars, before and after topical anesthesia, on the temporal linkage between the oral and pharyngeal components of the swallow. We hypothesized that if elicitation of the pharyngeal swallow were dependent upon stimulation of faucial mucosal receptors this response would be facilitated by cold tactile stimulation and inhibited by topical anesthesia. In 14 healthy volunteers undergoing simultaneous videoradiography and manometry we measured and compared regional transit and clearance times, and the timing of hyoid motion, upper esophageal sphincter relaxation, and opening within the swallow sequence. There was a significant, volume-dependent forward shift in timings of hyoid motion, upper esophageal sphincter (UES) relaxation profile, and opening which were influenced neither by cold stimulation nor topical anesthesia. Regional transit and clearance times and UES coordination were not influenced by cold stimulation. Pharyngeal clearance time was prolonged by tonsillar pillar anesthesia due to earlier arrival of the bolus head at this region (p = 0.002). We conclude that the normal pharyngeal swallow response is neither facilitated nor inhibited by prior cold tactile stimulation or topical anesthesia to the tonsillar pillars, respectively. These observations do not support the hypothesis that elicitation of the pharyngeal swallow response is dependent upon stimulation of mucosal receptors in the tonsillar arches.

Adenoids↗

PubMed1989

Graphic representation of pharyngeal wall motion during swallow: technical note.

Movements of the pharyngeal wall were measured at 12 transverse levels, on consecutive cineradiograms obtained during swallowing of thin, liquid barium, in a single nondysphagic volunteer. By graphic representation of these measurements on the IBM personal computer, it was possible to analyze in detail pharyngeal motor activity in terms of displacement of the pharyngeal wall. The contraction created a fairly steep narrowing of the lumen. The peristaltic wave was more difficult to analyze. Movements of the pharyngeal wall in posteroanterior projection gave good information about the constrictors. Although this technique has several inherent methodologic difficulties, its use may expand our knowledge of pharyngeal peristalsis.

Cineradiography↗

PubMed2006

Pharyngeal pouch: associations and complications.

The aetiopathogenesis of pharyngeal pouch remains obscure. This review highlights the associations and complications of pharyngeal pouch to better understand the pathogenesis and management of the pouch. A search of the MEDLINE was conducted to identify studies that looked at associations and/or complications of the pharyngeal pouch. The Medical Subject Headings (MeSH) included Zenker's diverticulum and hypopharyngeal diverticulum. A total of 64 papers were included for the analysis. They consisted mainly of single case reports, case series and review articles and one case control study. A summary of evidence from the literature is discussed. This review shows the various associations and complications that can occur with pharyngeal pouches. It is important to be aware that pharyngeal pouch can co-exist with other pathologies and treatment needs to be altered to incorporate the treatment of the associated pathology too. Surgeons should also be aware of the complications that can occur within and outside the pouch.

Comorbidity↗

PubMed2005

Hoxa3 regulates the proliferation and differentiation of the third pharyngeal arch mesenchyme in mice.

Genetic disruption of Hoxa3 results in bilateral defects of the common carotid artery, which is derived from the third branchial arch artery. The tunica media of the great arteries derived from the arch arteries is formed by the ectomesenchymal neural crest cells. To examine the etiology of the regression of the third arch artery, we generated Hoxa3 homozygous null mutant embryos that expressed a lacZ marker transgene driven by a connexin43 (Cx43): promoter in the neural crest cells. The expression of beta-galactosidase in these mouse embryos was examined by both whole-mount X-gal staining and immunohistochemistry with the monoclonal beta-galactosidase antibody on sections. The migration of neural crest cells from the neural tube to the third branchial arch was not affected in the Hoxa3 homozygotes. The initial formation of the third arch artery was also not disturbed. The artery, however, regressed at embryonic day 11.5 (E11.5), when differentiation of the third pharyngeal arch began. The internal and external carotid arteries arose from the dorsal aorta in E12.5 null mutants, which showed an abnormal persistence of the ductus caroticus. The third pharyngeal arch of wild-type mice fuses with the fourth and second arches at E12.0. In the Hoxa3 null mutants, however, the fusion was delayed, and the hypoplastic third pharyngeal arch was still discerned at E12.5. Moreover, the number of proliferating cells in the third arch of the null mutants was small compared with that in the wild-type. Thus, Hoxa3 is required for the growth and differentiation of the third pharyngeal arch. The defective development of the third pharyngeal arch may induce the anomalies of the carotid artery system.

Animals↗

PubMed1985

Facial growth following pharyngeal flap surgery: skeletal assessment on serial lateral cephalometric radiographs.

The purpose of this study was to evaluate the effect of pharyngeal flap surgery on subsequent facial growth in patients with cleft lip and/or palate. Pharyngeal flap surgery is used in such patients to partially obliterate the velopharyngeal port, reducing hypernasal speech. Thirty-four patients (18 with cleft palate only, 16 with unilateral cleft lip and palate) were selected from the longitudinal growth study of the H.K. Cooper Clinic. Seventeen of these (9 with cleft palate only, 8 with unilateral cleft lip and palate) underwent pharyngeal flap surgery between the ages of 5 and 7 years. The other seventeen patients did not undergo pharyngeal flap surgery and served as a control group for this study. Serial lateral cephalometric radiographs were traced and digitized (ages 3 to 5, preflap; ages 7-10, postflap). Fourteen skeletodental measurements (six angular, six linear, two derived) were taken to determine whether pharyngeal flap surgery may be related to subsequent facial growth changes. The data from the 17 flap patients were compared with control data taken from the other seventeen patients. The groups were matched for sex, cleft type, and similarity of presurgical mandibular growth direction (facial axis angle). Results obtained demonstrate several significant areas of change following flap surgery, including a decrease in facial axis angle, an increase in Frankfort-mandibular plane angle, an increase in incremental gains in lower anterior face height, and increased retroclination of upper and lower incisors in the flap group as compared to their matched controls.

Cephalometry↗

PubMedDate not supplied

Pharyngeal diverticulum as a sequela of anterior cervical fusion.

A rarely diagnosed etiology of dysphagia is a pharyngeal diverticula occurring after anterior cervical fusion. Here we review 2 cases where patients developed pharyngeal diverticula following anterior cervical fusion. The first patient was a 28-year-old female who presented with regurgitation following C5 through C6 cervical fusion. She was diagnosed with a pharyngeal diverticulum and underwent open repair, but began to experience symptoms again a few months later. A barium swallow showed a recurrent pharyngeal diverticulum. Endoscopic repair was attempted; however, because of the thick scar band between the diverticulum and the esophagus, the operation had to be converted to an open repair with cricopharyngeal myotomy. The second case involved a 63-year-old male who presented with dysphagia and regurgitation 6 months after anterior cervical fusion. Esophagram demonstrated a small diverticulum at the right lateral border of the upper esophagus. Open repair of the diverticulum with cricopharyngeal myotomy was successfully performed. Pharyngeal diverticula after anterior cevical fusion have only been reported in 2 prior cases in the literature. Here we describe 2 additional cases at our institution, both requiring open repair. Radiographic studies demonstrate the diverticulum at the site of scarring from the cervical fusion. Because of the thick scar band and the atypical location of these diverticula, endoscopic repair with stapping (as done for Zenker's diverticula) may not be feasible. These cases highlight the importance of considering a diverticulum in the differential of posoperative patients presenting to the otolaryngologists with complaints of dysphagia following cevical spine surgery.

Adult↗

PubMed2006

Speech outcome after cranial-based pharyngeal flap in children born with total cleft, cleft palate, or primary velopharyngeal insufficiency.

PURPOSE: The aim of this study was to compare the effect of a cranial-based pharyngeal flap on the speech of children born with a unilateral cleft lip and palate (UCLP), bilateral cleft lip and palate (BCLP), cleft palate (CP), or primary velopharyngeal insufficiency (VPI) without cleft. PATIENTS AND METHODS: A total of 234 children born with clefts and 22 children born with primary VPI were evaluated. Children with associated abnormalities were excluded from this study. The Borel-Maisonny classification system was used to evaluate the velar insufficiency. The cranial-based pharyngeal flap was performed using the Sanvenero-Rosselli technique. RESULTS: Between 1984 and 2001, 74 children underwent pharyngeal flap for VPI. The mean follow-up period was 7 years. Borel-Maisonny scores after pharyngeal flap surgery were as follows: children with UCLP (n = 22), 59.1% type 1, 36.4% type 1/2, and 4.5% type 2; children with BCLP (n = 18), 44.4% type 1, 27.8% type 1/2, 16.7% type 2, and 11.1% type 2/3; children with CP (n = 17), 64.7% type 1, 23.5% type 1/2, and 11.8% type 2; children with primary VPI (n = 17), 29.4% type 1, 29.4% type 1/2, 29.4% type 2/3, and 11.8% type 3. There were significant differences in outcome among the 4 groups (P = .029; Fisher exact test). CONCLUSIONS: The positive effect on speech of a cranial-based pharyngeal flap is greater in children born with a UCLP or CP than in those born with a BCLP. In children born with primary VPI, this operation has only a slightly positive effect on speech that shows compensatory misarticulations; in such cases, alternative surgical choices or secondary procedures may be indicated. This information should be clearly conveyed to the parents in presurgical consultation so that they know what to expect from the procedure and postoperative adjuvant therapy.

Age Factors↗

PubMed2004

Zebrafish gcmb is required for pharyngeal cartilage formation.

The glial cells missing (gcm) gene in Drosophila encodes a GCM-motif transcription factor that functions as a binary switch to select between glial and neuronal cell fates. To understand the function of gcm in vertebrates, we isolated the zebrafish gcmb and analyzed the function of this gene using antisense morpholino oligonucleotides against gcmb mRNA (gcmb-MO) and transgenic overexpression. Zebrafish gcmb is expressed in the pharyngeal arch epithelium and in cells of the macrophage lineage. gcmb-MO-injected larvae show significantly reduced branchial arch cartilages. fgf3-MO-injected larvae display a similar phenotype to that of gcmb-MO-injected larvae with respect to the lack of pharyngeal cartilage formation. In addition, gcmb expression in the pharyngeal arches is down-regulated in fgf3-MO-injected larvae. The gcmb transgenic larvae show a protrusion of the lower jaw and abnormal spatial arrangement of the pharyngeal cartilage elements. These results suggest that gcmb is required for normal pharyngeal cartilage formation in zebrafish and that its expression is dependent on fgf3 activity.

Amino Acid Sequence↗

PubMed2004

Abnormalities of caudal pharyngeal pouch development in Pbx1 knockout mice mimic loss of Hox3 paralogs.

Pbx1 is a TALE-class homeodomain protein that functions in part as a cofactor for Hox class homeodomain proteins. Previous analysis of the in vivo functions of Pbx1 by targeted mutagenesis in mice has revealed roles for this gene in skeletal patterning and development and in the organogenesis of multiple systems. Both RNA expression and protein localization studies have suggested a possible role for Pbx1 in pharyngeal region development. As several Hox mutants have distinct phenotypes in this region, we investigated the potential requirement for Pbx1 in the development of the pharyngeal arches and pouches and their organ derivatives. Pbx1 homozygous mutants exhibited delayed or absent formation of the caudal pharyngeal pouches, and disorganized patterning of the third pharyngeal pouch. Formation of the third pouch-derived thymus/parathyroid primordia was also affected, with absent or hypoplastic primordia, delayed expression of organ-specific differentiation markers, and reduced proliferation of thymic epithelium. The fourth pouch and the fourth pouch-derived ultimobranchial bodies were usually absent. These phenotypes are similar to those previously reported in Hoxa3(-/-) single mutants and Hoxa1(-/-);Hoxb1(-/-) or Hoxa3(+/-);Hoxb3(-/-);Hoxd3(-/-) compound mutants, suggesting that Pbx1 acts together with multiple Hox proteins in the development of the caudal pharyngeal region. However, some aspects of the Pbx1 mutant phenotype included specific defects that were less severe than those found in known Hox mutant mice, suggesting that some functions of Hox proteins in this region are Pbx1-independent.

Animals↗

PubMed2004

Zebrafish gcm2 is required for gill filament budding from pharyngeal ectoderm.

The pharyngeal arches give rise to multiple organs critical for diverse processes, including the thymus, thyroid and parathyroids. Several molecular regulators of thymus and thyroid organogenesis are strikingly conserved between mammals and zebrafish. However, land animals have parathyroids whereas fish have gills. The murine transcription factor Glial cells missing 2 (Gcm2) is expressed specifically in the parathyroid primordium in the endodermal epithelium of the third pharyngeal pouch, and in both mice and humans is required for normal development of parathyroid glands. The molecular regulation of fish gill organogenesis remains to be described. We report the expression of gcm2 in the zebrafish pharyngeal epithelium and a requirement for Hox group 3 paralogs for gcm2 expression. Strikingly, zebrafish gcm2 is expressed in the ectodermal portion of the pharyngeal epithelium and is required for the development of the gill filament buds, precursors of fish-specific gill filaments. This study identifies yet another role for a GCM gene in embryonic development and indicates a role for gcm2 during the evolution of divergent pharyngeal morphologies.

Amino Acid Sequence↗

PubMed2005

Loss of Gbx2 results in neural crest cell patterning and pharyngeal arch artery defects in the mouse embryo.

Several syndromes characterized by defects in cardiovascular and craniofacial development are associated with a hemizygous deletion of chromosome 22q11 in humans and involve defects in pharyngeal arch and neural crest cell development. Recent efforts have focused on identifying 22q11 deletion syndrome modifying loci. In this study, we show that mouse embryos deficient for Gbx2 display aberrant neural crest cell patterning and defects in pharyngeal arch-derived structures. Gbx2(-/-) embryos exhibit cardiovascular defects associated with aberrant development of the fourth pharyngeal arch arteries including interrupted aortic arch type B, right aortic arch, and retroesophageal right subclavian artery. Other developmental abnormalities include overriding aorta, ventricular septal defects, cranial nerve, and craniofacial skeletal patterning defects. Recently, Fgf8 has been proposed as a candidate modifier for 22q11 deletion syndromes. Here, we demonstrate that Fgf8 and Gbx2 expression overlaps in regions of the developing pharyngeal arches and that they interact genetically during pharyngeal arch and cardiovascular development.

Animals↗

PubMed2006

C. elegans pharyngeal morphogenesis requires both de novo synthesis of pyrimidines and synthesis of heparan sulfate proteoglycans.

The C. elegans pharynx undergoes elongation and morphogenesis to its characteristic bi-lobed shape between the 2- and 3-fold stages of embryogenesis. During this period, the pharyngeal muscles and marginal cells forming the isthmus between the anterior and posterior pharyngeal bulbs elongate and narrow. We have identified the spontaneous mutant pyr-1(cu8) exhibiting defective pharyngeal isthmus elongation, cytoskeletal organization defects, and maternal effect lethality. pyr-1 encodes CAD, a trifunctional enzyme required for de novo pyrimidine synthesis, and pyr-1(cu8) mutants are rescued by supplying exogenous pyrimidines. Similar pharyngeal defects and maternal effect lethality were found in sqv-1, sqv-8, rib-1 and rib-2 mutants, which affect enzymes involved in heparan sulfate proteoglycan (HSPG) synthesis. rib-1 mutant lethality was enhanced in a pyr-1 mutant background, indicating that HSPG synthesis is very sensitive to decreased pyrimidine pools, and HS disaccharides are moderately decreased in both rib-1 and pyr-1 mutants. We hypothesize that HSPGs are necessary for pharyngeal isthmus elongation, and pyr-1 functions upstream of proteoglycan synthesizing enzymes by providing precursors of UDP-sugars essential for HSPG synthesis.

Amino Acid Sequence↗

PubMed2002

Neoglottic formation from posterior pharyngeal wall conserved in surgery for hypopharyngeal cancer.

OBJECTIVE: To describe a new treatment modality of hypopharyngeal cancer consisting of total laryngectomy plus partial pharyngectomy (TLPP) conserving the posterior wall of the pharynx vertically for voice restoration. METHODS: Review of hospital charts, TLPP was undertaken in 15 of 54 patients. Surgical modalities of reconstruction subsequent to TLPP were indicated on the basis of the width of posterior pharyngeal wall conserved during surgery. Posterior pharyngeal walls of width 3 cm or larger were sutured in primary closure. If the width of posterior wall was less than 3 cm, a free forearm flap or free jejunal flap was patched to the wall. Tracheo-esophageal shunt with a voice prosthesis was performed 3 weeks after surgery. RESULTS: The Kaplan-Meier method indicated no difference in survival rate between patients with TLPP (46.4%) and the remaining patients (47.4%). Nine of 15 patients with TLPP (two patients with primary closure, three with free forearm flap, and four with free jejunal flap) were examined for voice restoration and fluoroscopy of the neopharynx. Eight of the nine patients, in whom more than 2 cm of the posterior pharyngeal wall had been conserved, demonstrated a good speech rating, maximum phonation time and neoglottic formation by the posterior pharyngeal wall. CONCLUSION: The combination of conservation of the posterior pharyngeal wall, patch graft and a voice prosthesis is a useful method that offers sufficient quality of phonation without deterioration of survival rate for patients with hypopharyngeal cancer.

Adult↗