Published online Jun 27, 2026. doi: 10.4240/wjgs.118552
Revised: February 11, 2026
Accepted: March 23, 2026
Published online: June 27, 2026
Processing time: 169 Days and 18.8 Hours
Dysphagia is a common symptom that can lead to serious complications such as nutritional deficits, aspiration pneumonia, and even death, particularly in older adults. Oropharyngeal dysphagia is more prevalent than esophageal dysphagia, and the optimal treatment relies on the established cause. In this study, we pre
Patient 1 was a 79-year-old man admitted with a 1-week history of worsening dysphagia alongside coughing and choking. Patient 2 was a 65-year-old man who presented with a 2-year history of progressive dysphagia that was also ac
Cervical spondylosis is an uncommon cause of dysphagia at the OEJ, and or
Core Tip: This study reports cervical spondylosis at the oropharyngeal-esophageal junction as a rare but treatable cause of oropharyngeal dysphagia in two elderly patients. By presenting these uncommon cases, the study demonstrates that this etiology should be considered when common causes are ruled out. Dysphagia was resolved through orthopedic surgery and subsequent rehabilitation in both patients. Collectively, these findings highlight the importance of recognizing cervical spondylosis as a potential cause of dysphagia and facilitating appropriate intervention to prevent serious complications and improve clinical outcomes, thereby contributing to better management of dysphagia.
- Citation: Li XH, Sun YY, Chen TT, Yang F, Lai ZB, He J. Surgical management of dysphagia at the oropharyngeal-esophageal junction due to cervical spondylosis: Two case reports. World J Gastrointest Surg 2026; 18(6): 118552
- URL: https://www.wjgnet.com/1948-9366/full/v18/i6/118552.htm
- DOI: https://dx.doi.org/10.4240/wjgs.118552
Dysphagia is a highly prevalent condition characterized by an obstructed or disrupted normal swallowing process[1]. This frequently underreported condition can impact quality of life, resulting in symptoms that range from mild discomfort to severe nutritional deficits[2,3]. Additionally, dysphagia is associated with an increased risk of pneumonia and even death, particularly in the older population[2,4].
The etiologies of dysphagia are diverse. Major common causes include benign or malignant tumors of the esophagus or cardia, gastroesophageal reflux disease, achalasia, diffuse esophageal spasm, benign iatrogenic strictures, external compression of the esophagus, and central nervous system diseases[1,3,5]. A precise diagnosis of the underlying cause of dysphagia is essential for implementing effective treatment strategies[6]. In the Department of Gastroenterology at our hospital, we have managed numerous patients with dysphagia. Recently, we encountered two uncommon cases of dysphagia in which cervical spondylosis was found to compress the esophagus and pharynx, leading to dysphagia at the oropharyngeal-esophageal junction (OEJ) through mechanical obstruction or functional impairment.
Given the rarity of this presentation, we present this case series to highlight cervical spondylosis as a cause of dys
Case 1: The patient was a 79-year-old man who was admitted to our hospital with a complaint of progressively worsening difficult swallowing or dysphagia accompanied by coughing and choking for one week.
Case 2: The patient was a 65-year-old man who presented to our outpatient clinic with a complaint of progressive dysphagia accompanied by coughing and choking during meals for two years.
Case 1: Prior to the onset of these symptoms, the patient received neck Tuina massage therapy for cervical spondylosis at an unlicensed chiropractic clinic. Five days before admission, nasopharyngoscopy performed at an external hospital revealed a bulge in the posterior wall of the lower pharynx. Additionally, esophagography/esophagogram revealed aspiration of contrast agent into the trachea and bronchi attributable to severe coughing (Figure 1A).
Case 2: The patient reported no obvious triggers of symptom onset.
Case 1: The patient denied any history of other chronic diseases, previous surgeries, or trauma.
Case 2: Previous examinations at another hospital, including computed tomography (CT) of the chest and neck and gastroscopy, were unremarkable.
Cases 1 and 2 reported no personal or family history of dysphagia or malignancies.
On physical examination, cases 1 and 2 exhibited normal vital signs.
Case 1: Laboratory tumor marker tests revealed the following findings: Carbohydrate antigen 125, 18.00 U/mL; carbohydrate antigen 19-9 < 2.00 U/mL; carcinoembryonic antigen, 4.75 ng/mL; and alpha-fetoprotein, 3.27 ng/mL.
Case 2: Laboratory tumor marker tests revealed the following findings: Carbohydrate antigen 125, 15.00 U/mL; carbohydrate antigen 19-9 < 5.00 U/mL; carcinoembryonic antigen, 2.35 ng/mL; and alpha-fetoprotein, 4.05 ng/mL.
Case 1: Gastroscopy identified an area of extrinsic compression or an extrinsic pressure-type bulge on the posterior wall of the hypopharynx and esophageal inlet (Figure 1B). Nasopharyngoscopy uncovered a protruding lesion on the posterior pharyngeal wall along with evidence of pharyngitis. Magnetic resonance imaging (MRI) of the head and cervical spine demonstrated intervertebral disc herniation at the C3-C4, C4-C5, C5-C6, and C6-C7 levels (Figure 1C). Laboratory tests and imaging eliminated common causes of dysphagia, including pharyngeal or esophageal tumors, motility disorders, and cerebrovascular diseases. Nasopharyngoscopy demonstrated normal epiglottic function; however, both nasopharyngoscopy and gastroscopy identified a bulge on the posterior wall of the hypopharynx. Cervical MRI highlighted multiple disc herniations and osteophyte formation, suggesting that swallowing difficulty might have been exacerbated by external compression from cervical spine issues, which were potentially worsened or even triggered by neck Tuina massage therapy. An orthopedic consultation confirmed that the bulge, resulting from cervical disc herniation and osteophyte formation, caused pharyngeal narrowing and acute dysphagia.
Case 2: Gastroscopy was conducted at our hospital, revealing a large bulging extrinsic compressive lesion on the posterior wall of the hypopharynx, with the epiglottis closely adjacent to the lesion (Figure 2A). Contrast-enhanced CT of the neck disclosed slight thickening of the nasopharyngeal roof and posterior wall, as well as mild thickening of the upper esophageal wall. Cervical CT demonstrated multiple bony bridges at the margins of the cervical and thoracic vertebrae, and sagittal reconstruction revealed posterior compression of the oropharynx, hypopharynx, and posterior wall of the cervical esophagus, suggestive of diffuse idiopathic skeletal hyperostosis (Figure 2B).
The final diagnosis for cases 1 and 2 was dysphagia at the OEJ.
The patient was treated with surgical intervention.
The patient underwent resection of a large anterior osteophyte at C3-C6, subtotal corpectomy of C4-C5, and implantation and fixation of a self-stabilizing three dimensions-printed artificial vertebral body.
Postoperatively, the patient wore a cervical collar, and he could tolerate a liquid diet without difficulty by the second day with no reported choking incidents (Figure 3A and B). Fiberoptic endoscopic evaluation of swallowing (FEES), which assessed the degree of airway involvement during swallowing according to the Rosenbek aspiration-penetration scale, demonstrated a marked improvement in swallowing function, with the FEES grade decreasing from 7 pre-treatment (August 20, 2025) to 1 post-treatment (September 1, 2025).
On the second day after surgery, the patient was able to consume liquid diets, but he experienced difficulty swallowing solid foods. The FEES grade decreased from 6 before treatment (March 7, 2024) to 2 after treatment (June 15, 2024). After subsequent neck and swallowing rehabilitation training, the patient was able to eat solid foods 6 months later, and he reported smooth swallowing with no additional symptoms related to the cervical and thoracic vertebral osteophytes. Follow-up CT after 1 year confirmed the resolution of the cervical and thoracic vertebral osteophytes (Figure 3C).
Dysphagia resulting from cervical spondylosis compressing the esophagus is relatively rare[7]. This condition typically arises from intervertebral disc degeneration, which can lead to a cascade of pathophysiological changes, including annular tears, hemorrhage, calcification, and the formation of osteophytes beneath the anterior longitudinal ligament and periosteum. These anteriorly protruding osteophytes can subsequently exert pressure on the esophagus, leading to dysphagia. Because of the infrequency of this condition, it is often misdiagnosed or underdiagnosed[8,9]. This study presents two unique cases of dysphagia localized to the OEJ that were caused by cervical spondylosis. To our knowledge, there are limited reports detailing the diagnosis and treatment of dysphagia at the OEJ specifically associated with cervical spondylosis.
Both patients presented with dysphagia at our department, and gastroscopy revealed a protruding lesion on the posterior hypopharyngeal wall. Subsequent neck CT and MRI confirmed that cervical vertebral hyperplasia, osteophyte formation, and intervertebral disc displacement were compressing the posterior hypopharyngeal wall, thereby narrowing the pharyngeal space. This compression impeded epiglottic closure, leading to dysphagia and episodes of choking. Following surgical intervention[10], including osteophyte resection or subtotal vertebrectomy performed in the Department of Orthopedics in our hospital, along with stabilization using anastomotic nails or a self-stabilizing three dimensions-printed artificial vertebral body, intraoperative assessments indicated no damage to the surrounding muscles or recurrent laryngeal nerve. Case 1 experienced a rapid recovery from dysphagia. In comparison, case 2 experienced a longer duration of symptoms and sustained compression from the cervical osteophyte, which resulted in damage to both the muscles and recurrent laryngeal nerve. Consequently, recovery from dysphagia for this patient required 6 months. After undergoing postoperative rehabilitation training, case 2 successfully resumed the consumption of solid foods and recovered from symptoms of dysphagia.
Although our patients were managed with surgical intervention, patients with dysphagia caused by cervical diffuse idiopathic skeletal hyperostosis can often be effectively treated with non-surgical methods, such as dietary modifications, muscle relaxants, anti-inflammatory medications, posture adjustments during eating, and swallowing rehabilitation training[11]. For those with dysphagia from pharyngoesophageal junction cervical spondylosis, especially older patients at higher surgical risk, we recommend starting with non-surgical approaches such as swallowing rehabilitation. This training should evaluate the patient’s physical condition and swallowing function to ensure safety and effectiveness, focusing on oral muscle training, swallowing posture adjustments, sensory stimulation, and respiratory exercises, all of which should be maintained long-term. If conservative treatments fail, then surgical removal of osteophytes might alleviate or resolve dysphagia symptoms[12,13].
We propose several potential pathophysiological mechanisms by which cervical spondylosis can lead to OEJ dysphagia: (1) Direct compression: Osteophytes or intervertebral disc herniation can compress the posterior wall of the pharynx and esophagus, leading to narrowing of the pharyngoesophageal lumen. This obstruction might impede the passage of food into the esophagus and can interfere with laryngeal movement, resulting in dysphagia[14]; (2) Tissue irritation and inflammation: Osteophytes can irritate the anterior margin of the vertebral body, inducing inflammation and edema in the surrounding tissues at the pharyngoesophageal junction. This inflammatory response can lead to the formation of adhesions, further narrowing the lumen and restricting the contraction of the cricopharyngeal muscle, which impairs swallowing and potentially causes dysphagia[8]; (3) Nerve plexus damage: Prolonged compression of the pharyngoesophageal junction by large osteophytes can damage the local nerve plexus, resulting in decreased peristalsis and contributing to dysphagia; and (4) Restricted cervical motion: The formation of an anterior cervical bony bridge can limit cervical spine mobility, adversely affecting the swallowing function of both the pharynx and esophagus.
In conclusion, cervical spondylosis is a rare yet treatable cause of dysphagia at the OEJ. Our experience underscores the importance of considering cervical spondylosis after common causes have been excluded. A multidisciplinary approach integrating imaging and laboratory tests to establish the cause and guide treatment through surgery and rehabilitation is essential. Reporting such cases might enrich our understanding and ultimately improve care for patients with dysphagia. We also acknowledge that surgical success in our cases does not guarantee similar outcomes for all patients.
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