Endoscopic treatment of benign esophageal strictures: Advances and challenges

Abstract

Benign esophageal stricture is characterized by the narrowing of the digestive tract lumen due to multiple factors. Endoscopic treatment is the first treatment choice and includes endoscopic dilatation, drug injection, stenosis incision, stent implantation, stem cell flap transplantation, etc. However, there are currently no specific clinical standards or guidelines to quantify a series of specific parameters in the treatment of benign esophageal stricture, such as the frequency of drug administration, dosage, dilation inner diameter, and number of treatments. This leads to operator bias in clinical practice and inconsistent treatment outcomes among patients. Therefore, this article reviews the current advances and existing challenges in the endoscopic treatment of benign esophageal stricture, with the aim of exploring the possibility of achieving precision and standardization in the endoscopic treatment of this disease.

Key Words: Benign esophageal strictures; Esophageal stricture; Oesophageal strictures; Endoscopic treatment; Endoluminal functional luminal imaging probe; Advances and challenges

Core Tip: Endoscopic treatment is the first-line approach for benign esophageal strictures, including dilation, medication, incision, and stenting. However, the lack of standardized protocols (e.g., drug dosage, dilation parameters) leads to inconsistent outcomes. Future advancements should integrate precision assessment tools like endoluminal functional luminal imaging probe to standardize treatment, reduce operator bias, and optimize individualized strategies.

INTRODUCTION

Esophageal stricture is the narrowing of the esophageal lumen due to various diseases and factors. The causes of esophageal stricture can be divided into benign and malignant. Patients with esophageal stricture usually experience symptoms such as dysphagia, chest pain, and vomiting, and may also present with systemic manifestations such as emaciation and malnutrition. These symptoms seriously affect the quality of life of patients. In Western populations, the majority of benign esophageal stricture cases are attributed to chronic gastroesophageal reflux disease (GERD) (60%-70%), followed by eosinophilic esophagitis (15%-30%), which has emerged as a leading cause of dysphagia in patients under 40 years[1,2]. Iatrogenic injury (e.g., post-surgical anastomotic strictures, endoscopic mucosal resection, or radiation therapy) accounts for 10%-20% of cases, while caustic ingestion remains prevalent in regions with limited access to healthcare[3]. Management of benign esophageal strictures necessitates a dual approach: Mechanical dilation to relieve luminal obstruction and targeted therapy addressing the underlying etiology. For example, in GERD-related strictures, sustained acid suppression with proton pump inhibitors or potassium-competitive acid blockers (e.g., vonoprazan) is critical to mitigate inflammation and fibrosis, thereby reducing the need for repeated dilations. Similarly, eosinophilic esophagitis mandates topical corticosteroids to reverse eosinophilic infiltration. Currently, the dilation therapies for benign esophageal strictures include surgery, medication, and endoscopic treatment. Of these, endoscopic treatment has become the first-line treatment for benign esophageal stenosis due to its minimally invasive nature and definite efficacy. With the rapid development of endoscopic technology, techniques such as endoscopic dilation, local drug injection, endoscopic incision, stent placement, stem cell transplantation, and skin flap transplantation have been applied in clinical practice[4]. However, due to the wide variety and complexity of endoscopic accessories and differences in doctors’ operating habits, the specific parameters of many operations have not yet been quantified and unified, resulting in uneven treatment effects in clinical practice. This article reviews the progress and current challenges of endoscopic treatment for benign esophageal stenosis, aiming to explore the possibility of standardization and precision of some endoscopic surgical treatments.

PATHOPHYSIOLOGY OF BENIGN ESOPHAGEAL STRICTURES

The esophagus is a tube that extends from the pharynx to the stomach, transporting food and water from the mouth to the stomach. Histologically, the esophagus can be divided into four layers in cross-section: The mucosa, submucosa, muscular layer, and serosa. The mucosa is further subdivided into the mucosal epithelium, consisting of non-keratinized squamous epithelial cells, the lamina propria, and the muscularis mucosae. The muscular layer of the esophagus includes two layers of inner circular and outer longitudinal muscles, composed of skeletal muscle cells in the upper one-third and smooth muscle cells in the lower one-third, with a mixture in the middle. Currently, it is believed that esophageal stenosis is often the result of multiple biological mechanisms occurring in parallel or in a cross-cascading manner. Fibrosis, inflammation, or esophageal epithelial barrier (EEB) injury are not independent individual causes of esophageal stenosis[5]. Benign esophageal stenosis is thought to be caused by scar tissue formation and fibrosis around the wound. Biomechanical changes in the submucosa and alterations in collagen components are also involved in the pathogenesis of esophageal stenosis[6]. Doupé et al[7] explored the mechanism of esophageal wound healing in mice and believed that the same epithelial progenitor cells involved in tissue homeostasis play an important role in the healing process of small-area wounds. However, for larger wounds, such as those after endoscopic mucosal resection greater than 3/4 of the circumference, due to the absence of the muscularis mucosae and/or submucosal glands, the wound cannot heal smoothly using the above-mentioned methods; thus, a high stenosis rate usually occurs after the operation. The mainstream view holds that the formation of benign esophageal stenosis consists of the following steps: The first step is the loss of barrier function after epithelial injury, exposing the submucosal space to various stimuli. The second step involves multiple local stimuli activating the immune system, inducing an inflammatory response that promotes the formation of granulation tissue, including inflammatory cell infiltration and palisading angiogenesis. The third step is that after extensive esophageal mucosal injury, resident fibroblasts and pericytes differentiate into myofibroblasts required for scar formation under the action of fibrogenic cytokines. At the same time, myofibroblasts drive the formation of scar tissue by synthesizing type I collagen. This series of processes ultimately leads to the formation of scar tissue and the occurrence of esophageal stenosis. Liu et al[8] reported an experimental study on a pig model and showed that if the mucosa on the esophagus is resected, severe stenosis will form, while if the mucosa is only incised but not resected, esophageal stenosis will not form. This indicates that the degree of loss of esophageal mucosa, rather than just injury to the esophageal mucosa, is a key factor in esophageal stenosis. The rat model study by Wu et al[6] also supports this view.

In general, the occurrence of esophageal stenosis can be divided into three stages: EEB structure injury, chronic inflammation, and severe fibrosis. Among them, EEB dysfunction or injury is the initiating mechanism leading to esophageal stenosis. Re-epithelialization is crucial for the treatment and prevention of esophageal stenosis. Further research on the mechanism of esophageal stenosis will help clinicians or scientists develop more effective techniques in the future.

ENDOSCOPIC TREATMENT OF BENIGN ESOPHAGEAL STRICTURES

Endoscopic dilation

In the 17^th century, Sir Thomas Willis, a British anatomist and physician, first used a specially-made whalebone to dilate the esophagus and treated a patient with severe dysphagia[9]. Since then, dilation treatment for esophageal stenosis has gradually evolved and improved over a long period and has become the first-line treatment for benign esophageal stenosis under endoscopy[10]. To date, this technology has become more and more visualized and precise. In addition, with the rapid development of materials science, more and more tools for endoscopic use have emerged. Commonly used tools include endoscopic balloon dilators, push-type dilating bougies, tapered dilators, etc[11]. These common methods of endoscopic treatment tools each have their own advantages and disadvantages, which are now summarized in Table 1.

Table 1 Common methods of endoscopic dilation for benign esophageal stenosis.

Treatment methods	Indications	Whether to use radiation assistance	Advantages	Disadvantages
Guide-wire-free bougie	Simple stenosis of the distal esophagus	No	Simple to operate, and patients can use it at home	It is only applicable in simple linear stenosis
Guide-wire-assisted bougie	Complex stenosis of the distal esophagus	Yes	Cost-effective and reusable. Guidance by a guide wire makes it safer	It is not applicable in severe stenosis
Endoscopic balloon	Complex or severe stenosis of the esophagus	Yes	Dilation effect is definite, and it can be applied in a wider range of scenarios	Cost is high and the operation process is relatively complex

Endoscopic dilation treatment acts on esophageal stenosis through the expansion force of a rigid object, causing the muscular layer of the stenotic segment to tear, relax, and expand the esophagus lumen that has been constricted to varying degrees, restoring its patency, and thus achieving the purpose of alleviating and improving the patient’s clinical symptoms. Currently, the two main types of tools used clinically are mechanical (bougie) dilators and balloon dilators. Mechanical (bougie) dilators are divided into two categories according to whether a guide wire and/or fluoroscopic guidance is required. These include the Hurst bougie and Maloney bougie without a guide wire, the Savary-Gilliard dilator with a guide wire, etc. The bougies that do not require guide wire guidance are filled with mercury or tungsten. Under the action of gravity, they can pass through the stenotic area of the esophagus. These bougies are generally conical and are available in various sizes. For simple stenoses located at the distal end of the esophagus, these bougies are effective, safe, and can be used for home treatment by patients. Another type of dilator with guide wire guidance first uses the guide wire to pass through the stenotic area before dilation, and then gradually passes the dilating bougie through the stenotic segment of the esophagus under the guidance of the guide wire to dilate the affected area. This method is safer due to the use of guide wire guidance. These two types of bougies are respectively suitable for different types of esophageal stenosis, and there is no significant difference in clinical efficacy.

Balloon dilation uses a balloon dilator. Under the direct visual guidance of a gastroscope (or in combination with an X-ray), the balloon is inserted into the stenotic orifice, with the waist of the balloon located in the center of the stenosis. Normal saline or contrast agent is then slowly injected into the balloon to continuously squeeze the stenotic area, causing mechanical tearing at this section to increase the diameter of the stenotic area. During the operation, the stenotic area is marked as “waist-shaped” or “hourglass-shaped” in the center of the balloon, and this state is maintained until the waist-shape disappears, and is then maintained for several seconds to several minutes. If the diameter of the narrow segment does not reach the target (usually ≥ 13 mm) after the first balloon dilation, the balloon size needs to be gradually upgraded. This process is repeated several times until the target diameter is reached. During dilation treatment, the classic “rule of three” should be followed, that is, at most 3 mechanical dilators are used in one dilation process, and the lumen diameter increases by no more than 3 mm after dilation[12]. However, in clinical practice, the “rule of three” is not strictly implemented. Many clinical studies have confirmed that a single dilation of > 3 mm does not increase the probability of complications[13-15]. Currently, there is no single rule or technique that stipulates the best way and degree of esophageal dilation. The only rule is based on clinical judgment, which varies according to the nature of the disease and the patient’s condition[16]. In summary, the treatment of esophageal dilation has a long history and is easy to operate. However, there is currently no unified standard to regulate the duration of dilation, the specific diameter after dilation, and the choice of balloon or bougie use. Most clinical judgments are based on the experience of the operating doctor or the patient’s tolerance, so there are certain differences in the treatment effects.

Endoscopic drug treatment

In addition to endoscopic dilation therapy, drug-based intervention can also be carried out to target the formation process of benign esophageal stenosis. Severe inflammation, scar hyperplasia and contracture, fibrosis, and excessive collagen deposition are all associated with the occurrence of benign esophageal stenosis. In view of these causes, drugs such as corticosteroids, statins, botulinum toxin A, and mitomycin C can be used clinically for treatment.

Steroid hormones have a powerful and wide-ranging anti-inflammatory effect. They can relieve symptoms such as redness, swelling, heat, and pain in the early stage of inflammation, and prevent tissue adhesion and scar formation in the later stage of inflammation. The anti-inflammatory mechanism of steroid hormones is mainly through the gene effect (also known as the genomic effect), which inhibits the expression of CHST15, transforming growth factor-β1 (TGF-β1) and collagen I regulated by it, thereby suppressing esophageal fibrosis and preventing the formation of esophageal stenosis[17]. As long-term and high-dose steroid hormone use can cause many adverse reactions, including osteoporosis, osteonecrosis, myopathy, and immunosuppression[18], local injection or topical application of tissue gel can be used clinically for prevention. Compared with oral administration of hormones, local esophageal injection can effectively increase the drug concentration in tissues, reduce the adverse reactions of systemic administration, shorten the dosing cycle, and improve patient compliance. Hashimoto et al[19] conducted a study on the prevention of esophageal stenosis by multiple local injections of triamcinolone acetonide. They injected 18-62 mg of triamcinolone acetonide on the 3^rd, 7^th, and 10^th day, respectively. The study found that after local injection, the incidence of esophageal stenosis could be reduced to 19%. Inspired by the treatment of skin injuries with emulsion gel, Zhang et al[20] mixed aluminum phosphate gel with hydrocortisone sodium succinate, which was then dissolved in normal saline to prepare an oral gel medicine, and carried out a randomized controlled trial with local injection of triamcinolone acetonide. The results showed that the oral gel had a better effect in preventing esophageal stenosis after extensive endoscopic submucosal dissection (ESD), with an incidence of stenosis of 9.4%, while that in the triamcinolone acetonide injection group was 35.5%. Statins exert an anti-fibrotic effect by inhibiting the production of connective tissue growth factor and α-smooth muscle actin induced by TGF-β1[21]. Wang et al[22] conducted a retrospective cohort study comparing statins with a variety of other drugs to prevent post-ESD stenosis. They believed that statins are a potential method for preventing esophageal stenosis after ESD, and their effect is superior to that of oral corticosteroids and local injection of triamcinolone acetonide. Botulinum toxin A promotes the expression of the apoptotic factor caspase-3 in fibroblasts by inhibiting the expression of TGF-β1, inhibits the proliferation of fibroblasts, and promotes fibroblast apoptosis, thereby suppressing scar formation[23]. Mitomycin C has an anti-fibrotic effect. It regulates apoptosis and autophagy by inhibiting the expression of long non-coding RNA-ATB and upregulating the expression of microRNA-200b, thus playing a role in preventing the formation of postoperative esophageal fibrosis[24]. In summary, the main mechanism of action of these drugs in preventing esophageal stenosis is to reduce local inflammatory responses, thereby inhibiting tissue fibrosis and achieving the goal of reducing the degree of scarring. However, due to the relatively numerous side effects associated with long-term drug use, they are often not used as a single treatment method.

Endoscopic radial incision

In 2012, Muto et al[25] reported endoscopic longitudinal incision. This method uses a mucosal cutting knife to make longitudinal incisions in the area of benign esophageal stenosis, aiming to disrupt the structure of the stenotic area and expand the diameter of the lumen. Compared to conventional longitudinal incisions, radial incisions create 4 to 6 radial cuts at multiple positions (e.g., 3:00, 6:00, 9:00, 12:00 directions) around the stricture ring, forming a stellate pattern to thoroughly release the annular fibrotic scar. This approach achieves more uniform tension relief of the circumferential scar, reducing restenosis rates. Additionally, radial incisions avoid potential complications such as eccentric under-dilation or diverticulum-like deformities caused by single longitudinal incisions. Jimoh et al[26] Schatzki compared radial incision with endoscopic dilation. The analysis showed that compared with dilation, patients who received endoscopic radial incision (ERI) had a reduced overall risk of stenosis recurrence [odds ratio (OR) = 0.35, 95% confidence interval (CI): 0.13-0.92, P = 0.03; I² = 71%], and a reduced risk of initial stenosis recurrence (OR = 0.32, 95%CI: 0.17-0.59, P = 0.0003; I² = 0%). Compared with dilation alone, patients who received ERI + dilation had a significantly increased recurrence-free duration (mean difference = 42.76, 95%CI: 12.41-73.11, P = 0.006). This also confirms that this technique, whether used alone or in combination with treatment methods such as steroid injection and balloon dilation, has very good application prospects, especially in patients with severe dysphagia and vomiting. Symptoms can be improved more rapidly by endoscopic incision of the stenotic area.

Endoscopic stent placement

Esophageal stent treatment for benign esophageal stenosis is mainly used in patients with refractory or recurrent stenosis. According to the definitions of refractory and recurrent esophageal stenosis by Kochman et al[27], they refer to cases where the target diameter of 14 mm cannot be achieved after treatment with dilation every two weeks within 5 weeks, or the target diameter cannot be maintained within 4 weeks after the last dilation. Although it is currently believed that the continuous dilating force of the esophageal stent on the stenotic area may promote remodeling of the stenotic site, due to its relatively high incidence of adverse events and cost, esophageal stent placement is currently only used as a second-line treatment method for benign stenosis[28]. Lu et al[29] compared esophageal stent placement with dilation treatment. The analysis found that the success rate of patients treated with dilation was 70.9% (39 of 55), which was higher than that of patients treated with stents (35%, 7 of 20). During the follow-up period, the dysphagia-free period for patients treated with dilation was 3.7 months (95%CI: 2.7-5), while that for patients treated with stents was 2.3 months (95%CI: 1.5-3). Moreover, stent placement caused more adverse events than dilation treatment. In the study, 31.6% (6/19) of the patients had stent displacement, 47.4% (9/19) of the patients had stent-related adverse events, and 8% (6/75) of the patients developed esophageal fistula. At present, there is a wide variety of stents on the market, with different characteristics such as different materials (plastic or metal), covered or uncovered, different diameters, degradability, and anti-displacement properties. Partially covered self-expandable metal stents and fully covered self-expandable metal stents are the most commonly used in clinical practice. However, as neither of them can be permanently implanted in the body, it may be difficult to remove the stents after long-term use. Therefore, biodegradable stents have gradually attracted significant attention. Compared with traditional stents, the advantages of biodegradable stents are that they can maintain their integrity and radial expansion force within 6-8 weeks after implantation and disintegrate within 11-12 weeks[30], eliminating the need for secondary removal. In addition, there are currently biodegradable paclitaxel (PTX)- poly (lactic-co-glycolic acid) (PLGA)-coated magnesium stents, etc. have been successfully used in animal experiments and in vitro studies for the treatment of benign esophageal strictures. PTX-PLGA is a biodegradable composite stent, having PLGA containing PTX coated the surface of the magnesium-based braided stent. Liu et al[30] evaluated the in vitro and in vivo characteristics of magnesium esophageal stents with PLGA coatings and different concentrations of PTX and stents with uncoated PLGA. It was found that PTX-PLGA stents had a higher radial force than uncoated stents, a faster degradation rate in acidic medium, and effectively promoted fibroblast apoptosis in in vitro experiments. In a rabbit model using PTX-PLGA stents, compared with the control group, the esophageal lumen increased and esophageal wall inflammation decreased. In summary, due to the various serious complications associated with stent placement and the lack of a unified standard for material selection, this method is commonly used for malignant esophageal stenosis and has not become a first-line treatment for benign esophageal stenosis.

Endoscopic stem cell injection and flap transplantation

In recent years, there have been an increasing number of studies on endoscopic stem cell injection and flap transplantation for preventing esophageal stenosis after ESD. In 2012, Ohki et al[31] from Japan obtained epithelial cell sheets with a diameter of 23.4 mm by culturing oral mucosal tissue samples in vitro. These engineered cell sheets were successfully implanted onto the esophageal wound site through endoscopic transplantation. In subsequent endoscopic follow-up, the wound healed well, and no symptoms of esophageal stenosis occurred. In 2018, Chai et al[32] from China innovatively transplanted the skin from a patient’s right thigh to the postoperative wound site and fixed it with a stent, which was removed one month later. It was observed that the survival rate of the transplanted skin was 80%, and the incidence of stenosis was 37.5%. Autologous flap transplantation has created new ideas for the treatment of esophageal stenosis. This method not only provides a new treatment approach for esophageal stenosis after ESD of large-area esophageal lesions but also offers a new way to treat refractory esophageal stenosis. However, how to use this method to improve the success rate of treating refractory esophageal stenosis and how to further optimize and perfect this technique require relevant basic and clinical research support. In addition to flap transplantation, there is also the method of stem cell transplantation. Stem cells, as incompletely differentiated, immature cells with self-replicating ability, have pluripotency. Chung et al[33] developed an injectable and self-crosslinking hyaluronic acid hydrogel (EISCH), and mixed adipose-derived stem cells (ADSCs) to prepare an EISCH-ADSC mixture. Subsequently, a detailed controlled experiment was carried out in a pig model, and the response to esophageal stenosis was evaluated in the early, middle, and late stages. The experimental results showed that the ADSC-EISCH group exhibited a better effect in preventing esophageal stenosis. Although stem cell transplantation, as a new technology, has only achieved initial success in animal experiments, it is believed that with the continued advancement of regenerative medicine technologies, stem cell-based therapies may eventually evolve into viable options for preventing esophageal stenosis, though their clinical implementation would need to be carefully evaluated through phased translational research. In summary, it can be seen that the current endoscopic treatment methods for benign esophageal strictures include dilation, medication, stenosis incision, stent placement, and flap transplantation. These methods have different applicable scenarios, advantages, and disadvantages, which are summarized in Table 2.

Table 2 Summary of endoscopic treatment for benign esophageal stenosis.

Treatment methods	Applicable scenarios	Advantages	Disadvantages
Dilation	The vast majority of benign esophageal stenoses	The first-choice treatment method with a wide range of applicable scenarios	High recurrence rate after dilation, requiring repeated treatments
Medication	Reflux-related stenosis or stenosis after ESD	Can intervene in the early process of esophageal stenosis and has a certain preventive effect	The effect of drug alone is not definite and it is often used in combination with dilation and other methods
Stenosis incision	Refractory Schatzki ring and short-segment anastomotic stenosis (< 1 cm)	Definite effect and good effect on annular stenosis	Difficult to operate, high risk of perforation, and the scar after cutting is prone to causing restenosis
Stenting	Refractory or recurrent stenosis, sealing benign esophageal leaks and perforations	It can control potential inflammation, and the scar tissue may also undergo remodeling, thus achieving continuous lumen patency	The long-term effect of the stent is not good. About one-third of patients have a poor effect in terms of long-term relief of dysphagia, and the displacement rate is relatively high
Flap transplantation	Prevention of stenosis after ESD for large-area esophageal lesions	Significantly reduces the incidence of stenosis after endoscopic circumferential mucosal resection of the esophagus. Flap transplantation avoids repeated dilation of esophageal stenosis and damage to the esophagus	Is a cutting-edge technology, less carried out, and requires relevant basic and clinical research for further verification

ESD: Endoscopic submucosal dissection.

PROBLEMS ASSOCIATED WITH ENDOSCOPIC TREATMENT

At present, benign esophageal stenosis still poses a challenge to gastroenterologists. The above text reviews the current mainstream endoscopic treatment methods, including dilation, medication, incision, stenting, transplantation, etc. Generally speaking, balloon dilation or bougie dilation remains the first-line treatment. For stenosis caused by reflux esophagitis and stenosis after ESD, a treatment method combining dilation with local steroid injection can be considered. For corrosive stenosis, intralesional injection of mitomycin C may be an effective option. For some experienced doctors, incision treatment is a safe and effective method for Schatzki rings and anastomotic stenosis. The long-term effect of esophageal stent placement is disappointing, with a relatively high overall displacement and recurrence rate. Therefore, careful consideration and individualized selection should be made in clinical practice. At the same time, the experience of the endoscopist and the characteristics of the patient’s stenosis should also be taken into account.

From the perspective of operational details, most of the above-mentioned methods lack objective and unified standards. The treatment methods selected for different patients vary greatly, and even different doctors may choose different treatment methods for the same patient. For example, in endoscopic injection treatment, the operation methods in terms of injection dose, the number of injection sites, or injection time are all different. In balloon dilation, there is no unified standard for the selection of balloon diameter, the pressure of balloon dilation, and the duration of balloon dilation. Moreover, there is a lack of strong clinical data support for research on the details of these processes, such as the optimal dilation duration and the most appropriate pressure. For example, the dilation time in Sweden ranges from 30 seconds to 5 minutes, with an average of 2 minutes. In addition, there is no strict requirement for the balloon pressure during dilation, which is only selected based on the doctor’s experience. In China, when using balloon dilation to treat esophageal stenosis, the pressure is usually maintained at 3-8 atmospheres according to the condition of the patient, and it is maintained for 2-3 minutes, judged by the patient’s tolerance. This may lead to different clinical outcomes during the treatment process due to different dilation intensities or durations, and may even cause serious complications such as perforation and bleeding. In 2013, Wallner and Wallner[34] prospectively compared the number of times required to reach a post-dilation diameter of 20 mm during the balloon dilation process with an inflation time of 10 seconds and 2 minutes in 20 symptomatic patients with benign esophageal stenosis following random grouping. They also followed up the patients at 1 week, 1 month, 3 months, and 1 year after dilation. The results showed that the 10-second group required an average of 1.4 dilations per patient, and the 2-minute group required an average of 1.5 dilations per patient to achieve the expected therapeutic effect. This preliminary study indicates that a 10-second dilation time is as effective as 2 minutes. Also, as both gastroscopy and dilation can cause patient discomfort, and even symptoms such as vomiting and pain, reducing the dilation duration is important and beneficial to patients. Similar problems also exist in the selection of schemes such as the peak dilation pressure and the number of dilations. Thus, different treatment strategies may be crucial to the patient’s postoperative outcome. Therefore, there is an urgent need for a precise and controllable method to assist clinicians in formulating treatment plans.

SUMMARY AND PROSPECTS

In the current era of precision medicine, using advanced technologies such as endoscopic pressure measurement or pressure mapping to make pre-treatment judgments on esophageal stenosis sites and planning in advance the peak pressure and duration during dilation will become the trend in future development. Recently, the functional luminal imaging probe (FLIP) has achieved good results in evaluating esophageal sphincter function, esophageal wall stiffness, and esophageal motility[35]. FLIP consists of a catheter with a distal balloon. Inside the balloon, there are 16 pairs of impedance plane electrodes and a solid-state pressure sensor. During endoscopy, FLIP is placed in the esophagus, and by gradually inflating the balloon, it measures changes in the cross-sectional area and pressure of the esophageal lumen. It can detect parameters such as the diameter, volume, pressure changes in the esophageal lumen, compliance of the esophageal wall, the opening kinetics of the lower esophageal sphincter, the distensibility index of the lower esophageal sphincter, and the hardness of the esophageal wall, thus evaluating esophageal motility, sphincter function, and the physical properties of the esophageal wall, and guiding the diagnosis and treatment of esophageal-related diseases. Kwiatek et al[36] applied the FLIP [endoluminal FLIP (EndoFLIP)] to analyze the mechanical properties of the esophagus in patients with eosinophilic esophagitis. The study included 33 eosinophilic esophagitis patients and 15 controls. Using the luminal imaging probe, it was found that EndoFLIP could successfully display the geometry of the tubular esophagus and mark the location of the stenosis through pressure mapping. The study found that during the balloon dilation treatment process, after the balloon reaches a certain pressure, it will enter a dilation plateau phase. At this time, even if the pressure inside the balloon is further increased, the minimum cross-sectional area of the esophagus remains unchanged, which proves that the peak pressure of balloon dilation can be predicted by EndoFLIP. The study also found that mucosal eosinophil count, age, gender, and current proton-pump inhibitor treatment cannot achieve such a prediction, while EndoFLIP can provide us with an objective means to measure the results of medical or dilation therapy.

CONCLUSION

There are still many problems in the treatment of benign esophageal stenosis. The main issue is the lack of effective outcome measurement methods to objectively reflect the final results of tissue remodeling and fibrosis. Currently, clinical assessment mainly relies on imaging and endoscopic indicators to qualitatively evaluate the degree of esophageal fibrosis and compliance. However, it is obvious that these tools are significantly subjective and cannot test the distensibility of the esophageal wall, thus are unable to measure the pressure-geometric relationship of the esophageal lumen. The current EndoFLIP technology can make up for this deficiency. It is believed that in the future, more technologies and tools will be applied to digestive endoscopy, providing further assistance in the diagnosis and treatment of digestive system diseases.