Published online Nov 15, 2026. doi: 10.4251/wjgo.121634
Revised: June 25, 2026
Accepted: October 9, 2026
Published online: November 15, 2026
Processing time: 216 Days and 22.2 Hours
Esophageal epidermoid metaplasia, also known as esophageal keratosis, can occur on the normal esophageal epithelium and surface of esophageal squamous cell carcinoma (ESCC). However, its endoscopic characteristics and clinical significance in early ESCC remain underexplored.
To investigate endoscopic characteristics and clinical significance of keratosis in early ESCC and assess its impact on endoscopic assessment accuracy.
This retrospective cross-sectional study included 107 consecutive patients (121 pathologically confirmed early ESCC lesions) treated at Sichuan University Affiliated Chengdu Second People’s Hospital between January 2022 and De
Among the 121 early ESCC lesions, esophageal keratosis was detected in 46 (38.02%). Age > 60 years and history of smoking and alcohol consumption were associated with a higher incidence of esophageal keratosis (P < 0.05). Infiltrative lesions were more frequently associated with keratosis and showed increased lamina propria invasion (P < 0.05), with a trend toward better differentiation (P = 0.086). Sex, family history, tumor size, anatomical location, and morphology showed no significant differences between the groups. Keratinized area ≥ 30% reduced preoperative endoscopic diagnostic accuracy (P < 0.05). When we further compared groups based on the proportion of keratinized area, we found that larger esophageal lesions had greater keratinized areas, although there was no significant difference (P = 0.06).
Keratosis is associated with tumor infiltration. The accuracy of preoperative endoscopy is reliable for most early ESCCs but may decrease when the keratinized area exceeds 30% of the lesion.
Core Tip: Esophageal keratosis in early esophageal squamous cell carcinoma (ESCC) is associated with tumor infiltration and may reflect invasion depth. Preoperative endoscopic assessment based on intraluminal papillary capillary loop morphology in nonkeratinized areas is reliable for most early ESCCs; however, its accuracy may decrease when the keratinized area accounts for ≥ 30% of the lesion. The extent of keratinization may also be related to lesion size, although further studies are needed to confirm these associations.
- Citation: Zhang YJ, Wen W, Li F, Yuan J, Zou DH, Shi HP, Liang C, Yang Y. Proportion of esophageal keratinized area ≥ 30% reduces accuracy of preoperative endoscopic evaluation in early esophageal squamous cell carcinoma. World J Gastrointest Oncol 2026; 18(11): 121634
- URL: https://www.wjgnet.com/1948-5204/full/v18/i11/121634.htm
- DOI: https://dx.doi.org/10.4251/wjgo.121634
In recent years, rapid advances in endoscopic technology have significantly improved the early detection and diagnosis of esophageal squamous cell carcinoma (ESCC); a predominant pathological subtype of esophageal cancer in China. In current practice, the morphology of intraluminal papillary capillary loops (IPCLs) in esophageal lesions is observed using narrow-band imaging with magnifying endoscopy (NBI-ME), with or without iodine staining, to determine the lesion type and invasion depth before treatment[1]. During endoscopic examination of early esophageal cancer, white plaques are sometimes observed adhering to the lesion surface and are difficult to remove with water irrigation. These plaques are called esophageal epidermoid metaplasia; also known as esophageal keratosis[2]. Esophageal keratosis can occur on the surface of the normal esophageal epithelium and on ESCC lesions, and reports of its detection on the surface of ESCC are increasing[3,4]. However, endoscopic features of esophageal keratinization and their clinical significance have not been fully elucidated[5,6]. The presence of these white plaques may obscure IPCL morphology and result in pale or unstained areas during iodine staining. Accordingly, they can increase the difficulty of preoperative endoscopic assessment and may lead to inaccurate evaluation and inappropriate treatment selection. However, the endoscopic characteristics and clinical significance of esophageal keratosis in early ESCC remain underexplored. Therefore, we retrospectively analyzed the endoscopic, pathological, and clinical characteristics of 121 early ESCCs (107 patients) to clarify the endoscopic features and clinical significance of esophageal keratosis and to help guide accurate diagnosis and treatment selection.
We enrolled 107 consecutive patients (121 early ESCCs) who received endoscopic or surgical treatment at Sichuan University Affiliated Chengdu Second People’s Hospital between January 2022 and December 2024. Early ESCCs were defined as lesions confined to the mucosa and submucosa, regardless of lymph-node metastasis, based on postoperative pathological results[7].
As determined under white light endoscopy (WLE), the cases were divided into epithelial and nonepithelial keratosis groups. Patient data collected included: Sex; age; smoking history (≥ 10 years, ≥ 5 cigarettes/day); alcohol consumption history (≥ 10 years, ≥ 100 g/day); family history (first-degree relatives with gastrointestinal malignancies); and lesion location, size, and infiltration depth.
Inclusion criteria were: (1) Suspected early ESCC on preoperative endoscopy with subsequent pathological con
This study was approved by the Ethics Committee of Affiliated Chengdu Second People’s Hospital of Sichuan University prior to data collection, and the requirement for informed consent from participants was waived, No. [KY] PJ2026049.
Our study followed the diagnostic criteria of the Japanese Gastroenterological Endoscopy Society Guidelines Committee[8]. Lesions confined to the mucosal epithelium were classified as high-grade intraepithelial neoplasia (HGIN) or intramucosal carcinoma (M1). Lesions infiltrating the mucosal propria were classified as M2, those infiltrating the muscularis mucosa but not beyond as M3, and those infiltrating the submucosa but not the muscularis propria as SM.
Standard colonoscopes (GIF H260Z, GIF Q260, or GIF HQ290; Olympus, Tokyo, Japan) and open biopsy forceps with a 7-mm deployed diameter (QYQ-AXC2.3X2300; Changchun Huichun Medical Devices, Changzhou, China) were used.
Endoscopic imaging data were reviewed, and unclear or controversial records were clarified by an experienced doctor. Lesion location and size, morphological classification under WLE, and morphology of IPCLs under NBI-ME were an
Lesion size was estimated in vivo using open biopsy forceps with a 7-mm deployed diameter. Growth morphology was categorized according to the Paris classification of early gastrointestinal lesions[10] as protuberant (0-I), flat (0-II), and depressed (0-III). Type 0-II was predominant in our study and included three subtypes: 0-IIa (superficial protuberance type), in which the lesion was higher than the surrounding mucosa, usually < 1.2 mm; 0-IIb (superficial flat type), in which the lesion was at the same height as the surrounding mucosa, without apparent elevation, although surface roughness or color change may have been present; and 0-IIc (superficial depression type), in which the lesion was lower than the surrounding mucosa, usually with a depth of < 0.5 mm.
Esophageal keratosis can occur on the surface of the normal esophageal epithelium (Figure 1A) and on esophageal cancer. Common characteristics[11] include: (1) Clear boundaries; (2) Elevated, white, flat-topped keratotic plaques that are not easily washed away with water; (3) Absent or pale Lugol iodine staining; and (4) Unclear or invisible IPCLs under NBI-ME. There are other distinguishing features[12]. For example, on the normal esophageal mucosa, keratotic plaques are often translucent, scaly, and relatively smooth, with adjacent hyperkeratotic foci of similar size and uniform height. Meanwhile, esophageal keratosis on early esophageal cancer is often porcelain white or milk white, with rough or irregular surfaces, dregs-like appearance, and poor transparency; adjacent hyperkeratotic plaques vary in size and height and can merge with each other. The area surrounding esophageal keratosis on the normal esophageal mucosa appears normal without apparent erosion, roughness, or redness. However, esophageal keratosis on early esophageal cancer is often accompanied by surrounding mucosal roughness, redness, erosion, or nodular protuberance lesions, and uno
All cases were early ESCCs. Invasive depth was estimated in SM-stage cancers, especially specimens resected using endoscopic submucosal dissection. Curative endoscopic resection was defined by the following criteria[13]: (1) R0 resection, no tumor cells at horizontal and vertical resection margins on microscopic examination; (2) M-stage or SM-stage cancer with submucosal invasion depth < 0.2 mm; (3) No lymphatic or vascular invasion; and (4) Tumor budding grade < 2. Based on postoperative pathological findings, resection was considered curative when all of the above conditions were met. Patients who underwent noncurative resection were advised on further treatment (Figure 2). Follow-up endoscopy was set at 3 months (short), 6 years (intermediate), and 1 year (long). Local tumor recurrence and metastasis were recorded.
Statistical analyses were performed by a biomedical statistician using IBM SPSS version 25.0 (IBM Corp., Armonk, NY, United States). Categorical data are expressed as counts. Basic characteristics were analyzed using Fisher’s exact tests, χ2 tests, and χ2 tests of R × C table data. Logistic regression analysis was performed to assess the associations of esophageal keratosis with age, tumor infiltration, smoking history, and alcohol consumption history. Statistical significance was set at P < 0.05. Statistical methods were reviewed by Jing Yuan from the Department of Scientific Training of Affiliated Chengdu Second People’s Hospital of Sichuan University.
Between January 2022 and December 2024, 107 consecutive patients (121 early ESCCs) who received endoscopic (n = 94) or surgical (n = 13) treatment at Sichuan University Affiliated Chengdu Second People’s Hospital were enrolled. Early ESCCs were confirmed according to postoperative pathology results. To date, no recurrence or metastasis has been observed post-treatment.
Of 121 early ESCCs, 46 were associated with esophageal keratosis, with a detection rate of 38.02%. Fourteen patients (13.08%) had two early esophageal cancers simultaneously. The overall male-to-female ratio was 85:22, and the patient ages ranged from 18 to 80 years (64.09 ± 7.42 years). Compared with patients in the nonkeratosis group, more patients in the epithelial keratosis group were aged > 60 years (age > 60 vs ≤ 60 years: 32/41 vs 38/65 patients) (P = 0.038) and had a history of smoking (with vs without: 27/41 vs 22/65 patients) (P = 0.001) and alcohol consumption (with vs without: 26/41 vs 20/65 patients) (P = 0.001) (Table 1). Based on pathological results for the resected specimens, among those who received initial endoscopic therapy, four failed to achieve curative therapy (1, vertical margin positive; 2, deep submucosal invasion; 1, lymphatic invasion). Of the four patients with noncurative resection, three underwent additional surgery, and one (lymphatic invasion) opted for close follow-up. None of these patients has developed tumor recurrence or metastasis to date.
| Variable | Esophageal keratosis (n = 41) | Nonesophageal keratosis (n = 65) | P value | |
| Alcohol consumption history | 26 (63.41) | 20 (30.77) | 0.001 | |
| Smoking history | 27 (65.85) | 22 (33.85) | 0.001 | |
| Family history | 3 (7.32) | 6 (9.23) | 0.199 | |
| Age (year) | > 60 | 32 (78.05) | 38 (58.46) | 0.038 |
| ≤ 60 | 9 (21.95) | 27 (41.54) | ||
| Sex | Female | 8 (19.51) | 14 (21.54) | 0.802 |
| Male | 33 (80.49) | 51 (78.46) | ||
Most lesions occurred in the middle and lower segments of the esophagus. No significant differences in lesion location were observed between early ESCCs with esophageal keratosis and those without (2/21/23 vs 7/31/37) (Table 2). Lesion size ranged from approximately 0.5 cm × 0.5 cm to 6.0 cm × 5.5 cm. The most common growth pattern was 0-IIb. Mixed lesions were classified according to the main lesion type; for example, 0-IIa+IIb was recorded as 0-IIa, and 0-IIb+IIc as 0-IIb. No significant difference in lesion size or morphology was observed between the two groups (Table 2).
| Variable | Esophageal keratosis (n = 46) | Nonesophageal keratosis (n = 75) | P value | |
| Morphology | 0-IIa | 7 (15.22) | 11 (14.67) | 0.722 |
| 0-IIb | 37 (80.43) | 58 (77.33) | ||
| 0-IIc | 2 (4.35) | 6 (8) | ||
| Location | Upper thoracic esophagus | 2 (4.35) | 7 (9.33) | 0.561 |
| Middle thoracic esophagus | 21 (45.65) | 31 (41.33) | ||
| Lower thoracic esophagus | 23 (50) | 37 (49.34) | ||
| Size (cm) | ≥ 2 | 30 (65.22) | 40 (53.33) | 0.199 |
| < 2 | 16 (34.78) | 35 (46.67) | ||
Based on pathological findings and the presence of invasion, early ESCC was classified into two main categories: (1) Noninvasive early ESCC, including HGIN and carcinoma in situ, in which the tumor did not penetrate the basement membrane and was therefore considered to carry no risk of metastasis; and (2) Invasive early ESCC, including intra
| Variable | Esophageal keratosis (n = 29) | Nonesophageal keratosis (n = 27) | P value | |
| Depth of tumor infiltration | M2 | 20 (68.97) | 10 (37.04) | 0.038 |
| M3 | 6 (20.69) | 8 (29.63) | ||
| SM | 3 (10.34) | 9 (33.33) | ||
| Degree of tumor differentiation | High | 19 (65.52) | 10 (37.04) | 0.086 |
| Medium-high | 8 (27.59) | 12 (44.44) | ||
| Medium-low | 2 (6.89) | 5 (18.52) |
Most tumors were well differentiated, with the highest proportion classified as highly differentiated, followed by high–moderate and moderate–low differentiation. Tumors in the esophageal keratosis ESCC group showed a higher degree of differentiation; however, this difference did not reach significance (P = 0.086) (Table 4). The tumor budding grade was less than G2 in both groups. Lymphatic invasion was observed in one case in each group, with no significant difference between groups.
The accuracy of preoperative evaluation based on the observed IPCL morphology in the nonkeratosis group was approximately 85.33%. The other two groups showed significantly lower accuracy (P = 0.022) (Table 5). Pairwise comparisons showed that the presence of epithelial keratosis with a keratosis area < 30% had little effect on the accuracy of preoperative endoscopic evaluation for most lesions (P = 0.653) (Table 6). However, when the keratinized area exceeded 30% of the tumor, preoperative endoscopic diagnostic accuracy was significantly lower than that for nonepithelial keratosis early ESCC (P = 0.008) (Table 6). When we further compared groups based on the proportion of keratinized area, we found that larger esophageal lesions had greater keratinized areas, although the difference was not significant (P = 0.06) (Table 7); thus, further studies are required to confirm this finding.
| Variable | Evaluation accuracy | Total (n) | P value | |
| (+) | (-) | |||
| Keratosis area ≥ 30% | 9 (52.94) | 8 (47.06) | 17 | 0.008 |
| Nonkeratosis | 64 (85.33) | 11 (14.67) | 75 | |
| Keratosis area ≥ 30% | 9 (52.94) | 8 (47.06) | 17 | 0.061 |
| Keratosis area < 30% | 23 (79.31) | 6 (20.69) | 29 | |
| Keratosis area < 30% | 23 (79.31) | 6 (20.69) | 29 | 0.653 |
| Nonkeratosis | 64 (85.33) | 11 (14.67) | 75 | |
| Variable | Keratosis area ≥ 30% (n = 17) | Keratosis area < 30% (n = 29) | P value | |
| Noninvasive ESCCs | 7 (41.18) | 10 (34.48) | 0.65 | |
| Invasive ESCCs | 10 (58.82) | 19 (65.52) | ||
| Size (cm) | ≥ 2 | 14 (82.35) | 16 (55.17) | 0.06 |
| < 2 | 3 (17.65) | 13 (44.83) | ||
| Location | Upper thoracic esophagus | 1 (5.89) | 1 (34.48) | 0.91 |
| Middle thoracic esophagus | 7 (41.18) | 14 (48.28) | ||
| lower thoracic esophagus | 9 (52.94) | 14 (48.28) | ||
| Morphology | 0-IIa | 4 (23.53) | 3 (10.34) | 0.13 |
| 0-IIb | 13 (76.47) | 24 (82.76) | ||
| 0-IIc | 0 | 2 (6.9) | ||
Patients aged > 60 years, those with a history of smoking and alcohol consumption, and those with invasive early ESCCs had a significantly higher incidence of esophageal keratosis. Further logistic regression analyses identified tumor infiltration as an independent risk factor for esophageal keratosis in early esophageal cancer (Table 8).
| Variable | Wald | OR (95%CI) | P value |
| Age (> 60/≤ 60 years) | 3.137 | 0.465 (0.199-1.085) | 0.077 |
| Infiltration (+/-) | 7.464 | 3.183 (1.387-7.304) | 0.006 |
| History of smoking | 2.093 | 0.475 (0.173-1.303) | 0.148 |
| History of alcohol consumption | 0.356 | 0.738 (0.272-2.002) | 0.551 |
Esophageal cancer is a common malignant tumor in clinical practice, and its prognosis is closely related to tumor stage[14,15]. Early detection and diagnosis are crucial for improving outcomes. Early ESCC typically presents under WLE as localized mucosal roughness, erythema, erosion, and interruption of the submucosal vascular network. For many endoscopists, detecting this mucosal change is critical yet difficult under WLE, and further evaluation involving NBI or iodine staining is performed. NBI-ME is used to evaluate IPCL morphology in esophageal lesions before surgery, and iodine staining is often used to evaluate the lesion nature and invasion depth. With the rapid development of endoscopic technology, the early diagnosis rate of ESCC has increased annually. Keratosis is obvious and easily detected under WLE; accordingly, the combination of early esophageal cancer with keratosis can improve lesion detection by endoscopists. Currently, esophageal keratosis can occur on the normal esophageal epithelium and ESCC[16-18], and its incidence is significantly higher in patients with ESCC[3,19]. Pathologically, it is characterized by a hyperplastic epithelium, prominent granular cell layer, and focal incomplete keratinization. In recent years, esophageal keratosis has attracted increasing attention as a potentially precancerous lesion that is not yet fully understood. However, esophageal keratosis in early ESCC is rarely reported and may have distinct endoscopic features and clinical significance. For example, it is often associated with surrounding mucosal roughness, redness, erosion, or nodular protrusions. Areas not obscured under NBI may appear tea-colored, rough or irregular, dreg-like, and poorly transparent. The affected mucosa is prone to bleeding, especially with manipulation or repeated insufflation and aspiration. Pathologically, tumor cells are often observed around and beneath keratinized areas (Figure 3).
To avoid the effect of a biopsy-induced white coating on ulcer surfaces, a complete endoscopic evaluation was performed prior to biopsy. The detection rate of keratinization in early ESCC reached 38.02%, which is markedly higher than that in the normal population[4], suggesting a close association with early ESCC. This high rate may also be related to the higher prevalence of smoking and alcohol consumption in this cohort; consistent with previous findings[20,21]. It is possible that long-term alcohol consumption repeatedly irritates the esophageal mucosal epithelial cells, causing chronic inflammation. This makes cells prone to abnormal differentiation during the process of damage and repair, leading to abnormal keratinization and even dysplasia and carcinogenesis. Furthermore, harmful substances in tobacco can damage the microvessels of the esophageal mucosa, affecting the supply and absorption of substances, exacerbating the aforementioned risks. Keratinization was more commonly observed in middle-aged patients but was independent of sex, and lesion location, size, or growth pattern. ESCCs with keratosis were more likely to exhibit invasion, often into the mucosal propria, suggesting that keratinization is more likely to occur during tumor infiltration rather than at precancerous or early stages, distinguishing it from keratosis on the normal epithelium. Moreover, there was a trend toward an asso
Advances in computer vision indicate that different types of occlusion variably affect detection performance, with occlusion > 10% impairing accuracy and occlusion > 30% causing a substantial reduction. To assess the impact of ke
This study had some limitations. First, although iodine staining is useful for assessing lesion type and invasion depth, its use is declining because NBI-ME combined with WLE can improve real-time detection rates during the surveillance of high-risk patients, and some patients may be allergic to iodine[22]. We observed that esophageal keratinization may have influenced iodine staining. For example, similar to cancerous or precancerous tissue, keratinized tissue remains unstained in the Lugol’s chromoendoscopy of the esophagus owing to a lack of glycogen, while healthy esophageal tissue absorbs iodine and turns dark brown. In addition, we found that the size of the keratinized area may have affected the outcome of the “TaTami sign” (i.e., the larger the keratinized area, the more likely the disappearance of the “TaTami sign”). However, no “Pink-Color Sign” was observed in the keratinized tissue after iodine staining, and further research is needed to validate this observation. Second, different types and degrees of occlusion may have had varying effects on detection; however, stratified analyses were not feasible owing to sample limitations. Finally, this was a single-center retrospective study with inherent limitations, including a small sample size and potential bias.
In future studies, we plan to expand the sample size, perform more detailed stratified analyses to investigate effects of different types of keratosis-related occlusion (e.g., central vs peripheral) in early ESCC, and evaluate the contribution of genetic factors to keratosis and ESCC.
Esophageal keratosis is a common endoscopic feature of early ESCC, with distinct characteristics and clinical significance compared with those of keratosis on the normal esophageal mucosal epithelium. For most early ESCCs with epithelial keratosis, assessing lesion nature and invasion depth by evaluating IPCL morphology in exposed, nonkeratinized areas during preoperative endoscopy is a reliable approach. However, when keratinization involves ≥ 30% of the lesion area, the accuracy of this assessment may decrease. Esophageal keratosis is also associated with tumor infiltration in early ESCC.
We thank Professor Hu Bing of West China Hospital, Sichuan University, for giving scientific guidance.
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