# Oral Glycogenic Acanthosis: A Clinicopathological Analysis of 13 Cases and Narrative Literature Review

**Authors:** Gisele N. Mainville, Safae Benali Lietefti, Antonio Nanci, Catherine Laliberté, Adel Kauzman

PMC · DOI: 10.1007/s12105-026-01891-6 · Head and Neck Pathology · 2026-02-19

## TL;DR

This study analyzes 13 cases of oral glycogenic acanthosis, a rare benign condition that mimics leukoplakia, to improve its clinical recognition and understanding.

## Contribution

The study presents the largest case series of oral glycogenic acanthosis and proposes diagnostic features to distinguish it from similar conditions.

## Key findings

- Oral GA typically appears as asymptomatic white plaques on the tongue or soft palate and is often mistaken for leukoplakia.
- Histologically, GA shows glycogen-rich clear cells without dysplasia, and most cases remain stable over time.
- One case regressed without treatment, while another progressed to mild dysplasia in a patient with HIV and a history of smoking.

## Abstract

Glycogenic acanthosis (GA) is a benign epithelial lesion characterized by intracellular glycogen accumulation, most seen in the esophagus. In the oral cavity, it is rarely reported and clinical recognition is low.

We retrospectively analyzed 13 cases of oral GA diagnosed between 2017 and 2025, assessing clinical presentation, histopathological characteristics and follow-up data.

Thirteen cases were identified, with a median age of 61 years (range: 34–71) and a male predominance (76.9%). Lesions were asymptomatic, thin, homogeneous, often well-demarcated milky white plaques, located on the lateral or ventral surfaces of the tongue (84.6%) or the soft palate (15.4%), all mimicking oral leukoplakia. All patients reported alcohol use; 46.2% were never smokers. Histologically, lesions showed glycogen-rich clear cells in the spinous layer of epithelium, without dysplasia. Follow-up data (available in 9 cases, 3 months to 8 years) showed that most lesions remained stable following initial diagnosis, except for one case that regressed by 80% without treatment after nearly 4 years, and another that focally progressed to mild dysplasia after 7 years in a smoking patient with HIV.

This study presents the largest series of oral GA to date and proposes a list of distinguishing clinical and histopathological features to assist in the diagnosis of this condition. Our findings are consistent with the seven previously published reports, further supporting that oral GA is an under-recognized lesion that can clinically mimic homogenous leukoplakia. While current evidence suggests a benign long-term course, additional studies using standardized diagnostic criteria and molecular approaches are needed to better understand its pathogenesis and prognosis. Greater clinician awareness is essential to minimize misdiagnosis and ensure appropriate management.

The online version contains supplementary material available at 10.1007/s12105-026-01891-6.

## Full-text entities

- **Diseases:** cancer (MESH:D009369), Dyskeratosis (MESH:C565079), diabetes (MESH:D003920), infection (MESH:D007239), mucosal irritation (MESH:D001523), oedema (MESH:C536897), GA lesion (MESH:D006008), atrophy (MESH:D001284), abnormalities in glucose metabolism (MESH:D044882), hyperkeratosis (MESH:D017488), keratosis (MESH:D007642), Head and Neck (MESH:D006258), Inflammation (MESH:D007249), GERD (MESH:D005764), trauma (MESH:D014947), tobacco pouch keratosis (MESH:D014029), mucosal diseases (MESH:D004194), clear cell acanthoma (MESH:D049309), architectural dysplasia (MESH:D015792), verruciform xanthoma (MESH:D014973), oral hairy leucoplakia (MESH:D017733), OL (MESH:D007972), dyslipidemia (MESH:D050171), basilar (MESH:D014715), CS (MESH:D006223), hypertension (MESH:D006973), basal cell hyperplasia (MESH:D002280), Leukoplakia (MESH:D007971), basal hyperplasia (MESH:D006965), erythema (MESH:D004890), parakeratosis (MESH:D010241), OPMD (MESH:C537245), GA (MESH:D000052), HIV infection (MESH:D015658), , prostate, and skin (MESH:D011472), leukoedema (MESH:D007967), linea alba (MESH:C567402), reactive white lesions (MESH:D000085343), OSCC (MESH:D000077195), squamous cell carcinoma (MESH:D002294), depression (MESH:D003866), reactive (frictional) keratosis (MESH:D000275), OED (MESH:C567703), oral lesions (MESH:D009059), oral (MESH:D020820), oral cancer (MESH:D009062), COPD (MESH:D029424)
- **Chemicals:** H&amp;E (MESH:D006371), GA (-), Alcohol (MESH:D000438), ETOH (MESH:D000431), Glycogen (MESH:D006003)
- **Species:** Homo sapiens (human, species) [taxon 9606], Human papillomavirus (species) [taxon 10566], Human immunodeficiency virus (species) [taxon 12721], Human immunodeficiency virus 1 (no rank) [taxon 11676], Nicotiana tabacum (American tobacco, species) [taxon 4097], Areca catechu (areca-nut, species) [taxon 184783]
- **Mutations:** P18 A

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12921078/full.md

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12921078/full.md

## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12921078/full.md

---
Source: https://tomesphere.com/paper/PMC12921078