Differential diagnosis of rare diseases presenting as palatal ulcers: a case series

Introduction

Palatal ulcers are common in oral medicine. Their causes range from self-limiting benign conditions to life-threatening systemic diseases, making diagnosis challenging. Common causes include herpetic gingival stomatitis, candidiasis, major aphthous ulcer, lichen planus, and pemphigus (1,2). These can usually be diagnosed based on clinical features. However, when ulcers are refractory, atypical, or unresponsive to conventional treatment, clinicians should broaden their diagnostic thinking and consider underlying systemic diseases.

Palatal ulcers can be the first sign of many rare systemic diseases. These include inflammatory disorders, lymphoproliferative diseases, infectious conditions, histiocytic disorders, immunodeficiencies, and inflammatory bowel disease-associated conditions. Necrotizing sialometaplasia is a rare self-limiting inflammatory disease. About 79% of cases occur on the palate, presenting as a crater-like ulcer that is easily misdiagnosed as malignancy (3). Extranodal natural killer (NK)/T-cell lymphoma, nasal type, is an aggressive lymphoma closely associated with Epstein-Barr virus (EBV). It often involves midline facial structures. Palatal involvement is a prominent oral manifestation, usually presenting as destructive ulcerative lesions that can be confused with traumatic ulcers or squamous cell carcinoma (4,5). Furthermore, oral tuberculosis can occur without a known history of tuberculosis or pulmonary symptoms. It is difficult to diagnose and requires extensive differential diagnosis and systematic evaluation (6); STAT1 gain-of-function mutation-induced chronic mucocutaneous candidiasis (CMC) predisposes patients to Candida susceptibility, manifesting as persistent oral ulcers (7); the gingiva and hard palate are the most frequently involved sites in oral soft tissue lesions of Langerhans cell histiocytosis (LCH) (8); pyostomatitis vegetans (PSV) is closely associated with inflammatory bowel disease, and its characteristic “snail track” ulcers are an important clinical clue (9). Peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), is extremely rare as an isolated oral manifestation. It usually presents as destructive, infiltrative, painful ulcers with a very poor prognosis (10).

However, no systematic comparative study has yet been conducted on the multiple rare diseases presenting initially with palatal ulcers. Based on clinical experience and literature review, we developed a diagnostic algorithm for palatal ulcers (Figure 1). It integrates clinical morphology, systematic history taking, histopathology, microbiology, and molecular genetics. This approach guides clinicians from routine differential diagnosis to in-depth investigation and final etiological clarification.

Figure 1 Diagnostic process of palatal ulcers. The five cases are marked with red numbered ① to ⑤ in the figure. ANCA, antineutrophil cytoplasmic antibody; CMC, chronic mucocutaneous candidiasis; CT, computed tomography; EBER, Epstein-Barr virus-encoded RNA; EBV, Epstein-Barr virus; EBV-MCU, Epstein-Barr virus-positive mucocutaneous ulcer; ENKTL, extranodal natural killer/T-cell lymphoma; GPA, granulomatosis with polyangiitis; HE, hematoxylin and eosin; HIV, human immunodeficiency virus; IBD, inflammatory bowel disease; IHC, immunohistochemistry; LCH, Langerhans cell histiocytosis; MDT, multidisciplinary team; PCR, polymerase chain reaction; PSV, pyostomatitis vegetans; PTCL-NOS, peripheral T-cell lymphoma, not otherwise specified.

This study retrospectively analyzed five cases of rare diseases with palatal ulcers as the initial manifestation at our hospital from 2022 to 2024. We summarize their clinical and pathological features to help clinicians reduce misdiagnosis and missed diagnosis. We present this article in accordance with the AME Case Series reporting checklist (available at https://fomm.amegroups.com/article/view/10.21037/fomm-2025-1-48/rc).

Case presentation

This study is a single-center retrospective case series study. All five cases were selected from patients who initially presented with oral ulcers that primarily or secondarily involved the palate at the Department of Oral Medicine, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, between 2022 and 2024. The case selection criteria were as follows: (I) oral ulcers involving the palate as the primary or prominent clinical feature; (II) a final diagnosis of a rare systemic disease confirmed by histopathology, microbiology, genetic testing, or a combination thereof; (III) complete clinical records. Exclusion criteria were: (I) common etiologies of palatal ulcers confirmed by routine investigations (e.g., traumatic ulcers, recurrent aphthous stomatitis, herpes simplex infection); (II) incomplete diagnostic workup; (III) loss to follow-up before a definitive diagnosis was established. The clinical data were obtained from combined records of the Department of Oral Medicine and the Department of Oral Pathology.

Case 1

A 76-year-old man presented with swelling in the upper left posterior gingiva for 7 months and ulceration for 1 month. Anti-inflammatory treatment was ineffective. His medical history included hypertension, coronary artery disease, psoriasis, and anemia. Physical examination revealed ulcers on the left upper gingiva and buccal mucosa extending to the hard palate, covered with a pseudomembrane and yellow exudate (Figure 2). Contrast-enhanced computed tomography (CT) showed soft tissue thickening and bilateral cervical lymphadenopathy. Histopathological examination of the ulcer excision specimens demonstrated characteristic granulomatous lesions with tuberculous nodules, showing central caseous necrosis surrounded by epithelioid cells and an outer layer of lymphocytic infiltration (Figure 2). The T-SPOT test was positive. Following infectious disease consultation, a diagnosis of oral tuberculosis was established. The patient received anti-tuberculosis treatment: isoniazid, rifampicin, and pyrazinamide for 2 months, followed by isoniazid and rifampicin for over 4 months. At 6-month telephone follow-up, pain was significantly relieved and oral erosions had healed.

Figure 2 Case 1: a 76-year-old male diagnosed with tuberculous ulcer of the oral mucosa. (A) Ulceration on the left maxillary gingiva and buccal mucosa, presenting with mildly elevated borders, a surface covered by pseudomembrane and yellow exudate. (B) HE staining (×200) reveals granulomatous lesions with characteristic tuberculous nodules, demonstrating central caseous necrosis surrounded by epithelioid cells and an outer layer of lymphocytic infiltration. HE, hematoxylin and eosin.

Case 2

A 23-year-old woman presented with recurrent palatal erosions covered by white pseudomembrane for 2 months. She had recurrent oral ulcers since age 4, with facial erythema and nail lesions. Six months earlier, she was diagnosed with Candida albicans infection at an outside hospital. Oral itraconazole gave temporary improvement, but symptoms recurred after discontinuation and re-treatment failed. Intraoral examination showed extensive white pseudomembranes on the palate, maxillary palatal gingiva, and soft palate. When wiped off, the underlying mucosa was congested and eroded. Scattered pseudomembranes were also seen on the dorsal tongue and lower lip vermilion, without significant pain (Figure 3). Lymphocyte subsets showed undetectable Th17 cells and decreased NK cells (4.80%). Other subsets and immunoglobulins were normal. Screening for hepatitis B, human immunodeficiency virus (HIV), hepatitis C, and syphilis was negative. Fungal culture confirmed Candida albicans. Whole-exome sequencing identified a heterozygous STAT1 mutation, c.800C>T (p.A267V) (Figure 3). The diagnosis was CMC due to STAT1 mutation. The patient received oral fluconazole (100 mg/d) and 1% sodium bicarbonate mouthwash. At 3 months, fungal culture was negative and oral symptoms resolved, with no recurrence during this period. However, over nearly 2 years of follow-up, multiple recurrences were observed.

Figure 3 Case 2: a 23-year-old female with CMC due to a STAT1 mutation. (A) Widespread erythema and erosion on the palatal mucosa, covered by a white pseudomembrane. (B) Sequence chromatogram revealing the heterozygous STAT1 c.800C>T variant (NM_007315.4), resulting in the amino acid substitution p.A267V. The arrow indicates the heterozygous mutation site of c.800C>T in STAT1. CMC, chronic mucocutaneous candidiasis.

Case 3

A 20-year-old woman presented with recurrent oral ulcers accompanied by loose teeth and tooth loss for more than 2 years. She had self-medicated with anti-inflammatory drugs (specifics unknown) without significant improvement. She had short stature, a history of otitis media, central diabetes insipidus, and growth hormone-deficiency dwarfism. Intraoral examination revealed extensive palatal erythema with scattered erosions covered by pseudomembrane. Multiple mandibular posterior teeth were missing, and the remaining teeth exhibited a “floating” sensation with deep periodontal pockets (Figure 4). Histopathological examination with hematoxylin-eosin staining showed aggregation of Langerhans cells, macrophages, lymphocytes, eosinophils, granulocytes, and giant cells in the lesional tissue. Immunohistochemical staining demonstrated CD1a (+), S-100 (+), and Langerin (CD207) (+), supporting the diagnosis of LCH (Figure 4). After diagnosis, the patient underwent low-dose radiotherapy to the head and neck region (10 sessions, total dose 20 Gy). At 1-month follow-up, the palatal erosions had decreased in area with slight residual erythema and tenderness, and no new ulcers had developed. Radiotherapy was continued as scheduled.

Figure 4 Case 3: a 20-year-old female diagnosed with LCH. (A) Extensive erythema and erosion on the palatal mucosa, with multiple scattered ulcers exhibiting raised borders and covered by a yellowish pseudomembrane. (B) Widespread erythema and swelling of the gingiva, with gingival margins showing moth-eaten-like destruction and eroded interdental papillae. (C) HE staining (×400) showing sheets and nests of Langerhans cells. These cells are medium-sized with abundant pale cytoplasm and exhibit round, oval, or lobulated nuclei possessing characteristic nuclear grooves. They show mild nuclear atypia and conspicuous nucleoli, and are accompanied by an infiltrate of lymphocytes and eosinophils. (D-F) Immunohistochemical staining shows CD1a (+), S-100 (+), and Langerin (CD207) (+) (D: original magnification ×20; E,F: original magnification ×40). HE, hematoxylin and eosin; LCH, Langerhans cell histiocytosis.

Case 4

A 25-year-old man with palatal ulceration and hyperemia for 3 months. Palatal lesions are characterized by multiple yellow or white pustules that may rupture, leaving erosions and a characteristic “snail track” appearance, and exudative or crusted vegetating plaques on flexural areas (Figure 5). Detailed history revealed a 3-year history of ulcerative colitis, with loose stools (2–3 times daily), occasional hematochezia, and ongoing maintenance therapy with mesalazine (1.5 g daily). There were abnormal laboratory findings, including elevated eosinophils (13.0%; absolute count 1.51×10⁹/L), elevated erythrocyte sedimentation rate (ESR) (25.0 mm/h), and positive fecal occult blood, while the C-reactive protein (CRP) level was within the normal range. Screening for hepatitis B, HIV, hepatitis C, and syphilis yielded negative results. Histopathological examination of the intestinal mucosa revealed epithelial hyperplasia with dense mixed inflammatory cell infiltration in the deeper layers of the lamina propria, along with intraepithelial and subepithelial microabscesses predominantly composed of eosinophils and neutrophils (Figure 5). Based on clinical phenotype and intestinal pathology, a diagnosis of PSV was established. Treatment was adjusted to mesalazine (1 g three times daily) combined with azathioprine (150 mg daily) and 2% sodium bicarbonate mouthwash. At 2-month follow-up, the ulcers were well controlled.

Figure 5 Case 4: a 25-year-old male diagnosed with PSV. (A) The palate exhibits widespread yellow-white pustules, which have ruptured leaving extensive ulcerations and erosions with a characteristic “snail-track” appearance. (B) HE staining (×400) of the intestinal mucosa revealed epithelial hyperplasia with dense mixed inflammatory cell infiltration in the deeper layers of the lamina propria, along with intraepithelial and subepithelial microabscesses predominantly composed of eosinophils and neutrophils. HE, hematoxylin and eosin; PSV, pyostomatitis vegetans.

Case 5

A 44-year-old man presented with a persistent palatal ulcer for over 4 months. The lesion was initially mung bean-sized, with submandibular lymphadenopathy and fatigue. Intraoral examination revealed an irregular mid-palate ulcer, approximately 3.5 cm × 3.0 cm, with an uneven base, raised erythematous margins, thick yellowish-white pseudomembrane, and tenderness (Figure 6). Magnetic resonance imaging (MRI) showed a palatal mass and cervical lymphadenopathy. Biopsy confirmed PTCL-NOS, cytotoxic phenotype. Immunohistochemistry was positive for CD3, CD56, granzyme B, TIA1, CD2, CD5, CD7, CD8, and focal CD30 (60–70%); Epstein-Barr virus-encoded small RNA (EBER) was negative. TCR gene rearrangement was monoclonal. Positron emission tomography (PET)-CT showed hard palate thickening (3.0 cm × 2.5 cm × 1.8 cm) extending to the nasal floor with bone resorption, and bilateral cervical lymphadenopathy. Bone marrow showed scattered CD3⁺ T cells. The Hematology Department diagnosed PTCL-NOS, cytotoxic phenotype [stage IVB, International Prognostic Index (IPI) score 1]. The patient received CHOP chemotherapy. At 1-month follow-up after the first cycle, the ulcer had reduced to 2.0 cm × 1.2 cm. During the second cycle, he developed hemophagocytic syndrome; chemotherapy was immediately discontinued, and he was treated with dexamethasone, etoposide, and meropenem. Two weeks after the start of the second cycle, palatal perforation developed. After 2 months of treatment at our hospital, he returned to his local hospital for continued care. At the last follow-up the following year, his family reported that he had died.

Figure 6 Case 5: a 44-year-old male diagnosed with PTCL-NOS. (A) An irregular ulcer, approximately 3.5 cm × 3.0 cm, located in the mid-palate. The lesion presents with an uneven base, raised and erythematous borders, and is covered by a thick yellowish-white pseudomembrane. It was tender on palpation. (B) HE staining (×100) revealing a polymorphous lymphoid infiltrate. The infiltrate is composed of medium to large cells with irregular nuclear contours, set against a background of small lymphocytes, plasma cells, eosinophils, and histiocytes. (C,D) Immunohistochemical staining demonstrates that the atypical lymphoid cells are positive for CD3 (+) and CD2 (+). HE, hematoxylin and eosin; PTCL-NOS, peripheral T-cell lymphoma, not otherwise specified.

Ethical considerations

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Publication of this case report and accompanying images was waived from patient consent according to the Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine ethics committee/institutional review board.

Discussion

The five rare diseases presenting initially with palatal ulcers in this report highlight the core value of structured diagnostic thinking. To provide a comprehensive overview and facilitate comparison among these five cases, we have summarized their key clinical features, diagnostic findings, treatments, and outcomes in Table 1.

When histopathology shows granulomas composed of epithelioid cells and multinucleated giant cells, the diagnostic focus shifts from common aphthous ulcers to specific infectious or granulomatous diseases, as seen in Case 1. A positive T-SPOT provides supportive evidence, but the gold standard for tuberculosis diagnosis remains culture or molecular detection of Mycobacterium tuberculosis. Oral tuberculosis is a rare manifestation of extrapulmonary tuberculosis. Oral involvement is relatively uncommon, with approximately 0.1% to 5% of patients exhibiting oral symptoms. Tuberculous ulcers are commonly found on the lips and tongue, and rarely on the palate. Few cases of palatal tuberculous ulcers have been reported (11). The case reported by Arul Devah et al. of a 28-year-old woman with palatal tuberculosis is highly similar to our case: erythematous granulomatous lesions on the hard palate, histopathology showing necrotizing granulomatous inflammation with positive acid-fast staining. Their report emphasizes that oral tuberculosis can occur without a known history of tuberculosis or pulmonary symptoms, requiring extensive differential diagnosis and systematic evaluation (6). The adolescent case of oral and laryngeal tuberculosis reported by Medhi et al. further confirms the diversity of clinical presentations of oral tuberculosis (12). For palatal ulcers presenting with granulomatous proliferation, irregular borders, and unresponsiveness to antibiotic therapy, tuberculosis should be included in the differential diagnosis.

STAT1 gain-of-function mutations lead to both innate and adaptive immunodeficiency. These include impaired T-cell receptor diversity, reduced numbers of T cells, memory B cells, and NK cells, and defective production of interleukin-17A (IL-17A) and interferon-gamma. To date, over 100 STAT1 gain-of-function mutation sites have been reported worldwide. They are mainly located in the coiled-coil domain (CCD) and DNA-binding domain (DBD). About 62% are in the CCD, with A267V, R274Q, and R274W being the most common. About 35% are in the DBD, with T385M being the most frequent. The remaining 3% are outside these domains (13). The pediatric case reported by Xiang et al. (7) and the immunophenotypes of five patients analyzed by Lei et al. (14) are highly consistent with the clinical phenotype of our case with the c.800C>T (p.A267V) mutation. Together, they suggest that STAT1 gain-of-function mutations cause impaired IL-17 immunity as the pathogenic mechanism. As a rare immunodeficiency disorder, early diagnosis of CMC is crucial. In clinical practice, after excluding triggers such as immunosuppression or prolonged broad-spectrum antibiotic use, comprehensive genetic testing is essential for early definitive diagnosis.

The presence of osteolytic lesions with histopathology showing abnormal proliferation of LCH. LCH can involve a single organ or multiple systems. The skeletal system and skin are the most commonly affected sites. Among oral soft tissue lesions, the gingiva and hard palate are the most frequently involved (8,15,16). Previous reports on LCH mostly focused on skin lesions. Few reports mention palatal ulcers. The case of a 32-year-old edentulous woman reported by Yashoda-Devi et al. (17) and the 63-year-old woman reported by Neves-Silva et al. (18) both presented with palatal ulcers as the initial or main manifestation. Oral findings can precede systemic symptoms. In the differential diagnosis, LCH must be distinguished from infectious, inflammatory, and neoplastic lesions (19). Pathologically, LCH is characterized by an increase in Langerhans cells mixed with eosinophils, lymphocytes, and macrophages (8,19). These cases collectively suggest that in the presence of severe inflammation and tooth loosening without obvious periodontal etiology, LCH should be considered.

The diagnosis of PSV in Case 4 underscores the pivotal role of a thorough and detailed systemic history in the diagnostic process. The palatal ulceration and the characteristic surrounding ‘snail track’ lesions provided crucial morphological clues pointing towards this condition. However, the key factor that definitively distinguished PSV from other pustular diseases was the elicited history of ulcerative colitis, which aligns with the well-established classical association between PSV and inflammatory bowel disease(20-22).

PTCL is an aggressive malignancy of mature T lymphocytes, accounting for 10–12% of non-Hodgkin lymphomas (23). PTCL-NOS is the most common subtype and usually presents with nodal disease. About one-third of patients have systemic B symptoms (23,24). Oral PTCL is rare and hard to diagnose. As shown in Case 5, oral lesions can be persistent, progressively enlarging ulcers with lymphadenopathy, mimicking benign diseases. Reported oral sites include the tongue, palate, buccal mucosa, gingiva, and tonsils (25,26). Currently, only a limited number of international case reports exist. de Oliveira et al. reported five PTCL-NOS cases with aggressive presentation, three with palatal ulcers. All expressed CD3, and four died during follow-up (10). Our patient also had a poor outcome, developing palatal perforation despite chemotherapy. de Oliveira emphasized that EBER testing is needed to rule out extranodal NK/T-cell lymphoma. Histopathologically, PTCL-NOS shows polymorphous lymphoid infiltrates of medium to large cells with irregular nuclei, often with mitotic figures (27). Immunophenotypically, the neoplastic cells typically express pan-T-cell antigens (e.g., CD2, CD3) (28,29). The key to diagnosis lies in comprehensive immunohistochemical analysis. PTCL-NOS follows an aggressive course, as seen in our patient’s rapid progression and palatal perforation, highlighting treatment challenges.

This study is the first to systematically compare five rare diseases presenting initially with palatal ulcers and proposes a structured diagnostic pathway, offering significant clinical value. However, as a single-center retrospective study, it has limitations, including a small number of cases, lack of family verification in Case 2, and absence of BRAF V600E mutation analysis in Case 3. These limitations warrant improvement in future multicenter prospective studies.

Conclusions

Diagnosing and differentiating diseases that manifest as palatal ulcers is challenging due to the wide range of etiologies and potential systemic involvement. This case series highlights that rare diseases such as oral tuberculosis, CMC, LCH, PSV, and PTCL-NOS can initially present as refractory palatal ulcers. A definitive diagnosis relies not only on histopathology but, crucially, on a systematic approach integrating detailed history, comprehensive physical examination, and appropriate auxiliary tests, including genetic and microbiological assays.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the AME Case Series reporting checklist. Available at https://fomm.amegroups.com/article/view/10.21037/fomm-2025-1-48/rc

Peer Review File: Available at https://fomm.amegroups.com/article/view/10.21037/fomm-2025-1-48/prf

Funding: This work was supported by Science, Technology and Innovation Commission of Shenzhen Municipality (No. JCYJ20190809141807492) and Shanghai Municipal Health Commission (No. ZHYYZXYYD-202511)

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://fomm.amegroups.com/article/view/10.21037/fomm-2025-1-48/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Publication of this case report and accompanying images was waived from patient consent according to the Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine ethics committee/institutional review board.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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