A 30-year-old man presented to clinic with mid-facial swelling and painful palatal ulceration (panel A). Facial swelling first appeared 4 months earlier following drainage of a periodontal abscess with extraction of the maxillary teeth, and it gradually worsened over time. No constitutional symptoms were present, and physical examination revealed a tender, fluctuant, gray-white palatal ulcer. Maxillofacial computed tomography scans showed extensive inflammation involving hemifacial subcutaneous soft tissue with opacification of right sinuses and obstruction of right nasal airway (panel B). The patient’s complete blood count was unremarkable, cultures were negative for pathogenic organisms, and lactate dehydrogenase was elevated to 1117 U/L. Biopsy of the palatal ulcer showed diffuse inflammatory necrosis with infiltration by large atypical lymphoid cells (panel C, hematoxylin and eosin (H&E) stain; 40× objective) with vesicular chromatin and abundant pale cytoplasm proliferating in an angiodestructive growth pattern (panel D, H&E stain; 40× objective). Immunohistochemical stains performed on the lymphoid neoplasm were positive for CD2, CD3, CD7, CD43, CD45, CD56 (panel E, CD56 stain; 20× objective), TIA-1, granzyme B, and perforin, and returned negative for CD4, CD5, CD8, CD20, and keratin. Additionally, in situ hybridization identified Epstein-Barr virus in neoplastic cells [panel F, in situ hybridisation for EBV (EBER); 20× objective], together supporting the diagnosis of extranodal natural killer/T-cell lymphoma of the palate.

This relatively subtle presentation emphasizes the importance of cytomorphological evaluation of lymphoid infiltrates that may be otherwise overlooked as simple inflammatory processes.

A 30-year-old man presented to clinic with mid-facial swelling and painful palatal ulceration (panel A). Facial swelling first appeared 4 months earlier following drainage of a periodontal abscess with extraction of the maxillary teeth, and it gradually worsened over time. No constitutional symptoms were present, and physical examination revealed a tender, fluctuant, gray-white palatal ulcer. Maxillofacial computed tomography scans showed extensive inflammation involving hemifacial subcutaneous soft tissue with opacification of right sinuses and obstruction of right nasal airway (panel B). The patient’s complete blood count was unremarkable, cultures were negative for pathogenic organisms, and lactate dehydrogenase was elevated to 1117 U/L. Biopsy of the palatal ulcer showed diffuse inflammatory necrosis with infiltration by large atypical lymphoid cells (panel C, hematoxylin and eosin (H&E) stain; 40× objective) with vesicular chromatin and abundant pale cytoplasm proliferating in an angiodestructive growth pattern (panel D, H&E stain; 40× objective). Immunohistochemical stains performed on the lymphoid neoplasm were positive for CD2, CD3, CD7, CD43, CD45, CD56 (panel E, CD56 stain; 20× objective), TIA-1, granzyme B, and perforin, and returned negative for CD4, CD5, CD8, CD20, and keratin. Additionally, in situ hybridization identified Epstein-Barr virus in neoplastic cells [panel F, in situ hybridisation for EBV (EBER); 20× objective], together supporting the diagnosis of extranodal natural killer/T-cell lymphoma of the palate.

This relatively subtle presentation emphasizes the importance of cytomorphological evaluation of lymphoid infiltrates that may be otherwise overlooked as simple inflammatory processes.

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