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This article discusses a case study of a patient with a rare condition called Russell body oral mucositis. Russell bodies are abnormal collections of immunoglobulins within plasma cells, and they can be seen in various chronic inflammatory conditions and autoimmune diseases. The patient in this case study had a large ulcerative lesion on the tongue, which was diagnosed as Mott cell-rich lymphoplasmacytic infiltrate. The lesion healed completely after 2 months of follow-up. The article also mentions similar cases of Russell body formation in the gastrointestinal tract and emphasizes the importance of recognizing this condition due to its prognostic impact. [Extracted from the article]

The study evaluated the regenerative responses of the lacrimal functional unit (LFU) after lacrimal gland (LG) ablation. The LG of Wistar rats was submitted to G1) partial LG ablation, G2) partial ablation and transplantation of an allogeneic LG, or G3) total LG ablation, (n = 7–10/group). The eye wipe test, slit lamp image, tear flow, and histology were evaluated. RT-PCR analyzed inflammatory and proliferation mediators. The findings were compared to naïve controls after 1 and 2 months (M1 and M2). G3 presented increased corneal sensitivity, and the 3 groups showed corneal neovascularization. Histology revealed changes in the LG and corneal inflammation. In the LG, there was an increase in MMP-9 mRNA of G1 and G2 at M1 and M2, in RUNX-1 at M1 and M2 in G1, in RUNX-3 mRNA at M1 in G1, and at M2 in G2. TNF-α mRNA rose in the corneas of G1 and G2 at M2. There was an increase in the IL-1β mRNA in the trigeminal ganglion of G1 at M1. Without changes in tear flow or evidence of LG regeneration, LG ablation and grafting are unreliable models for dry eye or LG repair in rats. The surgical manipulation extended inflammation to the LFU. [ABSTRACT FROM AUTHOR]

Objective: Lysosome‐associated membrane protein 3 (LAMP3) misexpression in salivary gland epithelial cells plays a causal role in the development of salivary gland dysfunction and autoimmunity associated with Sjögren's disease (SjD). This study aimed to clarify how epithelial LAMP3 misexpression is induced in SjD. Methods: To explore upstream signaling pathways associated with LAMP3 expression, we conducted multiple RNA sequencing analyses of minor salivary glands from patients with SjD, submandibular glands from a mouse model of SjD, and salivary gland epithelial cell lines. A hypothesis generated by the RNA sequencing analyses was further tested by in vitro and in vivo assays with gene manipulation. Results: Transcriptome analysis suggested LAMP3 expression was associated with enhanced type I interferon (IFN) and IFNγ signaling pathways in patients with SjD. In vitro studies showed that type I IFN but not IFNγ stimulation could induce LAMP3 expression in salivary gland epithelial cells. Moreover, we discovered that LAMP3 overexpression could induce ectopic Toll‐like receptor 7 (TLR‐7) expression and type I IFN production in salivary gland epithelial cells both in vitro and in vivo. TLR‐7 knockout mice did not develop any SjD‐related symptoms following LAMP3 induction. Conclusion: Epithelial LAMP3 misexpression can be induced through enhanced type I IFN response in salivary glands. In addition, LAMP3 can promote type I IFN production via ectopic TLR‐7 expression in salivary gland epithelial cells. This positive feedback loop can contribute to maintaining LAMP3 misexpression and amplifying type I IFN production in salivary glands, which plays an essential role in the pathophysiology of SjD. [ABSTRACT FROM AUTHOR]

The article examines ectopic germinal centers (GCs) in Sjögren's syndrome (SS) and non-SS non-sicca patients, revealing similarities in GC frequency. Topics discussed include the significance of GCs in SS severity, the diagnostic implications of marker expression differences, and the histomorphological variations between the two patient populations.

The article details an exuberant nodular parotid gland lesion, focusing on its clinical and pathological characteristics, diagnostic challenges, and treatment implications.

Syphilis can mimic, clinically and microscopically, many other diseases. By microscopy, typically syphilis presents with plasma cell infiltration, admixed with lymphocytes and macrophages, in lichenoid and/or perivascular/perineural distribution pattern. When exuberant, this inflammatory infiltrate can mimic a lymphoproliferative disorder (LPD), notably plasma cell neoplasia or lymphoma. To date, about 12 cases of secondary syphilis, all but one in extraoral location, suggesting initially a LPD, have been published. Here, to our knowledge, we report an unusual case of intraoral primary syphilis initially suggesting LPD, notably lymphoid hyperplasia (pseudolymphoma); however, mucosa‐associated lymphoid tissue (MALT) lymphoma and follicular lymphoma could not be disregarded. Polyclonality of plasma cells on immunohistochemistry, in strict clinical correlation, was essential to arrive at the correct diagnosis. [ABSTRACT FROM AUTHOR]

We describe two cases of extensive indolent calvarial osteomyelitis after rhino-orbital-mucormycosis in diabetic patients previously diagnosed with COVID-19. Both patients presented with acute rhino-orbital symptoms about one month after being diagnosed with COVID-19. Treatment with intravenous liposomal Amphotericin B and prompt radical surgical debridement was instituted, but calvarial osteomyelitis ensued and persisted chronically despite maintenance of antifungal therapy and partial debridement of necrotic calvarial bone. The patients were discharged to continue antifungal therapy on a day-hospital regime. After more than 8 months of treatment, they remain with radiological signs of osteomyelitis but with no symptoms or intracranial extension of the infection. Calvarial indolent osteomyelitis secondary to mucormycosis is extremely rare, and little is known regarding its treatment. We believe it can be controlled with medical treatment and partial bony debridement although more studies are necessary to better define therapy. [ABSTRACT FROM AUTHOR]

Summary: Progression to aggressive secondary acute myeloid leukaemia (sAML) poses a significant challenge in the management of myeloproliferative neoplasms (MPNs). Since the physiopathology of MPN is closely linked to the activation of interferon (IFN) signalling and that AML initiation and aggressiveness is driven by leukaemia stem cells (LSCs), we investigated these pathways in MPN to sAML progression. We found that high IFN signalling correlated with low LSC signalling in MPN and AML samples, while MPN progression and AML transformation were characterized by decreased IFN signalling and increased LSC signature. A high LSC to IFN expression ratio in MPN patients was associated with adverse clinical prognosis and higher colony forming potential. Moreover, treatment with hypomethylating agents (HMAs) activates the IFN signalling pathway in MPN cells by inducing a viral mimicry response. This response is characterized by double‐stranded RNA (dsRNA) formation and MDA5/RIG‐I activation. The HMA‐induced IFN response leads to a reduction in LSC signature, resulting in decreased stemness. These findings reveal the frequent evasion of viral mimicry during MPN‐to‐sAML progression, establish the LSC‐to‐IFN expression ratio as a progression biomarker, and suggests that HMAs treatment can lead to haematological response in murine models by re‐activating dsRNA‐associated IFN signalling. [ABSTRACT FROM AUTHOR]

Background: Psoriasis is a common cutaneous disease; however, information about psoriasis‐related oral mucosal lesions is scarce in the literature. Case Description: We report a case of a 73‐year‐old male patient with cutaneous and oral palatal alterations. An incisional biopsy of these lesions revealed psoriasis. Conclusion: The current case highlights the importance of a systematic examination of the oral cavity in psoriasis patients for the appropriate diagnosis and management on the control of these lesions. [ABSTRACT FROM AUTHOR]

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We report the case of a 64-year-old male patient with a 5 month history of proptosis, motility limitation and vision loss in OD. Visual acuity (VA) was 20/200 in OD and 20/20 in OS. CT showed a large, round, intraconal lesion, with bony density and no apparent connection to adjacent orbital walls. MRI showed a T1-weighted hypointense lesion surrounded by a contrast enhancing capsule. The orbital tumor was excised through a lateral orbitotomy revealing a nodular, round, osseous structure. Histological examination disclosed well-formed lamellar bone trabeculae, with no necrosis or mitosis figures. Immunohistochemical staining was negative for MDM2 and CDK4. After 3 years, there was no evidence of tumor recurrence and VA had improved to 20/30. Intraconal osteomas with no clear attachment to orbital walls are extremely rare. We are aware of a few reported cases in the lid, hand, thigh, tongue, pterygopalatine fossa and brain. To the authors' knowledge, this is the first report in English literature of an orbital intraconal osteoma without any visible relation to the orbital walls. [ABSTRACT FROM AUTHOR]