Autoimmune diseases (AIDs) emerge due to an irregular immune response towards self- and non-self-antigens. Inflammation commonly accompanies these conditions, with inflammatory factors and inflammasomes playing pivotal roles in their progression. Key concepts in molecular biology, inflammation, and molecular mimicry are crucial to understanding AID development. Exposure to foreign antigens can cause inflammation, potentially leading to AIDs through molecular mimicry triggered by cross-reactive epitopes. Molecular mimicry emerges as a key mechanism by which infectious or chemical agents trigger autoimmunity. In certain susceptible individuals, autoreactive T or B cells may be activated by a foreign antigen due to resemblances between foreign and self-peptides. Chronic inflammation, typically driven by abnormal immune responses, is strongly associated with AID pathogenesis. Inflammasomes, which are vital cytosolic multiprotein complexes assembled in response to infections and stress, are crucial to activating inflammatory processes in macrophages. Chronic inflammation, characterized by prolonged tissue injury and repair cycles, can significantly damage tissues, thereby increasing the risk of AIDs. Inhibiting inflammasomes, particularly in autoinflammatory disorders, has garnered significant interest, with pharmaceutical advancements targeting cytokines and inflammasomes showing promise in AID management.

Erosive oral lichen planus (EOLP) represents a significant challenge in dental and medical management due to its chronic inflammatory nature, painful symptoms, and impact on quality of life. This study aims to evaluate the current diagnostic approach with novel non-invasive techniques, such as dermoscopy, and also the landscape of treatment options for EOLP, focusing on its efficacy, safety, and the challenges that it present in clinical practice. Through a comprehensive literature review, we explored the use of topical corticosteroids, systemic immunosuppressants, biologics, and Janus kinase (JAK) inhibitors in treating EOLP, alongside examining patient compliance, psychological impacts, and the risk of adverse effects and recurrence. Our findings reveal that while topical corticosteroids are the cornerstone of EOLP treatment, offering symptomatic relief, their long-term use is limited by side effects and tolerance development. Systemic therapies and biologics provide alternatives for refractory cases but necessitate careful adverse effect monitoring. JAK inhibitors show promise as an innovative treatment avenue but require more evidence on long-term safety and efficacy. This study highlights the necessity of personalized treatment approaches due to the variable disease course and response to treatment, underscoring the importance of a multidisciplinary strategy in managing EOLP. The complexity of EOLP treatment, compounded by its psychological and quality of life impacts, demands ongoing research into targeted therapies, the establishment of standardized treatment protocols, and the development of effective outcome measures to improve patient care and treatment outcomes.

Background and Objectives: Oral cancer remains a critical global health concern, with oral squamous cell carcinoma (OSCC) being the most prevalent form. Oral potentially malignant disorders (OPMDs), such as oral leukoplakia (OLK), oral lichen planus (OLP), and actinic cheilitis (AC), often precede OSCC. Identifying reliable biomarkers is vital for assessing malignant transformation risk. The present study aimed to evaluate the immunohistochemical expression of differentiated embryonic chondrocyte 1 (DEC1), a marker of dysplasia severity, and cluster of differentiation 44 (CD44), which is associated with cancer progression, in OPMD and OSCC tissues. Materials and Methods: A retrospective analysis was conducted on 145 biopsy specimens from January 2015 to January 2023, comprising normal mucosa (NM), OLK, OLP, AC, and OSCC. DEC1 and CD44 expression levels were assessed using immunohistochemical staining. Positivity scores were determined based on staining intensity and extent, with statistical analyses performed using SPSS software (SPSS Inc., Chicago, IL, USA, version 29.0 for Windows). Results: It was found that CD44 expression significantly increased across OPMD and OSCC compared to NM (p < 0.001). Conversely, DEC1 expression was consistent across lesion types and dysplasia levels. CD44 expression was the highest in AC and OSCC, underscoring its potential role as a progression marker. Conclusions: The results indicate that CD44 is a more sensitive marker for assessing dysplastic severity and malignant transformation, while DEC1 may serve as a complementary marker for early-stage evaluation. Further research involving larger cohorts is needed to confirm these findings.

Background/Objectives: Oral potentially malignant disorders (OPMDs), including oral leukoplakia (OLK), oral lichen planus (OLP), and actinic cheilitis (AC), have varying risks of progression to oral squamous cell carcinoma (OSCC). Biomarkers such as aldehyde dehydrogenase 1 (ALDH1) and mammary serine protease inhibitor (Maspin) have shown potential for diagnostic and prognostic use in oral cancer. The present study aimed to evaluate the immunoexpression of aldehyde dehydrogenase 1, a cancer stem cell marker associated with aggressiveness, and the mammary serine protease inhibitor, a potential tumor suppressor, in OPMD and OSCC tissues. Methods: A retrospective analysis was performed on 145 biopsy specimens collected from January 2015 to January 2023, including normal epithelium, OPMDs (OLK, OLP, AC), and OSCC. ALDH1 and Maspin expression levels were evaluated using immunohistochemistry, considering both the percentage of positive cells and staining intensity. Statistical analyses were carried out using the Statistical Package for the Social Sciences (SPSS, version 29.0; IBM Corp., Chicago, IL, USA). Results: Normal oral epithelium showed no expression of ALDH1, whereas 40.6% of OPMDs and 44.4% of OSCC samples exhibited high cytoplasmic ALDH1 expression. Nuclear ALDH1 expression was elevated in 29.7% of OPMDs and 38.9% of OSCCs (p < 0.001). Nuclear Maspin expression was high in 95.2% of normal tissues, in 67.2% of OPMDs and in 55.6% of OSCCs (p < 0.001). Maspin showed strong nuclear and cytoplasmic expression in normal tissue, but its expression decreased in OPMDs and OSCCs, with statistically significant reductions in both compartments (p < 0.001). Conclusions: The results indicate that ALDH1 upregulation and Maspin downregulation are hallmark events in oral carcinogenesis. Their combined evaluation provides a powerful tool for assessing dysplastic severity and malignant transformation risk in OPMDs. Future studies on larger cohorts are needed to confirm the prognostic utility of this dual-marker model.

Background and Objectives: Oral lichen planus (OLP) is a chronic immune-mediated disorder in which the need for systemic therapy remains difficult to predict using standardized clinical criteria. This retrospective two-center cohort study aimed to develop a multivariable clinical prediction model for systemic therapy escalation in patients with histopathologically confirmed OLP. Material and Methods: Medical records of 141 adult patients treated between 2022 and 2025 were reviewed. Baseline demographic, clinical, and laboratory variables were analyzed using univariate analyses, followed by multivariable logistic regression with backward stepwise selection and Firth penalized likelihood estimation. Discrimination was assessed by the area under the ROC curve (AUC), and internal validation was performed by bootstrap resampling (1000 samples) with repetition of the full selection procedure. Results: Four independent predictors of systemic therapy were identified: concomitant cutaneous lichen planus (penalized odds ratio (OR) 13.96, 95% CI 3.94–55.84), autoimmune thyroiditis (OR 12.67, 3.26–54.88), genital lichen planus (OR 10.21, 2.36–51.57) and oral Candida superinfection (OR 4.48, 1.10–18.82). The apparent AUC was 0.889 (95% CI 0.801–0.976); after bootstrap internal validation, the optimism-corrected AUC was 0.84 and the calibration slope 0.73, indicating moderate overfitting. Candida superinfection was the least stable predictor (selected in 43% of bootstrap samples). A prognostic risk matrix was developed to estimate the probability of systemic therapy escalation according to different combinations of predictors. Conclusions: The identified clinical factors and derived risk matrix may provide a preliminary framework for risk stratification and individualized therapeutic decision-making in patients with OLP. However, given the retrospective design and limited number of outcome events, these findings should be interpreted cautiously. Prospective external validation in larger independent cohorts is required before the model can be considered for routine clinical use.