Abstract The objective of the present study was to investigate the frequency of oral leukoplakia and oral erythroplakia among young patients from three Brazilian reference centers in Oral and Maxillofacial Pathology. A retrospective study was carried out from 2011 to 2021 on 861 patients diagnosed with oral leukoplakia and oral erythroplakia. Demographic and clinicopathological data were evaluated. Fisher’s exact test was used to evaluate the association among sex, age, anatomical location, and histopathological diagnosis. A total of 83 (9.64%) cases involved young patients (aged <40 years). Among these, biopsy records were included in 31 (37.34%) cases, all of which received a clinical diagnosis of oral leukoplakia. Seventeen (54.84%) patients were female, mostly in their fourth decade of life (n = 22/70.97%), and their mean age at diagnosis was 32.61(± 5.21) years. Among informed cases, seven (22.58%) patients were smokers. The lateral border of the tongue (n = 9/29.03%) was the most affected site. In 13 (41.94%) cases, oral leukoplakias showed a homogeneous appearance. The mean size of the lesions was 1.47 cm (0.2–3.0 cm) and the mean time of disease progression was 64.37 (± 65.90) months. The histopathological analysis showed that 11 cases (35.48%) exhibited some degree of epithelial dysplasia. Acanthosis and/or hyperkeratosis were observed in 20 cases (64.52%). No significant associations were observed between sex and anatomical location, age and anatomical location, nor between sex and histological diagnosis (p > 0.05). Oral leukoplakia and oral erythroplakia are uncommon diseases in young patients. In this population, oral leukoplakia shows a slight predilection for women aged between 30 and 39 years. Pathology 201 202 86 evaluated Fishers Fisher s location 8 9.64% 964 9 64 (9.64% 40 <4 years . years) these 3 37.34% 3734 37 34 (37.34% 54.84% 5484 54 84 (54.84% female n 22/70.97%, 227097 22/70.97% , 22 70 97 22/70.97%) 32.61± 3261 32.61 ± 32 61 32.61( 5.21 521 5 21 22.58% 2258 58 (22.58% smokers 9/29.03% 92903 29 03 site 1 41.94% 4194 41 94 (41.94% appearance 147 47 1.4 0.2–3.0 0230 0 2 (0.2–3. 6437 64.3 ( 65.90 6590 65 90 months 35.48% 3548 35 48 (35.48% dysplasia andor or 64.52%. 6452 64.52% 52 (64.52%) p 0.05. 005 0.05 05 0.05) population 9.64 96 6 (9.64 4 < 37.34 373 (37.34 54.84 548 (54.84 22709 22/70.97 7 326 32.6 5.2 22.58 225 (22.58 9/29.03 9290 41.94 419 (41.94 14 1. 0.2–3. 023 (0.2–3 643 64. 65.9 659 35.48 354 (35.48 645 64.52 (64.52% 00 0.0 9.6 (9.6 37.3 (37.3 54.8 (54.8 2270 22/70.9 32. 5. 22.5 (22.5 9/29.0 929 41.9 (41.9 0.2–3 02 (0.2– 65. 35.4 (35.4 64.5 (64.52 0. 9. (9. 37. (37. 54. (54. 227 22/70. 22. (22. 9/29. 92 41. (41. 0.2– (0.2 35. (35. (64.5 (9 (37 (54 22/70 (22 9/29 (41 0.2 (0. (35 (64. (3 (5 22/7 (2 9/2 (4 (0 (64 22/ 9/ (6

Abstract Oral cancer is a multifactorial disease involving genetic, epigenetic, and environmental factors. The literature indicates that inflammatory cells at the advancing front of the tumor induce a host immune response, preventing the spread of the tumor. However, cancer cells adopt various continued strategies to circumvent this immune surveillance. The complexity of immune mechanisms suggests that there must be virtually individual patterns of anti-tumor immune responses. Due to this important interaction of cancer with the immune system, the objective of the present study was to provide an up-to-date overview of immuno-oncology focused on oral cancer, summarizing the basic immunology, the classic risk factors, immunotherapy, and future treatment and prognostic perspectives. genetic epigenetic factors response However surveillance antitumor anti responses system uptodate up date immunooncology immuno oncology immunology immunotherapy perspectives

Abstract Scientific evidence about genetic and molecular changes in oral squamous cell carcinoma (OSCC) among smokers and non-smokers is inconclusive. This systematic review and meta-analysis assessed the effects of tobacco on the DNA of individuals with OSCC based on protein mutations. Electronic searches were conducted on PubMed, Ovid, Web of Science, and Scopus to identify observational studies published up to January/2022. The Joanna Briggs Institute tool was used for the critical appraisal of studies. The certainty of the evidence was evaluated. Twenty-three studies assessing 4,060 individuals (2,967 smokers vs. 1,093 non-smokers) were included in this review. Fifteen groups of proteins/genes were investigated. Analysis of the quality of articles revealed low risk of bias in most studies. The certainty of the evidence was very low. The meta-analysis confirmed no significant difference between smokers and non-smokers with respect to damage to GSTM1 (OR: 0.60; 95%CI: 0.30–1.18), GSTT1 (OR: 1.18; 95%CI:0.49–2.83), hydrolase proteins (Ku70 and Ku80) (OR: 0.74; 95%CI: 0.18–3.05), and transferase proteins (GSTM1, GSTT1, GSTM3) (OR: 0.74; 95%CI: 0.47–1.18). Most of the studies included showed that smokers are more likely to exhibit genetic instability. However, the meta-analysis revealed that smokers do not necessarily have more genetic alterations in the DNA than non-smokers. (OSCC nonsmokers non inconclusive metaanalysis meta analysis mutations PubMed Ovid Science January2022 January 2022 January/2022 evaluated Twentythree Twenty three 4060 4 060 4,06 2,967 2967 2 967 (2,96 vs 1093 1 093 1,09 proteinsgenes genes investigated GSTM OR (OR 0.60 0 60 95%CI 95CI CI 95 0.30–1.18, 030118 0.30–1.18 , 30 18 0.30–1.18) GSTT 1.18 118 95%CI0.49–2.83, 95CI049283 0.49–2.83 49 83 95%CI:0.49–2.83) Ku70 Ku (Ku7 Ku80 0.74 074 74 0.18–3.05, 018305 0.18–3.05 3 05 0.18–3.05) GSTM1, (GSTM1 GSTM3 0.47–1.18. 047118 0.47–1.18 . 47 0.47–1.18) instability However nonsmokers. smokers. January202 202 January/202 406 06 4,0 2,96 296 96 (2,9 109 09 1,0 0.6 6 9 03011 0.30–1.1 1.1 11 CI0 95%CI0.49–2.83 95CI04928 049283 0.49–2.8 8 95%CI:0.49–2.83 Ku7 (Ku Ku8 0.7 07 7 01830 0.18–3.0 (GSTM 04711 0.47–1.1 January20 20 January/20 40 4, 2,9 29 (2, 10 1, 0. 0301 0.30–1. 1. 95%CI0.49–2.8 95CI0492 04928 0.49–2. 95%CI:0.49–2.8 0183 0.18–3. 0471 0.47–1. January2 January/2 2, (2 030 0.30–1 95%CI0.49–2. 95CI049 0492 0.49–2 95%CI:0.49–2. 018 0.18–3 047 0.47–1 January/ ( 03 0.30– 95%CI0.49–2 95CI04 049 0.49– 95%CI:0.49–2 01 0.18– 04 0.47– 0.30 95%CI0.49– 95CI0 0.49 95%CI:0.49– 0.18 0.47 0.3 95%CI0.49 0.4 95%CI:0.49 0.1 95%CI0.4 95%CI:0.4 95%CI0. 95%CI:0. 95%CI0 95%CI:0

Abstract The aim of this study was to describe the prevalence, clinicopathological, and prognostic features of acinic cell carcinoma (AciCC) of the oral and maxillofacial region. AciCC cases were retrospectively retrieved from 11 pathology centers of three different countries. Medical records were examined to extract demographic, clinical, pathologic, and follow-up information. A total of 75 cases were included. Females (65.33%) with a mean age of 45.51 years were mostly affected. The lesions usually presented as an asymptomatic (64.28%) nodule (95.66%) in the parotid gland (70.68%). The association of two histopathological patterns was the most common finding (48.93%) and the tumors presented mainly conventional histopathological grades (86.11%). Surgical treatment was performed in the majority of the cases (59.19%). Local recurrence was observed in 20% of the informed cases, regional metastasis in 30.43%, and distant metastasis in 12.50%. The statistical analysis showed that the cases with a solid histopathological pattern (p=0.01), high-grade transformation (p=0.008), recurrence (p=0.007), and regional metastasis (p=0.03) were associated with poor survival. In conclusion, high histopathological transformation, presence of nodal metastasis, and recurrence were prognostic factors for AciCC of the oral and maxillofacial region. prevalence clinicopathological (AciCC region 1 countries demographic clinical pathologic followup follow up information 7 included 65.33% 6533 65 33 (65.33% 4551 45 51 45.5 affected 64.28% 6428 64 28 (64.28% 95.66% 9566 95 66 (95.66% 70.68%. 7068 70.68% . 70 68 (70.68%) 48.93% 4893 48 93 (48.93% 86.11%. 8611 86.11% 86 (86.11%) 59.19%. 5919 59.19% 59 19 (59.19%) 20 3043 30 43 30.43% 1250 12 50 12.50% p=0.01, p001 p p=0.01 , 0 01 (p=0.01) highgrade grade p=0.008, p0008 p=0.008 008 (p=0.008) p=0.007, p0007 p=0.007 007 (p=0.007) p=0.03 p003 03 (p=0.03 survival conclusion 65.33 653 6 3 (65.33 455 4 5 45. 64.28 642 2 (64.28 95.66 956 9 (95.66 706 70.68 (70.68% 48.93 489 (48.93 861 86.11 8 (86.11% 591 59.19 (59.19% 304 30.43 125 12.50 p00 p=0.0 (p=0.01 p000 p=0.00 00 (p=0.008 (p=0.007 (p=0.0 65.3 (65.3 64.2 (64.2 95.6 (95.6 70.6 (70.68 48.9 (48.9 86.1 (86.11 59.1 (59.19 30.4 12.5 p0 p=0. (p=0.00 (p=0. 65. (65. 64. (64. 95. (95. 70. (70.6 48. (48. 86. (86.1 59. (59.1 30. 12. p=0 (p=0 (65 (64 (95 (70. (48 (86. (59. p= (p= (6 (9 (70 (4 (86 (59 (p ( (7 (8 (5

Abstract: The aim of the present study was to analyze the relationship of OM with possible risk factors such as oral health condition, immunological status and IL-1β profile in patients submitted to hematopoietic stem cell transplantation (HSCT). Fifty-four individuals submitted to HSCT were included. All patients received previous dental treatment and photobiomodulation (PBM) as the institutional OM preventive protocol. OM scores, immune status, and IL-1β levels were determined during the conditioning period and at D+3 and D+8 after HSC infusion. IL-1β gene polymorphism was also analyzed during conditioning. Possible associations of OM with risk factors were analyzed using conditional Fisher's exact test. OM was observed in 34 patients (62.9%) classified as Grade 1 (13 patients/24.1%), Grade 2 (14 patients/25.9%), Grade 3 (3 patients/5.5%), and Grade 4 (4 patients/7.4%). Allogeneic HSCT individuals exhibited a higher OM grade than autologous subjects. Moreover, an association was observed between severe OM and severe gingivitis (p = 0.01), neutropenia (p = 0.03), and leukopenia (p = 0.04). A significant association between OM and lower IL-1β levels was detected at three time points, i.e., conditioning (p = 0.048), D+3 (p = 0.01), and D+8 (p = 0.005). The results showed that IL-1β gene polymorphism was not associated with OM. Our study provided important insights into the scope of OM risk factors in the setting of HSCT. Patients submitted to HSCT with severe gingivitis prior to chemotherapy and with severe neutropenia and leukopenia exhibited a higher OM grade. Further investigation will be necessary to better understand the exact role of IL-1β in the context of OM pathobiology and to validate cytokine analysis in larger cohorts.

Abstract: Tobacco smoking involves a high risk of human malignancies, including oral cancer, because it contains multiple carcinogens that cause genetic instability. Thus, a worse prognosis would be expected for cancer patients who are smokers. The aim of this study was to assess the DNA damage response through the expression of checkpoint kinase 2 (CHK2), H2A histone family member X (H2AX), and P53 among smokers and non-smokers with oral squamous cell carcinoma (OSCC). Associations between immunoexpression of proteins and clinicopathological data and histopathological grading were also analyzed. A total of 35 individuals (18 non-smokers and 17 smokers) with OSCC of the tongue and/or floor of the mouth were included. Immunohistochemistry for H2AX was conducted for the identification of double-strand breaks, CHK2, and P53 to evaluate the expression of this protein in cell cycle regulation. The sample consisted of 22 males and 13 females, with a mean age of 63.9±11.8 years. OSCC of non-smokers were well-differentiated tumors in 50% of the cases, and those of smokers were equally distributed into moderately differentiated and poorly differentiated tumors (35.3% each). Overall, 31 (88.6%) cases were CHK2-positive, 27 (77.1%) were H2AX-positive, and 23 (65.7%) were P53-positive, with no difference between smokers and non-smokers (p > 0.05). No association was found between proteins and clinicopathologic data (p > 0.05). Similarities in CHK2, H2AX, and P53 immunohistochemical staining patterns were observed between smokers and non-smokers, and immunoexpression was not associated with clinicopathological parameters. However, the findings indicated consistent expression of these proteins in OSCC.

Abstract: The aim of this study was to determine the presence of immature CD1a+ and mature CD83+ dendritic cells in oral squamous cell carcinoma, to compare immunoreactivity between smokers and nonsmokers, and to correlate the results with histopathological grading. In this observational study, twenty-eight paraffin-embedded biopsies of oral squamous cell carcinoma were retrospectively retrieved and submitted to immunohistochemistry for immature CD1a+ and mature CD83+. Descriptive and statistical analyses were performed. The sample consisted of 18 man (64.3%) and 10 women (35.7%), with a mean age of 64.6 years in the nonsmoker group and 53.2 years in the smoker group. The tongue (11 cases, 39.2%) was the most commonly affected anatomical site, followed by gingiva (6 cases, 21.4%). Histopathological grading revealed 7 low-grade and 7 high-grade malignancy cases in each group, and no correlation with the number of positive DCs. The number of immature CD1a+ was not significantly different between smoker and nonsmoker groups, while a lower number of mature CD83+ was detected in the smoker group (p = 0.001). Smoking changes the oral immune system and decreases the ability to activate and mature dendritic cells, which may influence the development and progression of oral squamous cell carcinoma.