A great number of lichenoid lesions have overlapping clinicopathological features, so the use of adjunct tests to establish definitive diagnosis is recommended for correct management and prognosis of the lesions. In this context, direct immunofluorescence (DIF) can be a useful tool. Thus, this study aimed to characterize the clinical, histopathological, and DIF pattern in patients with oral lichen planus (OLP) and patients with oral lichenoid lesions (OLLs). Patients with OLP and patients with OLL were characterized and compared with patients with mucous membrane pemphigoid, pemphigus vulgaris, and fibrous hyperplasia through a cross-sectional study. Patients with OLP (n = 30) and patients with OLL (n = 26) were mostly white women in the fifth decade of age, with reticular lesions mainly on the buccal mucosa. All patients with OLP and half of the patients with OLL showed liquefaction degeneration at the basal cell layer and a band-like lymphocytic infiltrate in the subepithelial tissue. Twenty-two patients with OLP (73.3%), 10 with OLL (38.4%), 25 with mucous membrane pemphigoid (96.1%), and all with pemphigus vulgaris (100%) had positive DIF. There was no positive DIF in patients with fibrous hyperplasia. The most frequent DIF pattern in patients with OLP and patients with OLL was linear fibrinogen at the basement membrane zone, and a logistic regression model for positive DIF found statistically significant difference in OLP versus OLL (odds ratio, 3.73; confidence interval, 1.23–11.38). Although clinical and histopathological features are sufficient for diagnosing most of the patients with OLP and OLL, DIF is a key tool in differentiating some lichenoid lesions and could improve the diagnosis of OLP and OLL, especially in lesions showing typical clinical and histological features of OLP.

Persistent infection with Human papillomavirus (HPV) is the main etiologic factor for pre-malignant and malignant cervical lesions. Moreover, HPV is also associated with oropharynx and other anogenital carcinomas. Cancer-causing HPV viruses classified as group 1 carcinogens include 12 HPV types, with HPV 16 and 18 being the most prevalent. High-risk HPVs express two oncoproteins, E6 and E7, the products of which are responsible for the inhibition of p53 and pRB proteins, respectively, in human keratinocytes and cellular immortalization. p53 and pRB are pleiotropic proteins that regulate the activity of several signaling pathways and gene expression. Among the important factors that are augmented in HPV-mediated carcinogenesis, proteases not only control processes involved in cellular carcinogenesis but also control the microenvironment. For instance, genetic polymorphisms of matrix metalloproteinase 1 (MMP-1) are associated with carcinoma invasiveness. Similarly, the serine protease inhibitors hepatocyte growth factor activator inhibitor-1 (HAI-1) and -2 (HAI-2) have been identified as prognostic markers for HPV-dependent cervical carcinomas. This review highlights the most crucial mechanisms involved in HPV-dependent carcinogenesis, and includes a section on the proteolytic cascades that are important for the progression of this disease and their impact on patient health, treatment, and survival.

Head and neck squamous cell carcinoma remains challenging to treat with no improvement in survival rates over the past 50 years. Thus, there is an urgent need to discover more reliable therapeutic targets and biomarkers for HNSCC. Matriptase, a type-II transmembrane serine protease, induces malignant transformation in epithelial stem cells through proteolytic activation of pro-HGF and PAR-2, triggering PI3K-AKT-mTOR and NFKB signaling. The serine protease inhibitor lympho-epithelial Kazal-type-related inhibitor (LEKTI) inhibits the matriptase-driven proteolytic pathway, directly blocking kallikreins in epithelial differentiation. Hence, we hypothesized LEKTI could inhibit matriptase-dependent squamous cell carcinogenesis, thus implicating kallikreins in this process. Double-transgenic mice with simultaneous expression of matriptase and LEKTI under the keratin-5 promoter showed a prominent rescue of K5-Matriptase^+/0 premalignant phenotype. Notably, in DMBA-induced SCC, heterotopic co-expression of LEKTI and matriptase delayed matriptase-driven tumor incidence and progression. Co-expression of LEKTI reverted altered Kallikrein-5 expression observed in the skin of K5-Matriptase^+/0 mice, indicating that matriptase-dependent proteolytic pathway inhibition by LEKTI occurs through kallikreins. Moreover, we showed that Kallikrein-5 is necessary for PAR-2-mediated IL-8 release, YAP1-TAZ/TEAD activation, and matriptase-mediated oral squamous cell carcinoma migration. Collectively, our data identify a third signaling pathway for matriptase-dependent carcinogenesis in vivo. These findings are critical for the identification of more reliable biomarkers and effective therapeutic targets in Head and Neck cancer.

Background: Juvenile spongiotic gingival hyperplasia (JSGH) is a benign proliferation of non-keratinised stratified squamous epithelium with evident spongiosis, exocytosis leukocytes and dilated vessels with varying numbers of inflammatory cells. Although uncertain, it has been suggested that the epithelial proliferation is probably related to trauma and local irritants. It emerges as a painless erythematous patch or papule with an irregular surface. Case reports: We present a series of eight cases and a literature review of the clinical presentation and treatment approaches for JSGH. This series includes four females and four males with a mean age of 11.6 years, all com-plaining of injury to the gums. All lesions were painless and not bleeding. One patient associated the lesion with the onset of trauma and another with a previous history of an eruption cyst. Periapical radiographs of the adjacent area did not show any alteration of bone or teeth. Based on these findings, the diagnostic hypotheses were a non-neoplastic proliferative process or a factitious injury. Incisional biopsy was performed and histopathologic diagno-sis was conclusive for JSGH. Surgical excision was conducted in three cases, and the other five cases were supported by clinical observation and plaque control in order to prevent gingival recession defects. After a follow-up period of 11 months (mean), no recurrence was observed for surgically treated cases and mild improvement was achieved with periodontal treatment. Conclusion: This case series illustrates the importance of diagnosis and follow-up of patients with JSGH. A conser-vative approach consisting of basic periodontal support instead of surgical excision may be indicated because of the risk of aesthetic defects at the involved areas.

Introduction Epidemiological studies focused on prognostic factors associated with laryngeal cancer in the Brazilian population are poorly reported in the literature. Objective To evaluate the influence of certain risk factors on the survival rates of patients with squamous cell carcinoma (SCC) of the larynx. Methods This retrospective study was conducted on adult patients who were admitted to the outpatient clinic of the head and neck department in a tertiary care hospital. Evaluation of the influence of risk factors on the survival rates of patients registered in the hospital with laryngeal SCC was performed based on age, sex, initial stage, time of evolution, habits, educational levels and relapse and death. Overall survival (OS), disease-free survival (DFS) and clinical-demographic data were analyzed using the Kaplan-Meier method, Log-rank test and Cox regression. Results A total of 107 patients with a mean age of 59.8 years (range 19–81) were included in this study. Stages III and IV were associated with decreased DFS (p = 0.02) and OS (p = 0.02). Smoking patients had a greater period of disease evolution than non-smoking patients (p = 0.003). Alcohol consumption in smokers increased the risk of death by 2.8 (p = 0.002) compared with non-drinking smokers. Male patients presented lower DFS average when compared with female patients (p = 0.04). Conclusion Our study confirms that male gender, smoking habit combined with alcohol consumption, and advanced stages were strongly associated with poor prognosis.