The limitation of markers for chronic oral diseases such as oral lichen planus (OLP) and burning mouth syndrome (BMS) is a diagnostic challenge for clinicians. The pathogenesis of OLP and BMS is not yet fully understood. Therefore, diagnoses are mainly based on the observation of clinical features and history, rather than established markers. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are used to determine the state of inflammation; however, these markers have some limitations. Recently, a new inflammatory marker, pentraxin-3 (PTX3), has been identified in other systemic inflammatory diseases. PTX3 is a member of the pentraxin family and is classified as a long pentraxin. PTX3 is found in various human tissues, whereas the classical short pentraxin, CRP, is secreted only in the liver. PTX3 is a marker of autoimmune diseases and periodontitis. However, there are no studies on PTX3 in OLP and BMS; therefore, we sought to determine if PTX3 can be a diagnostic marker for OLP and BMS. PTX3 was found to be correlated with other inflammatory markers, suggesting its diagnostic value for inflammatory oral diseases. We also found that the PTX3 levels were lower in patients with OLP and BMS. ESR levels were elevated in the OLP and BMS groups, but CRP levels were not. Despite these associations, no correlation was found between PTX3 expression and other known clinical features of OLP and BMS. We suggest that PTX3 plays a role in the immunological and neurological pathways involved in the complex pathogenesis of OLP and BMS.

Oral lichen planus (OLP) is a chronic inflammatory disease observed in approximately 0.5–2.2% of the population, and it is recognized as a premalignant lesion that can progress into oral squamous cell carcinoma (OSCC). The rate of malignant transformation is approximately 1.09–2.3%, and the risk factors for malignant transformation are age, female, erosive type, and tongue site location. Malignant transformation of OLP is likely related to the low frequency of apoptotic phenomena. Therefore, apoptosis-related genetic factors, like p53, BCL-2, and BAX are reviewed. Increased p53 expression and altered expression of BCL-2 and BAX were observed in OLP patients, and the malignant transformation rate in these patients was relatively higher. The involvement of microRNA (miRNA) in the malignant transformation of OLP is also reviewed. Because autophagy is involved in cell survival and death through the regulation of various cellular processes, autophagy-related genetic factors may function as factors for malignant transformation. In OLP, decreased levels of ATG9B mRNA and a higher expression of IGF1 were observed, suggesting a reduction in cell death and autophagic response. Activated IGF1-PI3K/AKT/mTor cascade may play an important role in a signaling pathway related to the malignant transformation of OLP to OSCC. Recent research has shown that miRNAs, such as miR-199 and miR-122, activate the cascade, increasing the prosurvival and proproliferative signals.

Numerous reports on the immunopathogenesis of an oral lichen planus (OLP) have shown some inconsistency in terms of the role and distribution of CD4+ and CD8+ T cells, and Langerhans cells (LC). This has led to the hypothesis that although the clinical and histopathological manifestations of OLPs appear similar, they can be grouped into CD4+ predominant lesions and CD8+ ones on the varied immunopathogenesis or clinical progress. This study investigated the distribution of CD4+ T cells, CD8+ T cells, LC and the ratio of CD4/CD8 and defined the important immunocompetent cells. In addition, the clinicopathological and histopathological correlation with those immunocompetent cells were investigated. Frozen sections of 16 OLPs and 5 normal buccal mucosae were immunostained. Quantification was done using KAPPA Imagebase software and statistical analysis using SPSS 10.0 statistical package. CD8+ T cells were consistently more abundant in the epithelium of the OLP than CD4+ T cells, but no difference between the two cells was detected in the lamina propria. The intra-epithelial CD4+ T cells revealed a positive linear correlation with the intra-epithelial CD8+ T cells. In the lamina propria, the number of LC had a positive linear correlation with CD4/CD8 ratio. The number of LCs was higher in the reticular type of OLP compared to the erosive type. The histopathological features such as hyperkeratosis, acanthosis, the band-like infiltration of mononuclear cells, and liquefaction degeneration did not show significant correlation with the CD4/CD8 ratio. The results suggest that CD8+ T cells play major role in immunopathogenesis of OLP. The immunopathogenesis of OLP appears to vary from lesion to lesion in relation to the clinical progress.

Oral lichen planus (OLP) is an atypically keratinized and ulcerative lesion, producing severe pain and discomforts in the involved patients. Nevertheless, the etiological factor or the pathogenetic mechanism has not been clearly elucidated. In the present study, the different gene expressions were screened in 21 cases of OLP by immunohistochemical (IHC) array method using 80 antibodies, and found that the pathway of E-cadherin/β-catenin was abnormally expressed compared to the other essential genetic pathways. Particularly, the expressions of eIF5A, DHS, and DOHH, which are the biomarkers of protein translation, were remarkably reduced, nevertheless the expression of β-catenin was strongly positive in the 7 cases among 21 cases of OLP. The other expressions of p53, BCL-2, MDM-2, PAKT, BAX, BAK, BAD, NFkB, HO-1, etc, were usually weak or sparse, while the expressions of PCNA, CDK4, and HSP-70 were markedly increased. Taken together, it is presumed that the overexpression of β-catenin indicates the derangement of E-cad/β-catenin/NFkB pathway, causing the transcription of cellular proliferating genes in downstream events, i.e., PCNA and CDK4, and that it may be eventually relevant to the malignant potential of OLP epithelial cells. It is also suggested that the activation of β-catenin/TCF/LEF1 pathway be closely relevant to the immunological reaction of OLP with the accumulation of T-cells underneath the mucosal epithelium.