ABSTRACT
Despite significant efforts in developing new diagnostic and therapeutic modalities, oral squamous cell carcinomas (OSCCs) still exhibit a high recurrence rate, a low five-year survival rate, and an increasing prevalence. Toll-like receptors (TLRs), which initiate and perpetuate immune mechanisms upon activation, have been linked to immune surveillance and the antitumor immune response. The aim of this study was to investigate the association between the polymorphisms of the TLR7 rs3853839 and TLR9 rs187084 genes and OSCC risk, clinicopathological features, and survival. Genotyping was assessed by real-time polymerase chain reaction (PCR) in 95 HPV-negative OSCC patients and 107 age- and sex-matched healthy controls. Patients with lymph node metastases had higher frequencies of the TLR9 rs187084 CC variant genotype compared to the major TT genotype (P = 0.020) and to T-allele carriers (combined TT + CT genotypes, P = 0.015). A higher prevalence of advanced stage III was observed in patients with the TLR9 rs187084 variant CC genotype compared to TT (P = 0.047) and to T-allele carriers (TT + CT, P = 0.037). Kaplan-Meier analysis revealed a lower overall survival rate in patients with the TLR9 rs187084 variant CC genotype compared to TT genotype (P = 0.010, log-rank test) and to T-allele carriers (TT + CT, P = 0.002), though it was not an independent predictor of overall survival. Both TLR9 rs187084 and TLR7 rs3853839 polymorphisms were associated with high alcohol consumption (P = 0.027 and P = 0.001, respectively). The investigated genetic variations were not associated with OSCC susceptibility. The variant CC genotype of the TLR9 rs187084 polymorphism might be a marker of poor survival and tumor progression in OSCC.
ABSTRACT
BACKGROUND/AIM: Periodontal disease affects gingival tissue and supporting apparatus of the teeth leading to its decay. The aim of this study was to highlight and precisely determine his- tological changes in the gum tissue. METHODS: Gingival biopsy samples from 53 healthy and parodontopathy-affected patients were used. Clinical staging of the disease was performed. Tissue specimens were fixed and routinely processed. Sections, 5 µm thin, were stained with hematoxylin and eosin, histochemical Van-Gieson for the collagen content, Spicer method for mast-cells and immunochemical method with anti-CD68 and anti-CD38 for the labelling of the macrophages and plasma-cells. Morphometric analysis was performed by a M42 test system. RESULTS: While the disease advanced, collagen and fibroblast volume density decreased almost twice in the severe cases compared to the control ones, but a significant variation was observed within the investigated groups. The mast-cell number increased nearly two times, while the macrophage content was up to three times higher in severe parodontopathy than in healthy gingival tissue. However, the relative proportion of these cells stayed around 6% in all cases. Plasma-cells had the most prominent increase in the number (over 8 times) compared to the control, but again, a variation within investigated groups was very high. CONCLUSION: Gingival tissue destruction caused by inflammatory process leads to significant changes in collagen density and population of resident connective tissue cells. Although inflammatory cells dominated with the disease advancing, a high variation within the same investigated groups suggests fluctuation of the pathological process.
