Immunoexpression of VEGFR-3, but not the immunoexpression of VEGF-C or lymphatic density, is correlated with metastasis in lower lip squamous cell carcinoma.

The purpose of this study was to evaluate the immunoexpression of vascular endothelial growth factor C (VEGF-C) and VEGF receptor 3 (VEGFR-3) and their correlation with intratumoural lymphatic density (ILD) and peritumoural lymphatic density (PLD) in metastatic and non-metastatic lower lip squamous cell carcinoma (LLSCC). Twenty-five LLSCC with regional nodal metastasis and 25 LLSCC without metastasis were selected. The percentages of VEGF-C and VEGFR-3 staining in each tumour core and at the deep invasive front were assessed. PLD and ILD were determined using anti-podoplanin antibody. Immunohistochemical findings were correlated with nodal metastasis, clinical staging, local recurrence, clinical outcome, and histological grade. Cytoplasmic immunoexpression of VEGFR-3 in the tumour core was associated with metastasis (P=0.009), patient death (P=0.008), and histological grade (P<0.005). PLD, ILD, and VEGF-C expression showed no significant associations with clinicopathological parameters (P>0.05). PLD and ILD were not significantly correlated with the immunoexpression of VEGF-C or VEGFR-3 (P>0.05). There was a significant positive correlation between PLD and ILD (P=0.004), and between cytoplasmic immunoreactivity of VEGF-C and VEGFR-3 (P=0.011). These results suggest an important role for VEGFR-3 in the progression of LLSCC, and highlight the possible influence of its expression on the prognosis of these tumours. ILD and PLD may not be associated with lymph node metastasis in LLSCC.

Molecular survey of atheromatous plaques for the presence of DNA from periodontal bacterial pathogens, archaea and fungi.

BACKGROUND AND OBJECTIVE: Chronic infections, such as periodontitis, have been associated with the development and progression of atherosclerosis. The mechanisms through which this occurs have yet to be elucidated. This study was carried out to detect periodontopathic bacteria as well as archaea and fungi in atheromatous plaques and search for factors associated with their occurrence in atheromas. MATERIAL AND METHODS: A cross-sectional study was carried out including 30 patients diagnosed with atherosclerosis in the carotid, coronary or femoral arteries. Plaques were collected during surgery and analysed using PCR to detect Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola and members of the Synergistetes group. Samples were also surveyed with universal primers for bacterial, archaeal and fungal DNA. Patients responded to a questionnaire to determine factors associated with PCR results. RESULTS: All dentate individuals (66.7%) had periodontal disease, 95% of which was severe and 65% extensive. None of the targeted periodontopathic bacteria was found in the atheromas. No sample yielded positive results for fungal and archaeal DNA. Four samples (13%) were positive for the presence of bacterial DNA. Of these, three participants were dentate (two with severely chronic generalized periodontitis and one with severely chronic localized periodontitis). CONCLUSION: This study did not confirm previous findings of periodontal pathogens in atheromas, making it impossible to establish factors associated with their presence in plaques. Presence of bacterial DNA in some samples indicates that periodontal or nonoral bacterial species other than the ones targeted in this study may be involved with some cases of atherosclerosis.