Microscopic aspects of angiogenesis and lymphangiogenesis in oral squamous cell carcinoma

Vol. 54 No. 3 Suppl., 2013
This supplement was not sponsored by Outside Organizations.


Adina Bunget, A. Fronie, Emilia Afrem, Dorina Corlan Puscu, H. Manolea, Anca Rodica Dan, Malina Coman, Vanda Roxana Nimigean

Despite various great scientific and financial efforts, head and neck carcinomas represent a public health problem, being the eighth cause of cancer death worldwidely. The rate of tumor growth, its local expansion, as well as the metastasis of cancerous cells depend on the tumor vascularization, on the ability of blood vessels to provide a constant supply of nourishing substances and oxygen and to eliminate the residual products resulted from tumor growth. That is why angiogenesis and lymphogenesis are considered to be essential processes within the neoplastic process. The assessment of tumoral neoformed blood vessels in oral squamous carcinomas, using the CD34 antibody, showed a significant growth of the microvascular density, the average number being 504.66+/-177.65 vessels/mm(2). The diameter of angiogenesis vessels varied between 3.42 and 121.27 micro-m. The density of lymphogenesis vessels was 508.78+/-235.93 vessels/mm(2), while the diameter varied from 2.82 to 165.28 micro-m. Both angiogenesis and lymphogenesis vessels were more numerous in the areas where the inflammatory infiltrate was more abundant, which suggests that chronic inflammation plays the part of a promoter factor of neoplastic lesions.

Corresponding author: Adrian Fronie, Assistant Professor, MD, PhD; e-mail: adrianfronie@yahoo.com

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Anca Chiriac, Liliana Foia, Anca E. Chiriac, Codrina Ancuta, Paloma Manea, Lenuta Profire, Florina Filip

Objectives: Biologic therapy such as Etanercept, which is a tumor necrosis factor alpha (TNF-alpha) inhibitor, has been extensively used as election therapy in rheumatoid arthritis. The purpose of this case presentation was to inform about the possibility that lichen planus lesions could potentially become complicated by secondary infections in patients treated with Etanercept. Furthermore, we aimed at analyzing if the complication of the cutaneous lesion was coincidental or it was due to the immunosuppressive systemic therapy, and whether the infected lesion would respond to antibiotic therapy. Case summary: The patient was a 59-year-old woman with rheumatoid arthritis and that have had lichen planus lesions for approximately 25 years. Only recently, she had been received immunosuppressive therapy (Etanercept and Methotrexate). Further on, the lichen planus flared up with a secondary infection determined by a Methicillin-sensitive Staphylococcus aureus. Uncommon myocardial complications were also characteristic of this case. Results: While a case report described already the appearance of lichen planus following Etanercept therapy (Battistella M et al., 2008), the possibility that the lesion could become secondary complicated following this therapy was never reported before, according to our knowledge. Additionally, we describe in this case the interplay between Etanercept therapy and hypertrophic cardiomyopathy. Conclusions: Our case is not a lichen planus induced by Etanercept, but it is aggravated and secondary infected with Methicillin-sensitive Staphylococcus during the therapy. The additional cardiac complication (hypertrophic cardiomyopathy) may represent solely an evolutive sign of rheumatoid arthritis and therefore not influenced by Etanercept.

Corresponding author: Liliana Foia, Professor, MD, PhD; e-mail: lilifoia@yahoo.co.uk

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