Jugular fossa tumors are uncommon diseases. During the surgery and due to the interposition of the facial nerve in the tumor approach, the facial nerve must be elevated from the fallopian canal and placed permanently into an anterior position. Although this maneuver provides a wide exposure, most of the patients suffer a long-term total or partial facial palsy. The purpose of this article is to check whether the infratemporal fossa approach without transposition of the facial nerve is equivalent to the approach with rerouting of the facial nerve regarding postsurgical morbidity. The clinical records of 52 patients who underwent an infratemporal fossa approach were reviewed in which 34 patients were segregated into two comparable groups regarding the presence or absence of transposition of the facial nerve. There were 19 women and 15 males. The majority of the patients (73%) had jugular paragangliomas. The mean follow-up of the full series was 66 months. It was statistically significant that the worst facial nerve function at hospital discharge was in the patients who underwent facial nerve transposition (p = 0.001). Equally the facial nerve function in the no-rerouting group 1 year after the surgery was significantly much better than in the rerouting group (p = 0.003). Regarding to survival, recurrence or complications no significant differences were observed between both groups. Our study suggests that most of cases avoiding facial nerve transposition allow significant better functional results thereof without affecting other parameters such as recurrence, complications or survival.
Background
Squamous epithelia of the head and neck undergo continuous cell renewal and are continuously exposed to mutagenic hazard, the main cause of cancer. How they maintain homeostasis upon cell cycle deregulation is unclear.
Methods
To elucidate how head and neck epithelia respond to cell cycle stress, we studied human keratinocytes from various locations (oral mucosa, tonsil, pharynx, larynx, and trachea). We made use of genotoxic or mitotic drugs (doxorubicin [DOXO], paclitaxel, and nocodazole), or chemical inhibitors of the mitotic checkpoint kinases, Aurora B and polo‐like‐1. We further tested the response to inactivation of p53, ectopic cyclin E, or to the chemical carcinogen 7,12‐dimethylbenz[a]anthracene (DMBA).
Results
All treatments provoked DNA damage or mitosis impairment and strikingly triggered squamous differentiation and polyploidization, resulting in irreversible loss of clonogenic capacity.
Conclusion
Keratinocytes from head and neck epithelia share a cell‐autonomous squamous DNA damage‐differentiation response that is common to the epidermis and might continuously protect them from cancer.
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