Evaluation of trigeminal nerve injuries in relation to third molar surgery in a prospective patient cohort. Recommendations for prevention.

Trigeminal nerve injury is the most problematic consequence of dental surgical procedures with major medico-legal implications. This study reports the signs and symptoms that are the features of trigeminal nerve injuries caused by mandibular third molar (M3M) surgery. 120 patients with nerve injury following M3M surgery were assessed. All data were analysed using the SPSS statistical programme and Microsoft Excel. 53 (44.2%) inferior alveolar nerve (IAN) injury cases and 67 (55.8%) lingual nerve injury (LNI) cases were caused by third molar surgery (TMS). Neuropathy was demonstrable in all patients with varying degrees of paraesthesia, dysaesthesia (in the form of burning pain), allodynia and hyperalgesia. Pain was one of the presenting signs and symptoms in 70% of all cases. Significantly more females had IAN injuries and LNIs (p<0.05). The mean ages of the two groups of patients were similar. Speech and eating were significantly more problematic for patients with LNIs. In conclusion, chronic pain is often a symptom after TMS-related nerve injury, resulting in significant functional problems. Better dissemination of good practice in TMS will significantly minimize these complex nerve injuries and prevent unnecessary suffering.

The antiangiogenic agent ZD4190 prevents tumour outgrowth in a model of minimal residual carcinoma in deep tissues.

BACKGROUND: Tumour cells may persist at the operative site after seemingly adequate surgery. Radiotherapy is often given in an attempt to prevent repopulation, but this modality cannot be relied upon to prevent locoregional recurrence. An alternative strategy is to take advantage of the requirement of tumour cells to develop an independent blood supply and block this process to prevent recurrence. METHODS: In this study, we evaluate the effect of the angiogenesis inhibitor, ZD4190, using a rodent model of residual carcinoma in deep tissues, mimicking the clinical scenario where low numbers of malignant cells persist at the operative site. RESULTS: The tumour burden that could be eliminated was dependent on the site where the cells were implanted. Immediate treatment with ZD4190 prevented outgrowth of up to 2.5 x 10(5) cells in the rectus muscle and 1 x 10(5) in the gastrocnemius, whereas control animals developed large tumours. When more than 2.5 x 10(6) cells were implanted into the rectus or 1 x 10(6) into the gastrocnemius and treatment was maintained for 3 weeks, the carcinomas that developed in ZD4190-treated animals showed a reduced microvessel density and increased necrosis when compared with the vehicle-treated controls, but an infiltrative growth pattern was common. CONCLUSION: These findings suggest that antiangiogenic agents have a role to play in preventing outgrowth of residual carcinoma and are likely to be most effective when the tumour burden is minimal.

Tissue engineering of oral dysplasia.

Keratinocytes and fibroblasts isolated from dysplastic oral lesions were combined to provide a renewable source of epithelia. A dysplasia-scoring index was devised to compare the architectural and cytological features and used together with robust immunophenotyping to show that the engineered epithelia showed most of the characteristics of the clinical lesions. The strains of dysplastic oral keratinocytes with an extended or immortal lifespan provided a reproducible resource of epithelia showing mild (DOK), moderate (POE9n) or severe (D20) dysplasia when maintained under defined conditions. The dysplasia score was influenced by growth conditions, with KGF polarizing proliferation to the basal layer and reducing the severity of dysplasia. When compared to the normal counterparts, dysplasia-associated fibroblasts expressed MMP9, secreted more HGF, increased the dysplasia score for epithelia generated with mortal dysplastic keratinocytes and induced morphological changes in normal keratinocytes, highlighting the role of the microenvironment in determining the phenotype of dysplastic epithelia.