Influence of laser light on bioimplants used in otorhinolaryngology.

In otorhinolaryngology, dermatology and reconstructive surgery biomaterials as implants and a variety of lasers are used. Laser light applied near to an implant could have the risk to damage these materials. Therefore, their resistance exposed to laser light is of interest. A diode laser emitting at 940 nm and a CO2 laser were used to investigate its effects to the biomaterials Bioverit®, Medpor® and Palacos®, and in addition, an excised implant containing Medpor® and nasal turbinate tissue, excised and fixed in formalin. The macro- and microscopic changes of the material, temperature development during laser energy application in dependency to distance of fibre and material, time of exposure and applied power were investigated. Interaction of diode laser light with Bioverit® (0 mm distance, 360 s, 10 W, 3,600 J) resulted in minimal microscopic effects in direct contact of with the fibre. Using Medpor® (1 mm, 10s, 10 W, 100 J) resulted in melting and perforation. In the case of Palacos® (0.6 mm, 10s, 10 W, 100 J), melting occurred creating a flat excavation. The effect to Medpor® in nasal turbinate (1-2 mm, 10s, 10 W, 100 J) showed tissue denaturation and carbonisation and creation of a hole. The interaction of the CO2 laser with Bioverit® (3 cm, 0.5, 1 and 5 s, 2, 10 or 20 W) induced melting and discolouring resulting finally in a perforating hole. Depending on the material, first damage starts 10 s after an impact of 100 J (threshold value). So interaction between laser energy and biomaterials occurs. This should be carefully considered during clinical laser treatments especially nearby implants.

p16 methylation does not affect protein expression in cervical carcinogenesis.

Previous studies have reported a frequency range of 19-61% for p16 methylation in cervical cancers. However, p16 is strongly expressed in over 90% of cervical cancers and pre-cancers, due to interactions of HPV oncogenes with p53 and pRb. In order to clarify these controversial findings, we developed a new bisulphite sequencing protocol to determine the methylation status of p16. DNA extracted from 17 cell lines and 94 microdissected clinical samples was subjected to methylation analysis. p16 expression was confirmed in Western blot and immunohistochemistry. Complete methylation of p16 was found in none of the dysplastic lesions, but in 26% of the cervical carcinomas. However, immunohistochemistry showed strong p16 expression in all cancers. These findings indicate that p16 methylation does not implicate loss of p16 expression in HPV-induced tumours. In cervical cancer, methylation of p16 does not seem to be an underlying pathogenic mechanism, but may be a result of increasing genetic and epigenetic instability.