UV radiation increases carcinogenic risks for oral tissues compared to skin.

People can expose their oral cavities to UV (290-400 nm) by simply opening their mouths while outdoors. They can also have their oral cavities exposed to UV indoors to different UV-emitting devices used for diagnoses, treatments and procedures like teeth whitening. Because the World Health Organization declared UV radiation as a complete human carcinogen in 2009, we asked if oral tissues are at a similar or higher carcinogenic risk compared to skin tissue. To understand the UVB (290-320 nm)-related carcinogenic risks to these tissues, we measured initial DNA damage in the form of cyclobutane pyrimidine dimers (CPD), the repair rate of CPD (24 h) and the number of apoptotic dead cells over time resulting from increasing doses of erythemally weighted UV radiation. We used commercially available 3D-engineered models of human skin (EpiDerm™), gingival (EpiGingival™) and oral (EpiOral™) tissues and developed an analytical approach for our tri-labeling fluorescent procedure to identify total DNA, CPD and apoptotic cells so we can simultaneously quantify DNA repair rates and dead cells. Both DNA repair and apoptotic cell numbers are significantly lower in oral cells compared with skin cells. The combined results suggest UVB-exposed oral tissues are at a significantly higher carcinogenic risk than skin tissues.

UVB-induced inflammatory cytokine release, DNA damage and apoptosis of human oral compared with skin tissue equivalents.

People can get oral cancers from UV (290-400 nm) exposures. Besides high outdoor UV exposures, high indoor UV exposures to oral tissues can occur when consumers use UV-emitting tanning devices to either tan or whiten their teeth. We compared the carcinogenic risks of skin to oral tissue cells after UVB (290-320 nm) exposures using commercially available 3D-engineered models for human skin (EpiDerm™), gingival (EpiGing™) and oral (EpiOral™) tissues. To compare the relative carcinogenic risks, we investigated the release of cytokines, initial DNA damage in the form of cyclobutane pyrimidine dimers (CPDs), repair of CPDs and apoptotic cell numbers. We measured cytokine release using cytometric beads with flow cytometry and previously developed a fluorescent immunohistochemical assay to quantify simultaneously CPD repair rates and apoptotic cell numbers. We found that interleukin-8 (IL-8) release and the initial CPDs are significantly higher, whereas the CPD repair rates and apoptotic cell numbers are significantly lower for oral compared with skin tissue cells. Thus, the increased release of the inflammatory cytokine IL-8 along with inefficient CPD repair and decreased death rates for oral compared with skin tissue cells suggests that mutations are accumulating in the surviving population of oral cells increasing people's risks for getting oral cancers.