Does wound healing contribute to the eradication of basal cell carcinoma following curettage and electrodessication?

BACKGROUND: Histologic studies indicate that C&D fails to mechanically remove all the tumor in a percentage of cases that far exceeds the 5-year recurrence rate. This raises the question that if C&D does not mechanically remove the tumor in a significant number of patients, why don't we observe tumor recurrence in most of these patients? Our previous study indicates that inflammation occurring over 1 month following C&D does not clear residual tumor. It may be some other process, requiring more time, that clears the residual tumor. Perhaps the proliferative or maturation phase of wound healing or, alternatively, a slow-acting process such as a low-grade immune response set in motion earlier, clears the residual tumor. OBJECTIVE: To test the hypothesis that wound healing and maturation following C&D clear residual tumor that has not mechanically removed by the procedure. METHODS: The frequency of residual BCC detected histologically immediately following C&D was compared with the frequency 3 months after the C&D, an amount of time in which the maturation phase of wound healing is well under way. RESULTS: Twenty-two of 29 primary BCC less than 1 cm in size were tumor-free immediately following the procedure (clearance rate 75.9%). Twelve primary BCC <1 cm were treated by C&D, allowed to heal for 3 months, and then excised and checked histologically. Ten of the twelve BCC were free of tumor, for a clearance rate of 83.3%, which is not a statistically significant difference (p = 0.7187). CONCLUSION: By 3 months, the proliferative phase of wound healing is complete, and our study indicates that this phase has no effect on clearing the tumor. The maturation phase is well under way three months following C&D, and no statistically significant effect was observed.

A high SPF sunscreen's effects on UVB-induced immunosuppression of DNCB contact hypersensitivity.

Several studies in mice of the protection afforded by sunscreens from UVB-induced suppression of contact hypersensitivity have yielded conflicting reports ranging from complete protection to no protection. Firstly, we sought to determine the effects of sunscreen and UVB on Langerhans cells; secondly we sought to determine whether the effect of preapplication of sunscreen with a sun protection factor of 30 could prevent local UVB-induced suppression of contact hypersensitivity to dinitrochlorobenzene in humans. In the first part of the study we compared a control group with a sunscreen plus UVB group and enumerated the number of Langerhans cells in each group. In the second part of the study we had four groups: a control group, a UVB group, a sunscreen group, and a sunscreen plus UVB group. Our results show that application of a sunscreen prior to UVB can prevent the decrease in number of Langerhans cells in an irradiated site. In the second part of the study, our results indicate that sunscreen, in itself, does not interfere with contact hypersensitivity, and that a high SPF sunscreen applied prior to UVB irradiation partially prevents suppression of contact hypersensitivity.