LiCl Promotes Recovery of Radiation-Induced Oral Mucositis and Dysgeusia

Oral mucositis and taste dysfunction are frequently complained by patients with head and neck cancer receiving radiotherapy, challenging the clinical outcome of cancer treatment. Recent studies have indicated the protective role of Wnt/beta-catenin signaling in radiation-induced oral mucositis (RIOM) and its pivotal role in the development and self-renewal of taste buds. The current study hypothesizes that lithium chloride (LiCl), a potent activator of the Wnt/beta-catenin signaling pathway, can promote the postirradiation restoration of oral mucosa integrity and taste function. To validate this hypothesis, we established a RIOM mouse model and evaluated the treatment efficacy of LiCl on oral mucositis and taste dysfunction in comparison with keratinocyte growth factor (KGF), an agent approved by the US Food and Drug Administration for oral mucositis. The results showed that LiCl alleviated the weight loss and tongue ulceration of RIOM mice, promoted proliferation of basal epithelial cells, and inhibited epithelial-mesenchymal transition in tongue mucosa. More important, elevated taste bud renewal and dysgeusia recovery toward sweetness were observed in RIOM mice treated with LiCl as compared to those treated by KGF. Collectively, our data demonstrate that LiCl can mitigate oral mucositis and rescue taste alteration induced by irradiation, and activation of Wnt/beta-catenin signaling may represent a promising therapy to improve the quality of life of patients receiving radiotherapy.

Automated summary

Recent studies suggest that lithium chloride can alleviate radiation-induced oral mucositis and taste dysfunction, promoting restoration of oral mucosa and taste bud function post-irradiation. Activation of Wnt/beta-catenin signaling pathway may represent a promising therapy to improve the quality of life of patients receiving radiotherapy.