OM is a common adverse effect of anticancer therapy, typically occurring within 1 week of undergoing chemotherapy. In addition to causing discomfort and pain, OM may affect the quality of life of cancer patients by prolonging hospitalisation and increasing financial expenses. Therefore, it is increasingly important to understand the mechanisms of OM lesions to provide effective prevention and treatment. The primary cause of OM is the cytotoxicity of chemotherapeutics on the rapidly dividing oral epithelium . Studies have shown that the pathogenesis of OM is a biologically complex process involving amplified inflammatory responses, reduced cell proliferation, increased cell senescence/apoptosis, and impaired regenerative potential in both the mucosal and submucosal compartments [1,5–6].
Clinically, different chemotherapy regimens can cause different degrees of OM. Current research indicates that antimetabolites, which affect DNA synthesis, are associated with 40–60% of OM incidences, with the use of 5-FU and platinum derivatives (cisplatin and oxaliplatin) resulting in more severe OM [15–17]. Although no evidence for a cumulative effect with repeated chemotherapy cycles has been found, considering the use of the same drugs and the sensitivity of the body, it remains necessary to consider using prophylactic drugs for patients with a history of severe OM .
Prevention and treatment of OM is necessary to relieve symptoms, accelerate tissue repair, and promote successful chemotherapy. Many treatments, including basic oral care, antimicrobial agents, and natural medicine using substances such as honey, aim to reduce both the incidence and severity of OM [2,10,19–20]. However, these treatments have their own limitations, including cariogenic effects and adherence to teeth following prolonged ingestion of honey . Previous studies suggest that preventive oral spray can delay the occurrence of OM [9,22].
RhIL-11 is a pleiotropic cytokine which stimulates myeloid, erythroid, and megakaryocyte differentiation, modulates macrophage and T cell inflammatory functions, and protects the function of the mucosal epithelium [11–12,18]. It is also known to promote mitosis and proliferation by inhibiting apoptosis and improving the mitotic activity of small intestinal villi stem progenitor cells, and it has a good protective effect on gastrointestinal tract injuries caused by radiotherapy and chemotherapy. The oral mucosa is similar to the intestinal mucosa in terms of continuous self-renewal and rapid proliferation . Thus, rhIL-11 has the potential to reduce chemotherapy-related OM. Moreover, epithelial cells contain the colony-stimulating factor receptor, which is bound by rhIL-11 to stimulate the migration and proliferation of epithelial cells and promote the growth of keratinocytes and fibroblasts . Thus, rhIL-11 may promote the proliferation and maturation of endothelial cells to accelerate the healing of OM caused by chemotherapy.
Our data were collected prospectively, eliminating potential recall bias and increasing credibility compared to a retrospective design. Prior research in an animal model found that rhIL-11 favourably modulates acute radiation-induced mucositis by attenuating pro-inflammatory cytokine expression . Unfortunately, there is no relevant prospective research to support these findings. In the present study, rhIL-11 therapy significantly reduced the recovery time of OM and improved the efficiency of treatments compared with the control treatment, supporting the ability of rhIL‐11 to accelerate recovery from OM. In addition, this study demonstrates there was no significant difference in the efficacy of rhIL-11 or Rehabilitation New Liquid in the first few days, but after 1 week of treatment, the efficacy of rhIL-11 in OM was better than Rehabilitation New Liquid. This further indicates that rhIL-11 may shorten the treatment time of severe OM. This study also found that no advantage of rhIL-11 treatment in preventing OM, both the incidence and degree of oral mucositis. At present, many studies have shown that low-intensity laser therapy, honey and probiotics play a role in prevention.
However, there are few a samples after radiotherapy in this study. According to previous studies, the incidence of OM related to radiotherapy of head and neck tumours is high and the treatment time is long, which need to be further investigated. Moreover, the severity of chemotherapy-induced OM in this study is low, which may offset the results. In addition, the main limitation of our experiment is the small sample size of this study; therefore, larger studies are needed to verify our conclusions.