ABSTRACT
BACKGROUND: There is little information available in the mechanism of radiation-induced salivary gland injury, and its treatment and prevention are still at the exploratory stage.OBJECTIVE: To establish a rat model of radiation-induced xerostomia with 18 Gy electron beam and to observe the pathological changes of the submandibular gland and changes in saliva ingredients.METHODS: Totally 115 Wistar rats were randomly divided into exposure and control groups: the rats in the exposure group were subjected to anesthesia, and the submandibular gland received 18 Gy electron beam radiation to establish the model of radiation-induced xerostomia. The rats in the control group were only anesthetized but not exposed to radiation. The water intake was recorded at 21 dys after modeling. The saliva was collected and the submandibular gland was removed at 1, 3, 7, 14, 21, 28, 35 and 42 days to detect the saliva volume and submandibular gland index,and the morphological changes of the submandibular gland were observed by hematoxylin-eosin staining.RESULTS AND CONCLUSION: At 1-21 days after modeling, the average daily water intake was (6.42±1.91) mL in the exposure group and (4.82±1.20) mL in the control group, respectively (P < 0.05). During 42 days after modeling, the saliva secretion volume in the exposure group was lower than that in the control group, which was the lowest on day 7,and the difference was significant at 7, 21, 28 and 42 days after modeling between two groups (P < 0.05). The submandibular gland index in the exposure group was significantly lower than that in the control group at 1 and 21-42 days after modeling (P < 0.05). Hematoxylin-eosin staining results showed that in the exposure group, the rat submandibular gland appeared with inflammatory infiltration, glandular atrophy and karyopyknosis that were aggravated with time until day 42. To conclude, the rat model of radiation-induced xerostomia is established successfully with 18 Gy beam, characterized as increased water intake, decreased saliva volume and progressive aggravation of pathological injury of the submandibular gland.