Salivary biomarkers are promising molecules for diagnosing systemic diseases. Cytidine/uridine monophosphate kinase 2 (CMPK2) is associated with various systemic diseases. However, little is known about the role of the CMPK2 gene in saliva and dyslipidemia. This study investigated the relationship between serum lipid levels and Cmpk2 mRNA expression in the saliva of dyslipidemic mice. Additionally, immunofluorescence staining was employed to assess the localization of the CMPK2 protein in the submandibular gland. Two types of dyslipidemic mice were utilized: mice fed a high-fat and high-cholesterol (HFHC) diet and genetically dyslipidemic ApoE-deficient mice. The mice at 9 to 46 weeks were analyzed for serum lipid levels, Cmpk2 mRNA expression in saliva, and CMPK2 protein localization in the submandibular glands. Both dyslipidemic mice displayed elevated low-density lipoprotein cholesterol and total cholesterol in serum. ApoE-deficient mice apparently exhibited increased Cmpk2 expression in saliva. Immunofluorescence staining indicated that CMPK2 proteins were primarily localized in the serous acini, potentially associated with the secretion of Cmpk2 mRNA in saliva. These findings suggest that Cmpk2 mRNA increases and is detectable in the saliva of dyslipidemic mice, providing a viable experimental model to assess the potential use of CMPK2 as a biomarker for dyslipidemia.

Diabetes is a significant risk factor for bisphosphonate-related osteonecrosis of the jaw (BRONJ), a severe oral complication with limited treatment options. Salivary testing offers a noninvasive approach for monitoring BRONJ risk; however, few studies have investigated salivary biomarkers in BRONJ. This study screened salivary biomarkers that reflect the progression of BRONJ under diabetic conditions. A diabetic BRONJ rat model was established to screen for diabetes-related biochemical biomarkers in saliva. Streptozotocin (STZ) administration elevated blood glucose and glycated albumin levels and altered lipid and renal function markers, confirming diabetes induction. Subsequent zoledronic acid (ZA) administration and extraction of the maxillary first molar delayed epithelialization, inflammatory cell infiltration, bone exposure, and necrosis in extraction sockets, indicating successful establishment of a diabetic BRONJ model. This model showed reductions in submandibular and sublingual gland size, as well as in acinar cell number. Although salivary secretion volume was reduced, saliva samples were successfully collected from all groups. Screening identified elevated urea nitrogen (UN) and total ketone bodies (T-KB) in the STZ + ZA group. These findings suggest that salivary UN and T-KB may reflect disease progression and serve as potential biomarkers for predicting BRONJ risk under diabetic conditions.