[Skip to Navigation]
October 1996

Parotid Gland Dysfunction in an Animal Model of Chronic Graft-vs-Host Disease

Author Affiliations

From the Department of Oral and Maxillofacial Surgery, Rambam Medical Center and Faculty of Medicine, Technion—Israel Institute of Technology, Haifa (Drs R. Nagler and Laufer); and Bone Marrow Transplantation Department, Hadassah University Hospital, Jerusalem, Israel (Dr A. Nagler).

Arch Otolaryngol Head Neck Surg. 1996;122(10):1057-1060. doi:10.1001/archotol.1996.01890220025005

Background:  Xerostomia is observed in 85% of patients suffering from chronic graft-vs-host disease (cGVHD). The pathophysiological mechanism of the major salivary gland dysfunction is unclear.

Objective:  To evaluate parotid gland function in a mouse model of cGVHD.

Design:  The volume, flow rate, lag phase, and composition of secreted saliva were assessed in mice with cGVHD after pilocarpine stimulation (5mg/kg) by cannulation of the main parotid excretory duct with polyethylene tubing.

Results:  Significant reduction in the secreted saliva volume was observed in the mice with cGVHD compared with the syngeneic controls (39.1± 2.9 μL/30 minutes and 71.2±5.7 μL/30 minutes, respectively) (P<.05). In addition, we observed a flattening of the normal salivary flow rate curve in the mice with cGVHD. The lag phase (time between pilocarpine stimulation and saliva secretion) was significantly longer in the cGVHD group than in the controls (2.5±0.3 vs 1.9±0.2 minutes) (P<.05). Sialochemical analysis showed a significant decrease in sodium level (42.1±1.9 vs 61.4±4.8 mmol/L) (P<.01) and a significant increase in potassium level (20.0±1.2 vs 15.1±1.2 mmol/L) (P<.05) in the saliva of the mice with cGVHD compared with syngeneic mice. Histopathological evaluation of the parotid glands demonstrated moderate lymphocyte infiltration and parenchymal destruction.

Conclusion:  The parotid gland dysfunctions leading to xerostomia observed in a mouse model of cGVHD may be of clinical importance.Arch Otolaryngol Head Neck Surg. 1996;122:1057-1060

Add or change institution