Pharmacotherapy of Xerostomia in Primary Sjogren's Syndrome

Geoffrey C. Wall, Pharm.D., Michelle L. Magarity, Pharm.D., Jeffrey W. Jundt, M.D.

Disclosures

Pharmacotherapy. 2002;22(5) 

In This Article

Pathogenesis

Sjögren's syndrome is characterized by intense lymphocytic infiltration of exocrine glands.[10] This can destroy much of the glands, making it difficult for them to produce natural fluids for regular function.[1,11] Acinar cells in these glands must first be stimulated by acetylcholine, which is released from nerve endings at M3 muscarinic receptors on glandular epithelial cells in order to produce saliva. The five muscarinic receptors have different tissue distribution. Stimulation at muscarinic receptors together with a secondary signal generated by other receptors on the cell matrix activates production of adenosine triphosphatase (ATPase), which is necessary for secretion of saliva. A decrease in acinar cell production of ATPase caused by lymphocytic infiltration results in decreased saliva production.

Immune factors also have a significant effect on the salivary process. Cytokines, especially tumor necrosis factor and interleukin-1, cause a dramatic decline in acetylcholine release by autonomic nerve and postreceptor signals in response to acetylcholine. This results in impairment of both glandular function and microvasculature response to autonomic nerve stimulation.[12] It appears that a combination of direct invasion by lymphocytes resulting in local tissue inflammation and fibrosis, as well as autoimmune-mediated interference with neurotransmitters and receptors, may be responsible for clinical manifestations of SJS.

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