Image analysis of fibrosis in labial salivary glands of patients with systemic autoimmune diseases. Close correlation of lobular fibrosis to seropositive rheumatoid arthritis and increased anti-CCP and RF titres in the serum

TGF-β1 Triggers Salivary Hypofunction via Attenuating Protein Secretion and AQP5 Expression in Human Submandibular Gland Cells

“…6−9 In recent years, salivary gland fibrosis received a lot of attention due to its frequent occurrence in various pathologic and physiologic conditions covering chronic inflammation, infections, physical trauma, irradiation, ductal obstruction, autoimmune disease, and aging of course. 1,10,11 The accumulated evidence suggests that abnormal active TGF-β signaling is the primary driving factor for fibrosis events, limited to not only pulmonary fibrosis, 12 hepatic fibrosis, 13 renal fibrosis, 14 and cardiac fibrosis 15 but also salivary gland fibrosis. 16 For instance, in TGF-β1-overexpressed transgenic adulthood mice, salivary gland fibrosis and acinar atrophy are markedly observed, thereby leading to hyposalivation, 17 indicative of the decreased flow rate.…”

“…Previous evidence suggests that degenerative changes in the histology of salivary glands widely occur with age. In terms of morphologies, aging salivary glands are characterized by acinar cell atrophy, ductal cell atrophy, cytoplasmic vacuolization, lymphocyte infiltration, increased tissue fibrosis, and decreased volume of acinus tissue but increased volume of duct tissue with more periductal fibrosis. − In recent years, salivary gland fibrosis received a lot of attention due to its frequent occurrence in various pathologic and physiologic conditions covering chronic inflammation, infections, physical trauma, irradiation, ductal obstruction, autoimmune disease, and aging of course. ,, The accumulated evidence suggests that abnormal active TGF-β signaling is the primary driving factor for fibrosis events, limited to not only pulmonary fibrosis, hepatic fibrosis, renal fibrosis, and cardiac fibrosis but also salivary gland fibrosis . For instance, in TGF-β1-overexpressed transgenic adulthood mice, salivary gland fibrosis and acinar atrophy are markedly observed, thereby leading to hyposalivation, indicative of the decreased flow rate.…”