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References [1] Aragona P, Di Pietro R, Spinella R, Mobrici M. Conjuctival epithelium improvement after systemic pilocarpine in patients with Sjögren’s syndrome. Br J Ophthalmol 2006,90:166-170. [2] Bjerrum KB. Tests and symptoms in keratoconjuctivitis sicca and their correlation. Acta Ophtalmol Scan. 1996;74:436-441. [3] Buyon JP. Congenital heart block. Lupus. 1993;2:291-295. [4] Cohen EJ. Punctal occlusion. Arch Ophthalmol. 1999;117:389-390. [5] Constantopoulos SH, Tsianos EV, Moutsopoulos HM. Pulmonary and gastrointertinal manifestations of Sjögren’s syndrome

1 Introduction Sjogren’s syndrome (SS) is an autoimmune disease that mainly affects the exocrine glands leading to ocular and oral dryness alongside with other systemic manifestations, which are reported to occur in a quarter of patients.[ 1 ] The histological hallmark of SS is the lymphoplasmacytic infiltration of lacrimal and salivary glands. Though the origin of this is unknown, it is believed that an intrinsic activation of glandular epithelial cells leads to an increased rate of apoptosis of these cells and migration of the Ro-60 antigen on the cell surface

References 1. Binard A, Devauchelle-Pensec V, Fautrel B, Jousse S, Youinou P, Saraux A. (2007) Epidemiology of Sjogren’s syndrome: where are we now? Clin Exp Rheumatol. 25:1-4. 2. Fox RI. (2005) Sjogren’s syndrome. Lancet. 366:321-331. 3. Delaleu N, Jonsson R, Koller MM. (2005). Sjogren’s syndrome. Eur J Oral Sci. 113: 101-113. 4. Both T, Dalm VA, van Hagen PM, van Daele PL. (2017) Reviewing primary Sjögren’s syndrome: beyond the dryness - From pathophysiology to diagnosis and treatment. Int J Med Sci. 4(3):191-200. 5. Reksten TR, Lessard CJ, Sivils KL. Genetics

REFERENCES 1. FISHER B.A., BROWN R.M., BOWMAN S.J., BARONE F. A review of salivary gland histopathology in primary Sjögren’s syndrome with a focus on its potential as a clinical trials biomarker. Ann Rheum Dis. 2015; 74 :1645–50. 2. CHERIF E., BOUKHRIS I., HAJJI R., HASSINE LB., AZZABI S., KECHAOU I. et al. Extra-glandular manifestations of primary Sjögren’s syndrome. Eur J Intern Med. 2013; 24 :e119. 3. ATTWOOD W., POSER CM. Neurologic complications of Sjogren’s syndrome. Neurology. 1961; 11 :1034–41. 4. PAVLAKIS P.P., ALEXOPOULOS H., KOSMIDIS M

Introduction Primary Sjögren’s syndrome (pSS) is a chronic inflammatory autoimmune disease, which is most common in middle or elderly women. pSS is characterized by keratoconjunctivitis sicca and xerostomia due to focal lymphocytic infiltration to exocrine glands. The disease was originally considered benign at a stable phase. Now pSS is more thought of as a systemic disorder with the development of autoimmune cytopenia, synovitis, interstitial lung disease, neuropathy, renal disease, and vasculitis. [ 1 ] Activated B lymphocytes are a hallmark of the disease

;50(4):693-699. 11. Kim C.S., Choi Y.D., Choi J.S., Bae E.H., Ma S.K. , Kim S.W. - EBV-positive diffuse large B-cell lymphoma in a patient with primary Sjogren’s syndrome and membranous glomerulonephritis. BMC Nephrol., 2012;13:149. doi: 10.1186/1471-2369-12-149. 12. Tadashi T. - Primary diffuse large B-cell lymphoma of the submandibular gland. Int J Clin Exp Pathol., 2012;5(2):179-181. 13. Freeman C., Berg J.W., Cutler S.J. - Occurrence and prognosis of extranodal lymphomas. Cancer, 1972;29(1):252-260. 14. Choi W.W., Weisenburger D.D., Greiner T.C., Piris M.A., Banham A

review. J Oral Rehabil, 2016;43:388-399. 11. Isidor F, Brondum K, Hansen HJ, Jensen J, Sindet-Pedersen S. Outcome of treatment with implant-retained dental prostheses in patients with Sjogren syndrome. Int J Oral Maxillofac Implants, 1999;14:736-743. 12. Korfage A, Raghoebar GM, Arends S, Meiners PM, Visser A, Kroese GMF et al. Dental Implants in Patients with Sjogren’s Syndrome. Clin Implant Dent Relat Res. 2016;18:937-945. 13. Oczakir C, Balmer S, Mericske-Stern R. Implantprosthodontic treatment for special care patients: a case series study. Int J Prosthodont, 2005

, they evaluate 181 patient samples taken from their Autoimmune Serum Collection, along with their follow-up medical records and history. These patients were suspected of having ANA associated autoimmune rheumatic disease and were positive for ANA but negative for anti-ENA. The oldest available serum for each patient was used for the study. The follow-up time of these cases was up to 10 years (mean 4.75 years). The final diagnoses in this cohort included SLE (n = 44), Sjogren’s syndrome (n = 23), systemic sclerosis (n = 18) and non-ANA related autoimmune rheumatic

tissue disease complicated Klinefelter´s syndrome. Intern med, 1997, 33: 714-717 [37] Fujimoto M, Ikeda K, Nakamuri T, Iwamoto T, Furuta S, Nakajima H. Development of mixed connective tissue disease and Sjogren´s syndrome in a patient with trisomy X. Lupus, 2015, 11: 1217-20 [38] Miyagawa S, Matsura E, Kitamura W et al. Systemic lupus erythematosus and anticardiolipin antibodies in Klinefelter´s syndrome. Lupus, 1995, 4: 236-8 [39] Amstrong RD, McFarlane DG, Panyi GS. Ankylosing spondylarthritis and Klinefelter´s syndrome: does the X chromosome modify disease

References 1. Frederick B Vivino, Vatinee Y Bunya, Gacomina Massaro-Giardo, Chadwick R Joher, Jing He, Julian L Ambrus Jr. Sjögren’s syndrome: an update on disease pathogenesis, clinical manifestations and treatment. Clin Immunol. 2019; 203:81-121. 2. Stewart CM, Berg KM, et al. Salivary dysfunction and quality of life in Sjögren’s syndrome: a critical oral-systemic connection. J Am Dent Assoc.2008;139:291–299. 3. Wei Wei, Syed Sayeed Ahmad, Shuang Chi, Yu Xie, Jiang Li. From molecular mechanism to the etiology of Sjögren syndrome. Curr Phar Des. 2018; 24