Sclerostin levels in blood and saliva in patients with scleroderma

Systemic sclerosis (SSc) is a chronic autoimmune inflammatory disease characterized by extensive fibrosis of skin and visceral organs. Although the exact etiology of the SSc could not be clarified, genetic and environmental factors account for its etiology. The exact pathogenesis is unknown. The disease is thought to result from the factors affecting collagen synthesis, capillary changes and interactions between immunological mechanism. It is accompanied by significant psycho-social problems since it predominantly occurs in young women and affects the quality of life of patients. Skin changes and contractures in SSc substantially affect morbidity while visceral organ involvement substantially affects morbidity and mortality. The sclerostin molecule is a glycopeptide product of the SOST gene and is primarily expresssed by osteocytes. It is also expressed by renal and vascular cells. Sclerostin acts as an inhibitor in the Wnt signaling pathway. Wnt signaling pathway is known to play a role in the development of embryonic stem cells, bone metabolism and normal homeostasis in adults. Our study aims to investigate and determine the sclerostin level in blood and saliva of SSc patients and to compare their levels with those of healthy volunteers. In the literature, a sufficient number of studies that demonstrate the association between SSc and sclerostin are not available. Sclerostin is thought to be able to play o role in the pathogenesis of SSc. In our study, a group of 35 SSc patients was compared to a group of 35 healthy volunteers. The level of sclerostin in blood and saliva of the SSc group was found significantly higher than the control group (p<0,001). In conclusion, the level of sclerostin increases in SSc that is a chronic autoimmune disease. Sclerostin, an inhibitor of Wnt signaling pathway, does not have a known role in the pathogenesis of SSc. Further studies involving more participants are needed in order to verify the findings of our study. Key words: Systemic sclerosis, Sclerostin, Wnt signaling pathway