Background: The gradual deterioration of articular cartilage was thought to be the central event in osteoarthritis (OA), but recent studies demonstrated importance of low-grade synovitis in progression of OA. Syndecan (SDC) family of membrane proteoglicans is known to be involved in regulation of inflammation but there is a limited evidence considering the role of syndecans in OA synovitis. The aim of my study was to investigate hip OA synovial membrane expression patterns (intimal and subintimal) of syndecan-1 (SDC1), syndecan-2 (SDC2), and syndecan-4 (SDC4) as well as exostosins (EXT) and sulfotransferases (NDST) (enzymes involved in polimerisation and modification of syndecans’ heparan-sulfat chains). Methods: surgically collected synovial membrane samples of patients with OA were divided into two groups according to their Krenn synovitis score grading. Immunohistochemical expression of SDC1, SDC2, SDC4, EXT1, EXT2, NDST1, and NDST2 in synovial intima and subintima was then analyzed and compared with control group (patients with femoral neck fracture, without OA). Additionally, I investigated the association of the expression of these molecules with clinical and radiological indicators of hip osteoarthritis severity. Results: according to my study, immunoexpression of SDC1, NDST1 and EXT2 is significantly increased in intimal cells of OA synovial membrane in patients with lower histological synovitis score, and SDC4 in patients with higher synovitis score, in comparison with non-OA controls. Difference in expression of SDC2 among OA and non-OA group is insignificant. Contrary, clinical and radiological indicators of OA severity correlate best with syndecan-2 expression, of all investigated molecules, both in intimal and subintimal layers of synovial membrane. Conclusions: SDC1, SDC4, NDST1 and EXT2 seem to be involved as inflammation moderators in low-grade OA synovitis. The interpretation of the results is difficult due to the delicate interactions between the tested molecules and their potential pro- and anti-inflammatory effects. However, I am of the opinion that the results of my study prove that syndecan related inflammation pathways should be further investigated as potential markers of disease progression and therapeutic goal in OA.