Syndecans and enzymes for heparan sulfate biosynthesis and modification differentially correlate with presence of inflammatory infiltrate in periodontitis

Abstract

Periodontitis is a common degenerative disease initiated by the bacteria in subgingival biofilm. The exposure to bacterial biofilm triggers host inflammatory response whose dysregulation is ultimately responsible for the destruction of hard and soft periodontal tissues resulting in tooth loss. To date, significant effort has been invested in the research of the involvement of host cells and inflammatory mediators in regulation of inflammatory response in periodontitis. Syndecans (Sdcs) belong to a four-member family of heparan sulfate proteoglycans (HSPGs). Sdcs are compound molecules comprised of the core protein to which several heparan sulfate (HS) glycosaminoglycan (GAG) chains are attached. The role of Sdcs in pathogenesis of periodontitis is poorly investigated despite the numerous reports from experimental studies about the critical involvement of these factors in modulation of various aspects of inflammatory response, such as the formation of inflammatory mediators gradients, leukocyte recruitment and extracellular matrix remodeling in resolution of inflammation. Most of these functions of Sdcs are HS-related and, thus, dependent upon the structure of HS. This, in turn, is determined by the combinatorial action of enzymes for biosynthesis and modification of HS such as exostosis (EXTs), sulfotransferases (NDSTs), and heparanase 1 (HPSE1). The data presented in this study clearly indicate that some Sdcs display different expression profiles in healthy and diseased periodontal tissue. Additionally, the differences in expression profiles of HS GAG biosynthesis and modification enzymes (EXTs, NDSTs, and HPSE1) in healthy and diseased periodontal tissue imply that changes in HS GAG content and structure might also take place during periodontitis. Most notably, expression profiles of Sdcs, EXTs, NDSTs, and HPSE1 differentially correlate with the presence of inflammatory infiltrate in healthy and diseased periodontal tissue, which might imply that these factors could also be involved in modulation of inflammatory response in periodontitis.