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.
Highlights
IntroductionPeriodontitis is a chronic disease which affects tooth supporting tissue (gingiva, alveolar bone, periodontal ligament) causing its gradual degradation to the point where masticatory function of the teeth (or their resilience to occlusal forces) is permanently lost
Periodontitis is a chronic disease which affects tooth supporting tissue causing its gradual degradation to the point where masticatory function of the teeth is permanently lost
This is further accompanied by the differences in expression profiles of enzymes involved in biosynthesis and modification of heparan sulfate (HS) GAG side chains (EXTs, NDSTs, and heparanase 1 (HPSE1)), which are comparable to a certain degree with those described in other chronic degenerative diseases such as osteoarthritis (Chanalaris et al, 2019)
Summary
Periodontitis is a chronic disease which affects tooth supporting tissue (gingiva, alveolar bone, periodontal ligament) causing its gradual degradation to the point where masticatory function of the teeth (or their resilience to occlusal forces) is permanently lost. Syndecans (Sdcs) belong to a four-member family (Sdc1-4) of cell surface heparan sulfate proteoglycans (HSPGs). With regard to functional versatility of Sdcs and, their roles in regulation of inflammatory response, there are several important aspects which need to be considered, some of which are more exclusive to Sdcs, and some of which can be broadly associated to HSPGs. In adult tissues, Sdcs are widely distributed, the expression domains of individual Sdcs do not completely overlap – Sdc is predominantly expressed in stratified and simple epithelia, Sdc in connective tissue and endothelial cells, Sdc in neural tissue, whereas Sdc is expressed ubiquitously. Studies on Sdc1−/− and Sdc4−/− single knockout mice have revealed that these animals develop normally, meaning that Sdc and Sdc are functionally redundant in organogenesis. When adult Sdc1−/− or Sdc4−/− knockouts are challenged by diseaseinstigating agents they, depending on the type of challenge, display impaired regulation of various segments of inflammatory response – from formation of chemokine/cytokine gradients and leukocyte recruitment, to ECM remodeling in resolution of inflammatory response (Floer et al, 2010; Teng et al, 2012)
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