Effect of proteoglycans at interfaces as related to location, architecture, and mechanical cues

Abstract

IntroductionCovalently bound functional GAGs orchestrate tissue mechanics through time-dependent characteristics. ObjectiveThe role of specific glycosaminoglycans (GAGs) at the ligament–cementum and cementum–dentin interfaces within a human periodontal complex were examined. Matrix swelling and resistance to compression under health and modeled diseased states was investigated. Materials and methodsThe presence of keratin sulfate (KS) and chondroitin sulfate (CS) GAGs at the ligament–cementum and cementum–dentin interfaces in human molars (N=5) was illustrated by using enzymes, atomic force microscopy (AFM), and AFM-based nanoindentation. The change in physical characteristics of modeled diseased states through sequential digestion of keratin sulfate (KS) and chondroitin sulfate (CS) GAGs was investigated. One-way ANOVA tests with P<0.05 were performed to determine significant differences between groups. Additionally, the presence of mineral within the seemingly hygroscopic interfaces was investigated using transmission electron microscopy. ResultsImmunohistochemistry (N=3) indicated presence of biglycan and fibromodulin small leucine rich proteoglycans at the interfaces. Digestion of matrices with enzymes confirmed the presence of KS and CS GAGs at the interfaces by illustrating a change in tissue architecture and mechanics. A significant increase in height (nm), decrease in elastic modulus (GPa), and tissue deformation rate (nm/s) of the PDL-C attachment site (215±63–424±94nm; 1.5±0.7–0.4±0.2GPa; 21±7–48±22nm/s), and cementum–dentin interface (122±69–360±159nm; 2.9±1.3–0.7±0.3GPa; 18±4–30±6nm/s) was observed. ConclusionsThe sequential removal of GAGs indicated loss in intricate structural hierarchy of hygroscopic interfaces. From a mechanics perspective, GAGs provide tissue recovery/resilience. The results of this study provide insights into the role of GAGs toward conserved tooth movement in the socket in response to mechanical loads, and modulation of potentially deleterious strain at tissue interfaces.