Paediatric Dentist, Dental Section, Department of Surgery, Faculty of Health Sciences, Medical College, The Aga Khan University Karachi, Karachi, Pakistan
*Corresponding Author: Saleha Shah, Paediatric Dentist, Dental Section, Department of Surgery, Faculty of Health Sciences, Medical College, The Aga Khan University Karachi, Karachi, Pakistan.
Received: March 30, 2018; Published: May 21, 2018
Citation: Saleha Shah. “Statherin-Role in Biomimetic Early Caries Management”. Acta Scientific Dental Sciences 2.6 (2018).
Dental enamel is a highly mineralized acellular tissue comprising of individual crystallites which are larger and more oriented than other mineralized tissues of the body. Morphologically dental enamel is formed by matrix-mediated biomineralization. Precipitation of enamel crystallites from a supersaturated solution within a well-delineated biological compartment lead to enamel lattice crystallization. The enamel crystal comprises of carbonated apatite which dissolves by organic acids (lactic and acetic) produced by the cellular action of plaque bacteria on dietary carbohydrates. Demineralization occurs when pH levels fall to 5.7. Salivary proteins slow down enamel demineralization by inhibiting calcium hydroxyapatite (HA) demineralization. Remineralization allows loss of calcium, phosphate, and fluoride ions to be replaced by fluorapatite crystals which are more resistant to acid dissolution and are substantially larger than the original crystals, thereby providing a more favorable (smaller) surface to volume ratio. Hence larger apatite crystals in remineralized enamel are more resistant to enamel breakdown by the resident organic acids. Statherin (StN43), a 43 residue phosphorylated salivary protein with primary sequence similarities to osteopontin and caseins, binds calcium and HA. The identification of the minimum length of the functional domain of the statherin molecule augments the understanding of cariostatic functions by measuring the efficacy of peptides of progressively shorter length (i.e. containing only the N‐terminal 21 (StN21), 15 (StN15), 10 (StN10), or 5 (StN5) residues) to reduce HA demineralization rates (RDHA). The mechanism by which statherin-like peptides reduce Hydroxyapatite demineralization rates may be associated with their binding to HA surfaces. Overview of previously published binding energies of statherin to HA also suggest that statherin-like peptides containing 21 and 15 N-terminal residues or more are required for binding suggesting a link between binding and demineralization reduction. The short chain statherin N-Terminal residues do not exert a cariostatic effect owing to the inability to undergo helical changes on adsorption to hydroxyapatite crystals. Different remineralization strategies using fluoride, electrolytic deposition, hydroxyapatite nanoparticles, amorphous calcium phosphates, and hydrogen peroxide have been developed recently and synthetic peptides are being employed in biomimetic hard tissue remineralization processes. Further in vivo studies are needed to develop salivary biomimetic peptides for anti-caries applications.
Keywords: Statherin; Biomimetic; Hydroxyapatite
Copyright: © 2018 Saleha Shah. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.