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Collagen Drawing
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By Manuel ToledanoManuel Toledano SciProfiles Scilit Preprints.org Google Scholar 1, Manuel Toledano-OsorioManuel Toledano-Osorio SciProfiles Scilit Preprints.org Google Scholar 1, * , Matthias HannigMatthias Hannig SciProfiles Scilit Preprints mona SciProfiles Scilit Preprints.org Google Scholar 1, María T. OsorioMaría T. Osorio SciProfiles Scilit Preprints.org Google Scholar 3 , Franklin García-GodoyFranklin García-Godoy SciProfiles Scilit Preprints.org Google Scholar 4 , Inmaculfile Cabello Sciorg Scholar 5, 6 and Raquel OsorioRaquel Osorio SciProfiles Scilit Preprints.org Google Scholar 1
Submitted: 24 December 2021 / Revised: 2 February 2022 / Accepted: 4 February 2022 / Published: 8 February 2022
Schematic Of Cell-independent Orthogonality Of Collagen Fibril…
This is a narrative review of the literature evaluating the potential efficacy of polymer dentin adhesives doped with zinc compounds. To improve adhesion efficiency mineral regeneration and prevent deterioration A literature search was performed using electronic databases such as PubMed, MEDLINE, DIMDI, and Web of Science. We found literature showing that Zn-doped dentin adhesive improves the protection and remineralization of the resin-dentin interface. Increased biological activity also leads to clogging of the dentinal tubules with crystal precipitation. which helps improve the efficiency of rehabilitation Zinc dentin adhesive increases mineral crystallinity and collagen crosslinking. The main role of zinc in dentin glue is to prevent collagen protein breakdown. We conclude that zinc exerts a protective effect through binding at the junction of collagen-sensitive matrix metalloproteinases (MMPs), which contributes to the stability of the dentin matrix. Zinc may not only act as an MMP inhibitor, but also influence signaling pathways and stimulate metabolic effects in dentin mineralization and remineralization. Zn-doped adhesive prolongs dentin bonding through MMP inhibition. Zn provides a remineralization strategy in demineralized dentin.
Dentin bond formation is achieved by two main strategies. It is based on the use of etching and washing glue or self-etching glue. By using both techniques Gradient diffusion of resin monomers in acid-etched dentin beneath the hybrid layer results in a demineralized collagen matrix phase [ 1 , 2 ] (Fig. 1) This region is sensitive to the proteolytic activity of host or exogenous enzymes such as matrix metalloproteinases (MMPs) [3] found in dentin [4, 5, 6]. MMP was responsible for the higher collagen cleavage in dentin etched with phosphoric acid (PA). However, it inhibited collagen degradation. Gen in the hybrid layer [7] has been observed due to the presence of hydrophobic/hydrophilic resin monomers. This leads to promoting higher protection through self-bonding methods [8].
A common practice in dentistry is to bond with adhesives to irregular dentin surfaces, such as dentin with caries. During clinical treatment Caries-affected dentin must be preserved. Because it can return minerals It becomes a precursor for dentin adhesion [ 9 ]. Finally, demineralization can be caused by attack by acidic bacteria or acidic foods and drinks [ 10 ]. Enzymes of bacterial origin can cause Biodegrades collagen without visible minerals. They are not protected by fibrillar minerals. This is because mineral deposits can fossilize activated MMPs and promote further nucleation. Reincorporation of minerals into the demineralizing matrix from the dentin is therefore a determining factor [11], as it causes inactivation of MMPs and allows continued remineralization. Alternatively, the structural integrity of collagen fibrils may be damaged by acidic conditions. for long-lasting adhesion The dentin adhesive must remineralize and protect the interface between the resin and dentin. The release of active molecules results in the bioactive properties of dentin [12]. Dentin remineralization is the process of restoring the inorganic matrix. It has been used clinically to protect the resin-dentin diffusion zone [13] from caries and hypersensitivity. and as a preventive strategy [14, 15] among the dentin sites that require collagen remineralization strategies. Exposed fibrils include root caries. Cervical erosion and dentin affected by caries [10] Physiologically This process occurs on the surface of demineralized dentin. on these surfaces Broken crystals are regenerated. and various minerals will be absorbed back into The dynamics of dentin regeneration are characterized by high complexity.
Kim et al [10] stated that promoting the growth core center in dentin remineralization is An intact collagen structure is required. In addition to the mineral crystals remaining The highly negatively charged mobile diffusion structure forms in a way that is densely packed with nuclear clusters. The chemical and structural structure for mineral deposits is provided by dentin. Dentin is composed of approximately 18% (w/w) organic matter. Approximately 10% of this content corresponds to non-collagenous proteins, while the other 90% is collagen. Among the non-collagenous proteins, Phosphoproteins are the most representative. The anionic nature of these phosphoproteins may play a role in their biomineralization [16]. Removal of the soluble portion of the organic matrix containing phosphoproteins using various staining agents [ 17] is an important part in the remineralization of demineralized dentin [18, 19]. An insoluble phosphoprotein found in decalcified collagen. It has been speculated that it stimulates remineralization in vitro due to its role as a nuclear reservoir for mineral accumulation [16] .
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In some positions, dentin acts as a scaffold in the process of mineral deposition [20] at the edges of gaps and overlapping zones. Collagen fibrils display nano-sized positively charged regions. It can be used for mineral infiltration or electrical charge attraction [21, 22], which in turn produces higher local energy [23] (Fig. 2). Specific macromolecules are required in situ to act as nuclei of crystal to control the size of crystals Stabilizes the mineral phase and direct crystal orientation [24]. Some demineralized dentin exhibits mineral-inducing properties due to the presence of polyanionic proteins. which is a small part Instead, it binds tightly to the collagen matrix [25]. Mineralization is induced by a set of peptides found in the two collagen-binding sites [20]. Therefore, the natural process of Mineralization is then imitated by biomimetic mineralization. By simulating the natural formation process of mineral crystals on the surface of organic and inorganic matrices without the use of harsh conditions [26], it was found that dentin plays an important role in the tissue repair process even in the absence of cells. Anyway The presence of growth factors, enzymes, and bioactive molecules that bind to the released matrix and are activated through different mechanisms supports the repair process [27]. Therefore, nanometer-sized hydroxyapatite (HAP) then grows and develops at the nuclear region [28]. This causes the formation of the main template of collagen fibrils. which can prevent enzymatic and hydrolytic degradation. It partially recreates the mechanical properties of the tissue. These properties are determined by factors such as the position of the mineral in the organic matrix. mineral density and microstructure [29]
Hard tissues that contain collagen (such as bone and dentin) have mineral phases classified as intrafibrillar apatite or extracellular apatite. The former is stored near or in the gap zone of the collagen molecule and can extend through the microfibril gaps in the fibrils. While the latter is found in the interstitial space that separates collagen fibrils (Fig. 2c and Fig. 3), intravascular apatite appears to play an important role in the mechanical properties of mineralized tissues [28, 30. ]
The presence of zinc is known to maintain the efficiency of dentin adhesion [14, 32] and increase the mineral absorption of hard tissues [33, 34]. Zinc has not only been shown to be a matrix inhibitor. metalloproteinase (MMP) that reduces MMP-mediated collagen degradation [35], but is also a stimulator of mineral precipitation in hard tissues [36, 37] and an inhibitor of tissue demineralization. Teeth [38] – Zinc affects mineral metabolism in hard tissues. which affects signal transduction pathways [32, 37]. Zinc improves the adhesion between materials and tissues. It causes some biological reactions at the interface [39] when zinc is included in the adhesive composition. This increases the mineral content in some demineralized fiber. [9] Zinc has anti-inflammatory and anti-inflammatory properties.