Gingival Wound Healing

Ph, Smith; Cáceres, Mónica; Martínez, Constanza; Oyarzún, Alejandro; Martı́nez, Jorge

doi:10.1177/0022034514563750

Cited by 63 publications

(38 citation statements)

References 58 publications

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“…TIMP-1, COL1A1, and COL3A1 mainly participate in the proliferative and remodeling phases of periodontal wound healing. TIMP functions as a matrix metalloproteinase (MMP) inhibitor, and plays an important role in the remodeling phase by inhibiting extracellular matrix and collagen breakdown 46 . Collagen is a basic component of the periodontium.…”

Section: Discussionmentioning

confidence: 99%

Autologous platelet-rich fibrin stimulates canine periodontal regeneration

Kornsuthisopon

Pirarat

Osathanon

et al. 2020

Sci Rep

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Platelet-rich fibrin (PRF) provides a scaffold for cell migration and growth factors for promoting wound healing and tissue regeneration. Here, we report using PRF in periodontal healing after open flap debridement (OFD) in canine periodontitis. A split-mouth design was performed in twenty dogs. Forty periodontitis surgical sites were randomly categorized into 2 groups; OFD alone and OFD with PRF treatment. Clinical parameters of periodontal pocket depth, gingival index, and the cemento-enamel junction-alveolar bone levels/root length ratio were improved in the OFD + PRF group. The OFD + pRf group also demonstrated a dramatically decreased inflammatory score compared with the OFD group. Collagen accumulation was improved in the OFD + PRF group at later time points compared with baseline. PRF application also significantly reduced inflammatory cytokine expression (TNFA and IL1B), and promoted the expression of collagen production-related genes (COL1A1, COL3A1, and TIMP1) and growth factors (PDGFB, TGFB1, and VEGFA). These findings suggest that PRF combined with OFD provides a new strategy to enhance the overall improvement of canine periodontitis treatment outcomes, especially in terms of inflammation and soft tissue healing. Therefore, PRF use in treating periodontitis could play an important role as a regenerative material to improve canine periodontitis treatment.

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Section: Discussionmentioning

confidence: 99%

Autologous platelet-rich fibrin stimulates canine periodontal regeneration

Kornsuthisopon

Pirarat

Osathanon

et al. 2020

Sci Rep

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“…In this study, two cell types, GFs and DPMCs, originating from different anatomical sites and having distinctive roles in regeneration and healing of damaged periodontal (Sisman, Aksoy, Yalcin, & Karaoz, 2016;Smith, Caceres, Martinez, Oyarzun, & Martinez, 2015) and dental pulp tissues (Patil et al, 2014;Rodas-Junco, Canul-Chan, Rojas-Herrera, De-la-Pena, & Nic-Can, 2017;Sonoyama et al, 2008) were assessed for their potential to regenerate gingival connective tissues (lamina propria) (Chiquet et al, 2015) and dental pulp (Huang, Gronthos, & Shi, 2009) in vitro. Such assessment is seen as necessary in predicting a success of restoration of deciduous teeth or traumatized tissues and the formation of tertiary dentin as a protective barrier for dental pulp.…”

Section: Discussionmentioning

confidence: 99%

Assessing the effect of triethyleneglycol dimethacrylate on tissue repair in 3D organotypic cultures

Tigani

Škrtić

Valerio

et al. 2018

J of Applied Toxicology

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Leachables from dental restoratives induce toxicity in gingival and pulp tissues and affect tissue regeneration/healing. Appropriate testing of these materials requires a platform that mimics the in vivo environment and allows the architectural self-assembly of cells into tissue constructs. In this study, we employ a new 3D model to assess the impact of triethyleneglycol dimethacrylate (TEGDMA) on early organization and advanced recruitment/accumulation of immortalized mouse gingival fibroblasts (GFs) and dental papilla mesenchymal cells (DPMCs) in extracellular matrix. We hypothesize that TEGDMA (1) interferes with the developmental architecture of GFs and DPMCs, and (2) inhibits the deposition of mineral. To test these hypotheses, GFs and DPMCs were incubated with the soluble TEGDMA at concentrations (0-2.5) mmol/L. Diameter and thickness of the constructs were determined by microscopic analysis. Cell differentiation was assessed by immunocytochemistry and the secreted mineral detected by alizarin-red staining. TEGDMA interfered with the development of GFs and/or DPMCs microtissues in a dose-dependent manner by inhibiting growth of inter-spherical cell layers and decreasing spheroid size (four to six times). At low/moderate TEGDMA levels, GFs organoids retained their structures while reducing thickness up to 21%. In contrast, at low TEGDMA doses, architecture of DPMC organoids was altered and thickness decreased almost twofold. Overall, developmental ability of TEGDMA-exposed GFs and DPMCs depended on TEGDMA level. GFs constructs were more resistant to structural modifications. The employed 3D platform was proven as an efficient tool for quantifying the effects of leachables on tissue repair capacities of gingiva and dental pulp.

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“…If expression of these mediators persists, however, inflammation becomes sustained in the pulp, creating uncontrolled cell proliferation, angiogenesis, and collagen synthesis. 3,74 On the converse, another study reported increased wound healing in the absence of neutrophils. 75 These reports imply that at least under sterile conditions neutrophils are either not essential or perhaps detrimental for wound repair.…”

Section: Early Phase Of Wound Healingmentioning

confidence: 99%

Wound repair: role of immune–epithelial interactions

Leoni¹,

Neumann²,

et al. 2015

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The epithelium serves as a highly selective barrier at mucosal surfaces. Upon injury, epithelial wound closure is orchestrated by a series of events that emanate from the epithelium itself as well as by the temporal recruitment of immune cells into the wound bed. Epithelial cells adjoining the wound flatten out, migrate, and proliferate to rapidly cover denuded surfaces and re-establish mucosal homeostasis. This process is highly regulated by proteins and lipids, proresolving mediators such as Annexin A1 protein and resolvins released into the epithelial milieu by the epithelium itself and infiltrating innate immune cells including neutrophils and macrophages. Failure to achieve these finely tuned processes is observed in chronic inflammatory diseases that are associated with non-healing wounds. An improved understanding of mechanisms that mediate repair is important in the development of therapeutics aimed to promote mucosal wound repair.

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Gingival Wound Healing

Cited by 63 publications

References 58 publications

Autologous platelet-rich fibrin stimulates canine periodontal regeneration

Autologous platelet-rich fibrin stimulates canine periodontal regeneration

Assessing the effect of triethyleneglycol dimethacrylate on tissue repair in 3D organotypic cultures

Wound repair: role of immune–epithelial interactions

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