Browsing by Subject "Repair"

Now showing 1 - 7 of 7
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    Bioactivity of Dental Restorative Materials: FDI Policy Statement
    (Elsevier, 2023) Schmalz, Gottfried; Hickel, Reinhard; Price, Richard Bengt; Platt, Jeffrey A.; Biomedical Sciences and Comprehensive Care, School of Dentistry
    The term bioactivity is being increasingly used in medicine and dentistry. Due to its positive connotation, it is frequently utilised for advertising dental restorative materials. However, there is confusion about what the term means, and concerns have been raised about its potential overuse. Therefore, FDI decided to publish a Policy Statement about the bioactivity of dental restorative materials to clarify the term and provide some caveats for its use in advertising. Background information for this Policy Statement was taken from the current literature, mainly from the PubMed database and the internet. Bioactive restorative materials should have beneficial/desired effects. These effects should be local, intended, and nontoxic and should not interfere with a material's principal purpose, namely dental tissue replacement. Three mechanisms for the bioactivity of such materials have been identified: purely biological, mixed biological/chemical, or strictly chemical. Therefore, when the term bioactivity is used in an advertisement or in a description of a dental restorative material, scientific evidence (in vitro or in situ, and preferably in clinical studies) should be provided describing the mechanism of action, the duration of the effect (especially for materials releasing antibacterial substances), and the lack of significant adverse biological side effects (including the development and spread of antimicrobial resistance). Finally, it should be documented that the prime purpose, for instance, to be used to rebuild the form and function of lost tooth substance or lost teeth, is not impaired, as demonstrated by data from in vitro and clinical studies. The use of the term bioactive dental restorative material in material advertisement/information should be restricted to materials that fulfil all the requirements as described in the FDI Policy Statement.
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    Coordinated induction of cell survival signaling in the inflamed microenvironment of the prostate
    (Wiley, 2016-06) McIlwain, David W.; Zoetemelk, Marloes; Myers, Jason D.; Edwards, Marshé T.; Snider, Brandy M.; Jerde, Travis J.; Pharmacology and Toxicology, School of Medicine
    PURPOSE: Both prostate cancer and benign prostatic hyperplasia are associated with inflammatory microenvironments. Inflammation is damaging to tissues, but it is unclear how the inflammatory microenvironment protects specialized epithelial cells that function to proliferate and repair the tissue. The objective of this study is to characterize the cell death and cell survival response of the prostatic epithelium in response to inflammation. METHODS: We assessed induction of cell death (TNF, TRAIL, TWEAK, FasL) and cell survival factors (IGFs, hedgehogs, IL-6, FGFs, and TGFs) in inflamed and control mouse prostates by ELISA. Cell death mechanisms were determined by immunoblotting and immunofluorescence for cleavage of caspases and TUNEL. Survival pathway activation was assessed by immunoblotting and immunofluorescence for Mcl-1, Bcl-2, Bcl-XL, and survivin. Autophagy was determined by immunoblotting and immunofluorescence for free and membrane associated light chain 3 (LC-3). RESULTS: Cleavage of all four caspases was significantly increased during the first 2 days of inflammation, and survival protein expression was substantially increased subsequently, maximizing at 3 days. By 5 days of inflammation, 50% of prostatic epithelial cells expressed survivin. Autophagy was also evident during the recovery phase (3 days). Finally, immunofluorescent staining of human specimens indicates strong activation of survival proteins juxtaposed to inflammation in inflamed prostate specimens. CONCLUSIONS: The prostate responds to deleterious inflammation with induction of cell survival mechanisms, most notably survivin and autophagy, demonstrating a coordinated induction of survival factors that protects and expands a specialized set of prostatic epithelial cells as part of the repair and recovery process during inflammation.
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    Effect of surface treatments on microtensile bond strength of repaired aged silorane resin composite
    (2010) Palasuk, Jadesada; Platt, Jeffrey A., 1958-; Levon, John A.; Brown, David T.; Hovijitra, Suteera, 1944-; Cho, Sopanis D.
    Background: A silorane based resin composite, Filtek LS restorative, has been introduced to overcome the polymerization shrinkage of the methacrylate based resin composite. The repair of resin composite may hold clinical advantages. Currently, there is no available information regarding the repair potential of silorane resin composite with either silorane or methacrylate based resin composite. Objectives: The purpose of this study was to compare the repaired microtensile bond strength of aged silorane resin composite using different surface treatments and either silorane or methacrylate based resin composite. Methods: One hundred and eight silorane resin composite blocks (Filtek LS) were fabricated and aged by thermocycling between 8oC and 48oC (5000 cycles). A control (solid resin composite) and four surface treatment groups (no treatment, acid treatment, aluminum oxide sandblasting and diamond bur abrasion) were tested. Each treatment group was randomly divided in half and repaired with either silorane resin composite (LS adhesive) or methacrylate based resin composite (Filtek Z250/Single Bond Plus). Specimens were 12 blocks and 108 beams per group. After 24 hours in 37oC distilled water, microtensile bond strength testing was performed using a non-trimming technique. Fracture surfaces were examined using an optical microscopy (20X) to determine failure mode. Data was analyzed using Weibull-distribution survival analysis. Results: Aluminum oxide sandblasting followed by silorane or methacrylate based resin composite and acid treatment with methacrylate based resin composite provided insignificant differences from the control (p>0.05). All other groups were significantly lower than the control. Failure was primarily adhesive in all groups. Conclusion: Aluminum oxide sandblasting produced comparable microtensile bond strength compared to the cohesive strength of silorane resin composite. After aluminum oxide sandblasting, aged silorane resin composite can be repaired with either silorane resin composite with LS system adhesive or methacrylate based resin composite with methacrylate based dentin adhesive.
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    Interaction between Schwann cells and other cells during repair of peripheral nerve injury
    (Wolters Kluwer, 2021-01) Qu, Wen-Rui; Zhu, Zhe; Liu, Jun; Song, De-Biao; Tian, Heng; Chen, Bing-Peng; Li, Rui; Deng, Ling-Xiao; Neurological Surgery, School of Medicine
    Peripheral nerve injury (PNI) is common and, unlike damage to the central nervous system injured nerves can effectively regenerate depending on the location and severity of injury. Peripheral myelinating glia, Schwann cells (SCs), interact with various cells in and around the injury site and are important for debris elimination, repair, and nerve regeneration. Following PNI, Wallerian degeneration of the distal stump is rapidly initiated by degeneration of damaged axons followed by morphologic changes in SCs and the recruitment of circulating macrophages. Interaction with fibroblasts from the injured nerve microenvironment also plays a role in nerve repair. The replication and migration of injury-induced dedifferentiated SCs are also important in repairing the nerve. In particular, SC migration stimulates axonal regeneration and subsequent myelination of regenerated nerve fibers. This mobility increases SC interactions with other cells in the nerve and the exogenous environment, which influence SC behavior post-injury. Following PNI, SCs directly and indirectly interact with other SCs, fibroblasts, and macrophages. In addition, the inter- and intracellular mechanisms that underlie morphological and functional changes in SCs following PNI still require further research to explain known phenomena and less understood cell-specific roles in the repair of the injured peripheral nerve. This review provides a basic assessment of SC function post-PNI, as well as a more comprehensive evaluation of the literature concerning the SC interactions with macrophages and fibroblasts that can influence SC behavior and, ultimately, repair of the injured nerve.
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    Longevity of Crown Margin Repairs Using Glass Ionomer: A Retrospective Study
    (2020) Watson, Justin I.; Cook, N. Blaine; Thyvalikakath, Thankam; Diefenderfer, Kim E.; Capin, Oriana
    Objectives: Repair of crown margins may extend the functional life of existing crowns. However, the longevity of such treatment is unknown. This study determined the survival time of crown margin repairs (CMR) with glass-ionomer (GI) and resin-modified glass-ionomer cements. Methods: We queried axiUm (Exan Group, Coquitlam, BC, Canada) database for permanent teeth that underwent CMR in the Graduate Operative Dentistry Clinic, Indiana University School of Dentistry (IUSD), Indianapolis, Ind., USA, from January 1, 2006 through January 1, 2018. Since there is no CDT code for the CMR procedure, CDT codes for resin-composite and GI restorations (D23XX) were queried; these patients also had treatment notes that indicated CMR. The final data set included patient ID, birth date, gender, dates of treatments, CDT codes, tooth type, tooth surface and existing findings. Two examiners developed guidelines for record review and manually reviewed the clinical notes of patient records to confirm CMR. Only records that were confirmed with the presence of CMR were retained in the final dataset for survival analysis. Survival time was calculated by Kaplan-Meier statistics and a Cox Proportional Hazards model was performed to assess the influence of selected variables (p < 0.05). Results: 214 teeth (115 patients) with CMR were evaluated. Patient average age was 69.4  11.7 years old. Posterior teeth accounted for 78.5 percent (n = 168) of teeth treated. CMRs using GI had a projected 5-year survival rate of 62.9 percent (K-M Analysis) and an 8.9 percent annual failure rate. Cox Proportional Hazards Regression analysis revealed that none of the factors examined (age, gender, tooth type) affected time to failure. Conclusion: CMRs may extend the longevity of crowns with defective margins. Larger EHR studies or case control studies are needed to investigate other variables, such as the caries risk status or the severity of defects that may affect the survival rate of CMRs.
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    PPAR-γ in Macrophages Limits Pulmonary Inflammation and Promotes Host Recovery Following Respiratory Viral Infection
    (American Society for Microbiology, 2019-05-01) Huang, Su; Zhu, Bibo; Cheon, In Su; Goplen, Nick P.; Jiang, Li; Zhang, Ruixuan; Peebles, R. Stokes; Mack, Matthias; Kaplan, Mark H.; Limper, Andrew H.; Sun, Jie; Pediatrics, School of Medicine
    Alveolar macrophages (AM) play pivotal roles in modulating host defense, pulmonary inflammation, and tissue injury following respiratory viral infections. However, the transcriptional regulation of AM function during respiratory viral infections is still largely undefined. Here we have screened the expression of 84 transcription factors in AM in response to influenza A virus (IAV) infection. We found that the transcription factor PPAR-γ was downregulated following IAV infection in AM through type I interferon (IFN)-dependent signaling. PPAR-γ expression in AM was critical for the suppression of exaggerated antiviral and inflammatory responses of AM following IAV and respiratory syncytial virus (RSV) infections. Myeloid PPAR-γ deficiency resulted in enhanced host morbidity and increased pulmonary inflammation following both IAV and RSV infections, suggesting that macrophage PPAR-γ is vital for restricting severe host disease development. Using approaches to selectively deplete recruiting monocytes, we demonstrate that PPAR-γ expression in resident AM is likely important in regulating host disease development. Furthermore, we show that PPAR-γ was critical for the expression of wound healing genes in AM. As such, myeloid PPAR-γ deficiency resulted in impaired inflammation resolution and defective tissue repair following IAV infection. Our data suggest a critical role of PPAR-γ expression in lung macrophages in the modulation of pulmonary inflammation, the development of acute host diseases, and the proper restoration of tissue homeostasis following respiratory viral infections.IMPORTANCE Respiratory viral infections, like IAV and respiratory syncytial virus (RSV) infections, impose great challenges to public health. Alveolar macrophages (AM) are lung-resident immune cells that play important roles in protecting the host against IAV and RSV infections. However, the underlying molecular mechanisms by which AM modulate host inflammation, disease development, and tissue recovery are not very well understood. Here we identify that PPAR-γ expression in AM is crucial to suppress pulmonary inflammation and diseases and to promote fast host recovery from IAV and RSV infections. Our data suggest that targeting macrophage PPAR-γ may be a promising therapeutic option in the future to suppress acute inflammation and simultaneously promote recovery from severe diseases associated with respiratory viral infections.
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    A Qualitative Engineering Analysis of Occlusion Effects on Mandibular Fracture Repair Mechanics
    (SAGE-Hindawi, 2011-08) Katona, Thomas R.
    Objectives. The purpose of this analytical study was to examine and critique the engineering foundations of commonly accepted biomechanical principles of mandible fracture repair. Materials and Methods. Basic principles of static equilibrium were applied to intact and plated mandibles, but instead of the traditional lever forces, the mandibles were subjected to more realistic occlusal forces. Results. These loading conditions produced stress distributions within the intact mandible that were very different and more complex than the customary lever-based gradient. The analyses also demonstrated the entirely different mechanical environments within intact and plated mandibles. Conclusions. Because the loading and geometry of the lever-idealized mandible is incomplete, the associated widely accepted bone stress distribution (tension on top and compression on the bottom) should not be assumed. Furthermore, the stress gradients within the bone of an intact mandible should not be extrapolated to the mechanical environment within the plated regions of a fractured mandible.