Abstract:Corrosion resistance is a key feature of titanium biocompatibility. However, Ti surfaces exposed to critical environments (such as, chronic infection and inflammation) can undergo corrosion processes in vivo, leading to an unfavorable biological response and clinical failure, which remains poorly explored. In this study, we characterized an experimental model to replicate the surface features of Ti corrosion process observed within in vivo failures, and the cellular, tissue and molecular events associated with… Show more
“…Human macrophages develop a specific response to Ti particles. Upon contact, M1 exhibits increased production of pro-inflammatory cytokines, chemokines and growth factors, but a decreased phagocytic activity, while M2 macrophages have been suggested to mediate particle uptake ( 78 ). This could be related to the absence of MNGC or frustrated phagocytosis in the vicinity of titanium particles in granulation tissue harvested from peri-implantitis cases, as shown in a recent article, even though there was a significantly higher expression of CD68 ( 79 ).…”
Section: Stages Of Osseointegration Failurementioning
In the field of biomaterials, an endosseous implant is now recognized as an osteoimmunomodulatory but not bioinert biomaterial. Scientific advances in bone cell biology and in immunology have revealed a close relationship between the bone and immune systems resulting in a field of science called osteoimmunology. These discoveries have allowed for a novel interpretation of osseointegration as representing an osteoimmune reaction rather than a classic bone healing response, in which the activation state of macrophages ((M1–M2 polarization) appears to play a critical role. Through this viewpoint, the immune system is responsible for isolating the implant biomaterial foreign body by forming bone around the oral implant effectively shielding off the implant from the host bone system, i.e. osseointegration becomes a continuous and dynamic host defense reaction. At the same time, this has led to the proposal of a new model of osseointegration, the foreign body equilibrium (FBE). In addition, as an oral wound, the soft tissues are involved with all their innate immune characteristics. When implant integration is viewed as an osteoimmune reaction, this has implications for how marginal bone is regulated. For example, while bacteria are constitutive components of the soft tissue sulcus, if the inflammatory front and immune reaction is at some distance from the marginal bone, an equilibrium is established. If however, this inflammation approaches the marginal bone, an immune osteoclastic reaction occurs and marginal bone is removed. A number of clinical scenarios can be envisioned whereby the osteoimmune equilibrium is disturbed and marginal bone loss occurs, such as complications of aseptic nature and the synergistic activation of pro-inflammatory pathways (implant/wear debris, DAMPs, and PAMPs). Understanding that an implant is a foreign body and that the host reacts osteoimmunologically to shield off the implant allows for a distinction to be drawn between osteoimmunological conditions and peri-implant bone loss. This review will examine dental implant placement as an osteoimmune reaction and its implications for marginal bone loss.
“…Human macrophages develop a specific response to Ti particles. Upon contact, M1 exhibits increased production of pro-inflammatory cytokines, chemokines and growth factors, but a decreased phagocytic activity, while M2 macrophages have been suggested to mediate particle uptake ( 78 ). This could be related to the absence of MNGC or frustrated phagocytosis in the vicinity of titanium particles in granulation tissue harvested from peri-implantitis cases, as shown in a recent article, even though there was a significantly higher expression of CD68 ( 79 ).…”
Section: Stages Of Osseointegration Failurementioning
In the field of biomaterials, an endosseous implant is now recognized as an osteoimmunomodulatory but not bioinert biomaterial. Scientific advances in bone cell biology and in immunology have revealed a close relationship between the bone and immune systems resulting in a field of science called osteoimmunology. These discoveries have allowed for a novel interpretation of osseointegration as representing an osteoimmune reaction rather than a classic bone healing response, in which the activation state of macrophages ((M1–M2 polarization) appears to play a critical role. Through this viewpoint, the immune system is responsible for isolating the implant biomaterial foreign body by forming bone around the oral implant effectively shielding off the implant from the host bone system, i.e. osseointegration becomes a continuous and dynamic host defense reaction. At the same time, this has led to the proposal of a new model of osseointegration, the foreign body equilibrium (FBE). In addition, as an oral wound, the soft tissues are involved with all their innate immune characteristics. When implant integration is viewed as an osteoimmune reaction, this has implications for how marginal bone is regulated. For example, while bacteria are constitutive components of the soft tissue sulcus, if the inflammatory front and immune reaction is at some distance from the marginal bone, an equilibrium is established. If however, this inflammation approaches the marginal bone, an immune osteoclastic reaction occurs and marginal bone is removed. A number of clinical scenarios can be envisioned whereby the osteoimmune equilibrium is disturbed and marginal bone loss occurs, such as complications of aseptic nature and the synergistic activation of pro-inflammatory pathways (implant/wear debris, DAMPs, and PAMPs). Understanding that an implant is a foreign body and that the host reacts osteoimmunologically to shield off the implant allows for a distinction to be drawn between osteoimmunological conditions and peri-implant bone loss. This review will examine dental implant placement as an osteoimmune reaction and its implications for marginal bone loss.
“…The bacteria were counted using ImageJ software (version 1.53, MD, Bethesda, USA), and the plates without bacteria were qualitatively analyzed [ 18 ].…”
The present investigation was undertaken to evaluate the topographical and ultrastructural architecture of titanium plates coated with polylactic co-glycolic acid (PLGA), chitosan (CH), and/or meropenem (MEM) with or without Staphylococcus aureus (SA) or Pseudomonas aeruginosa (PA) bacteria. Single-hole segments of 0.4 mm thick, low-profile titanium plates were spray coated using an airbrush with polymeric carriers (PLGA or CH) loaded with MEM, in addition to the negative control group (uncoated titanium plates). The coated plates and the negative control group were subjected to bacterial biofilms through a cultivation process while being slowly stirred at 20 rpm for 24 h. The samples were fixed and processed for scanning electron microscopic study at 5, 10, and 20 k magnification. The data were statistically analyzed to compare within and between the different materials. Coating titanium plates with PLGA or CH with MEM appeared to enhance bacterial inhibition over uncoated plates, hindering biofilm formation and preventing bacterial proliferation. In the staphylococcus aureus group, the highest bacterial count was observed in the uncoated plates, whereas the lowest count was detected in meropenem-PLGA, followed by PLGA, chitosan, meropenem, and meropenem-chitosan, respectively. On the other hand, the Pseudomonas aeruginosa group with the uncoated plates had the highest bacterial count, whereas the lowest bacterial count was found related to CH, followed by PLGA, MP, MC, and MEM, respectively.
“…Histopathological/histomorphometric analysis of H&E and immunohistochemistry followed previously established procedures. 30 2.6. Quantitative Analysis of Capsule Thickness.…”
High Mobility Group Box 1 (HMGB1) is a redox-sensitive
molecule
that plays dual roles in tissue healing and inflammation. We previously
demonstrated that HMGB1 is stable when anchored by a well-characterized
imidazolium-based ionic liquid (IonL), which serves as a delivery
vehicle for exogenous HMGB1 to the site of injury and prevents denaturation
from surface adherence. However, HMGB1 exists in different isoforms
[fully reduced HMGB1 (FR), a recombinant version of FR resistant to
oxidation (3S), disulfide HMGB1 (DS), and inactive sulfonyl HMGB1(SO)]
that have distinct biological functions in health and disease. Thus,
the goal of this study was to evaluate the effects of different recombinant
HMGB1 isoforms on the host response using a rat subcutaneous implantation
model. A total of 12 male Lewis rats (12–15 weeks) were implanted
with titanium discs containing different treatments (n = 3/time point; Ti, Ti-IonL, Ti-IonL-DS, Ti-IonL-FR, and Ti-IonL-3S)
and assessed at 2 and 14 days. Histological (H&E and Goldner trichrome
staining), immunohistochemistry, and molecular analyses (qPCR) of
surrounding implant tissues were employed for analysis of inflammatory
cells, HMGB1 receptors, and healing markers. Ti-IonL-DS samples resulted
in the thickest capsule formation, increased pro-inflammatory, and
decreased anti-inflammatory cells, while Ti-IonL-3S samples demonstrated
suitable tissue healing similar to uncoated Ti discs, as well as an
upregulation of anti-inflammatory cells at 14 days compared to all
other treatments. Thus, results from this study demonstrated that
Ti-IonL-3S are safe alternatives for Ti biomaterials. Future studies
are necessary to investigate the healing potential of Ti-IonL-3S in
osseointegration scenarios.
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