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Surface | Coating type | Molecule | Study type | Effect | Ref. |
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Bioactive osseointegration | Covalent immobilization of osseointegration molecules | RGD peptide | In vitro | Supports osteoblast attachment and spreading, and significant mineralization after 14 and 21 days | [21] |
In vitro | Significantly improves the osteoblast adhesion, proliferation, and alkaline phosphatase (ALP) activity while retaining high antibacterial efficacy after aging for 21 days in PBS | [22] |
In vivo | Significant increase in bone formation after 4 weeks in vivo in rat femurs and in a rabbit model | [29, 30] |
BMP4 | In vitro | Induces significant alkaline phosphatase activity in pluripotent C3H10T1/2 cells | [24] |
BMP2 | In vitro | Only 8% of the immobilized BMP2 seems to be available for interaction with the cells and able to induce the signaling cascade with cytocompatible for C3H10T1/2 cells | [31] |
In vitro | Reduces the bacterial adhesion (S. aureus and S. epidermidis) and significantly promotes attachment, alkaline phosphatase activity, and calcium mineral deposition of both osteoblast and human bone marrow-derived mesenchymal stem cells | [20] |
In vivo | Titanium screw implants with nano-anchored oligonucleotides strands hybridized with conjugated rhBMP2 exhibited enhanced bone ingrowth into the perforations and increased bone implant contact after 1 and 4 weeks compared to controls. No difference was seen after 13 weeks. Bone density around the outer implant surface did not differ significantly at any of the intervals. Therefore, rhBMP2 immobilized on the surface of titanium implants through nanoanchored oligonucleotide strands can enhance bone implant contact | [32] |
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Antiadhesive | Polymer coating | PEG | In vitro | Inhibits salivary protein adsorption and the attachment of S. gordonii and S. mutans biofilm was easier to be detached | [25] |
PLL-g-PEG | In vitro | Human serum adsorbed was below the detection limit of the optical sensor technique (OWLS) (<1-2 ng/cm2). Reduces fibrinogen adsorption by 96%. Decreases S. aureus adhesion by 89–93% | [33, 34] |
PLL-g-PEG conjugated to catechols groups1 | In vitro | Suppresses fibrinogen adsorption. Resists attachment of the cyanobacterium Lyngbya spp. for at least 100 days | [35] |
PEG conjugate to catechols groups | In vitro | Resistant to serum proteins (<1 ng/cm2 to detection limit of OWLS). Almost free of blood protein adsorption. No cytotoxicity against bone-marrow stem cells. Reduces 95% of serum protein adsorption | [36–38] |
— | Multivalent PEGylated peptides | In vitro | 90% PEGylated peptides remain in surface. 90% reduction in S. aureus biofilm | [39] |
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Antibacterial | Metal ion incorporation | Silver | In vitro | Activity effects against periodontal and peri-implant pathogens, including P. gingivalis, P. intermedia, A. actinomycetemcomitans, F. nucleatum, Tannerella forsythia, and S. aureus | [40, 41] |
In vitro | Limits antibacterial activity against P. gingivalis and A. actinomycetemcomitans, probably due to the formation of silver compounds such as AgCl, Ag2O, and Ag2S | [42, 43] |
In vitro | Improves the antibacterial effect against S. aureus and preserves human gingival fibroblasts viability | [44] |
In vitro | Very strong (greater than 4-log or 99.99% reduction) antibacterial effect against P. aeruginosa for 24 h. Osteoblast adhesion, spread, and proliferation higher than bare-Ti and so does not cause cytotoxicity | [45] |
Zinc | In vitro | No antibacterial activity against the periodontal bacteria P. gingivalis and A. actinomycetemcomitans, possibly due to the formation of zinc halogens, oxides, or sulphides | [43] |
Copper | In vitro | Antimicrobial effect on E. coli and especially on S. aureus, with the lethal concentration for S. aureus of 5 µg/ml | [46] |
In vitro | Antibacterial activity (90%) against S. aureus | [47] |
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— | Biocidal release | Gentamicin into a degradable PDLLA | In vivo | Animals receiving systemic therapy alone had a recovery rate of about 15%, whereas animals receiving the gentamicin-coated implants had an 85% recovery rate. Human patient with infection-free after 1 year and no gentamycin levels in blood | [48] |
Mixtures of antibiotics or antiseptics into PLLA | In vitro and in vivo | Effective in eliminating S. aureus infection without cytotoxic effects | [49] |
Chlorhexidine into PLLA and politerefate | In vitro | Concentration of chlorhexidine remained at therapeutic levels for 200 h (8 days) before disappearing completely. Cytocompatible to hTERT fibroblast cells | [50] |
Gendine (chlorhexidine + gentian violet) | In vitro | Active against methicillin-resistant S. aureus (MRSA), preventing the formation of biofilm (90% reduction) | [51] |
Vancomycin into silica sol-gel thin film | In vitro | Releases drug above the MIC and degrades after about 2 weeks in vitro | [52] |
Minocycline and rifampicin | In vivo | In a rabbit model that induced infection by inoculating S. aureus in the femoral medullary canal, the coated implants had an infection rate of 38% compared with 100% for the noncoated | [53] |
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— | Covalent immobilization of biocidal | Vancomycin | In vitro and in vivo | Strong bactericidal activity against S. epidermidis and S. aureus over long periods of time (up to 6 weeks) in vitro. Stable bactericidal activity and reduced infection rates when implanted in an infected rat model | [54] |
Vancomycin conjugated to PEG-anachelin | In vitro | Only dead cells (B. subtilis) were detected on surface | [55] |
Gentamicin and penicillin | In vitro | The covalently immobilized antibiotics retain the antibacterial properties as indicated by a significant reduction in the viability of contacting S. aureus | [56] |
AMP Tet213 | In vitro | Activity against both Gram-positive (S. aureus) and Gram-negative (P. aeruginosa) bacteria with 106-fold reductions of both bacterial strains within 30 min | [57] |
AMP GL13K | In vitro | Significantly fewer live cells of P. gingivalis than disks coated with a control peptide and uncoated Ti under static culture conditions. This GL13K coating showed to be cytocompatible by an adequate proliferation of osteoblasts and human gingival fibroblasts. Kills bacteria and prevents formation and growth of S. gordonii biofilms in a drip-flow bioreactor and under regular mild-agitation conditions, with rupture of the cell wall | [58, 59] |
Tet-20 | In vitro and in vivo | Excellent activity against Gram-negative P. aeruginosa and Gram-positive S. aureus, as well as biofilm resistance in vitro. The coating had no toxicity to osteoblast-like cells and showed insignificant platelet activation and adhesion, and complement activation in human blood. Protects bacterial infection in vivo (rat model) against infected S. aureus | [60] |
hLf1-11 | In vitro | Reduction in bacterial adhesion, early-stage biofilm formation, and growth of planktonic of S. sanguinis and L. salivarius | [61] |
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