Review Article

Self-Assembled Monolayers for Dental Implants

Table 1

Bioactive osseointegration, antiadhesive, and antibacterial coatings on titanium.

SurfaceCoating typeMoleculeStudy typeEffectRef.

Bioactive osseointegrationCovalent immobilization of osseointegration moleculesRGD peptideIn vitroSupports osteoblast attachment and spreading, and significant mineralization after 14 and 21 days[21]
In vitroSignificantly improves the osteoblast adhesion, proliferation, and alkaline phosphatase (ALP) activity while retaining high antibacterial efficacy after aging for 21 days in PBS[22]
In vivoSignificant increase in bone formation after 4 weeks in vivo in rat femurs and in a rabbit model[29, 30]
BMP4In vitroInduces significant alkaline phosphatase activity in pluripotent C3H10T1/2 cells[24]
BMP2In vitroOnly 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 vitroReduces 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 vivoTitanium 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]

AntiadhesivePolymer coatingPEGIn vitroInhibits salivary protein adsorption and the attachment of S. gordonii and S. mutans biofilm was easier to be detached[25]
PLL-g-PEGIn vitroHuman 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 groups1In vitroSuppresses fibrinogen adsorption. Resists attachment of the cyanobacterium Lyngbya spp. for at least 100 days[35]
PEG conjugate to catechols groupsIn vitroResistant 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[3638]
Multivalent PEGylated peptidesIn vitro90% PEGylated peptides remain in surface. 90% reduction in S. aureus biofilm[39]

AntibacterialMetal ion incorporationSilverIn vitroActivity effects against periodontal and peri-implant pathogens, including P. gingivalis, P. intermedia, A. actinomycetemcomitans, F. nucleatum, Tannerella forsythia, and S. aureus[40, 41]
In vitroLimits 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 vitroImproves the antibacterial effect against S. aureus and preserves human gingival fibroblasts viability[44]
In vitroVery 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]
ZincIn vitroNo antibacterial activity against the periodontal bacteria P. gingivalis and A. actinomycetemcomitans, possibly due to the formation of zinc halogens, oxides, or sulphides[43]
CopperIn vitroAntimicrobial effect on E. coli and especially on S. aureus, with the lethal concentration for S. aureus of 5 µg/ml[46]
In vitroAntibacterial activity (90%) against S. aureus[47]

Biocidal releaseGentamicin into a degradable PDLLAIn vivoAnimals 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 PLLAIn vitro and in vivoEffective in eliminating S. aureus infection without cytotoxic effects[49]
Chlorhexidine into PLLA and politerefateIn vitroConcentration 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 vitroActive against methicillin-resistant S. aureus (MRSA), preventing the formation of biofilm (90% reduction)[51]
Vancomycin into silica sol-gel thin filmIn vitroReleases drug above the MIC and degrades after about 2 weeks in vitro[52]
Minocycline and rifampicinIn vivoIn 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]

Covalent immobilization of biocidalVancomycinIn vitro and in vivoStrong 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-anachelinIn vitroOnly dead cells (B. subtilis) were detected on surface[55]
Gentamicin and penicillinIn vitroThe covalently immobilized antibiotics retain the antibacterial properties as indicated by a significant reduction in the viability of contacting S. aureus[56]
AMP Tet213In vitroActivity 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 GL13KIn vitroSignificantly 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-20In vitro and in vivoExcellent 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]
hLf1-11In vitroReduction in bacterial adhesion, early-stage biofilm formation, and growth of planktonic of S. sanguinis and L. salivarius[61]