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Summary medical implants for biomedical engineering students
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Medical implantsLecture 1
23-2-2021
Surface coating = any non-native material to the surface can be classified as a surface coating. From a
biomaterial perspective, examples of surface coatings are:
- Salivary conditioning films (oral cavity).
- Protein/polysaccharide deposition.
- Antimicrobial coatings.
- Polymer brush coatings.
- Nanoparticle deposition.
No coating → infection can happen and a biofilm forms on the surface → can be treated with
antibiotics (sterilization of patient) or the implant has to be replaced.
Biofilm = a collective of one or more types of microorganisms that can grow on many different
surfaces. Microorganisms that form biofilms include bacteria, fungi and protists. Options for biofilm
control:
- Stop attachment: prevent bacteria from attaching.
- Stop growth: ones the bacteria adhere you can prevent them from growing.
- Mechanical removal: a biofilm like plaque on teeth can be removed with a toothbrush for
example.
- Promote detachment.
Preventing bacterial adhesion is easier than curing. There are different stages and ones a slime is
formed (maturation), the antibiotics will basically bounce off (when there is resistance in the biofilm).
As soon the bacteria start to interact or during expansion, the biofilm can be stopped forming, which
is easier than breaking down the eventual formed biofilm. It is hard to attack all bacteria in the
biofilm. If one of them stays alive, it will still replicate and form another biofilm colony that is
resistant to the antibiotics and they will bounce off.
Coatings that stop bacterial attachment:
- Antimicrobial coating (like an antibiotic coating)
- Polymer modification (at the surface)
- Hydrophobicity
- Surface roughness
- Surface charge
The difference between antimicrobial and antibacterial is that antimicrobial can also kill other
microbes besides bacteria, but they approximately the same effectiveness.
Current concepts and strategies of antibacterial biomaterials:
- Low adhesion / bacterial repulsion.
- Bactericidal activity (agent prevents the growth of bacteria / kills bacteria).
- Quorum quenching / enzymic biofilm disruption (bacteria can attach to the surface, but are
not able to form a biofilm).
- Modulation of host immune system
(attract macrophages and neutrophils
etc. to get rid of the bacteria).
- Bacterial interference (add a probiotic
or competing bacteria to the surface
that is not harmful for the host to
prevent the harmful bacterial from
attaching to the surface).
,Example antibacterial mechanism: silver
A surface coating containing silver nanoparticles will slowly release silver ions into the coating layer
and subsequently the solution. Silver ions will bind the bacterial membrane and proteins, causing cell
death.
Silver coating → bacteria attaches → silver ions released → bacteria dies due to high content silver,
causing cell death.
Issue mechanism: (1) the biofilm matrix remains. The dead bacteria remain on the surface. A bacteria
that might want to attach there will maybe not receive the same amount of silver ions and will not
die. The dead bacteria become attachment points for new bacteria. (2) the amount of silver
decreases. The coating is put in with a certain amount of antibiotic, but it is not able to continuously
produce this antibiotic, so there is only a certain level/amount within the system. The silver leaches
out and there is nothing left of the antibiotic after a certain period of time. After this period, the
silver coating becomes useless due to the antibiotics not being present anymore.
Example competition for adhesion: probiotic
A key contributing factor to the prevention of adhesion is the resident competitive microflora
(resident → not foreign to the body, it is adapted to its presence) in the human intestinal tract.
probiotics can be defined as bacteria (such as lactobacilli, bifidobacterial and enterococci) that are
part of the normal microflora, in both planktonic and sessile forms, that have a beneficial effect on
the health of the host. They compete against pathogens for limited space and nutrients.
Polymer modification
Forces of grafted polymer chains can prevent bacterial adhesion to
a surface. Polymers face upwards in long chains. The bacteria tries
to reach the surface, but the polymer chains get in the way. The
chains ‘bounce’ the bacteria away.
Layer density plays an important role → bigger coil per polymer,
more surface occupied and thus less density of the polymers /
smaller coil, less surface occupied and thus more density → the coil
becomes vertical to repel the bacteria.
Polymer brush surfaces:
A – the non-hydrated polymers are randomly packed on the surface.
B – they will create a tightly packed highly hydrated brush in aqueous environment.
C/D – microbes encountering the brush surface will be repelled.
Example hydrophobicity: Teflon/PFTE
Teflon = non-stick coating on a frying pan. ‘non-sticky’ is a property
called hydrophobicity → Teflon repels water. Water will have a
droplet shape on the surface instead of spreading out. Bacteria like
to be in water-based suspensions and do mostly not perform well
out of a water-based environment. If you have a hydrophobic
condition, there are less bacteria that will see the surface.
,Example surface roughness: voice prosthesis
Rough surfaces are more beneficial to biofilm formation, while smooth surface are less susceptible to
bacterial adhesion. Super smooth voice prosthesis showed less biofilm growth. The rough surfaces
create more area for the bacteria to attach than the smoot surfaces.
Surface charge
Electrostatic interactions determines initial bacterial adhesion. Bacteria carry a negative charge
under physiological conditions. Electrostatic repulsion is stronger for surfaces with a more negative
charge.
Change in adhesion rate during flow
During the flow, you can also change the adhesion. In a flow chamber you have the following
observations:
- Initially, little to no bacteria adhere to the surface.
- The bacteria are observed to move slowly near the surface, but do not stay.
- Later, new slow moving bacteria are near the surface and hit the same location, but stick.
➔ Reason: the first bacteria (A) leaves behind a small trail of its polysaccharides and (ECM)
proteins. This can happen when it slowly moves over the surface. This coating trail from
bacteria A creates a more favorable condition for adhesion for bacteria B.
In flow chamber, you do not see any attachment for a period of time in the beginning, but after a
while there will be attachment with changing any conditions in the chamber.
Conditioning film
This film can be removed with a scraper or other instruments in the oral cavity. However, since you
always produce saliva, there is always a conditioning film (bacteria keep secreting their proteins).
Important to note is that boundary layers or conditioning films do not only form between the surface
and the biofilm, but also between the biofilm and their environment.
EPS (=extracellular polymeric substances) has been proposed to play an important role in initial
adhesion, as well as secure anchoring, of bacteria to solid surfaces. However, there are also reports
which propose that for some bacteria EPS production does not enhance attachment and bay even be
a hindrance.
MSCRAMMS
= microbial surface components recognizing adhesive matrix molecules.
The attachment to human matrix proteins represents the first step of biofilm formation. S.
epidermidis and S. aureus express dozens of so-called MSCRAMMS that have the capacity:
- To bind to human matrix proteins, such as fibrinogen or fibronectin.
- To often combine binding capacity for several different matrix proteins.
Basically they are able to recognize and bind the matrix proteins to form a biofilm.
Bacteria are tricky buggers, they find any advantage against them and turn them to their advantage.
Bacillus and coccoid refer to the shape of the bacteria.
Bacillus = rod-shaped & coccoid = round.
Strepto = long chains & staphylo = cluster formation
A chain of two → diploid.
Alginate is important for the development of P. aeruginosa monospecies biofilms as it is the main
constituent of the glycocalyx. Glycocalyx = the peri-cellular matrix (basically extracellular materials
linked to the cellular membrane). Non-EPS-producing bacterial strains, including those of P.
aeruginosa, can attach to solid surfaces, but are unable to form mature biofilm.
- Mucoid P. aeruginosa strains (i.e. those that produce alginate) attach at higher frequencies
to hamster tracheal epithelial cells than nonmucoid (non-alginate produce) strains.
o Exogenously added alginate can enhance P. aeruginosa attachment.
, - Mucoid strains also attach better to inorganic substrates, such a s dacron fibers, when
compared to nonmucoid strains.
o This increase can be mitigated by the use of monoclonal antibodies to the alginate.
Surgery
When in implant, like a hip replacement or knee implant, is placed a lot of force is needed to locate it
in the right position. Sometimes tools like hammers are needed. Because of this, coatings do not
always work in theory. The coating is loosely attached to the surface, so when force is exerted on it
during the surgery, the coating can come off. For example the brush coating is a good solution as
coating in theory, but in reality it gets damaged and gets removed from the surface during the
placement. The coating needs to be able to withstand the surgery.
Longevity of surface coatings
Surface coatings are not designed to be everlasting. As mentioned earlier, even slowly moving
bacteria that never attach can alter a surface chemistry to allow adhesion from the next closest
encounter. Coatings only must serve purpose of protection against infection long enough to allow a
return to natural protective barriers. The mammalian cellular structures will return that prevent
bacterial adhesion. This taking over of the coating is known as ‘race for the surface’.
A problem is that when prevent bacterial adhesion can also prevent cellular adhesion, leading to
implant failure. Results in:
- No vascularization (blood/nutrient flow to the implant)
- No integration into the tissue, which can cause an adverse immune response.
Implants
All biomaterial implants and devices can be adversely affected by microbial contamination and
clinical infection. However, device coating strategies are often evaluated and applied without
considering important details unique or specific to each implant application. This is flawed for many
reasons.
Temporary implants
= feeding tubes, urinary or vascular catheters and contact lenses. They do not require tissue
integration.
Therefore, non-adhesive, antibiotic-releasing, silver-impregnated or coatings that kill bacteria
immediately upon their adhesion to the coating can prevent implant infection in these contexts (no
permanent solution needed). Regardless, infections arising from temporarily implanted medical
devices should not be considered less severe. Even infection caused by devices that can be easily
removed can result in a life-threatening situation. The physician has to balance the risks of infects vs.
the consequences of removing a potentially lifesaving device.
Permanent implants
Permanent, totally internal implants and devices are designed to selectively favor host tissue
integration over bacterial adhesion and biofilm growth is hard to achieve. Biomaterial surfaces
facilitating host cell adhesion, spreading and growth are also adhesive to microorganisms, because
microorganisms use many of the same adhesive mechanisms as host tissue cells.
An important example is the extracellular matrix proteins fibronectin (Fn). Fibronectin is a host
protein that adsorbs to implants and devices and is characterized by an integrin receptor-binding
motif, which is also recognized by staphylococci having Fn-binding proteins. Alternatively, surfaces
and coatings designed to prevent bacterial colonization do not effectively integrate with host cells
and tissues. Functional duplicity between friend and foe (promote cell adhesion and prevent bacteria
from adhering) has prompted increasing awareness of the futility of using monofunctional surfaces
to both repel and kill bacteria, while at the same time promoting tissue cell adhesion.
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