Biocompatibility: Host Response to Biomaterials Flashcards

1
Q

host responses to biomaterials

A

protein deposition
coagulation
inflammation
wound healing
matrix remodeling
tissue regeneration

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2
Q

the biomaterial surface

A

synthetic implant materials do not have biological content that cells can recognize

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3
Q

all biomaterials contact

A

body fluids
blood, saliva, tears, extracellular fluid
these fluids contain proteins

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4
Q

proteins are made of

A

amino acids, joined together to form peptides, and folded into precise structures

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5
Q

adsorption

A

two dissimilar surfaces will adhere to each other if there is attractive interactions between them
dissimilar molecules/macromolecules with respect to a surface will also absorb to the solid surface in the presence of attractive interactions

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6
Q

cohesion

A

when two surfaces with similar molecules are attached to each other

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7
Q

example of protein adsorption leading to reduced biocompatibility

A

disposable contact lenses
over time in the eye, proteins deposit with exposure to tears, needs periodic cleaning or replacement

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8
Q

if not removed, adsorbed proteins from disposable contact lenses can

A

clog pores on contact lenses, reduce oxygen permeability
mediate bacteria adhesion and lead to biofilm formation
contributes to loss of material function

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9
Q

biocompatibility testing looks to understand

A

the potential local and systemic toxicity to define potential incompatibility

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10
Q

wound healing

A

is a sequential process that is driven by non-specific immunity
interruption of the sequence can lead to chronic would (diabetic foot ulcer)

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11
Q

the stages of wound healing

A

hemostasis - blood clotting
inflammation - elimination of antigens and damage
proliferative - redeposit tissue architecture
remodeling - tissue maturation

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12
Q

would healing can be interrupted by

A

infection
wound bed disruption
blood supply

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13
Q

what stage of wound healing defines would outcomes, and is the stage most impacted by implants

A

inflammatory phase

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14
Q

granulocytes

A

contain small granules inside them to provide rapid soluble factor release
eosinophils, basophils, mast cells, neutrophils

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15
Q

phagocytes

A

consume and kill pathogens intracellularly, and some participate in adaptive immune engagement
neutrophils, macrophages, dendritic cells

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16
Q

immunity is effective because it is both

A

specific and non-specific

17
Q

non-specific responses

A

work quickly when they sense something that does not seem normal

18
Q

specific responses

A

work using memory, they are trained by non-specific responses to work more effectively with a second exposure - target response

19
Q

PAMPs

A

molecular signatures that are not present in normal mammals

20
Q

DAMPs

A

molecular patterns common to cell damage

21
Q

PAMPs and DAMPs are recognized by

A

pattern recognition receptors

22
Q

molecular patterns stimulate

A

an innate immune response, including cytokine and chemokine production

23
Q

blood - material interactions

A

blood is designed to form clots whenever it is not contacting normal endothelium - no synthetic or modified biological surface is as resistant to thrombosis as normal unperturbed endothelium

24
Q

materials can induce thrombosis through

A

blood plasma protein adsorption on the implant surface
adhesion of platelets and leukocytes
bulk fibrin formation

25
Q

coagulation is a

A

cascade
enzymes released from initiation propagates clot formation on implants

26
Q

clinical signs of inflammation

A

pain, heat, redness, swelling and loss of tissue function

27
Q

defining features of wound inflammation

A

clinical signs
the vascular component that is achieved through leaky vessels
cellular components: phase 1 and 2

28
Q

cellular component phase 1 of wound inflammation

A

extravasation of leukocytes from the blood occurs quickly - phagocytosis of foreign objects, debris, bacteria
attracted to the wound site by signaling molecules

29
Q

cellular component phase 2 of wound inflammation

A

monocytes, which differentiate into macrophages, further support this function and orchestrate the next stage of healing

30
Q

innate immune activation induces a cascade of

A

inflammation response - strength in collaboration and numbers