Biocompatibility: Host Response to Biomaterials Flashcards
host responses to biomaterials
protein deposition
coagulation
inflammation
wound healing
matrix remodeling
tissue regeneration
the biomaterial surface
synthetic implant materials do not have biological content that cells can recognize
all biomaterials contact
body fluids
blood, saliva, tears, extracellular fluid
these fluids contain proteins
proteins are made of
amino acids, joined together to form peptides, and folded into precise structures
adsorption
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
cohesion
when two surfaces with similar molecules are attached to each other
example of protein adsorption leading to reduced biocompatibility
disposable contact lenses
over time in the eye, proteins deposit with exposure to tears, needs periodic cleaning or replacement
if not removed, adsorbed proteins from disposable contact lenses can
clog pores on contact lenses, reduce oxygen permeability
mediate bacteria adhesion and lead to biofilm formation
contributes to loss of material function
biocompatibility testing looks to understand
the potential local and systemic toxicity to define potential incompatibility
wound healing
is a sequential process that is driven by non-specific immunity
interruption of the sequence can lead to chronic would (diabetic foot ulcer)
the stages of wound healing
hemostasis - blood clotting
inflammation - elimination of antigens and damage
proliferative - redeposit tissue architecture
remodeling - tissue maturation
would healing can be interrupted by
infection
wound bed disruption
blood supply
what stage of wound healing defines would outcomes, and is the stage most impacted by implants
inflammatory phase
granulocytes
contain small granules inside them to provide rapid soluble factor release
eosinophils, basophils, mast cells, neutrophils
phagocytes
consume and kill pathogens intracellularly, and some participate in adaptive immune engagement
neutrophils, macrophages, dendritic cells
immunity is effective because it is both
specific and non-specific
non-specific responses
work quickly when they sense something that does not seem normal
specific responses
work using memory, they are trained by non-specific responses to work more effectively with a second exposure - target response
PAMPs
molecular signatures that are not present in normal mammals
DAMPs
molecular patterns common to cell damage
PAMPs and DAMPs are recognized by
pattern recognition receptors
molecular patterns stimulate
an innate immune response, including cytokine and chemokine production
blood - material interactions
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
materials can induce thrombosis through
blood plasma protein adsorption on the implant surface
adhesion of platelets and leukocytes
bulk fibrin formation
coagulation is a
cascade
enzymes released from initiation propagates clot formation on implants
clinical signs of inflammation
pain, heat, redness, swelling and loss of tissue function
defining features of wound inflammation
clinical signs
the vascular component that is achieved through leaky vessels
cellular components: phase 1 and 2
cellular component phase 1 of wound inflammation
extravasation of leukocytes from the blood occurs quickly - phagocytosis of foreign objects, debris, bacteria
attracted to the wound site by signaling molecules
cellular component phase 2 of wound inflammation
monocytes, which differentiate into macrophages, further support this function and orchestrate the next stage of healing
innate immune activation induces a cascade of
inflammation response - strength in collaboration and numbers
