First phase of wound healing; usually occurs before immune response

Almost always occurs whenever an object is implanted (implantation causes systemic/vascular disruption, even if brief while not changing the material itself)

2 stages: vascular and cellular

Rubor (redness)

Tumor (swelling)

Calore (heating)

Dolore (pain)

Sometimes: loss of function

Blood vessels are normal

Occasional lymphocytes, macrophages present

Brief vasoconstriction followed by vasodilation (inc. blood flow, blood pooling create redness and warmth)

Increased microvascular permeability for plasma proteins and cells causes swelling; fluid loss leads to concentration of RBCs and slowed blood flow (stasis)

Leukocytes (i.e neutrophils) and plasma proteins migrate from the vessel (vessel becomes leaky)

Granulocytes (neutrophils, eosinphils, basophils) - 1st to inflammation site, majority of leukocytes; granular, phagocytic, aid in inflammation

Monocytes - Large phagocytic capacity (~5x that of neutrophils); mature to macrophages, which are even more effective

Lymphocytes (T and B cells) - Key roles in the acquired immune system; produce antibodies from acquired immunities

Megakaryocytes - Make platelets; no nucleus, found only in bone marrow; aid in clotting

Anatomical Barriers - skin and mucous membranes

Physiological Barriers - Body temp. and low stomach pH

Phagocytic cells

Inflammation (swelling, redness, heat, pain)

Leukocyte emigration from microcirculation to phagocytose debris, invaders

Coordinated event of rolling (slows the leukocyte), activation, arrest/adhesion, transendothelial migration out of the cell

Rolling is mediated by weak EC selectin and neutrophil proteoglycan interactions

For arrest and transEC migration, neutrophils must be activated by chemokines to induce conformational changes of integrins that have higher affinity to CaMs on EC surface

Phagocytosis: Engulfing and degradation/digestion of fragments of tissue or material

1) Pseudopoida surround the material

2) The cell ingests the material, forming a phagosome around it, which moves towards the lysosome

3) The phagosome and lysosome fuse; the lysosome releases enzymes, oxdiative factors that digest the material

4) The digestion products are released from the cell

Consequence of Inflammation due to Action by Neutrophils

Reactive oxygen species formed in intracellular granules through oxidative burst cause: increased oxygen consumption, increased glucose metabolism and oxidation, formation of superoxide ion

Radicals released to kill foreign organisms, but can also caused unwanted tissue oxidation, promote corrosion and oxidative degradation of biomaterials in the body

Neutrophils secrete a number of cytokines that have specific effects dep. on cell type

Inflammatory protein 1a/1b - Recruit monocytes to the area

IL-8: Attract more neutrophils (integrin presentation during extravasation)

IL-1 and TNF-alpha: promote cell migration by increasing expression of vascular endothelial CaMs

Many factors can also attract lymphocytes

Systemic effects: fever or coagulation, sepsis

Biomaterial particles that are smaller than cells resist degradation (cyclic process)

Microphages lyse after being unable to digest silica

Particles return to tissue, causing cytokines to release

Fibroblasts are stimulated to form fibrous tissue in the affected areas, imparing patient's oxygen production