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Actinic
relating to or exhibiting chemical changes produced by radiant energy, especially the visible ultraviolet parts of the spectrum; relating to exposure to ultraviolet rays of sunlight.
Angiogenesis
the formation of differentiation of blood cells.
Apoptosis
Programmed cell death as a part of an organisms growth or development.
Biochemical Mediators
chemicals in the body that activate responses.
Chemotaxis
the movement of white blood cells, as directed by biochemical mediators, to an area of injury.
C-reactive Protein
a nonspecific protein, produced in the liver, that becomes elevated during episodes of acute inflammation or infection.
Crenation
indentations or grooves, as seen on the side of the tongue, caused my irritation from adjacent teeth.
Cyst
an abnormal sac or cavity lined by epithelium and surrounded by fibrous connective tissue.
Demastication
when tooth wear is increased by chewing an abrasive substance.
Emigration
the passage of white blood cells through the walls of small blood vessels into injured tissue.
Fever
An elevation of the body temperature greater than the normal level of 37*C (98.6*F).
Fibroplasia
the formation of fibrous tissue as usually occurs in healing.
Fistula
an abnormal passage that leads from an abscess to an outside body surface.
Granulation Tissue
The initial connective tissue formed in healing.
Granuloma
a tumor-like mass of inflammatory tissue consisting of a central collection of macrophages , often including multi-nucleated giant cells, surrounded by lymphocytes.
Keloid
excessive scarring that mainly occurs in skin in some cases with healing.
Leukocytosis
increase in the number of white blood cells circulating in the blood.
Leukopenia
decrease in number of white blood cells circulating in the blood.
Macrophage
The second type of white blood cell to arrive at a site of injury that was originally a monocyte; it participates in phagocytosis during inflammation and continues to be active in the immune response.
Myofibroblasts
Fibroblasts that have some of the characteristics of smooth muscle cells, such as the ability to contract.
Neutrophil
the first white blood cell to arrive at a site of injury; the primary cell involved in acute inflammation; also called polymorphonuclear leukocyte.
Nodlike Receptors (NLR’s)
Intracellular sensors of pathogen-associated molecular patterns of molecules (PAMP’s) that enter the cell via phagocytosis or pores and danger-associates molecular patterns (DAMPs) that are associated with cell stress.
Opsonization
the enhancement of phagocytosis by a process in which a pathogen in marked, with opsonins for destruction by phagocytes.
Parulis
a collection of granulation tissue and abscessed material on the gingiva, which originates from a chronically inflamed tooth and spreads via fistulous tract; aka gum boil.
pavementing
the adherence of white blood cells to blood vessel walls during inflammation.
Perimolysis
dental erosion caused by gastric acid.
Pyrogens
fever inducing substances produced from either white blood cells or pathogenic organisms
Serous is a more watery based serum exudate as apposed to pus.
What is the difference between serous exudate and purulent exudate?
Specialized Proresolving Lipid Mediators (SPMs)
these endogenous autacoids are cell-signaling biological factors that are similar to hormones and serve to actively promote resolution or inflammation.
Tail Sign
involvement of the sublingual space/floor of the mouth area by a plunging ranula, as seen on three-dimensional imaging studies.
Toll-like Receptors (TLR’s)
the receptors usually expressed on cells such as macrophages and dendritic cells that recognize structurally conserved molecules derived from microbes.
Transudate
the extravascular fluid component of blood that passes through the endothelial cell walls of the microcirculation.
Waldeyer Ring
the ring of lymphatic tissue formed by the two palatine tonsils, the pharyngeal tonsils, the lingual tonsils, and the intervening lymphoid tissue.
Inflammation, Immunity, and Repair
What are the three basic responses of the body?
Necrosis
Less severe injury may result in reversible cellular responses such as hyperplasia, hypertrophy, and atrophy- while more severe injuries may result in irreversible tissue damage such as…?
Innate Defenses
Natural defenses of the body that provide protection against injury; inborn defenses present at birth and include skin or mucosa, cilia and mucus, and stomach acid…
-itis
inflammation to a specific tissue is denoted by the suffix…?
remove the source of injury.
How do you prevent an overwhelming inflammatory response from leading to further injury?
redness, heat, swelling, pain, and loss of normal level of tissue function.
What are the major clinical signs of inflammation?
fever, leukocytosis, lymphadenopathy, and elevated c-reactive protien.
What are major systemic signs of inflammation?
microcirculation, red and white blood cells, and biological modifiers.
The microscopic events of inflammation involve…
venules
Most of the plasma that leave the microcirculation reenters through..?
constriction of small blood vessels followed by dilation.
vessels increase permeability.
plasma with low protein levels leaves the microcirculation as a transudate, causing blood to increase in viscosity.
blood flow through the circulation slows down.
white blood cells marginate and pavement along the vessel walls.
as white blood cells emigrate from the microcirculation, they disrupt the basement membrane surrounding endothelial cells and increase vascular permeability.
plasma with high protein content leaves the microcirculation as an exudate.
white blood cells ingest foreign substances through phagocytosis.
What is the sequence of events for the inflammatory response in tissues?
Hyperemia
In the beginning stages of the inflammation the increased blood flow that fills the capillary beds in the injured tissue is called…?
HINT: this is responsible for the two clinical signs of inflammation- erythema and heat.
blood vessels of the microcirculation increase permeability.
What causes blood vessels to become “leaky” when hyperemia is occuring?
Margination
When vessels in the microcirculation become “leaky” endothelial cells contract and create spaces between cells which causes plasma fluid with low protein content to pass through and enter the vessels as transudate. This loss of fluid causes the blood to become thicker and eventually results in a decreased flow through the microcirculation.
As blood flow slows down the RBCs begin to pile up in the center of the vessels, while WBCs are displaced to the periphery of blood vessels- this process is called…?
opening of the cellular junctions of endothelial cells lining the blood vessels as the result of cells contracting in size in response to biochemical mediators.
Why does emigration of WBCs occur?
Neutrophils
Exudate that flows into injured tissue as a result of inflammation is primarily made up of what type of WBC’s?
helps to dilute injurious agents that may be present and carries them through the lymphatic system to lymph nodes where the immune response is stimulated.
What is the purpose of transudate/exudate in injured tissues?
from a chronically inflamed tooth to the gingiva, where it presents as a “gum boil”
where might a fistulous tract or fistula form in the oral cavity?
accumulation of exudate presses on the sensory nerves in the area
What part of the inflammation process causes pain in the injured area.
chemotactic factors
biochemical mediators that enhance the directed moevement of WBCs to injured tissues are called…?
2 weeks
about how long after injury does inflammation continue?
Hematopoietic Stem Cells (HSCs)
what cells are all WBC’s derived from?
60 to 70%
Neutrophils constitute what part of the entire WBC population?
they possess a granular cytoplasm that contains lysosomal enzymes that destroy substances after the cell has engulfed them, which is necessary for the repair process.
Why are neutrophils also called polymorphonuclear leukocytes (PMNs)?
M1 macrophages
macrophages that encourage inflammation.
M2 macrophages
macrophages that decrease inflammation and enhance tissue repair.
M1 has the ability to metabolize arginine to the “killer” molecule nitric oxide, while M2 can metabolize arginine to the “repair” molecule ornithine.
What makes M1 macrophage metabolism unique from M2 macrophages?
The Kinin System
This system biochemically mediates inflammation by causing increased dilation and increased permeability of the blood vessels at the site of injury.
rapidly activated by substances present in plasma and injured tissue.
limited to early phases of inflammation.
Kinins are rapidly degraded by kininases to limit the extent of inflammation.
The Clotting System
system helps stop bleeding by forming a fibrinous meshwork at the site of injury that protects adjacent tissue and keeps foreign substances contained at the site.
biochemically mediates inflammation because certain of its products that are activated when tissue is injured cause local vascular dilation and permeability by also activating the kinin system.
The Complement System
this system is composed of a series of plasma proteins that are activated in a cascading fashion.
components of this system can cause mast cells to release granules from their cytoplasm that contain the biochemical mediator histamine and other mediators into the surrounding tissue.
When histamine is released form mast cells, it causes an increase in vascular permeability and vasodilation, while other components of this system can cause cell death or necrosis by creating holes in the cell membrane.
Opsonization can also occur, where proteins of this system attach to the surface of bacteria, stimulating WBCs to phagocytize them; It plays a crucial role in amplifying the inflammatory response by marking pathogens for destruction and enhancing the ability of immune cells to clear pathogens.
Toll-Like Receptors (TLR’s)
single, membrane-spanning, noncatalytic receptors usually expressed on cells such as macrophages and dendritic cells, that recognize structurally conserved molecules derived from microbes- once these cells recognize these microbes they are able to activate immune cell responses.
Nodlike Receptors (NLRs)
intracellular sensors of pathogen-associated molecular patterns of molecules (PAMPs) that enter the cell via phagocytosis or pores and danger-associated molecular patterns (DAMPs) that are associated with cell stress; part of pattern recognition and play key roles in regulation of innate immune response.
DAMPs initiate and perpetuate a noninfectious inflammatory response, while PAMPs initiate and perpetuate the infectious pathogen-induced inflammatory response.
How do TLRs and NLRs work together to regulate inflammatory responses and apoptosis in cells?
prevent DAMP release, or neutralize/block DAMP receptors.
The application of therapeutics to treat disorders such as arthritis and cancer can target which type of NLR?
Fever, Leukocytosis, Lymphadenopathy, and Elevated levels of C-Reactive Protein.
The four systemic clinical signs of inflammation include…
Hypothalamic Thermoregulatory Center
Body temperature is controlled by what area of the brain?
Pyrogens
fever inducing substances produced by WBC’s and pathogenic organisms.
Pyrogens produce fever by increasing the synthesis and release of prostaglandins in the hypothalamus.
How do Pyrogens work?
Occurs in response to biochemical mediators and is an attempt to provide more cells for phagocytosis.
What is the purpose of Leukocytosis?
Both statements are false.
In a bacterial infection there is typically an increased number of lymphocytes. In a viral infection there is typically an increased number of neutrophils.
Liver
Where is C-Reactive Protein produced?
Granulomatous Inflammation
A distinctive form of chronic inflammation characterized by the formation of a granuloma, which causes antigens to evoke a cell-mediated hypersisnsitivity reaction and the body is unable to destroy them.
Instead the body will attempt to enclose them inside of masses of inflammatory cells, making treatment very difficult. Thus, granulomas destroy the surrounding tissue and tend to persist for long periods of time.
Fibrosis
A pathological condition resulting when excess connective tissue forms in an organ or tissue following chronic nonresolving inflammation.
Under the conditions associated with fibrosis