Ch 2: inflammation and repair

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71 Terms

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inflammation, immunity, and repair are the body’s response to _____.

injury

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inflammation

-Allows the body to eliminate injurious agents and injured tissue, control injuries, and begin the process of healing

-nonspecific response to injury

-Extent and duration of injury determines the extent and duration of inflammatory response

-can be local or systemic

-2 types: acute and chronic

- denoted by the suffix- itis combined with the name of the tissue

-not the same as infection

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injury

Is the result of an alteration in the environment that causes tissue damage or severe injury which may result in necrosis or a Less severe injury may result in reversible cellular response

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necrosis

the pathologic death of one or more cells or part of an organ as result of irreversible damage to the cells

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types of reversible cellular responses

-hyperplasia

-hypertrophy

-atrophy

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injury to the orofacial tissues may have different causes such as:

-physical injuries

-chemical injuries

-infections

-nutritional deficiencies

-toxicities

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physical injuries

-trauma

-can affect teeth, soft tissue, and bone

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chemical injuries

can occur from application of caustic substances

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infections

caused by microorganisms

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nutritional deficiencies

can render oral tissues more susceptible to injury from other sources

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toxicities

overdoes of some nutrients can also cause tissue damage (ex: illegal drugs)

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types of innate defenses

-physical barrier

-mechanical defense

-antibacterial activity

-removal of foreign substances

-inflammation process

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ex of physical barrier

intact skin or mucosa

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ex of mechanical defense

respiratory system’s cilia and mucus

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ex of antibacterial activity

enzymes in saliva

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ex of removal of foreign substances

flushing action of tears, saliva, urine and diarrhea

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ex of inflammation process

white blood cells

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body’s defense mechanisms

-tears

-skin

-large intestine

-saliva

-respiratory tract

-stomach

-bladder

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tears

-wash away irritating substances and microbes

-lysozyme kills many bacteria

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skin

-provides a physical barrier to the entrance of microbes

-acidic pH discourages the growth of organisms

-sweat and oil gland secretions kill many bacteria

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large intestine

normal bacterial inhabitants keep invaders in check

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saliva

washes microbes from the teeth and mucous membranes of the mouth

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respiratory tract

-mucus traps organisms

-cilia sweep away trapped microorganisms

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stomach

acid kills organisms

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bladder

urine washes microbes from urethra

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infection

implies an inflammatory response initiated by invasion of microbials

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acute inflammation

-minimal and brief

-the source is removed from tissue

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chronic inflammation

-longer lasting weeks, months, or indefinitely

-cause by persistent injuries

-repair can’t be completed until source of injury is removed

-more extensive tissue destruction, heals less readily

-stems from the immune system failing to turn off its response, often due to unresolved acute issues like infections or injuries, autoimmune disorders where the body attacks itself, long-term exposure to irritants (toxins, pollutants), or lifestyle factors like poor diet (high sugar/fat), smoking, obesity, lack of sleep, and chronic stress- It's a persistent, low-grade inflammation that damages tissues over time and underlies many serious conditions like diabetes, arthritis, and heart disease

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localized signs of inflammation

-pain

-heat

-redness

-swelling

-loss of normal tissue function

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4 major systemic signs of inflammation

-fever

-leukocytosis

-elevated C-reactive proteins (CRP)

-lymphadenopathy

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sequence of microscopic events of inflammation

  1. Constriction of microcirculation (immediate reflex)

2. Dilation of microcirculation →increased blood flow that fills the capillary beds: hyperemia → erythema and heat (local clinical sign)

3. Increase in permeability: vessels become leaky

4. Exudate leaves microcirculation, this extravascular fluid → transudate, supplies oxygen and nutrients

5. The loss of fluid leads to an increased blood viscosity (blood becomes thicker) and blood flow slows down

6. Decreased blood flow: RBC begin to pile up in the center of the blood vessel, and WBC primarily Neutrophils are displayed to periphery of blood vessel (Margination). The WBCs are now in position to adhere themselves to the wall of the injured blood vessel (Pavementing)

7. WBCs escape from the blood vessels and enter tissue → emigration → exudate and edema (local clinical sign). Exudate contains higher concentration of protein molecules than transudate.

8. Chemotaxis: directed movement of WBC toward the injury site by biochemical mediators

9. WBCs ingest foreign material → phagocytosis

10. The swelling and pain in tissue resulting from inflammation may cause a loss of normal tissue function (local clinical sign)

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transudate

the extravascular fluid component of blood that passes through the endothelial cell walls of the microcirculation

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margination

a process during inflammation in which WBC’s tend to move to the periphery of the BV at the site of injury

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pavementing

the adherence of WBC’s to BV walls during inflammation

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emigration

the passage of WBC’s through the walls of small BV’s and into injured tissue

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2 WBC’s that are initially involved in the inflammatory response

-neutrophils

-monocytes

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Neutrophils

-are the first type to arrive at the site of injury and the most commonly present during acute inflammation

-function is phagocytosis of substances such as pathogenic microorganisms and tissue debris. they possess lysosomal enzymes that destroy these substances and die shortly after phagocytosis

-As a result, the lysosomal enzymes are released from the dying cells, which can cause further tissue damage to the site when large numbers of this cell dies

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monocyte

-becomes a macrophage as it enter the surrounding tissue

-larger than neutrophils and also have a longer life span

-function is to assist in phagocytosis

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fever

-Controlled in the brain by the hypothalamus

-anything above the normal level of 98.6 degrees

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pyrogens

-Fever-inducing substances, produced by WBCs and pathogens

-act on the hypothalamus

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hypothalamus and fever

- increases body temperature by increasing the synthesis and release of prostaglandins

-The function of this increase in body temperature may be helpful in combating some infections as it may slow the growth of pathogenic microorganisms.

-However, the body cannot tolerate an extremely high fever for very long , thus drugs are given to reduce high fever by reducing systemic inflammation

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prostaglandins

substances involved in fever, pain, inflammation, blood clotting, menstruation and labor

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leukocytosis

-Normal number of WBCs per mm3 of blood: 4000 to 10,000

-In a systemic inflammatory response, the number increases to 10,000 to 30,000/mm3 of blood which is an increase in circulating WBCs

-It is the body’s attempt to provide more cells for phagocytosis

-The type of WBC that is increasing in number can aid in differential diagnosis

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viral infection will have an increase in _____

lymphocytes

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bacterial infection will have an increase in _____

neutrophils

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allergic reaction will have an increase in _____

eosinophils

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lymphadenopathy

-Enlarged and palpable superficial lymph nodes: it feels firmer and larger and may be tender

-enlarged nodes occur because of changes in lymphocytes

- usually occur during chronic inflammation and in neoplastic processes, such as lymphomas and metastatic spread of tumors to lymph nodes

-persistent or non resolving should be evaluated to determine a possible etiology

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lymphocytes

-primary cells of the immune response

-result in the change in size of the lymph node

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elevated levels of C-reactive protein (CRP)

-considered a proinflammatory marker

-a mucoprotein produced in the liver

-Levels can be used to help assess rheumatoid arthritis and systemic lupus erythematosus

-Used to monitor tissue healing

-Used as early infection detection system

-Chronically increased level is associated with an increased risk for cardiovascular disease

-Possible marker for periodontal disease

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cells involved in chronic inflammation

-neutrophils

-monocytes

-macrophages

-lymphocytes

-plasma cells

-fibroblasts

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granulomatous inflammation

- a distinctive form of chronic inflammation

-characterized by the formation of a granuloma which contains microscopic groupings of macrophages surrounded by lymphocytes

  • These macrophages group together to form multinucleated giant cells

  • The formation of granulomas is not preceded by an acute neutrophil-mediated inflammation, instead it may be caused by an antigen that persists at the site of inflammation

  • The body is unable to destroy the offending substance, and tries to enclose them in these masses of inflammatory cells. Granulomas destroy the surrounding tissue and tend to persist for a long time

  • Associated with foreign body reactions and some infections such as tuberculosis

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types of anti-inflammatory therapy

-nonsteroidal anti-inflammatory drugs (NSAIDs)

-steroidal anti-inflammatory drugs

-antihistamines

-cancer treatment drugs

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examples of NSAIDs

-Acetylsalicylic acid (aspirin)

-Ibuprofen

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examples of steroidal anti-inflammatory drugs

prednisone

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antihistamines

-used when response is initiated by an allergic reaction

-ex: Benadryl

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cancer treatment drugs

-Suppress the inflammatory response, used to treat inflammatory diseases but at significantly lower doses.

-ex: Methotrexate

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resolution of inflammation

-Leads to tissue remodeling and repair as well as, immune regulation and shutting off of acquired immune responses at lymph nodes and other lymphoid tissue.

-If tissue repair is not properly controlled it may lead to fibrosis and tissue scarring

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fibrosis

a pathologic condition that occurs when excess fibrous connective tissue forms in an organ or tissue

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shutting off process

Neutrophils recruitment ceases and programmed cell death occurs (apoptosis). Apoptotic neutrophils undergo phagocytosis by macrophages. Process ends by departure of macrophages through the lymphatics

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hyperplasia

-An increase in the number of cells, often in response to chronic irritation or abrasion

-May return to normal if the insult subsides, or may persist after removal of the irritant

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hypertrophy

-An increase in the size of cells

-May be seen in cardiac muscle as a response to hypertension

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atrophy

A decrease in size and function of a cell, tissue, organ, or entire body

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factors affecting the amount of scar tissue depends on:

-Heredity

-Strength and flexibility needed in the tissue

-Tissue type involved: oral mucosa is less prone to scar formation, because it is moist and a superficial scab does not form as in skin

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3 types of repair

-healing by primary intention

-healing by secondary intention

-healing by tertiary intention

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healing by primary intention

-Healing of an injury in which there is little loss of tissue, such as a surgical incision

-The margins are close together and very little granulation tissue forms, thus less scar tissue forms (scarring is minimized)

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healing by secondary intention

-Tissue loss is significant

-The edges of the injury cannot be joined during healing

-A large clot forms, resulting in increased granulation tissue

-Scar tissue formation can be excessive: A keloid

-Individuals with pigmented skin are more prone to forming keloids

-Example of healing by secondary intention is a tooth extraction site

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healing by tertiary intention

-if infection occurs at the site of a surgical incision that is healing by primary intention, this type of healing may result.

-This transformation occurs because of an enlargement of the injured area and an increase in the magnitude and duration of the inflammatory response triggered by the presence of pathologic microorganisms

-also known as delayed primary closure

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delayed primary closure

a wound healing technique that involves leaving a wound open to heal for a period of time before closing it

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when is tertiary intention used?

-When the wound is contaminated by bacteria (infection)

-A traumatic injury that may have debris in the wound

-When there is too much edema or infection that needs to improve

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local factors that impair healing

-Bacterial infection

-Tissue destruction and necrosis

-Hematoma

-Excessive movement of injured tissue

-Poor blood supply

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systemic factors that impair healing

-Malnutrition: protein, zinc, calcium and vitamin C severely reduced from diet

-Immunosuppression: because of steroid use or chemotherapy

-Genetic connective tissue disorders: Osteogenesis Imperfecta.

-Metabolic disorders: resulting from renal failure, diabetes.

-Alcohol, tobacco, recreational drugs also impair healing