DH215 Exam #2 Ch. 12/13 flashcards

Are periodontal pathogens alone enough to cause the tissue destruction seen in periodontitis?

No. Their presence alone is insufficient.

What causes nearly all of the destruction seen in periodontitis?

The body’s response to the periodontal pathogens.

The way the body responds to periodontal pathogens.

host response

What is the prime purpose of the human immune system?

To defend the life of the individual (the host).

In periodontal disease

is the body defending the tooth and periodontium?

All mechanisms that enable biofilm bacteria to colonize and damage tissues.

virulence factor

What two forms can virulence factors take?

Structural characteristics of bacteria or substances produced by bacteria.

Name the three primary virulence factors.

Presence of lipopolysaccharides (LPS) - Ability to invade tissues - Ability to produce enzymes

What is LPS

where is it found

Name two bacteria able to invade (penetrate) gingival tissue.

Porphyromonas gingivalis (P. gingivalis) and Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans).

What enzymes do bacteria produce

and what do they do?

How do host factors influence susceptibility to periodontal disease?

By modifying the host response or tissue metabolism.

Name the three categories of host factors

with examples.

What is the first line of defense against microbial invasion?

Acute inflammation.

What must the host be able to do after the microbial challenge is eliminated?

Shut down the response. Resolution of the acute inflammatory response must be effective.

What type of inflammation is periodontitis associated with?

Chronic inflammation.

Is resolution of inflammation passive or active?

Active; it is an actively regulated biologic process.

The return to homeostasis after inflammation.

catabasis

What is recruited during the acute phase

and what happens if it is overproduced?

What is the role of proresolving lipid mediators?

They are produced to terminate PMN recruitment.

When does chronic inflammation occur?

When the host is unable to stop recruitment of PMNs

Substances secreted by immune cells that activate “middlemen” and influence the immune response.

biochemical mediators.

Name the three inflammatory mediators of importance in periodontal disease.

Cytokines

Powerful mediators produced by immune cells that influence the behavior of other cells and signal the immune system to send more phagocytes to the infection site.

cytokines.

Which cells produce cytokines

and when?

Name the four cytokines important in periodontal disease.

IL-1

List three functions of cytokines.

Recruit PMNs and macrophages to the infection site - Increase vascular permeability so immune cells move into tissues - Initiate tissue destruction and bone loss in chronic infections

What are prostaglandins

and which cells produce them?

List three functions of prostaglandins.

Increase permeability and dilation of blood vessels - Trigger osteoclasts to destroy alveolar bone - Promote overproduction of destructive MMPs

Which prostaglandin series initiates most alveolar bone destruction in periodontitis?

The E series (PGE).

Bone-consuming (bone-resorbing) cells.

osteoclasts

A family of at least 12 enzymes that act together to break down the connective tissue matrix.

matrix metalloproteinases (MMPs).

Which cells produce MMPs

and what is the function of MMPs in health?

Why are MMPs released during chronic bacterial infection?

In an attempt to kill invading bacteria.

What results from overproduction (high levels) of MMPs?

Breakdown of periodontal connective tissue and extensive collagen destruction.

What are the clinical results of collagen loss in the periodontium?

Degradation of gingiva

Name the four histologic stages of periodontal disease

in order.

What is the clinical name of the initial lesion?

Clinically healthy/normal gingiva.

Initial lesion: what initiates the host response

and which cells release mediators?

Initial lesion: where is plaque located and how does the tissue look?

Plaque is located at the gingival margin. Clinically

Initial lesion: what do PMNs do?

They pass from blood vessels into gingival connective tissue

Initial lesion: name three tissue changes.

Increased gingival crevicular fluid

Initial lesion: what determines whether the host response is successful?

It is successful if most bacteria are destroyed and the body can repair any damage. If not controlled

What is the clinical name of the early lesion?

Early gingivitis.

Early lesion: what penetrates the JE?

Bacterial toxins and byproducts from the maturing biofilm.

Early lesion: what “wall” forms?

Increased vessel permeability lets more PMNs into connective tissue

Early lesion: what do macrophages release?

Cytokines

Early lesion: how much connective tissue is lost

and what causes it?

Early lesion: what epithelial changes occur?

Sulcular epithelium forms epithelial ridges and JE cells proliferate.

Early lesion: what is seen clinically

and is it reversible?

What is the clinical name of the established lesion?

Established gingivitis.

Established lesion: where does biofilm extend

and what does it disrupt?

Established lesion: what do plasma cells do?

They produce large quantities of antibodies to help control bacteria.

Established lesion: which cells are most numerous in the connective tissue?

Macrophages and lymphocytes. PMNs continue to fight bacteria in the sulcus.

Established lesion: why do epithelial ridges extend deeper?

To try to maintain epithelial integrity.

Established lesion: what does the JE transform into

and how is it different?

Established lesion: what interventions are vital?

Periodontal instrumentation and patient education for good self-care.

What is the clinical name of the advanced lesion?

Periodontitis.

Advanced lesion: how does the biofilm spread?

Laterally and apically along the root surface.

Advanced lesion: which cells destroy connective tissue and PDL fibers?

PMNs and macrophages.

Advanced lesion: how does PGE₂ destroy bone?

By stimulating large numbers of osteoclasts to resorb crestal bone.

Advanced lesion: what role does RANKL play?

Elevated RANKL levels modulate osteoclast activity

Advanced lesion: what happens to the gingival pocket?

It progresses to a periodontal pocket.

List the clinical signs of the advanced lesion.

Periodontal pockets

What is the hallmark of periodontitis?

The changes are not reversible.

Name the four phases of the bone remodeling cycle

in order.

What happens in the resorption phase?

Osteoclasts create erosion cavities in bone.

What happens in the reversal phase?

Osteogenic signals stimulate osteoclasts to cease action; mononuclear cells adhere to erosion cavities and signal to attract osteoblasts.

What happens in the formation phase?

Osteoblasts line the cavity and form new bone to replace the resorbed bone.

What is the resting phase?

The interval between cessation of bone resorption and bone remodeling.

What happens during the resting phase?

The bone remains in an inactive/resting interval until another remodeling cycle begins.

A network of different types of leukocytes and proteins that work together to defend the host from invasion; necessary for survival.

immune system

What are the two divisions of the immune system?

Innate immunity and adaptive (acquired) immunity.

When the immune system encounters a cell or molecule

what must it determine?

What is the primary purpose of the immune system?

To defend the life of the host by identifying foreign substances and defending against them.

Name the two ways the immune system defends against foreign substances.

(1) Deploying immune cells that target invaders; (2) producing biochemical substances that amplify the immune response and counteract invaders.

What is the host response?

The body's response to infection.

Give an example of a dysfunctional immune system and its effect

HIV disables a specific group of immune cells

Give an example of an overactive immune response.

Rheumatic heart disease: after Streptococcus pyogenes infection

What are leukocytes and where do they originate?

Colorless

How are leukocytes categorized?

By the presence or absence of cytoplasmic granules (granulocytes vs. agranulocytes).

Name the four granulocytes.

Neutrophils

Name the agranulocytes.

Lymphocytes and monocytes/macrophages.

What is a polymorphonuclear leukocyte (PML)?

A cell with a multilobulated nucleus. Mast cells are NOT included because they are mononuclear.

Which immune cells are deployed first and are the most abundant?

Neutrophils.

What is the primary role of eosinophils? Secondary role?

Primary: combat parasitic infections. Secondary: collaborate with mast cells and basophils to regulate the allergic response.

What do basophils primarily do?

Modulate the allergic response and coordinate physiologic activity against immune diseases.

What do mast cells do?

Protect against pathogens and release key inflammatory mediators that modulate the allergic response.

Describe four key features of neutrophils.

Phagocytose pathogens; pass through capillary walls via chemotaxis; cytoplasm contains bactericidal digestive enzymes; short-lived (die during phagocytosis).

What is the normal neutrophil count

and what are the terms for too few and too many?

Large phagocytes with a single irregular

kidney-shaped nucleus; two to three times larger than a red blood cell; lack granules (agranulocytes).

Largest leukocytes; highly phagocytic agranulocytes; slower to arrive than neutrophils; primarily function as antigen-presenting cells.

macrophages

Small mononuclear agranulocytes that recognize and neutralize foreign invaders.

lymphocytes

Name the three types of lymphocytes.

B-lymphocytes

Where do B-lymphocytes originate

and how do they compare in size?

What are the two subclasses of B-cells?

Plasma B-cells (produce antibodies) and memory B cells (remember previous exposures for a faster

Name the four subsets of T-lymphocytes.

T-helper (TH​)

What type of immune response do T-lymphocytes play a role in?

The adaptive immune response to pathogens.

Describe NK lymphocytes (large granular lymphocytes).

Larger than B- and T-cells; granules in cytoplasm; attributes of both innate and adaptive immunity; preprogrammed killers of virus-infected and tumor cells.

How do NK lymphocytes differ from NKT lymphocytes?

NK cells are a separate