perio exam idek just know everything

pathway of infection in horizontal bone loss

gingival connective tissue, alveolar bone, pdl

pathway of infection in vertical bone loss

gingival connective tissue, pdl, alveolar bone

cementum

-Protects the dentin of the root and anchors the end of the PDL fibers to the tooth so that the tooth stays in its socket

-thin, hard, mineralized

-light yellow

-does not have its own blood or nutrient supply

acellular cementum

no cells and is at cervical portion

cellular cementum

at apical portion of root and keeps forming

5 functions of pdl

supportive, sensory, nutritive, formative, resorptive

three forms of periodontitis

-necrotizing periodontal diseases

-periodontitis

-periodontitis as a manifestation of systemic disease

two classes of gingival disease and conditions

-gingivitis : dental biofilm induced

-gingival disease : non dental biofilm induced

what is the most common form of periodontal disease

dental biofilm induced

what does alveolar crest group do (or where is it)

extend apically from cervical cementum

what does alveolar crest group resist

resists horizontal and extrusive movement of the tooth

what does horizontal fiber group do (or where is it)

runs in horizontal direction - goes straight across - from cementum to bone

what does horizontal fiber group resist

horizontal pressure against crown of tooth

what does oblique fiber group do (or where is it)

runs diagonal direction

what does oblique fiber group resist

Vertical pressures that threaten to drive the root into its socket

what does apical fiber group do (or where is it)

extends from the tooth apex to bone

what does apical fiber group resist

Forces that might lift the tooth out of its socket

what does interradicular do

occurs only in multirooted teeth in the furcation area to stabilize the tooth in its socket

what is epithelial tissue characterized by

many cells, sparse ecm, avascular

what is connective tissue characterized by

sparse cells, many ecm, vascular

what is oral epithelium characterized by (boundary and keratinization?)

wavy boundary and keratinized (& partially nonkeratinized)

what is sulcular epithelium characterized by (boundary and keratinization?)

smooth boundary and nonkeratinized

what is JE characterized by (boundary and keratinization?)

smooth boundary and nonkeratinized

dentogingival fibers

extends from the cementum into the gingiva, providing support and attachment to the gingival tissue

circular fibers

encircle the tooth like a ring, helping maintain the gingival contour and position

if it is a 3 wall bony defect, how many walls are standing

3 walls

suprabony defect

JE is located coronal to the crest of alveolar bone

t or f: facultative cells can adapt

true

t or f: obligate anaeorbe cannot live in presence of o2

true

once attached to a surface, bacterium exhibit characteristics that are different from those that ...

it had as a free floating bacterium

more than 99% of all bacteria live as ...

attached bacteria

autograft

bone harvested from patient's own body (highest osteogenic potential)

allograft

bone harvested from another human (lowest osteogenic potential)

xenograft

bone harvested from another species

alloplast

synthetic bone like material

ostectomy

removal of tooth supporting bone

osteoplasty

reshaping of surface bone contours without removing tooth supporting bone

minocycline hydrochloride microspheres (arestin)

- Controlled-release mechanism delivers drug in powdered biodegradable microsphere form

-Broad-spectrum, semisynthetic tetracycline derivative that is bacteriostatic

healing by repair

formation of tissues that do not fully restore original architecture or original function

healing by reattachment

reunion of connective tissue and roots that had been separated by incision or injury, but not by disease

healing by new attachment

union of pathologically exposed root with connective tissue or epithelium

healing by regeneration

biologic process by which the architecture and function of lost tissue is completely restored

healing by primary intention

wound margins closely adapted to each other

healing by secondary intention

Wound margins not closely adapted

Healing by tertiary intention

wound cleared, deliberately left open to drain ; later closed

gingiva

Provides a tissue seal around the cervical portion of the tooth, covers the alveolar processes of the jaws, and holds the tissue against the tooth during mastication

alveolar bone

Surrounds and supports the roots of the tooth

pdl

Suspends and maintains the tooth in its socket

mmps

Involved in collagen destruction. In health they facilitate normal turnover of the connective tissue.

prostaglandins

Involved in alveolar bone destruction. Increase vascular permeability allowing immune cells and complement to move to the infection site.

cytokines

Initiate tissue destruction in bone loss. Recruit PMNs and macrophages to the infection site.

Proinflammation mediators in periodontitis:

Prostaglandins, thromboxanes, prostacyclins, and leukotrienes

with catabasis, pro-resolving lipid mediators work in programmed systemic process to:

▪Terminate PMN recruitment to site

▪Stimulate macrophages to remove dead cells

▪Promote antibacterial activities

-Promote tissue repair and regeneration

Key cytokines in periodontitis:

-IL-1

-IL-6

-IL-8

-TNF-α

Page and Schroeder in 1976 outlined pathogenesis of gingivitis and periodontitis with four histologic stages:

-initial lesion

-early lesion

-established lesion

-advanced lesion

gram negative bacteria activate ....

complement system

what is most important part of complement system

opsonization

four parts of complement system?

-immune clearance

-opsonization

-recruitment

-destroy pathogens

bone remodeling cycle steps

-resorption

-reversal

-resting

-formation

virulence factor: lipolysacchardies

•Mature biofilm contain Gram-negative bacteria

•Gram-negative bacteria have LPS on their outer membrane

•LPS initiates inflammation in periodontal tissues

a periodontal pocket is a pathologic deepening of the gingival sulcus as a result of ...

-apical migration of the JE

-destruction of periodontal ligament fibers

-destruction of alveolar bone

oral epithelium

covers the outer surface of the gingiva

sulcular epithelium

lines the gingival sulcus

je

forms base of sulcus and attaches the gingival epithelium to the tooth

important bacteria in periodontitis - all gram neg

-AA Aggregatibacter actinomycetemcomitans

-TF Tanerella Forsythia

-FN Fusobacterium nucleatum

-PG Porphryomonas gingivalis (MOST IMPORTANT)

5 steps of structure and colonization of oral biofilms

-initial attachment of microbes

-irreversible/permanent attachment

-mature phase 1 self protection

-mushroom shaped microcolonies

-dispersion

importance of early colonizers

-Free-floating periodontal pathogens cannot cause disease.

-Periodontal pathogens cannot colonize the biofilm until the nonpathogenic early colonizers attach to the tooth.

-If the biofilm is disrupted daily by self-care, the biofilm will always be reforming.

-Every time the biofilm is disrupted, the process must start all over again with the early colonizers.

early stages of bacterial colonization

-colonization of pellicle

-early gram +

-strep mitas

-s. oralis

sequence of attachment: within minutes

Pellicle film forms over the crown of the tooth and free-floating microbes attach to the surface

sequence of attachment: within 2-4 hours

Early colonizers attach supragingivally.

sequence of attachment: 6-12 hours

Microbes produce the initial extracellular protective matrix.

sequence of attachment: day 7

Mature supragingival biofilm forms

sequence of attachment: 3-12 weeks

Subgingival biofilm starts to form.

innate immune system

-present at birth

-not antigen specific

-does not improve with repeated exposure to infectious agent

adaptive immune system

—Develops throughout life

— Antigen specific

— Lag time between infection and response

— Memory develops which may provide lifelong

immunity to reinfection

pmns

neutrophils: rapid responders ; first line of defense

Five major classes of immunoglobulins are

- Immunoglobulin M (IgM)

- Immunoglobulin D (IgD)

- Immunoglobulin G (IgG)

- Immunoglobulin A (IgA)

- Immunoglobulin E (IgE)

Five Classic Signs of Acute Inflammation

heat, redness, swelling, pain, loss of function

Important mediators include: (inflammatory chemical mediators)

-IL-1, IL-6, and IL-8

-Leukotrienes

- Prostaglandins

- TNF-alpha

brushite

newly formed calculus deposit

octacalcium phosphate

primary form in deposits less than 6 months old

hydroxyapatite

primary form in deposits older than 6 months

association

▪Indicates relationship between two or more variables

▪Cannot explain how or why variables are related

causation

▪Means variable A causes or leads to variable B

▪Difficult to determine; may involve multitude of factors

peri implantitis

No single microorganism implicated as causative agent