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Perio > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Define Etiology

A

Etiology - the “science of origin,” studies all factors that may be involved in the development of disease

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2
Q

Etiological Factors with Respect to Perio Dx

A

etiological factors may cause, contribute of modify the development of perio dx

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3
Q

Importance of the Concept of Etiology

A
  • Understanding etiology is essential for a practitioner in order to direct, guide and focus: client education, prevention and treatment
  • Used in risk assessment
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4
Q

Define Risk Assessment and its importance

A
  • Identifying elements that either predispose a client to develop per dx or may influence the progression of disease that already exists
  • It is important in the decision making process in order to individualize treatment to improve client outcomes
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5
Q

How is Risk Assessment Used by Clinicians?

A
  • Use as a tool to predict who is at risk for period dx
  • Aids in diagnosis
  • Informs care planning
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6
Q

What are the two types of significant risk factors?

A

Local: pathogenic bacteria are considered a major local risk factor for inflammatory perio dx
Systemic: currently the most significant systemic risk factors for period dx are smoking tobacco, diabetes and genotype (positive status for a genetic marker related to the inflammatory mediator interleukin-1

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7
Q

Why Do We Focus on Oral PBF?

A
  • because it can help to contribute/initiate the inflammation response in perio dx
  • eliminating or controlling inflammatory perio dx (gingivitis and periodontitis) is highly dependent on plaque control and minimizing plaque retentive facotrs
  • addressing the host response is considered but it is more difficult to address directly
  • But we know that minimizing the role of PBF decreases the level of host response required to keep the host-bacteria interaction in favour of health
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8
Q

How do bacteria cause destruction in period dx?

A
  • Directly: by producing toxins, enzymes, bacterial antagonist, waste products and by direct invasion of gingival tissue
  • Indirectly: by initiating a host response
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9
Q

What are the variables that can upset the balance between bacteria and host?

A
  1. Presence of pathogenic bacteria: acinobacillus actinomycetemcomitans, porphyomonas gingivitis and tannerella forsythia
  2. Susceptibility of the host: partially hereditary, but can be influenced by environmental and behavioural factors (smoking, stress, diabetes, poverty
  3. Absence of or having a small proportion of beneficial bacteria: the presence of non-pathogenic bacteria counteracts or balances the effect of more pathogenic species
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10
Q

What are biofilms?

A
  • A living film containing a well organized community of bacteria that grows on a surface
  • Usually consists of many species of bacteria as well as other organisms and debris
  • Form rapidly on almost any surface that is wet
  • Found nearly everywhere in nature
  • Have major impact on human health
  • Environments: artifiical hip implants, contants lens case, teeth, etc
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11
Q

3 major stages in life cycle of biofilm.

A
  1. Attachment
  2. Growth: secrete a film known as the extracellular slime layer, which acts as a protective shield for the bacteria in the biofilm. The bacteria grow in a mushroom shaped structure that attach to the surface at a narrow base
  3. Detachment: clumps of biofilm break off, are carried away by the fluid and attach to other portions of a surface to form a new bacterial colony
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12
Q

Structural Elements of the Mature Biofilm

A
  • Bacterial micro-colonies
  • Extracellular slime layer
  • Fluid forces of the surrounding saliva
  • Fluid channels
  • Cell to Cell communication system
  • Bacterial signaling
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13
Q

Coaggregation of Bacteria

A

Coaggregation: the cell to cell adherence of one oral bacterium to another, it is not random, each bacterial strain only has a limited set of bacteria to which they are able to adhere
-The ability to adhere and congregate is important in the development of the bacterial biofilm

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14
Q

Supragingival PBF

A
  • Starts at or above the gingival margin and interdental spaces then spreads out evenly in a single layer towards the middle of the crown
  • Can also form in areas of irregularities on enamel surface
  • Is rime importance of initiating and causing gingivitis and participates in the formation of Supra-g calculus and has a greater relevance to caries
  • Uses components of the saliva as a prime nutrient source
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15
Q

Tooth-associated PBF

A
  • Bacteria attach to the tooth surface extending from the gingival margin to the JE at base of pocket
  • Has a greater direct relevance to caries
  • Consists if mostly gram + cocci and short rods in layers closest to the surface and gram - rods and filaments in the outer layer of the mature plaque mass
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16
Q

Subginigval PBF

A
  • Forms below the gingival margin and is more highly associated with periodontitis
  • Environment incomes flow of gingival crevicular fluid (GCF) in the sulcus
  • Nutrient source of these bacteria are the GCF, that several types metabolic byproducts from other bacteria and some host cells
  • Composition depends on pocket depth- apical areas dominated by spirochetes, cocci and rods, coronal areas have more filaments
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17
Q

Sub-g plaque types

A
  1. Sub-g tooth associate plaque: contributes to calculus and root caries
  2. Sub-g tissue-assoicated plaque: contributed to tissue destruction associated with periodontitis
  3. Free floating bacteria: the period pocket may also have free-floating, unattached bacteria that is not part of the biofilm
  4. Host and inflammatory cell influence the establishment and growth of sub-g plaque
  5. Sub-g bacteria have ability to invade dentinal tubules
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18
Q

Tissue-associated PBF

A
  • Bacteria adhere to the epith
  • Adhere loosely to pith of pocket wall
  • Distinctly different microorganisms from tooth-associated biofilms
  • Bacteria here can invade gingival CT, period CT and surface of alveolar bone
  • Contain a large number of spirochetes, flagellated bacteria, gram- cocci and rods
  • S. oralis, S. interdius, P. gingivalis, P. intermedia, T. forsythia, F. nucleatum
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19
Q

What variables influence PBF formation?

A
  • Surface micro-roughness and variations in dentition (mand vs max, ant vs post, interprox vs facial/lingual)
  • Diet
  • Smoking
  • Chemical composition of pellicle
  • Depth pockets
  • Antimicrobial factors in saliva
  • pH of saliva
  • Impact of gingival inflammation
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20
Q

Define Periodontal Dx

A
  • Perio dx encompasses all disease that are associated with the periodontium (gingiva PDL, alveolar bone and cementum)
  • It is essentially an inflammation of the periodontium
  • A perio dx classification system was adopted in 1999 at the international workshop for a classification of Perio DX and Condition organized by the American Academy of Periodontology (AAP)
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21
Q

Perio Classification is based on?

A
  • Etiology: bacteria, systemic influences, med
  • Development: rate of progression
  • Clinical manifestations: how does it present
  • Host response
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22
Q

Why bother with classification?

A

Provides necessary info in:

  1. Accurate communication with other dental professionals and insurance providers
  2. Presenting information to the client about their disease
  3. Formulating individualized treatment plans
  4. Predicting treatment outcomes (prognosis)
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23
Q

The Immune System

A

A complex body defense system that protects the body against bacteria, viruses, fungi, toxins and parasites

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24
Q

Two subdivisions of immune system

A
  1. Innate:
    - Present at birth
    - First line of defence
    - Not antigen specific
    - Present at all times and therefore response is quick
    - Does not improve with repeated exposure to infectious agent
  2. Adaptive:
    - Develops throughout life
    - Second line of defence
    - Antigen specific
    - Lag time between infection and response
    - Memory develops which may provide lifelong immunity to reinfection
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25
Q

Define Host Response

A

-The way an individuals body responds to the infection
-The body responds in 2 ways:
sending certain cells to the infection site and producing biochemical substances to counteract the foreign invaders

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26
Q

Define Overzealous Immune System

A

The immune system can become so intense in its response that it begins to hard the body that is it trying to protect. This response occurs in periodontitis

27
Q

Components of the Immune System that Play an Important Role in Combating Perio Dx

A
  • Cellular Defence (phagocytes, lymphocytes)

- The complement system

28
Q

Major events in the inflammatory response

A
  1. The inflammatory response is triggered by an invasion of a pathogen or injury
  2. Mast cells located in the CT near BV’s release chemicals that dilate the BV and increase vascular permeability
  3. Minutes after the injury there is an increase in blood flow (needed to deliver the cellular defenders) to the area and this higher blood volume heats the tissue and causes it to redden
  4. Within hours, leukocytes pass through the walls of the capillaries into the CT (transendothelial migration) and plasma proteins leak from capillaries and accumulate in the tissue
  5. Leukocytes and phagocytes invade pathogens and release inflammatory mediators that contribute to the inflammatory response
29
Q

Define Inflammatory Mediaters

A

These are biologically active compounds secreted by cells that activate the body’s inflammatory response. Mediators important to periodontitis include: Cytokines (CK), prostaglandins (PG) and metrix metalloproteinases (MMP’s)

30
Q

Describe Acute Inflammation

A
  • A short-term, normal process that protects and heals the body
  • The acute inflammation process is achieved by the increased movement of plasma and leukocytes from the blood into the injured tissues
31
Q

5 Signs of Acute Inflammation

A
  • Heat: a localized rise in temp due to an increased amount of blood at the site
  • Redness: the result of increased blood in the area
  • Swelling/Edema: the result of accumulation of plasma and leukocytes at the site
  • Pain: excessive fluid in tissues puts pressure on sensitive nerve endings, causing pain
  • Loss of function: the result of swelling and pain
32
Q

Describe the Acute Inflammation Response

A
  • The process of acute inflammation is initiated by the BV’s near the injured tissue which alter to allow the release of plasma proteins and leukocytes into the surround tissue
  • PMNs are the first cells to arrive at the site but are short-lived and act during the early stages of inflammation
  • PMNs released cytokines such as TNF and ILs
  • If the body succeed sin eliminating all the microorganisms, the tissue will heal and inflammation will cease
  • If acute inflammation response is not effecting the inflammatory response becomes chronic
33
Q

Describe Chronic Inflammation

A
  • Long-lived, out of control inflammatory response that continues for more than a few weeks
  • It is a pathological condition that can destroy healthy tissue and cause more damage than the original problem
  • Warning signs in acute inflammation are absent in chronic inflammation
  • The problem may go unnoticed by the host
34
Q

Why does Chronic Inflammation Occur?

A

Because the body is unable to rid itself from invading organism. These microorganisms are persistent and stimulate an exaggerated immune response

*when inflammation becomes chronic, the inflammatory response can become so intense that it does permanent damage to the bodies tissues (ex: periodontitis)

35
Q

Chronic Inflammatory Process

A
  • Characterized by an accumulation of macrophages
  • Macrophages engulf and digest microorganisms
  • Leukocytes release inflammatory mediated including IL-1, TNF-alpha and prostaglandins that perpetuate the inflammatory response
  • TNF-alpha contributes to the tissue destruction that characterizes chronic inflammation
  • If infection continues, inflammation can last months or years and if left unchecked the inflammatory response will attack healthy tissue
36
Q

Examples of Chronic Inflammation

A
  • Rheumatoid arthritis
  • Diabetes
  • Asthma
  • Gingivitis
  • Periodontitis
37
Q

Describe Early Cononizers (1)

A
  • First bacteria to colonize the tooth surface are nonpathogenic
  • The ability of early colonizers to attach to the tooth surface lays the foundation for growth of the biofilm
  • Periodontal pathogens are UNABLE to colonize the biofilm until the nonpathogenic species are attached
  • Perio pathogens reamin freely floating in the mouth until early colonizers attach to the tooth
  • The early colonizers send signals (chemicals) to pathogens when conditions are favourable for the pathogenic species to join the biofilm
  • They lay the foundation fro the growth of the biofilm by providing attachment sites and receptors for intermediate and late colonizers-this is called coadhesion
  • They also use up the O2 creating a anaerobic environment that favors the growth of gram - facultative species
38
Q

Who are these early colonizers?

A

These tend to be non-pathogenic aerobic gram +, primarily streptococcal songs and actinomyces viscosus

39
Q

Streptococcal Species

A
  • Early colonizers
  • Many streptococcal species have the ability to attach to the tooth pellicle and to each other
  • Other early colonizer cant attach to the pellicle, but have the ability to coaggregate with the streptococcal species
40
Q

Intermediate (2) and Late Colonizers (3)

A
  • Like the early colonizers, the intermediate and late bacterial colonizers must join the biofilm in the proper sequence
  • Many of the perio pathogens are late colonizers of the biofilm
41
Q

Sequence of Early, intermediate and late colonizers

A
  1. Early colonizers adhere to the pellicle coating the tooth
  2. Intermediate colonizers congregate with the early colonizers
  3. Late (secondary) colonized coaggregate with the intermediate colonizers
42
Q

Who are the intermediate and secondary colonizers?

A

-These tend to be anaerobic gram - living in a O2 deprived environment. Porphyromonas gingivalis, prevotella intermedia and fusobacterium nucleatum

43
Q

Explain the importance of early colonizers

A
  • Perio 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
  • Everytime the biofilm is disrupted, the process must start all over again with the early colonizers
44
Q

3 Ways Local Contributing Factors Increase the Risk of Disease

A
  1. Increase biofilm retention (rough edge on a restoration)
  2. Increase biofilm pathogenicity (biofilm covered calculus deposit)
  3. Cause direct damage to periodontium (heavy chewing forces on a tooth)
45
Q

Some examples of local contributing factors are:

A
  • Dental Calculus
  • Faulty dental restorations
  • Dental Decay
46
Q

Factors that increase biofilm retention

A

Dental calculus and tooth morphology

47
Q

How long can mineralized PBF form once PBF is matured?

A

48hr to 2 weeks after PBF formation

48
Q

Mechanisms of Increasing Plaque Retention Due to Calculus Deposits

A
  • As calculus builds up, it becomes irregular, forming ledges on the teeth
  • Plaque control becomes difficult or impossible in these areas
  • Plaque retention on irregular calculus increases risk for disease
49
Q

Types of Calculus

A
  1. Brushite Crystalline form: newly form calculus
  2. Octacalcium Phosphate crystalline form: less than 6 months old
  3. Hydroxyapatie crystalline form: mature deposits greater than 6 months old
50
Q

Composition of Calculus

A
  1. Inorganic about 70-90%, primarily calcium phosphate, but also contains some calcium carbonate and magnesium phosphate
  2. Organic about 10-30%, includes material derived from PBF, dead pith cells and dead WBCs
51
Q

3 Modes of Calculus attachment to the tooth surface

A
  1. Attachment to the pellicle
  2. Attachment to the tooth irregularities
  3. Attachment by direct contact to the tooth
52
Q

Tooth morphology and increased plaque retention

A

-Morphology is the study of anatomic surface features of teeth. Morphology that can increase biofilm retention include: poorly contoured restoration, untreated tooth decay, and groove or concavities in the tooth surface

53
Q

Define Pathogenicity

A

The ability of the bacteria in a biofilm to produce perio dx
-Mature PBF is more pathogenic than the biofilm first developed (changes from gram + aerobic cocci and rods (can cause gingivitis) to gram - anaerobic rods (which can cause periodontitis)

54
Q

Causes of direct damage to the periodontium

A
  • Food impaction (can strip gingiva, nutrient to tooth decay, alterations in gingival contour
  • Patient habits (improper use of self-care aids
  • Faulty restorations (a crown margin that is closer than 2mm to the crest of the alveolar bone can result in bone respiration
  • Occlusal forces
55
Q

Excessive Occlusal Forces

A

Parafunction occlusal forces result from tooth to tooth contact when not in the act of eating (ex: clenching and bruxism), which can cause bone resorption (causing a more rapid destruction by existing periodontitis)

56
Q

Signs of trauma from occlusion

A
  • Tooth mobility
  • Sensitivity to pressure
  • Migration of teeth
  • Enlarged, funnel shaped PDL space
  • Bone resorption
57
Q

Examples of systemic risk factors

A
  • Tobacco use
  • Diabete mellitus
  • Leukemia
  • HIV- infection
  • Osteoporosis
  • Hormonal variation
  • Genetic risk factors and down syndrome
  • Systemic medication
58
Q

Another name for gingiva, manifestation of HIV infection

A

Linear Gingival Erythema

59
Q

Functions of Prostaglandins

A
  • Powerful inflammatory mediates
  • Most cells can produce prostaglandins especially macrophages
  • Increase permeability and dilatation of Bv’s (increased redness and deem) to promote increased movement of immune cells and complement to the infection site
  • Trigger osteoclasts: bone consuming cells to destroy the alveolar bone
  • Promote the overproduction of destructive MMP enzymes
60
Q

Function of Prostaglandins E

A

PGE: initiate most of the alveolar bone destruction in periodontitis

61
Q

About Matrix Metalloproteinases (MMP)

A
  • Family of atlas 12 different enzymes
  • produced by PMNs, macrophages, fibroblasts and JE cells
  • Enzymes act together to breakdown CT matrix
62
Q

Functions of MMP (in health)

A

-In health, MMPs facilitate normal turnover of the perio CT matrix

63
Q

Function of MMP in Chronic Bacterial Infection

A
  • Large amounts of MMPs are released in an attempt to kill invading bacteria
  • Overproduction of MMPs results in breakdown of CT of the periodontium
  • High MMP levels results in extensive collagen destruction in perio tissues
  • Collagen provides the structural framework of all perio tissue, resulting in recession, pocket formation, attachement loss and tooth mobility

Perio (2 decks)

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