4. Chronic vs. Aggressive Periodontitis Flashcards

1
Q

Classifying Periodontal Diseases
• Clinical Characteristics paradigm (1870–1920)
• Classical Pathology paradigm (1920–70)
• Infection/Host Response paradigm (1970–present)

• Back 150 years ago periodontists didnt really understand the nature of the disease so they only used the clinical presentation to classify the disease.
• In 1920 there was more research and they started to realize there is more to the disease and they though that perhaps it had to do with an non-inflammatory destruction, a totally different animal. At that time it was called the ____ paradigm.
• After a few years people understood that there was still bacteria present. Both chronic/ aggressive perio involve infections and a host-response action
• Since 1970 this concept has been accepted.
• From 1970 to 2017 most people thought that aggressive/chronic perio were totally different
but now the evidence has shown that the pathogenesis is very ____, even if the bacteria differ slightly. There is no clear cut difference between these two diseases. The only difference is the degree of ____.

A

classical pathology
similar
host response

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2
Q

Historical background

  • Aggressive periodontitis was first noticed in the 1920s by Gottlieb who believed it was due to a ____ degeneration of the bone with some “impairment cementum deposition”
  • In 1950 AAP defined the disease as ____: degenerative and non-inflammatory destruction of the periodontium.
  • After 16 years AAP discarded this term because of lack of evidence of this non- inflammatory destruction. They started to notice it was related to bacteria and inflammation.
  • In 1967 they started the term ____ based on the clinical presentation of this happening mostly (not always) at a young age though.
A

non-inflammatory
periodontosis
juvenile periodontitis

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3
Q

Historical background cont.

• After a few years AAP classified this disease as ____. This was also subclassified based on the onset of the disease.
◦If the onset was before the age of 11, it was called ____ ◦If from 11-20 it was called ____
◦If from 20-30 it was called rapid ____.
• In 1999 they questioned: what if the patient is 50 years old but the disease is very aggressive? The AAP then decided to define the disease based on the rapid progression and not based on age. It was considered an age ____ disease but not age dependent.

They called it ____ which has been used for the last twenty years
• In 2017 AAP and EFP (the european counterpart) in a committee decided to combine chronic and aggressive periodontitis into the same group called ____. They use ____ to define the disease in more detail.

A
early onset periodontitis
prepubertal periodontitis
juvenile periodontitis
rapid progressive periodontitis
associated

aggressive periodontitis
periodontitis
staging and grading

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4
Q

• This was the 1989 classification before the 1999 armitage.
• You dont need to to know details of this but she wanted to show that this classification is
based on age. Adult periodontitis here is almost equal to chronic periodontitis with a slow rate of disease progression (except that the definition here requires that the onset occurs after age 35).
• Early onset periodontitis is a disease defined as the onset occurring before the age of ____
• Periodontitis associated with systemic disease is in the 1999 armitage and 2017
classification so it didnt change much
• We also still have necrotising ulcerative periodontitis in the 1999/2017 classification
• Refractory periodontitis was removed in the new classification
• So the 1989 classification is based on what? It was based on ____

A

35

age

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5
Q

American Academy of Periodontology International Workshop for Classification of Periodontal Diseases, 1999

• The disease periodontitis can be subclassified into the following four different types on the basis of clinical, radiographic, historical, and laboratory characteristics.
✓ ____
✓____
✓ Periodontitis as a manifestation of ____ disease
✓ ____

A

chronic periodontitis
aggressive periodontitis
systemic
necrotizing periodontitis

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6
Q

1999 Classification of Periodontal Diseases

• She sent us a copy of the 1999 paper as a reference but we dont have to read it.
• When she took the perio board this is the table she was grilled on in every case.
• Today she will focus on the periodontitis part. There is ____ forms of aggressive and chronic periodontitis but they each use different definitions
• Take a look at the periodontitis as a manifestation of systemic disease. If the patient is
defined as any of these and they also have periodontitis, your diagnosis shouldnt be chronic or aggressive perio but it should be defined as ____ as a manifestation of systemic disease

A

generalized and localized
periodontitis
periodontitis

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7
Q

Clinical Features

Chronic periodontitis is initiated and sustained by ____ but ____ mechanisms play an integral role in its pathogenesis

____ and subgingival plaque (and calculus)
Attachment loss
____ loss (angular/vertical or horizontal)
Root furcation involvement
Increased tooth ____
Change in tooth position
____ loss
Gingival swelling, redness, and loss of gingival stippling
Altered gingival ____ (rolled, flattened, cratered papillae, recessions)
Pocket formation
____ on probing

• This is the most ____ periodontitis
• It is initiated by bacterial plaque but the host defense plays an integral role in the disease
progression
• You have already seen these clinical features: you see some plaque, calculus, gingival
inflammation and you have deep pocket formation.
• You may have bleeding on probing and attachment/bone loss, which are the key factors for
periodontitis.
• When you go back to the posterior molars you will have root furcation involvement, tooth
mobility, change in tooth position, and eventually tooth loss

A

bacterial plaque
host defense

supragingival
bone
mobility
tooth
margins
bleeding
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8
Q
  • These are classic pictures of chronic periodontitis: you will see plaque and the patients oral hygiene is not good.
  • In the X ray you will ____ and bone loss as well as ____and furcation involvement
A

attachment

mesial tilting

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9
Q

• Gingivitis is when you have no ____ or bone lose and is ____
• Chronic periodontitis has bone/attachment loss and is ____
• Dr Wang mentioned she had a question on this in the last year final exam
• Not all sites with gingivitis progress will progress to periodontitis but all periodontitis
progresses from ____
• Difference between peri-implant mucositis and implantitis: If you have ____ then you
have periodontitis (irreversible) while peri implant mucositis is ____

A
attachment
reversible
irreversible
gingivitis
bone loss
reversible
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10
Q

Overall Characteristics

Prevalent in adults but can occur in ____ and adolescents
____ Specificity
Amount of periodontal destruction is ____ with the presence of local factors Subgingival biofilm varies between ____ & SITES
Subgingival calculus frequently found
____ rate of progression, with possible periods of rapid progression

Possibly modified by or associated with the following:
Local ____ factors (e.g., tooth-related or iatrogenic factors) ____ diseases (e.g., diabetes mellitus, HIV infection)
____ factors (e.g., cigarette
smoking, emotional stress)

• The overall characteristics of chronic periodontitis is that it usually occurs in adults, though not always (hence the name change in 1999)
• It is a site specific disease which means if you probe a tooth the deepest pocket is usually ____ because its hard to clean.
• Amount of periodontal destruction is consistent with the presence of local factors, which means that if you have more plaque/calculus you will have more disease progression
• Read rest of slide
• Iatrogenic factor example: an ill-fitting crown can accumulate alot of plaque.
• Tooth related example: furcation involvement means it will be hard to clean and cause further
progression of disease
• Systemic disease example: there is evidence which shows a bilateral relationship between ____ and periodontitis (this has been incorporated into the 2017 classification)
• Environment example: smoking has strong evidence “relating to” periodontitis

A
children
site
consistent
subjects
slow to moderate
predisposing
systemic
environmental

interproximally
diabetes

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11
Q

1999 AAP International Workshop
Chronic periodontitis can be further characterized by extent and severity

EXTENT:
- Localized: < ____% of sites involved
Generalized: > ____% of sites involved

SEVERITY:
Slight (Mild): ____ mm of clinical attachment loss Moderate: ____ mm of clinical attachment loss Severe: ≥ ____ mm of clinical attachment loss

• Also on the quiz: The definition of clinical attachment loss (CAL) is from ____ to the ____ (said it 3X). Note: we are probing from the ____ to the base of pocket
but this is NOT the CAL

A

30
30

1 to 2
3 to 4
5

CEJ
base of pocket

gingival margin

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12
Q

2015 AAP Task Force Report
• Task Force preferred to use the percentage of affected ____ rather than the percentage of affected sites as an extent descriptor for chronic periodontitis

Localized: < ____% of teeth involved
Generalized: > ____% of teeth involved

  • They still used 30% but used teeth involved instead of sites because it was too hard to calculate
  • If one tooth has one site greater than 5 mm CAL then it is counted as one tooth. If one tooth has six sites greater than 5mm CAL then it is still counted as one tooth
  • In the 2017 classification it is still based on the teeth involved instead of sites. They also introduce ____ depth, ____ on probing, and radiographic ____ to help define the severity of the disease. Some people just hate to calculate CAL so they would rather just use pocket depth because it is sometimes hard to detect the CEJ.
  • She said not to worry about the details here but just look at the the clinical attachment loss. There are the ____ numbers in the 2017 classification as the 1999 armitage.
A

teeth

30
30

pocket
bleeding
bone loss

same

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13
Q

Disease Progression

Continuous model
The disease progression is ____, with affected sites showing a ____ progressive rate of destruction throughout the duration of the disease

Random burst model
The periodontal disease progresses by ____ bursts of destruction followed by periods of no ____. This pattern of disease is ____ with respect to the tooth sites affected and the chronology of the disease process

Asynchronous multiple-burst model
The periodontal destruction occurs around affected teeth during ____ periods of life and that these bursts of activity are interspersed with periods of ____ or remission. The chronology of these bursts of disease is ____ for individual teeth or groups of teeth

A

slow and continuous
constantly

short
destruction
random

defined
inactivity
asynchronous

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14
Q

• The x axis is the attachment loss (I think she is referring to the vertical lines)
• Continuous model: (remember this is a site specific disease) some sites dont progress at all
but in this site it slowly and ____ increases.

• Random burst model: in this site, it starts to have attachment loss and then it is ____ for
a while and then it bursts then inactive and bursts again. So you never know when the disease will progress.

• Multiple burst model: this site repeatedly has ____ in a short period of time and is inactive for a long time. For example today you have 0.1mm CAL, and then after 2 months you have another 0.3mm CAL, and after 2 more months you have another 0.5mm attachment loss but consistent for ten years (Note: her example had other numerical values but then she corrects herself later to make it seem like the disease is not so rapid).

A

continuously
inactive
bursts

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15
Q

Epidemiology
• Chronic periodontitis is the most ____ occurring form of periodontal disease
• Increases in prevalence and severity with ____ (chronic periodontitis is a age-____ disease)
• Disease higher in ____, Mexican-Americans, smokers, pts living below the federal poverty level and those with less than a high school education

• So it is an age associated disease but not age dependent.

A

occurring
age
associated
men

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16
Q

NHANES 2009-2010

• NHANES is a nationwide survey to evaluate US population health and nutrition status.
• This survey has occurred multiple times but in this period it was found that ____% of Americans over ____ had ____ periodontitis (they did not differentiate
between the two).

Note: it says 64.7 million but that is 50%.
• Among the 50%, 30% have ____ periodontitis
• Probably 9% are mild or severe (**Not sure how this adds up)
• The graph shows you that the as people get older, the prevalence of periodontitis ____, especially moderate periodontitis

A
50
30
acute or chronic
moderate
increases
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17
Q

Pathology and Risk Factors

Microbiological aspects
- Microbial ____ (biofilm) is a crucial factor in inflammation of the periodontal tissues, but the progression of gingivitis to periodontitis is largely governed by ____ risk factors

Red complex—____, ____ & ____

Local factors

____-retentive factors are important for the development and progression of chronic periodontitis, because they retain microorganisms in proximity to the periodontal tissues, thereby providing an ecologic niche for biofilm maturation

Calculus , tooth morphology , overhanging margins 


  • Tooth morphology such as ____ and ____ involvement will influence the disease progression
  • Overhanging margins will also trap plaque and need to be corrected
A
plaque
host-based
prophyromonas gingivalis
tannerella forsythia
treponema denticola

plaque
palatal grooves
furcation involvement

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18
Q

Pathology and Risk Factors

Systemic factors
Chronic periodontitis also occurs with severe systemic diseases and systemic disorders
-
____ syndrome, Ehlers–Danlos syndrome, ____ syndrome, Cohen syndrome

____ mellitus, cardiovascular disorders, stroke, lung disorders

____, severe unbalanced diet, stress, dermatologic, hematologic, and neoplastic factors: interfere with periodontal inflammatory responses

Immunologic factors
• The onset, progression, and severity of the disease depend on the individual host’s ____
- Proinflammatory mediators modify innate and adaptive immune responses at periodontal sites ( ____, IL-6, IL-8, PGE2, TNF-alpha )
‣ ____: soft and hard tissue degradation

  • Alot of systemic diseases (especially syndromes) are related to chronic periodontitis. But if any of the patients have these syndromes, what is the diagnosis? Periodontitis associated to ____ diseases
  • Diabetes and other diseases related to inflammation are closely related to chronic periodontitis. Some of the diseases are bidirectional, ie diabetes.
  • Immune factors play a key because the host response is the key factor to disease progression, ie: proinflammatory cytokines will modify innate and adaptive immune responses at periodontal sites and are associated with periodontal disease
  • MMP and RANKL are one of the most of important factors that will cause soft and hard tissue degradation
A

papillon-lefevre
kindlers

diabetes
osteoporosis

immune response
IL1beta
MMPs & RANKL

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19
Q

Pathology and Risk Factors

•Genetic factors
Candidate genes studies (CGA) v.s. Genome-wide associations studies (GWAS)

Much attention has focused on polymorphisms associated with the genes involved in cytokine production; however, relation to chronic periodontitis has ____ been elucidated

Possible gene candidates include: ____ TNF-alpha, FC-gamma-R, Vitamin D receptor, IL-10

Environmental and behavioral factors

____ is a major risk factor for the development and progression of generalized chronic periodontitis (dose-dependent effect)

____ factors (e.g., stress, depression) also negatively influence the progression of chronic periodontitis

If you have a target gene you can use a candidate gene study but alot of focus is now is on the single nucleotide polymorphisms related to chronic/aggressive periodontitis but the evidence is still pretty weak.
• The reason for the weak evidence is because it is a ____ disease and its difficult to find direct correlations with single genes. This is why GWAS is used now because it can screen ____ genes to see relationships.
• She lists some candidate genes here: “but you saw that and it is enough”… (**Maybe it is not important?)
• Environment and behavioral factors: Smoking has the highest evidence and is a dose dependent effect. 1 pack-year is 20 cigarettes but the key number ____ cigarettes per day. If you smoke that much you are considered high risk compared to a former/non smoker.

A
not
IL1
smoking
psychological
multifactorial
multiple
10
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20
Q

Treatment of Chronic Periodontitis

Oral ____ instructions
Non-____ periodontal therapy
____ periodontal therapy Periodontal ____

A

hygiene
surgical
surgical
maintenance

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21
Q

Aggressive Periodontitis
• Aggressive periodontitis is much less ____ than chronic periodontitis and usually affects a narrower ____ of young patients
• Aggressive periodontitis may be further classified into ____forms
• Both forms of aggressive periodontitis are ____-induced infections, and ____ to plaque bacteria are responsible for most of the tissue destruction. The plaque biofilms are often clinically ____ than with chronic periodontitis. This is particularly true in cases of ____

A
common
range
localized and generalized
plaque
host responses
thinner
LAP
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22
Q

Primary Features of AgP
• Except for the presence of periodontitis, patients are otherwise clinically ____
• ____ attachment loss and bone destruction
• ____ aggregation

• Primary features means that all ____ perio, generalized or local, must meet
this criteria.

A

healthy
rapid
familial
aggressive

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23
Q

Secondary Features of AgP

• Amount of microbial deposits is ____ with severity of periodontal tissue destruction
• Increased proportions of ____ and, in some populations, ____ may be increased
• ____ (neutrophil) abnormalities
• ____-responsive macrophage phenotype
- Elevated production of ____ and interleukin-1β (IL-1β)
• Progression of attachment loss and bone loss may be ____

• Secondary features are not ____ present, though it is found in most cases
• Reads first line…usually you have a thin biotype with severe attachment and bone loss.
• Remember this bug: AA which is often mentioned whenever discussing localized aggressive
periodontitis
• AA is found in increased proportions in most of the cases (not all) and PG is mostly correlated
with AA
• PG however plays a role in both chronic and aggressive periodontitis
• This is why it is not ____ to use bacteria to differentiate between the two

A
inconsistent
actinobacillus actinomycetemcomitans
porphymonas gingivalis
phagocyte
hyper
PGE2
self-arresting

universally
best

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24
Q

Self-limiting (burn out)

• A 12 year old patient comes to the office. After taking x ray, you see severe bone loss
• When the patient comes back 4 years later the lesion doesnt ____ too much.
• This an example of self ____ and burn out that happens in only certain cases.
• The reason for this may have to do with ____ which control the disease (which
she says she will talk more about later)

A

progress
limitation
antibodies

25
Q

Localized Aggressive Periodontitis (LAP)

____ onset (11-13 yrs old)

Localized ____ presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first ____, and involving no more than two teeth other than first ____

Robust serum ____ response to infecting agents

• Read slide
• She refered to the second bullet as a “First Molar - Incisor Pattern”
• If you have involvement of three teeth other than first molar and incisor it is
considered ____.
• “They” dont use 30% to define localized perio they use this definition instead
• Third bullet: This is one of the theories to explain why it is localized
• Sometimes patients progress to generalize aggressive periodontitis but sometimes they have LAP for their entire lives

A

circumpubertal
first molar/incisor
molar
molars and incisors

antibody

generalized aggressive periodontitis

26
Q

LAP

• This is the classical presentation of LAP.
• Referring to the photos: this a young patient that looks clinically good other than than maybe the lower anteriors though there isnt really too much inflammation.
• However when looking at the blue block in the lower anteriors you can see
attachment loss of about ____% and you can see a vertical boney defect in the ____ area (blue box in molar area)
• When you bring the patient’s ____ in, she has a similar pattern and also has bone loss/vertical defect in the molar area

A

70
first molar
sister

27
Q

Clinical Features of LAP

Lack or ____ clinical inflammation

Amount of ____ inconsistent with the amount of periodontal destruction

Presence of ____ periodontal pockets

Elevated level of_ ___.

• Btw, What disease is usually not site specific? ____ because the
connective tissue orientation is different than a tooth. It is parallel, so it is easy for the disease to spread around the whole implant. Usually you don’t have one site with bone loss but its all around the implant. With chronic/aggressive you can have
a deep pocket in one area and it doesn’t spread around the whole tooth

A
minimal
plaque
deep
Aa
Pg
peri implantitis
28
Q
Radiographic Features of LAP
 - Typical pattern of bone loss
•Vertical bone loss around the \_\_\_\_
“\_\_\_\_” defects
“\_\_\_\_” pattern
Rate of bone loss is about \_\_\_\_ times faster than in chronic periodontitis

• The typical bone loss pattern is usually a vertical defect.
• To determine the bone loss pattern you use the CEJ of the adjacent teeth and you
draw a line between them. If the bone loss is parallel to the CEJ line then it is horizontal. When you take an x ray sometimes it isnt straight so dont use the term oblique or flat to define the bone loss.
• At the anterior area it usually starts as a vertical bone loss which can eventually become ____ as well.
• This is also sometimes called an “arch shape lesion”
• It can happen ____, which is called a “mirror image” pattern
• The rate of bone loss is 3-4 times faster than chronic

A

first molars and incisors
arc-shaped
mirror-image
3-4

horizontal
bilaterally

29
Q

Generalized Aggressive Periodontitis (GAP)

Usually affects people under ____ years old, but patients may be older

Generalized ____ attachment loss affecting at least ____
permanent teeth other than the ____

Pronounced episodic nature of the destruction of attachment and alveolar bone

____ serum antibody response to infecting agents

A
30
interproximal
three
first molars and incisors
poor
30
Q

GAP

• 32 year old patient
• When you first see this case you probably wont know if it is chronic or aggressive
perio but when you see the ____, it gives you a hint that it is probably aggressive perio.

A

age

31
Q

Clinical features of GAP

____ plaque, elevated ____.

2 gingival tissue responses
Destructive stage
Severe, acutely inflamed tissue that is often ____, ulcerated, and ____
____, suppuration, active loss of attachment & bone

Quiescence stage
Tissues appear pink, free of ____, & occasionally with some degree of ____
Deep pockets, bone & attachment levels relatively stable

• There are two gingival responses. If you are in the active disease stage it is the
destructive stage. The tissue can look inflamed, ulcerative, and bleeding on
probing. This corresponds to the bone loss.
• We talked about self limitation before (referring to the quiescence stage);
sometimes the disease will slow down and the tissue will look less inflamed and you can even get stippling, which is usually found in healthy gingiva (even if this tissue isnt healthy)
• You still will have bone loss but the levels are relatively stable

A

minimal
Pg, Tf, Aa

proliferating
fiery red
bleeding

inflammation
stippling

32
Q

Radiographic Features of GAP


Severe bone loss associated with the ____ number of teeth to advanced bone loss affecting the majority of teeth in the dentition

A

minimal

33
Q

Epidemiology

The diagnosis of aggressive periodontitis in epidemiological studies is ____, because all primary criteria for the disease, rapid progression, systemic health, and familiar aggregation are difficult to reliably assess in the setting of such a study 


A

difficult

34
Q

How To Distinguish Between “Chronic & Aggressive Periodontitis” in Epidemiology Study ?

• They propose an adaptation of the 2007 CDC/AAP definitions to incorporate an assessment of the loss of periodontal tissue in relation to ____, as follows.

• Aggressive periodontitis
• ≤ 25 years: the presence of two or more interproximal, nonadjacent sites with attachment
loss of ≥ ____ mm occurring at a minimum of two different teeth and accompanied by bleeding on probing
• 26 ~ 35 years: the presence of two or more interproximal, nonadjacent sites with attachment loss of ≥ ____ mm occurring at a minimum of two different teeth and accompanied by bleeding on probing

• They used ____ and amount of ____ to estimate the progression of the disease

A
age
4
6
age
attachment loss
35
Q

Prevalence

The prevalence of aggressive periodontitis varies significantly between different ____ locations and between different ____
• Aggressive periodontitis is most prevalent in ____ (1 to 5%)
In North America: 0.1–0.2% of Caucasians, 0.5–1.0% of Hispanics , 2.6% of Black

In the United States, a national survey of adolescents between the ages of 14 and 17 years
Localized juvenile periodontitis: ____% (greater prevalence in blacks)
Generalized juvenile periodontitis: ____%
The prevalence ratio among the two sexes is a ____ variable

A
locations
race/ethnicities
african populations
0.53
0.13
descriptive
36
Q

Does Aggressive Periodontitis Affect PRIMARY DENTITION ?

Some studies showed that the age onset of aggressive periodontitis may be during the ____ dentition (7-12 yrs old), and in these individuals the disease maybe affect both the ____ teeth

• If severe periodontal disease affecting primary dentition and leading to early tooth exfoliation
Usually interpreted as “periodontal manifestations of ____ disease”, like leukocyte adhesion deficiency

➡ Conclusion: The ____ teeth may also be affected, although early exfoliation of these teeth due to periodontal tissue loss is not ____

A

mixed
permanent
systemic

primary
common

37
Q

Microbiology
The deposition of ____ is a prerequisite to the initiation of aggressive periodontitis
____ is generally accepted as the primary etiologic agent in most but ____ all cases of localized aggressive periodontitis
The highly leukotoxic ____, was found to be directly related to the occurrence of LAP in children in Northern Africa
Human investigations have indicated that A.a. is able to ____ across the junctional epithelium and invade the underlying connective tissue
LAP is clearly not a monoinfection with A.a. but features a ____ biofilm. Supporting this notion are reports of confirmed cases of LAP that did not carry A.a.

• What is the JP2 clone of AA? They have a deletion at the leukotoxin ____ part.
This deletion causes 10-20 fold more leukotoxin production which is a key pathogenic factor of AA. This kills PMNs and ____ which is why it is directly related to the occurrence of LAP in northern Africa
• Another study found that AA can invade connective tissue and they do not just stay on the ____ surface. This is why some people believe you should use systemic antibiotics to treat LAP while simultaneously doing SRP, because you cannot kill the bacteria that has already invaded the tissue

A
dental plaque
Aa
not
Aa
translocate
polymicrobial

gene operon
macrophages
tooth

38
Q

Key Pathogens in Different Forms of Periodontitis

  • Take a look at AA, you can find it in 81.8% of LAP. This means about 20% of cases dont have it.
  • Aggressive periodontitis is referring to the generalized form. It is more related to ____
A

PG
PA
TF

39
Q

Host Response

____ neutrophil model or ____ neutrophil model

____-responsiveness of monocyte from localized aggressive periodontitis patients with respect to their production of PGE2 in response to LPS

The stronger activation of natural killer cells and natural killer T cells in patients with aggressive periodontitis was suggested to be ____ for the more pronounced tissue destruction

• The only difference between chronic and aggressive is the severity of ____. In aggressive perio the patient’s host response is most likely just more aggressive.
• There are a couple of models to explain this.
• In the impaired neutrophil model the neutrophil function is ____ which will influence the phagocytosis and intracellular killing ability of the PMN
• In the primed/hyperactive neutrophil model a hyperactive PMN will cause more ____ and will cause more destructive enzyme release. This means the ____e is causing periodontal destruction
• The monocyte also plays a key in the hyperreactiveness because it will produce more
PGE2 in response to LPS
• NK cells and NK T cells are closely related to aggressive periodontitis as well

A

impaired neutrophil
primed/hyperactive

hyper
causative
susceptibility

defective
oxidative stress
host response

40
Q

Genetic Factors

  • Aggressive periodontitis has a strong ____ component and it is more prevalent within ____ 

  • The likely mode of inheritance is ____ in AA populations

Immunologic PMN defects cluster in LAP families which indicated they might be related to ____ and ____

  • A study found that in African American populations, the population with the highest prevalence, is following a autosomal dominant pattern.
  • The PMN defect cluster in LAP families could be inherited
A

genetic
families

autosomal dominant

gene clusters
inherited

41
Q

Environmental Factors

____ are important factor that can influence the extent of destruction
Smoking is a ____-dependent factor


A

smoking

dose

42
Q

Treatment of AgP

Oral ____ instructions
Non-surgical and surgical periodontal therapy

Systemic antibiotics
Treatment may be empiric, or microbiological testing may be used for selection of appropriate antibiotics

____ planing + ____ + ____: may suppress A.a. more effectively than ____ antibiotic regimes
When pt is allergy to Amoxicillin: ____ + ____

Frequent ____ visits

The individuals with aggressive periodontitis, especially LAP, have to undergo surgical therapy more ____ than the average patient with periodontitis

Anti-infective therapy in patients with aggressive periodontitis seems to benefit strongly from the adjunctive use of ____ antibiotics

• Aggressive periodontitis has more vertical defects so it is more likely to be treated ____ when compared to chronic periodontitis

A

hygiene

scaling and root
metronidazole
amoxicillin
single
metronidazole
ciprofloxacin
maintenance

often

systemic

43
Q

2017 World Workshop

Limited consistent evidence of specific differences in cause of ____ between Aggressive periodontitis and chronic periodontitis

There is evidence that multiple factors (and interactions among them) result in different, clinically ____ phenotypes

• “Right now I am going to make you more confused… forget what I said”
• On an exam if you see the term chronic/aggressive, use the concept I taught you
previously
• In 2017 they changed the classification because they think that chronic and aggressive are not two different diseases
• Both are ____ diseases and all these factors interact with each other which makes
things complicated. This is why they decided to use ____ to describe the clinical presentation of the disease

A

pathophysiology
observable

multifactorial
staging and grading

44
Q

2017 Classification of Periodontal and Peri-Implant Disease and Conditions

• This is in the paper that she sent us. We can read it if we want. She just sent us the intro, and its actually a 300 page book
• This is presented by both AAP and EFP
• There are three big categories and they also added a category on implant diseases this year
• She only will focus on the periodontitis part
• The three categories in this group are: ____ disease, ____, and
periodontitis as a manifestation of ____ disease
• Chronic and aggressive perio “live together” as periodontitis

A

necrotizing periodontal
periodontitis
systemic

45
Q

Periodontitis Case Definition
1. Identification of a ____ as a periodontitis case

2. Identification of the specific ____ of periodontitis

3. Description of the ____ presentation and other elements that affect clinical management, prognosis,
and potentially broader ____ on both oral and systemic health 


A

patient
form
clinical
influences

46
Q

Tissue Loss Threshold for Periodontitis

Interdental CAL is detectable at ≥ ____ non-adjacent teeth, or
Buccal or lingual CAL ≥____ mm with pocketing >____ mm is detectable at ≥ ____ teeth

The observed CAL cannot be ascribed to non-periodontal causes such as:
____- induced gingival recession
Dental caries extending to the ____ area
____ lesions draining through the periodontium
CAL on the distal aspect of a ____ and associated with malposition or extraction of the ____
____ tooth fracture

• For this definition, the attachment loss must be ____ and not caused by
something else. For example if you do wisdom teeth extractions you may get attachment loss on your second molars. In that case, it would not be considered periodontitis.

A

2
3
3
2

trauma
cervical
endodontic
second molar
third molar
vertical

plaque induced

47
Q

A two-vector system to classify periodontics based on

____
____

A

stage

grade

48
Q

Periodontitis Stage

GOALS

Classify ____ of an individual based on currently measurable extent of ____ and damaged tissue attributable to periodontitis

Assess ____. Assess specific factors that may determine complexity of controlling current disease and managing long-term function and esthetics of the patient’s dentition

  • What is the goal with staging? It is used to classify the severity and extent by the current tissue and tooth lost
  • They also use ____ to assess the complexity of the treatment
A

severity and extent
destroyed
complexity
local factors

49
Q
  • The staging is based on severity, local factors (which assess complexity), and the extent and distribution
  • There are ____ stages

• ____ is still used and is similar to the 1999 armitage: mild (stage 1), moderate (stage 2), and
severe (stage 3+4) classification
• If CAL is not available you can use radiographic ____
• If the RBL=coronal third it is stage ____, if the RBL= middle third/apical it is stage ____

• They also considered ____ (only if related to periodontitis). The reason why this is here is
incase a patient only has two healthy teeth left after that patient lost them due to periodontitis. You need to consider the history of the disease. If you have more than 5 teeth lost it automatically stage ____, you dont need to consider anything else

A

four

CAL
bone loss
I or II
III or IV

tooth loss
IV

50
Q
  • Reads the complexity row: If anyone of these factors exist they ____ get that stage even if your attachment loss isnt that bad
  • Complex rehabilitation: if your patient loss multiple teeth and you have to send your patient to a prosthodontis then you are probably at stage ____ but they have severe periodontitis that can be managed then it probably will be at stage ____.
  • Extent and distribution: we still need to describe if it is ____. Remember it is teeth involved, not site. It could also be a molar incisor pattern. This is just a description for the stage but the ____ number is the most important factor.
A
automatically
IV
III
localized or generalized
stage
51
Q

Periodontitis Grade

GOALS

Estimate ____ of periodontitis progression and responsiveness to standard therapeutic principles, to guide intensity of therapy and monitoring

Estimate ____ on systemic disease and the reverse, to guide systemic monitoring and co-therapy with medical colleagues

A

future risk

potential health impact of periodontitis

52
Q

• They are evaluating the ____ of disease progression, response to ____, and potential impact on ____ health
• The first part is disease progression. There is ____ and indirect evidence.
• If you are fortunate you can follow the disease progression in the patient over 5 years and you can use direct evidence to define the rate of progression. This is the ____ evidence
• Most of the time you dont have this information so you use ____.
Example: you have a 20 year old patient and the bone loss is more than 20% then they
are a rapid rate. This is similar to formula that Dr. Papapanou used in his paper
• There is also case phenotype. For example if you have thin biofilm but extensive attachment lost then it is grade ____ (which is similar to the previous definition of aggressive periodontitis)

  • Then there are grade modifiers. For example if you smoke more than ____ cigarettes a day you are grade C even if your previous disease progression is slow
  • You are also grade c if you have diabetes and have a HbA1c>____%
A

rate
standard therapy
systemic

direct
best
% bone loss divided by age

C
10
7

53
Q

Three Steps to Staging and Grading a Patient

Step 1: Initial ____ of case
Screen ____ radiographs, FM ____ depths, missing teett

____Periodontitis

____ periodontitis

A

overview
FM
probing

mild to moderate
severe/very severe

54
Q

Three Steps to Staging and Grading a Patient

Step 2: Fine-tune Stage

Determine maximum ____ and BL
Confirm ____ patterns (horizontal/angular)

Assess periodontitis-related tooth loss
Determine case ____ (probing depths, furcation involvements, occlusion/function, need for extensive, multi-disciplinary tx)

STAGE I
STAGE II
STAGE III
STAGE IV

• Start to consider CAL and if you dont have CAL use RBL
• Then take a look at local factors such as bone loss. If you have vertical bone loss more than 3 then what is that? Stage ____. This is going to require memorization
• If your mouth has only 20 teeth then you are automatically stage ____. Even if the tooth
loss is not related to periodontitis then it is stage ____ because WHO believes you
need at least twenty teeth for masticatory function
• If you have a furcation involvement of 2/3 then it is automatically stage ____

A

CAL
bone loss
complexity

III
IV
IV
IV

55
Q

Three Steps to Staging and Grading a Patient

Step 3: Determine Grade

History/risk of ____ w/ respect to age
Risk factors / risk factor control
____ status / systemic inflammatory considerations

Response to initial tx
____
refine grade

DEFAULT GRADE
MOVE TO GRADE A or C, as indicated

• The default is grade B and then use evidence to move it to grade A or C because most
patients will be grade ____.
• If you can follow the history of your patient for five years then you can use ____
evidence. If not, you can just calculate the ____
• Question: Is this for a singe tooth or is it generalized? Answer: Every patient has one
stage and one grade
• Response of initial treatment is also considered

A

progression
health
compliance

B
direct
bone loss%/age

56
Q

Three Steps to Staging and Grading a Patient

Mild to moderate periodontitis
Stage ____
____ perio treatment

Severe/very severe periodontitis
Stage ____
____/multidisciplinary

GRADE A, B or C

A

I or II
standard

III or IV
complex

57
Q

LAP

• How much percent attachment loss? We focus on the ____ because it is more
severe than the ____. It is stage ____
• No mobility, no furcation, almost all teeth are present. You will not likely need to send your patient to a prosthodontist so it is probably a stage ____.

• Lets grade the case. Lets first consider grade B. We will use ____. She has
70% of bone loss and she is 15 years old. Much greater than one so it is definitely ____
.
• Define the extent of disease. It is a ____ pattern.

• The final answer: Stage ____, ____ pattern, ____ periodontitis

A

lower anteriors
first molar
III/IV
III

%bone loss/age
C

molar/incisor

III
molar/incisor
grade C

58
Q

Conclusion

Chronic v.s. Aggressive Periodontitis
( Concept from 2017 new classification )

Different ____ presentation (phenotype) of periodontitis, not a different disease
Same pathophysiology or mechanism of ____ loss Different rate of progression ( ____ ) v.s. different disease ____ approach is similar for both

  • To conclude: since 2017 we believe there are different clinical presentations of periodontitis. It is not two separate diseases since the pathogenesis is similar and the difference is in the severity.
  • They also have the same mechanism of bone and tissue loss why they may have different rates of progression
  • If you have LAP then you are most likely will be classified as a ____ pattern of stage ____ with grade ____
  • The treatment is similar for both. They both require oral hygiene instruction, surgical/non surgical therapy and possibly systemic antibiotics
  • The beauty of the new classification is that they built a framework with the ability to expand in the future since they expect more evidence to come out and things will change.
A

clinical
bone/attachment
grading
treatment

molar/incisor
III/IV
C