Periodontics Sheet 13 Hala Kanan

Aggressive Periodontitis

In this lecture we will talk about:

Localized and generalized are the types ofAggressive Periodontitis.

Clinical and graphical station
Immunology
Aggressive Periodontitis in details with its risk factors

Aggressive Periodontitis as the name implies has one distinctive feature: rapid destruction of the
bone or more precisely rapid rate of bone loss. In the panorama, it will be evident that there is a
severe bone loss around the teeth.

Case 1 shows generalized periodontitis.

The severity of the case can be seen through the probing depth. It is more severe when it is
deeper. This is just an example on aggressive periodontitis.

Aggressive periodontitis is an establisheddisease of the periodontium causing rapid bone loss

and periodontium destruction one or more pendant teeth along with a couple of healthy others.
This definition shows the primary features that distinguish the aggressive type from the others.
From 1923 till now this disease had changing names. When someone looks at older papers or
articles, it can be noticed that it had several names including periodontosis.

There are differences in the use between suffixes;itis means inflammation, -osis means
degenerative. That is why back in time people who called it Periodontosis thought it this a
degenerative disease and therefore causing loss of bone. They also called the types: localized
Juvenile, generalized Juvenile Periodontitis or rapidly progressive Periodontitis. These
classifications where made in 1999. However after 15 years, the common names are: Localized
aggressive and generalized aggressive periodontitis. Localized Juvenile is what we now call
Localized aggressive and generalized Juvenile is generalized aggressive. These two entities are
now called generalized aggressive.

Primary features of aggressive periodontitis (whether generalized or localized):

1. An otherwise healthy individual.

2. Rapid attachment loss.
3. Familial Aggregation.

These features can be used to distinguish if a patient has aggressive periodontitis or

periodontitis as a manifestation of systemic disease.

Secondary Features:
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1. The amount of Microbial deposits is inconsistent to the amount of destruction. Plaque or

calculus might be shown. However, there is no direct relationship between the amount of
Plaque or calculus and the disease or bone loss. For example, a patient might have heavy
calculus but does not have severe bone loss as shown on the X ray. It is not necessary that
the patient has the disease.
2. Elevated proportion of certain microbial profile but most likely AA
(Aggregatibacteractinomycetemcomitans), and sometimes PG (Porphyromonasgingivalis).
3. Phagocyte abnormalities. This means that there is a chemotactic defect. The phagocytes
are able to function on the foreign object, but there will be a chemotactic defect. This
means that the recruitment of the phagocytes will be defected; hyper responsive
macrophage phagocytes, elevated levels of cytokines, prostaglandins, the progression of
chemotactic response (not sure if the word is response) might be self arresting, only in
some cases.

Not all features will be there, which means that we dont need them all in order to formulate
the diagnosis. We do not need to do a microbiological sampling to check the presence of AA
and PG. But in general, this disease has: severe bone loss, healthy individual, the amount of
local factors does not explain the amount of bone loss and usually the patient is young
(secondary feature). A patient might be in his late thirties or early fourteens and might have
this disease. He is an older patient but might have the given features, for example if he was a
healthy individual with severe bone loss that is inconsistent with the amount of
microorganisms present and that has familial aggregation. Evidence might also be that
someone in the patients family has lost his/her teeth.

There cases which we call border line cases, in which periodontists would disagree on the
type of periodontitis. Some would say it is chronic and others will say it is aggressive. This is
because we still do not have a test that gives positive for the disease and negative for not. We
rely on features and multiple factors. There is a case, that will be shown if there is more time,
we have diagnosed and treated it as an aggressive case but when we sent it to the reviewer
there was a debate upon the type. Later it was accepted as an aggressive case. Border line
cases are mostly faced with older patients. There is no limit to distinguish between the two
types; long ago age was the distinguishing feature. Adult periodontitis (above 35 years) is the
name that used to be given to older people carrying the disease. For patients below 35 years,
it was called juvenile periodontitis. However, after the classification in 1999 it became no
longer the case because older people can have the disease from 8 years ago. It is not a proper
way to assign a disease category.

We are using a combination of clinical,radiographic, historical findings and sometimes lab

results (microbiology) to reach a diagnosis. That is why some cases are debatable. The good
thing is that the management may be similar.
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Localized aggressive usually the onset is at puberty (circumpubertal), strong antibody

response to elements for example AA, strong antibodyresponse to LPS (high titer of
antibodies), usually they affects the bone of first molars and incisors, interproximal
attachment loss of teeth of at least two permanent teeth, one of which is first molars and
involving no more than two teeth other than first molars and incisors. This means that this
disease affects first molars and any incisors and up to two more permanent teeth, if more
than two teeth it is a generalized. For example: maxillary first molar, lower lateral incisor and
two premolars = localized. Maxillary first molars, 7, 4, 5, 1 = generalized. The limit that
distinguishes local from generalized is done by consensus meeting (cut off point).There is a
difference from chronic and aggressive in the sense of distinguishing between the localized
and generalized.Remember that in chronic, 30 percent of the sites were the limit. The number
was the red flag in that case. Notice that there would be 8 teeth involved and it would
automatically be localized, but we can have 5 teeth involved and we can still call it
generalized. The idea is: when you have it localized to only these teeth, it is a different type of
disease. It usually happens on puberty, affects first molars and incisors and has a different
phenotype. There is no exact reason why 2 teeth not 3.

Why is it localized on first molars and incisors? This disease is one the most peculiar diseases;
why is that bone loss only occurs to first molars and incisors? Some said that because they are
the ones that stay for the longest period. But it does not vary with time. There are many
theories (no rigid explanation) for this particular subject:

1. The development of adequate defenses to bacteria such as AA after the initial colonization
of the teeth. After eruption of the teeth and the disease process takes place, defenses are
created to protect the remaining teeth. Therefore the ones that experienced bone loss are
the victims.
2. Another theory is: after the AA bacteria have established themselves and initiated the
disease, the patient starts having other types of bacteria that could neutralize the
pathogenic effect of the AA bacteria. This competition in the environment kind of limits
the ability of AA.
3. AA bacteria changes into becoming less pathogenic, losing some of its pathogenicity and
other types of bacteria starts to develop. And the defect in the cementum, i.e. the
defective cementum makes these teeth more susceptible to bone loss.

Features:

1. One of the vaulted features of the localized aggressive periodontitis is that there will be
minimal clinical information. When you actually look, you can notice that the patient has no
signs of inflammation such as swelling and redness. Minimal plaque, minimal mineralized
calculi and even we can barely notice any subgingival calculi. That is why in the localized
aggressive, the amount of local deposit does not coincide with the amount of disease.
General aggressive has much more deposits. The root could be clean, Something(couldnt
hear it) as well as rapid progression of the bone loss.
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Figure of a localized aggressive case: A severe bone loss, flat innovation, mostly clean roots no
calculi. Sometimes it is an incidental finding on an x-ray.

2. Clinical findings: Pathological tooth migration or distolabial migration of the maxillary

incisors. Diastema formation. There will be increases mobility, sensitivity, sometimes pain
(not that common), and abscesses. Abscesses do not fall in a 5mm pocket, we will have
deeper pockets. Figure shows distolabial migration.
3. Radiographic findings: vertical bone loss at the first molars and incisors, sometimes they are
arc shaped as opposed to the level of bone which is intact. It is like a saucer shape

Prevalence

In a libelous population (diverse society with less than 1 percent of the total population) in an
ethnic background it is less than 0.2% of the whites and about 2% in blacks. Thus there is a
higher prevalence in the black society. In the US more African Americans have Periodontitis than
the white. They are 10 times more. Historically, it was thought the female was thought to have
more of this disease, and then it was found that it is because of ascertainment bias. It actually
higher in black male followed by black female, white females and least in white males.
Management is the same, it goes in non-surgical therapy, surgical therapy (1)access surgery,
2)resective surgery, or regenerative surgery (graft)), oral hygiene instructions, and unique to
aggressive periodontitis is that we only use systemic antibiotics. Chronic periodontitis we can
also use systemic antibiotics. What do we use? For the longest time the antibiotic used was a
doxycycline 10 gram twice a day for 14 or 21 days. They used to think that the concentration of
the doxycycline in the GCF is high; it becomes more concentrated in the fluid rather than in the
plasma. Now, we know that it is not the case. Doxycycline is not the first line of choice for
antibiotics, but it could be given 100 milligrams twice a day for 14 days. What we do now is a
combination of amoxicillin500 three times a day for 10 days and metronidazole 250 3 times a
day for 10 days. This is the best option used to suppress the bacterial growth. Another option is
azithromycin 500mg once a day for three days or ciprofloxacin500mg twice a day for 10 days. Or
cephalosporin can be used but some studies showed its not preferable to use it.

Why do we use surgical methods if there is no sublingual calculus?

We try to regenerate some of the lost bone. The treatment is to graft, if its an isolated tooth.

Generalized aggressive

Usually affects individuals under the age of 30. Poor antibody response is found as opposed to
high antibody response. Minimum plaque is found but not as characteristic as for the localized.
What we see in the generalized aggressive is generalized interproximal attachment loss with at
least 3 permanent teeth other than the first molar and incisors.
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Two types of gingival response:

1. Severe inflamed tissue. (in comparison with the minimal inflammation seen in the localized
aggressive)
2. Tissues that appear pink and healthy.

We can have these two types of responses.

Sometimes Generalized AggressivePeriodontitis does not respond well to therapy. So despite

therapy, some cases continue to progress and lose teeth. In most of the cases they respond to
therapy. Usually when there is generalized disease, you have to do a medical workup. In the
localized, it is very distinct and well defined therefore there is no need to find a disease
category, no need to suspect a systemic background. It has a very typical presentation (first
molars, incisors) so you would not suspect there is an underlying medical condition. However in
the Generalized Aggressive Periodontitis, there is severe bone loss affecting the all the teeth
therefore you have to consider a medical background check. Patients might have conditions that
would affect their cases (mentioned later in another lecture). Although these patients can live
freely, yet they might have other medical issues. One of the manifestations of this medical
condition is generalized periodontal destruction. These patients are not diagnosed to have
generalized aggressive. One of the primary features for this disease is that these patients are
otherwise healthy. Thus you might need a consultation.

Figure: it could deceive you without an X-ray or a perio probe. The bone loss is everywhere.

One of the features of chronic periodontitis is usually horizontal bone loss. However this is not
exclusive. In the aggressive case it is usually a vertical bone loss. But then again that does not
mean that is the only way to bone loss.

Figure: a combination of horizontal and vertical bone loss. They are not mutually exclusive. They
could happen at the same time. Horizontal bone loss and the other tooth has a vertical defect
could occur at the same time.

Radiographic Presentations

Bone loss of various stabilities is present.If you have the access to previous X-rays, you can see
extreme rate (rapid) of bone loss. The problem is that when we see the patient for the first time,
we are seeing him/her for one point of time therefore we have no reference or base line to
compare. The annual rate of attachment of bone is about 0.5 mm in chronic periodontitis. In the
aggressive case it is from 0.1 to 1 mm. there is a big difference; twice the rate of attachment loss
we see in the chronic case.

Figure: vertical defect. Horizontal bone loss is also found

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Prevalence and distribution by Age and Gender

There has been a study conducted in the 1960s and ended in the 1970s and occurred in Sri
Lanka. They studied and examined the cases for about 10 years in a tea planation without
treating them. They went and examined people and came back after ten years to the same
people and compared their results to people in Norway. Norwegians have high dental
awareness, constantly receive dental prophylaxis and have excellent oral hygiene. While the Sri
Lanken Tea laborers have no dental hygiene and are the exact opposite of the Norwegians. To
monitor the differences, they compared the two extremes. So many studies came out of this,
one of which is the rate of bone detachment. Only 8% of these patients showed severe
progression attachment loss (0.1-1mm). 11% had absolutely no disease and no attachment loss.
81% had chronic periodontitis. These people (11%) did not practice any form of oral hygiene,
they still had no periodontitis. The patient has to be susceptible to the disease; it is not only
about the oral hygiene. Less than 1% of this age group had generalized aggressive periodontitis.
This is because they usually have localized.??

The prevalence is higher in black than white and in males than females.

The aggressive periodontitis has the same management; surgical and non-surgical. Non-surgical:
plaque control and systemic antibiotics.

Risk Factors for Aggressive Periodontitis:

1. Microbiological factors: AA has been implicated as a primary pathogen. Primary etiology of

Aggressive Periodontitis is bacteria (plaque). It is a plaque induced disease. Evidence that
AA is the primary etiology is (read off slide).

Secondary Risk Factors:

Some secondary risk factors like neutrophils defects and genetic factors. In some reports AA
was not detected, in other reports AA was detected in healthy sites. That is why it is not
absolutely specific. Some patients might not have AA but still have Aggressive Periodontitis. This
means it is not a cause effect.

1. Serotypes.

AA might have different types that have different machinery of producing different
proteins.Proteins, toxins or the way they stimulate the immune response could be different
between two different serotypes of the same species. They have found that serotype B is the
prevalent type of AA in the cases that have aggressive periodontitis in the US. And type A has
been shown to invade periodontal tissues. That is why we prescribe systemic antibiotics. There
is evidence that AA can be found within the periapical tissue that is why we prescribe
antibiotics, if it invaded the pocket or root tissues. After applying instrumentation on the root
surface or the pocket, the antibiotics will deal with the remaining bacteria (those which
remained in the tissues).
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2. Immunological factors. Chemotactic defects, functional defects in the PMNs or the

monocytes are found. There is a defect in permanent ability in the phagocytosis of
microorganisms as a functional defect in the PMNs or the phagocytes. Hyper responsiveness
can be also found. Most of the destruction that happens in periodontitis is due to the host
response. This means that the immune system gives an overzealous response to the
offending microbial biofilms.
3. Genetic factors: is it autosomal dominant inheritance of localized aggressive periodontitis
according to a clinical study on African americans. It maybe PMN defects they cluster in
certain families. This means that the PMNs defects may be genetic. Different patterns for
inheritance in other populations. The mode of inheritance in localized aggressive are within
the African American families. It could be autosomal recessive in other populations.
4. Environmental factors: smoking in generalized aggressive periodontitis patients is related to
bone loss and attachment loss. The impact of smoking on localized aggressive is not as clear.
It seems like it has less of an impact compared to Generalized Aggressive. It still is a risk
factor but it is more evident in Generalized.

Hala Kanan

Good luck