lecture 6 ,Periapical Periodontitis (script )

8/3/2019 lecture 6 ,Periapical Periodontitis (script )

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Periapical Periodontitis

The doctor started the lecture by telling us that she prefers to teach us directly from

the book without going back to the slides >>> So that meansU SHOULD STUDY FROM THE BOOK FOR UR OWN BENEFIT...

Periapical periodontitis means that the infection or bacteria enter the pulp & the

abscess occur & the toxics & bacteria products are inside the pulp. Bacteria may

leak out through the apex. Now we have the periapical area & it contains pain

receptors & proprioceptors which will localize the pain.

-So the first difference between the pulpitis & the Periapical periodontitis is: the

pain is well localized in Periapical periodontitis & poorly localized in pulpitis.

-The second is: the inflammatory response in the Periapical periodontitis area

differs from the response inside the pulp. In periapical area we have good blood

supply but a limited blood supply inside the pulp because the apex is narrow,,

which means if the problem in Periapical area was removed, the problem may

become reversible & the tissue could heal again not like the pulpitis because there

is no good blood supply inside the pulp.

The inflammatory response in Periapical area is DYNAMIC; it may become acute

then chronic (because of the defense) then acute exacerbation may occur.

So DYNAMIC means: Acute then Chronic the Acute then Chronic.

This Dynamic process depends on certain factors; one of them is the balance

between stimulus & the host defense, the stimulus is the bacteria, if the bacteria &

exudates were removed & the root was root canal treated & the pulp was removed

then healing (reversible) may occur. But in pulpitis -once it's severe- even if you

remove the caries the abscess or necrotic won't resolve.


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Etiology of Periapical periodontitis**

Why Periapical periodontitis may occur?? Like the pulpitis it's not only bacterial

origin, here we have:

1-Pulpitis & pulp necrotic: the most common cause of Periapical periodontitis is

to have caries or the beginning of necrotic pulp which will leak down through the

root canal to the periapical area & start causing Periapical periodontitis.

This is the most common cause,, bacterial toxins & product of inflammation.

2-Trauma:

A- If you have a new amalgam filling & it's occlusally high, & U bite suddenly

this sever sudden bite (occlusal trauma) will induce Periapical periodontitis.

B- Orthodontics treatment: when an excessive force is applied on one tooth,, this

cause Periapical periodontitis (inflammation) in periapical area

C- Biting on a hard body immediately: bite suddenly on a foreign body will cause

Periapical periodontitis (inflammation) in periapical area.

All of these factors will induce a TRAINSIET inflammation which means redness

& pain but it will be resolved & doesn't last for a long time because the cause will

be removed.

3-Endodontic treatment: we have mechanical instrumentation when inserting a

file to remove the pulp in RCT & if you go beyond the apex of the pulp & reach the

periapical area this will cause periapical periodontitis.

The chemical trauma in Endodontic treatment is the irrigation we use when

washing the canal after RCT & these chemicals will leak through the apex & reach

the periapical area.

The bacteria it self may be forced to leak through the apex due to instrumentation &

start causing inflammation in periapical area.

Acute Periapical Periodontitis:


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The bacteria & toxins are now in periapical area & they start forming the abscess,

but first they form exudates (fluid accumulation) then the abscess will be formed.

Here we have a confined space but it's no like the pulp. Here the abscess may leak

through the cancellous surrounding bone but relatively if you want to compare it

with soft tissue it's confined. So pressure will start acting on the nerves & you will

start feeling pain but the pain is localized.

What will induce the pain in periapical area?? Spontaneous due to continuous

pressure from acute exudates, may be palpation gentle touch may induce the pain-

sometimes you can't touch the patient's tooth because he's having acute periapical

periodontitis.

-Most likely (not always) the pulp is completely necrotic now. Why most likely

because in multi rooted teeth the pulp necrosis &abscess may leak through the apex

but part of the tooth is still vital.

-In general thermal (hot & cold) stimulation here isn't important factor but in

pulpitis hot & cold drinks are stimulating factors.

-Radio graphically:

Acute means severe pain occurring over a short period of time.

We have exudates & abscess in the periapical area & because there is no enough

time (short period of time) acute may be seen radio graphically eithernormal or

slight widening of the PDL. The bone doesn't have time to be resorbed so the

lamina dura may be slightly well defined.

Out comes of acute periapical periodontitis

1-Suppose the trauma was transient & the cause was removed it will resolve.

2-It may transform in to chronic periodontitis; if the bacteria or toxins persist there

the body will start the defense against them & now it's chronic periodontitis.

3-Exudates may become periapical abscess: first we should differentiate between

exudates & abscess.


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So here we have abscess accumulation with massive exudates formation, so we will

have pus collection >> exudates accompanied with abscess.

From the book: acute periapical abscess may develop directly from acute

apical periodontitis but most of them arise because of acute exacerbation with a

pre-existing periapical granuloma (chronic.(

Chronic periapical periodontitis

-Here we have persistent irritation, the bacteria is still there & the body is trying to

defend him self against it.

-Also we have granulation tissue formation which contains young fibroblast,

young blood vessels & young collagen fibers. All of this is called >>> periapical

granuloma.

So periapical granuloma means chronic periapical periodontitis

That means: we need time for the blood vessels & the collagen fibers & fibroblast

to be formed.

-Looking at the picture you can see a black

(space or radiolucent area) compared to thesurrounding bone. It contains (space) either

fluid or soft tissue. In this case its granuloma &

it needs bone to be resorbed first so it can take

its place. Resorption of bone needs time due to

inflammatory mediators.

Exudates: fluid leaks from blood vessels due

to inflammatory mediators or inflammation

Abscess: focal collection of neutrophiles & dead cells


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-Around the granuloma we have dense collagen bundles which try to form a

capsule at the periphery & it's attached to the root apex. So when extraction the

tooth you notice a soft tissue attached to the root apex which it's the granuloma.

-Periapical granuloma may be asymptomatic (patient isn't aware of it) ormild

(slight pain on percussion) & this differs from the acute periapical periodontitis

which has more severity of pain. We also noticed that in pulpitis: acute >> sever,

chronic >> dull & less sever.

Always the severity of pain in chronic is much less than acute

-We do - tenderness to percussion test when we have a heavily carious patient

using the inverted mirror & if the patient feels pain we say he might have chronicgranuloma

-Radio graphically:

-Well defined radiolucent area because it's chronic & it has time to form the

margin bundles. But when you have an ill defined margin that means it has been

form rapidly & there was not enough time to form the bundles in a well defined

shape, sometimes granuloma doesn't have a well defined margin.

-Cortication: formation of a dense layer of bone at the periphery of chronic

region. It surrounds periapical granuloma & periapical cyst & in minor causes it

surrounds the periapical abscess >> abscess leakage the surrounding tissue.

-It depends on the cellular activity if it's rapidly progressing or with acute

exacerbation. But in general chronic granuloma usually has well defined margin.

Sequelae of Periapical Granuloma:

-One of the periapical granuloma out come is osteosclerosis (bone deposition);

because the body defense is good, the infection is low grade. The body will have

time depending on specific type of inflammatory mediators which induce the

deposition of bone & start osteosclerosis to localize the infection & prevent further

spread.

This is one of the body mechanisms in fighting against chronic granuloma not

the acute because in acute there is no time to do any action.

-Sometimes the cementum will increase (hypercementosis) due to high occlusionor out of occlusion or the teeth may be hyper function, the pulp may be chronically


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inflamed with low grade infection that leak to the periapical area and induce

hypercementosis.

-There may be Equilibrium with host immunologic response: the granuloma

may stay static for years, the patient will continue doing follow up (not sure!!) the

tooth & the granuloma stays the same size. If the tooth was root canal treated (thecause was removed) the periapical granuloma may disappear >> healing may

occur, or it becomes slight widening in the periapical area.

-Acute exacerbation: because of the dynamic process sometimes chronic

granuloma will cause acute exacerbation, if the balance between the host defense &

the bacteria was disturbed (the bacteria are more) so acute exacerbation will occur

& the patient will have sever pain, sever tenderness to pain & acute symptoms.

?: Suppose the patient is having sever pain & when taking the radiograph wenoticed a well defined periapical region, how to diagnose this disease??

: I can't say acute because I have a well defined area, so we call it >> Acuteexacerbation of chronic periapical periodontitis& it can be treated byRCT.

> acuteexacerbation of chronicperiapical periodontitis

-Ill defined margins >> may be chronic periapical abscess

Abscess: is a fluid & may leak through the boundaries of granuloma

so it has ill defined margins

-Very big granuloma (more than 6 mm) >> cyst

-Cyst

In the periapical area we have epithelial cell rests of Malassez which form the rootsheath, when the inflammatory mediators reaches this area they induce proliferation


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of the epithelium & the collagen & fibroblasts & blood vessels >> all of them will

proliferate.

When the epithelium reaches a big sizes it won't have a blood supply to the centre

>> so it will start to be necrotic in the centre & a cavity will form >> formation of

the cyst.


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-Foam cells-lipid laden macrophages: when macrophages try to engulf

cholesterol which will be deposited in the cytoplasm, the macrophage will look like

foamy, like having bubbles inside the macrophages because they engulf lipid

material.

-Proliferation of epithelial rests of Malassez: the dark strands in this picture. This epithelium is the remnant of epithelium root

sheath.

&we have what's called Anastomosis of epithelial,

started as small strands then they become bigger &

bigger due to inflammatory mediators.

-All this is a granuloma... At the periphery we have

collagen bundlesthe new event here is having these

anastomozing strands which it's called proliferating

epithelium.

All of these things will be discussed in detailsin Cyst chapters. So don't worry about the

pathogenesis of cyst at this stage.

-Periapical Abscess:

-You may have acute periapical abscess forming directly from acute periapical

periodontitis-Or you may have acute periapical abscess forming within a chronic periapical

periodontitis

-Now we will take about abscess formation:

-Suppose we have pus and exudates in the periapical area both of them will leak

out through the canal orcancellous bone or through the PDL into gingival sulcus.

Now the pus wants to drain & the drainage will occur in areas with least resistance.

-Cancellous bone is less resistance that the cortical bone because it (cancellous)

contains a lot of marrow spaces.

-When the lingual root is close to the lingual side of the jaw this make the lingual

plate easier to perforate unless if it's very dense like in lower molars. But In

general Lingual plates are denser than buccal plates

-The origin of muscle is very important in the spread of pus; if the

perforation was above the origin the spread will reach it but below the origin the

spread will go in other direction


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-Looking at the picture & talking about the lower teeth

which have the buccinator M beside it.

Suppose the drainage happened through the cancellous

bone through the buccal space but above the buccinator M>> we see the abscess intra oral. But if the drainage

happened below muscle insertion >> we see extra oral

swelling & spread of abscess.

-If the pus drains through the lingual cortex which it's not

more likely to happen (because the lingual plate is thicker

than the buccal) & below the mylohayiod M >> we see

spread to the submandibular space.

-Now talking about the upper teeth, if the tooth is close to

maxillary sinus so the abscess may drain into the maxillary sinus.

-The abscess may drain into the palate if we are talking about a palatal roots (like

lateral incisors & maxillary molars). But the periosteoum in the palatal is very thick

so it's not easy for the pus to penetrate it so the pus spreads posteriorly.

.

-Here we have a crack, leakage of pus or abscess

through a crack in the cancellous bone then leakage

will occur in oral cavity. This gumball is called

parulis. The parulis is a granulation (inflammatory)

tissue marking the opening of the sinus tract.

-This clinical radiograph: the tooth here is non

vital, it's necrotic; it's having this small elevation.

It's parulis (granulation tissue), so we expect herewe have a sinus draining pus.

-Looking at this palatal abscess, suppose it came


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from the molar region & the pus accumulate. We don't have opening because the

periosteoum is very thick.

Cellulites &Soft Tissue Abscess

Cellulites means: spread of pus to the soft tissue, rapid spread of inflammation to

the soft tissue associated with a certain type of bacteria

(streptococcus.(

.

-Looking at this patient, U can see extra oral swelling

occurring in the submandibular area so the drainage occurred below the mylohyoid M.

-Spread of infection from the submandibular space to the

sublingual & submental spaces is called Ludwig's angina

which it's a sever cause of cellulites & the side effects of it are:

the tongue will rise up & posterior so suffocation may occur or infection of glottis

& patient may die.

-Here the patient has abscess in the mental area (lower pic in slide 22), so we

expect that the pus came from the lower anterior teeth & drained below the

mentalis M attachment so it will become (extra orally). If it drained above the

muscle attachment the abscess will become intra orally.

-Here the serious soft tissue infection & spread of pus &

edema.

-In the cellulites most of this is exudates (edema) not pus,

later on pus may occur why?? Because here we have ??!!!

body response to streptococcal infection.

-In cellulites we should have streptococcal infection & rapid

spread of inflammation in the soft tissue. Streptococcus has

special enzymes called streptokinase and hyaluronidase &

those two will facilitate the spread of exudates & this is serious because the inner

canthus of the eye drainage in the cavernous sinus in the brain so one of the

complication is cavernous sinus thrombosis. The patient will have: malaise,

elevated temperature & the condition is painful.


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-Last thing is about the Canine: the pus of the upper canine drainage above the

buccinators & above the orbicularis oris (lip M). So it will drain close to the angle

of the eye which it is serious if it happens because of the cavernous sinus

thrombosis.

The doctor insists that we should study from the book & read the key points(blue boxes) at the end of each topic.

Finished Alhamdulellah

I did my best... Forgive me for any mistakeDone By: Ayah Treef

And Joy is Everywhere;

It is in the Earth's green covering of grass;

In the blue serenity of the Sky;

In the reckless exuberance of Spring;

In the severe abstinence of gray Winter;

- Rabindranath Tagore

lecture 6 ,Periapical Periodontitis (script )

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