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 means ...U 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

**Etiology of Periapical periodontitis Why Periapical periodontitis may occur?? Like the pulpitis it's not only bacterial :origin, here we have Pulpitis & pulp necrotic: the most common cause of Periapical periodontitis is -1 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 :Trauma-2 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 Endodontic treatment: we have mechanical instrumentation when inserting a -3 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

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 painsometimes 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 either normal 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

.Suppose the trauma was transient & the cause was removed it will resolve -1 It may transform in to chronic periodontitis; if the bacteria or toxins persist there -2 .the body will start the defense against them & now it's chronic periodontitis Exudates may become periapical abscess: first we should differentiate between -3 .exudates & abscess

Exudates: fluid leaks from blood vessels due to inflammatory mediators or inflammation Abscess: focal collection of neutrophiles & dead cells 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 the surrounding 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

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) or mild (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 chronic granuloma

: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 occlusion or out of occlusion or the teeth may be hyper function, the pulp may be chronically

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 (the cause 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 we ?
??noticed 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 >> Acute
exacerbation of chronic periapical periodontitis & it can be treated by .RCT FOR the seek of exam & the coming years especially in oral diagnosis clinics U << should be able to distinguish between these different types of periapical << periodontitis

Well defined margins periapical area >> chronic granuloma Well defined margins with sever pain >> acute exacerbation of chronic periapical 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 root sheath, when the inflammatory mediators reaches this area they induce proliferation

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

So the out come of periapical periodontitis <<< :((Sequelae of Periapical Granuloma

Cyst formation -1 (Abscess formation (acute & chronic -2 Equilibrium or even healing -3 Osteosclerosis -4 Hypercementosis -5 Acute exacerbation of chronic periapical periodontitis -6

Histology of periapical granuloma

Root apex with necrotic pulp & products & bacteria...leaking out to the periapical area >> granulation tissue formation which contains proliferating fibroblast, blood vessels & a lot of inflammatory cells. Surrounding this granulation tissue we have fibrous tissue which it's a dense collagen bundles trying to confine the infection .within the granulation tissue We also have bone which does resorption & deposition. Resorption is due to inflammatory mediators. Deposition is due to body defense mechanism Looking at the picture U can see these needles like spaces & these spaces are empty because they contain cholesterol which has been lost during slide preparation & its called cholesterol cleft. Cholesterol comes from the cell walls of the destructed of RBC's & other cells in this area. The cholesterol is foreign to the body so there will be multinucleated giant cells accumulation on the wall of the clefts trying to .(engulf the cholesterol (foreign body The black dots are inflammatory cells .((lymphocytes, neutorophiles Granulation tissue which contains blood vessels, fibroblasts, macrophages, ...plasma cells .Haemosidren deposits which come from the destructed RBC's -

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 details in 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 or cancellous 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

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 The abscess happens in all teeth & not specific to the posterior ones. So in<< >> .anterior we may have trauma followed by necrosis & abscess formation 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 nonvital, it's necrotic; it's having this small elevation. It's parulis (granulation tissue), so we expect here .we have a sinus draining pus

Looking at this palatal abscess, suppose it came

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 he soft tissue associated with a certain type of bacteria .(streptococcus . Looking at this patient, U can see extra oral swelling ccurring in the submandibular area so the drainage .ccurred below the mylohyoid M t ( o o

Spread of infection from the submandibular space to the ublingual & submental spaces is called Ludwig's angina s hich it's a sever cause of cellulites & the side effects of it are: w 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 & rapidspread 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

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 mistake Done 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