Disorders of the dental pulp Pulpitis

Pulpitis = inflammation of the pulpal tissue regardless of the infective agent

Pulpitis is the most important and common disease process affecting the dental pulp It is a dynamic process and presents a spectrum of changes reflecting the interplay between its cause, the effectiveness of the host defenses, and a variety of other factors

What defense mechanisms dose the dental pulp have?!

o Tertiary dentine is the main defense mechanism and like any other tissues it has autoimmune mechanisms that's why it gets inflamed in the first place

How do we clinically know that the patient is having pulpitis?

o Pulpitis is characterized clinically by pain o The types of pulpitis are different according to the different clinical presentations and histopathological findings too ** We usually cant know the histopathological findings unless we extracted the tooth
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** We cant take biopsy from the pulp while the pulp is vital and the tooth is still in the socket ** So to diagnose pulpitis, we usually rely on the clinical features only o The pain that the patient reports to the dentist is variable ** Some patients report a localized type of pain in a specific tooth, while others report a non-

localized type of pain saying that all the teeth in one side hurt, but they dont know which tooth
is the offending one ** The pain might be severe, mild or moderate ** The pain might be throbbing, sharp or dull in nature ** The pain might be continuous (lasts for three to four hours continuously) or intermittent (comes and goes) ** The pain might be stimulated (by cold drinks, hot drinks or biting) or non-stimulated (spontaneous and comes by itself) ** The pain may disturb sleep, or affected by the posture (E.g. if the patient moves his head down, the pain increases. And if he moves his head up, the pain decreases)

Pulpitis has different clinical & pathological classifications which are artificial and confusing:
o Acute or chronic They are clinical diagnoses based on duration and severity of patients symptoms

Acute pulpitis = recent history of severe throbbing pain precipitated by hot or cold stimuli or on lying down and which often keeps the patient awake Chronic pulpitis = old history of spontaneous attacks of less severe dull aching pain which can last for an hour or more
** Patients coming with chronic pain usually have previous painful episodes (E.g. the patient will say that he had the same pain a year or two before)

o Open or closed

Closed pulpitis = pulpitis limited to the tooth structure and still surrounded by dentinal walls. Usually associated with very severe pain
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Open pulpitis = pulpitis open to the oral cavity because it isnt surrounded by the dentinal walls anymore. Usually associated with no or mild pain

o Symptomatic or asymptomatic o Reversible or irreversible

The most important clinical classification because it is the only one determining the treatment option

Reversible pulpitis = pulpitis that can be reversed back to normal and pulp will heal if drilling and filling are done before pulp gets exposed and irreversible pulpitis happens Irreversible pulpitis = pulpitis that can't be reversed back to normal and pulp won't heal because pulp is already exposed and RCT or extraction need to be done before pulp
necrosis happens ** Knowing that pulpitis is either reversible or irreversible depends MAINLY on clinical

symptoms IN ADDITION to other helpful investigations (e.g. Endo Ice, Electric Pulp Tester,
direct clinical observation and sometimes a Radiograph) ** Why dont we rely on the biopsy or the histopathological findings to decide

whether pulpitis is reversible or irreversible?

Because there a little or no correlation between the clinical features or symptoms

and the type and extent of inflammation seen microscopically in the pulp
E.g. sometimes the patient suffers from very severe type of pain that disturbs sleep, but the inflammation in the pulp is very much localized or minimal and just immediately at the point of pulp exposure It is okay to say More severe pain is most likely BUT NOT always associated with

more severe histopathological changes An absence of symptoms is NOT evidence of a normal pulp as pulp necrosis following pulpitis may occur with NO previous history of pain
Patients also differ in their pain thresholds (the stimulus that elicits pain for a patient may not do the same for another)

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** Radiographs don't show us the intra-pulpal changes going inside the pulp, because pulpal tissues are soft and all soft tissues appear black on the radiograph If we inject a florescent material intravenously so that it circulates in the blood and then it enters the blood of the pulp, and then we take a radiograph, we may see the pulp then BUT, this technique is NOT significant, and we don't know if they have done this before or not, because it is not easy to inject the patient with a florescent material and then taking a radiograph to view the vascular tissue of the pulp This technique can be done to view if someone has a cerebral stroke or not but not to view if pulpitis is reversible or irreversible

We have to decide:
o To restore the tooth (in cases of reversible pulpitis) o To remove the pulp (in cases of irreversible pulpitis and the tooth is restorable) o To remove the entire tooth (in cases of irreversible pulpitis and the tooth isn't restorable) ** So: we have to decide if the process is reversible or irreversible

Causes of pulpitis: 1. Bacterial:

Dental caries (coronal caries, root caries, recurrent caries due to marginal leakage of
restorations) ** When caries isn't extensive and bacteria aren't entering the pulp quickly, the pulp will have enough time to form tertiary dentine and protect itself from pulpitis ** When caries is extensive and bacteria are entering the pulp suddenly and quickly, the pulp won't have enough time to form tertiary dentine and thus pulpitis develops

Cracked tooth Periodontal pocket

** In here bacteria may reach the pulp through either the accessory canals or the root apex (if the pocket is very deep and approaches the apex) ** When bacteria enter the pulp and cause pulpitis due to periodontal pockets and in the absence of caries or crack then this is called Endo-Perio lesion

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Malformed teeth (Dense invaginatus, talon cusp and Leong premolars)

** Bacterial infection is the most important etiological factor in pulpitis ** Viruses never cause pulpitis ** Dental caries is the commonest cause of pulpitis

2. Traumatic:

Coronal fracture and exposure of the pulp Root fractures Partial avulsion Bruxism leading to attrition Abrasion
** Trauma can be either acute or chronic ** Chronic trauma when the pulp has enough time to form tertiary dentine and protect the pulp before pulpitis occurs (e.g. when there is attrition for a long period of time, there is low grade trauma to the pulp, so the pulp will have enough time to form reactionary dentin before having pulpitis) ** Acute trauma when the pulp doesn't have enough time to form tertiary dentine because injury to dentinal tubules was rapid and sudden so that pulpitis develops (e.g. when there is a fracture of the crown, large number of dentinal tubules are exposed rapidly and suddenly and this will speed up the inflammation, so the pulp wont have time to form the reactionary dentin)

3. Iatrogenic:

Heat generation (frictional heat without water coolant) Deep preparations Traumatic (iatrogenic) pulp exposures while operating on the tooth Filling materials Toxic disinfectants

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 Dental pulp is contained within a solid champer (Dentine) and this limits its ability to withstand edema and thus pressure rise (due to inflammation) will lead eventually to necrosis
** Inflammation process must cause edema and leakage of fluid from the systemic circulation ** Edema will press on nerves and vessels, leading to ischemia (cut of blood supply) and then local necrosis happens ** Sometimes pulpitis end up by necrosis because dental pulp doesn't have space to accommodate edema

Factors influencing pulpitis:

o Special anatomy of the pulp (Dental pulp is surrounded by hard dentinal wall that doesn't accommodate edema) o Nature, duration and severity of irritant (does it allow for tertiary dentine formation and pulp healing or not) o Host defense o Apical blood flow (e.g. open apex Vs. closed apex)

Dental pulp has limited blood supply through apical foramen Inflammation mechanism gets destructive and there will be:
o Dilatation of blood vessels o Leakage of fluid from blood vessels o Migration of cells

Histopathology of pulpal disease:

o There's spectrum of histological changes between normal and necrotic o Overview:

Low caries level lead to the mildest inflammatory response: Number and/or their virulence of bacteria entering the pulp is low (because caries hasn't reached pulp yet) inducing mild inflammation There's mild vasodilatation and congestion of blood vessels
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 There's diffuse infiltration of lymphocytes and macrophages (those chronic inflammatory cells aren't concentrated in one area forming an abscess, instead they are diffuse and spreading but necessarily involving the whole dental pulp)

There's NO edema or exudate or abscess formation

** So in here number and/or virulence of bacterial cells invading the pulp is low, severity of inflammation is mild, type of inflammatory cells is chronic, number of inflammatory cells is low, distribution of inflammatory cells is diffuse and there's NO abscess formation ** This inflammatory response is the initial response of the pulp to caries and it might be

reflected clinically like reversible pulpitis

** In this picture, dental caries is deep but it doesn't expose the pulp yet since we still have a thin layer of dentine overlying the pulp We can see some dilatation or congestion of the pulp blood vessels because of the inflammatory process First dilatation of blood vessels happens, then permeability of blood vessels increases and leakage of fluid from blood vessels occurs, then migration of white blood cells Here we have little vasodilatation and congestion, and few numbers of lymphocytes could leak and they are diffuse and not concentrated in one area (NO abscess formation)

If dental caries is drilled and removed, and carious lesion is restored, pulp status will reverse back to normal and healing will take place High caries level leads to more severe inflammatory response: Number and/or their virulence of bacteria entering the pulp is high (because caries has reached the pulp) inducing a more severe inflammation
There's more vasodilatation and congestion of blood vessels

There's edema or exudate formation

** Exudate = any fluid that filters from the circulatory system into lesions or areas of inflammation

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 There's localized infiltration of neutrophils (these acute inflammatory cells concentrate and accumulate around the bacteria trying to eat or kill them, leading to abscess formation) There's compression of blood vessels due to increased pressure in the limited area of the pulp

Ischemia and necrosis will then occur and this eventually leads to pulp abscess due
to progressive accumulation of neutrophils ** So in here number and/or virulence of bacterial cells invading the pulp is high, severity of inflammation is more, type of inflammatory cells is acute, number of inflammatory cells is high, distribution of inflammatory cells is localized and there's abscess formation ** This inflammatory response is the later response of the pulp to caries and it might be

reflected clinically like irreversible pulpitis

** Why do some people end up having abscess after pulpitis? Maybe because the stimulus will continue being there and the pus will continue forming to involve all of the pulp, and then the pus will leak out of the apex to spread in the periapical area Pulp reaction to this pus will be trying to localize its spread ** Usually skin pus has a well-formed capsule but pulpal pus doesnt have a

capsule (it is may be surrounded by some fibrous tissue but not a well-formed capsule)
** In this picture, caries is deep and it is exposing the pulp We can see dilatation or congestion of the pulp blood vessels because of the inflammatory process We can see some dilatation or congestion of the pulp blood vessels because of the inflammatory process First dilatation of blood vessels happens, then permeability of blood vessels increases and leakage of fluid from blood vessels occurs, then migration of white blood cells

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Here we have more vasodilatation and congestion, more edema and exudation, more compression and large numbers of neutrophils could leak and they are localized and concentrated in one area leading eventually to abscess formation

If dental caries is drilled and removed, and carious lesion is restored, pulp status will never reverse back to normal and healing will never take place RCT or EXTRACTION is our treatment option instead
** What are the outcomes of pulp abscess? 1. The pulp will try to localize the abscess (especially if the stimulus is removed or decreased for one reason or another and there's good pulp defense), so the pulp will start surrounding the abscess through the granulation tissue (and there will be increase in fibrous tissue content around the abscess without forming a capsule) and this will temporarily suspend the spread of the abscess BUT once there is another stimulus or an increase in the severity of the irritant, the spread of the abscess will start over again 2. The abscess will continue to expand until it involves the whole pulp (the whole pulp chamber and the whole root canals) and sometimes when we open this pulp in the emergency clinic the pulp will be necrotic, there wont be any bleeding and we won't be having fibrous tissue or anything, and if we insert the instrument, pulp will be empty (the pulp is all gone because of the continuous action of either the abscess or the necrosis) 3. The pus will drain from the opened carious cavity sometimes, and in here the patient will tell you that he feels a bad taste draining from the inside of his tooth ** What is the factor that will affect the drainage of the pus through

the carious cavity?!

The carious cavity has to be widely opened, and the pulpal exposure has to

be big

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 Reversible pulpitis:
o In reversible pulpitis the pulp is irritated o It represents the mildest form of inflammatory response where there's: Mild vasodilatation and congestion of blood vessels Some transudation (leakage of fluid from blood vessels) ** Transudate = extra-vascular fluid with low protein content containing mainly lymphocytes and macrophages that leave blood vessels due to their increased hydrostatic pressure Slight infiltration of lymphocytes (migration of lymphocytes)
Lymphocytes

o Treatment = drilling and filling o Pain symptoms:

Dilated blood vessels Elicited (stimulated) Sharp Lasts for 10-15 minutes Unaffected by posture (position of human body, such as: standing, bowing, lying down .) Easily localized

Irreversible pulpitis:
o In irreversible pulpitis there's wide spectrum of acute and chronic inflammatory changes o Treatment = removal of the pulp (RCT) or removal of

the tooth (Extraction)

o Pain symptoms: Spontaneous (unstimulated) Dull Lasts for more than 20 minutes Affected by body posture Difficult to localize
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 Pulpal Necrosis:
o Infected pulpal necrosis: Results from untreated irreversible pulpitis Acute and chronic symptoms maybe elicited There will be degeneration of nerve fibers There will be autolysis of pulpal tissue There will be irritation to the periodontal membrane There will be extensive pain (due the limited area of the pulp) and there will be extrusion of tooth out of its socket

o Non infected pulpal necrosis: There will be No symptoms for months There will be change in color of the tooth

Acute pulpitis:
o May be confined to one horn of dental pulp (focal acute pulpitis) or involve the whole pulp (total acute pulpitis)

o Causes:
Rapid bacterial invasion of dentinal tubules Overheating to the extent of rupturing blood vessels

o Acute pulpitis mainly affects children and adolescents o In acute pulpitis there's NO possibility of drainage and this causes build up of pressure o Pulp Abscess:

Core: (exudate): PMN cells, fibrin, necrotic cells, debris and RBC Zone of granulation tissue: newly formed blood vessels, young fibroblasts, plasma cells
and lymphocytes

No outer surrounding capsule

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 Chronic pulpitis:
o When there is little or no penetration into the pulp by large numbers of virulent types of bacteria o Chronic pulpitis mainly affects older teeth, where there are: Sclerotic dentin Reparative dentin formation

o Microscopically:
Loose connective tissue Dense Bundles of collagen Reduction in size and number of blood vessels and nerves Diffuse infiltrate of lymphocytes and plasma cells ** Known as pulp fibrosis Focal and diffuse calcifications may occur ** Pulp stones: spherical calcifications ** Dystrophic calcifications: linear calcifications

o Chronic hyperplastic pulpitis (pulp polyp):

The end result of an untreated pulpitis is total pulp

necrosis except in the case of chronic hyperplastic pulpitis because it has opened widely into the oral cavity
Chronic hyperplastic pulpitis is a special type of pulp response

What are the requirements of hyperplastic pulpitis?!

1) Low grade bacterial insult 2) Good defense and good apical blood supply 3) Wide opened carious cavity (because I have a polyp that wants to escape the pulp cavity) 4) Young patients

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 Why do some patients end up having a pulp polyp and others end up having necrosis?
Patients who are young and with low grade bacterial insult, a widely opened carious cavity and good defense will certainly end up having pulp polyp So in pulp polyp, the pulp (with the good defense it has) tries to protect itself by forming a lot of granulation tissue (that surrounds the abscess and localize it) and if there's an opened carious cavity occlusally, the granulation tissue will protrude out of this opened cavity into the oral cavity If the carious cavity isn't opened, patients will end up having necrosis, since there will be pressure on the pulp and accumulation of exudate and edema But the necrosis is variable, it may be localized or it may expand involving the whole pulp or it may leak out of the carious cavity Pulp polyp is usually seen in deciduous teeth or recently erupting permanent teeth with wide-open carious cavities and a good apical blood supply through a widely opened apical foramen The wide-open pulpitis prevents build-up of tissue pressure compromising pulpal blood flow and the good apical blood supply facilitates healing and repair (regenerative capacity of young pulpal tissue) There will be stimulation of pulp to proliferate leading to an excessive overgrowth that is fibrotic and deficient in nerves called (pulp polyp)

Pulp polyp = chronically inflamed hyperplastic granulation tissue that is devoid of sensation on
gentle probing (NOT painful to touch) This hyperplastic granulation tissue protrudes beyond the pulp chamber and may become

epithelialized
This epithelization comes from the oral cavity (gingiva and oral mucosa) BUT NOT from saliva (because if we have epithelium in the saliva, this epithelium can't proliferate and cover the pulp, since a basal layer is needed and this basal layer comes from the oral mucosa or from the gingiva ONLY)

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Epithelialized polyp
Epithelial tissue Pale in color Doesnt easily bleed Not painful to touch

Non-epithelialized polyp
Granulation tissue Dark red Easily bleeds Not painful to touch

Pulp response to restorative procedure:

Odontoblasts usually line the pulpal aspect of dentin

Features of pulp response to cavity preparation and restorative materials:

o If theres a stimulus that caused movement of dentinal fluids and edema in the pulp then there will be aspiration of odontoblasts so that they go inside the dentinal tubules and away from the pulp o Sometimes we may have dead tracts of the dentinal tubules immediately next to the pulp o Number of odontoblasts may decrease because the material may kill them Nowadays, they are doing researches and trying different materials for pulp capping, so they induce exposure in dogs teeth and they put a certain material on the exposure site to see what will the pulp response be if this material was used clinically, and then they will kill the dogs and take the teeth out from the jaw They found out that dogs do not survive if their canines are extracted!! Because dogs canines aren't longitudinal, but they are much curved so that a minor oral surgery is needed to extract them and dogs can't withstand a minor oral surgery, so that dogs are killed and their mandible is taken, and then their canines are cut and studied microscopically They observed the aspiration of odontoblast in these experiments, and they saw dead tracts of dentinal tubules and other features that occur in some materials more than others Glass ionomer was very toxic to be applied directly to the pulp also other types of materials

Healing of the pulp: If there is pulp exposure and we placed a good capping material over it, what will happen?
The calcium hydroxide (alkaline PH) will be placed immediately on the pulp exposure and it will start forming a necrotic zone
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The alkaline environment is good to kill bacteria, but it will form a necrotic zone immediately under the calcium hydroxide So after we put calcium hydroxide directly on the pulp, first there will be a necrotic zone, followed by a basophilic zone (which is considered as granules of calcified materials) and the ability of calcium hydroxide to form such a zone is a good feature, because the aim of all researches, is trying to find the best pulp capping material that will induce hard bridge formation to close the exposure, with minimal toxicity to the pulp Within 2 weeks of applying calcium hydroxide later, a layer of fibrous tissue immediately forms under the basophilic zone and this tissue is good because a sealing is to be formed to separate the exposure area from the underlying pulp tissue, so that NOT all of the pulp tissue gets inflamed at once Beneath this fibrous tissue, a layer of odontoblast-like cells appears These odontoblasts will not be at the periphery of exposure, so they will not come from the peripheries to the fibrous layer They found that these odontoblasts come from the pulp itself because it contains undifferentiated cells that may differentiate to form odontoblast And after a further 2 weeks a calcified barrier with the characteristics of dentine starts to develop to close the exposure ** Calcific barrier (Dentine Bridge) formation needs 4 weeks to be completed ** Calcific barrier is associated with a layer of odontoblast cells derived from undifferentiated stem cells in the pulp ** The quality of this calcific barrier is very variable and about 90% of calcific barriers contain multiple porosities which permit leakage of bacterial toxins into the pulp UNLESS the cavity has been

adequately sealed Why dont we do RCT directly instead of pulp capping?

The aim of pulp capping is to maintain the vitality of the pulp, because if the tooth gets non-vital then it will be brittle and it may fracture easily, and thats why they are trying different materials to try to keep the pulp vital as much as we can

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 Pulp calcification: Causes of pulp calcification:

1) 2) 3) 4) 5) Idiopathic Trauma Attrition or abrasion Pulpitis Restorative materials

Pulp stones (denticles) = calcified bodies with an organic core and occur most frequently in the coronal pulp True pulp stones are composed of tubular structure False pulp stones are composed of concentric layers of calcified material with NO tubular structure
surrounded by tertiary or secondary dentine)

Pulp stones can be according to their location in the pulp: free, adherent or interstitial (when Pulp stones are more numerous after operative procedures on the tooth
Pulp stones dont cause symptoms

Dystrophic calcification = granules of amorphous calcific material which may be scattered along collagen fibers or aggregated into larger masses and they are most commonly found in root canals
Pulp stones and dystrophic calcification may obstruct endodontic therapy Complete pulp obliteration may be seen in: dentinogenesis imperfecta, dentine dysplasia type 1 and following traumatic injury to the apical blood vessels which is NOT sufficient to cause necrosis

Age changes in the dental pulp:

Pulp size gets smaller More deposition of calcified tissue (Pulp stones do not increase with age) Odontoblast number will decrease with age Collagen content will increase (The elderly pulp will be more fibrous because there is a lot of collagen compared to the young pulp) Vascularity will decrease The reactionary dentin will form more and more with age leading to dentine sclerosis
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