Im note ..

I put the slides in a Bold so be happy read bolded sentences and ignore the rest :P Disorders of the Dental Pulp Pulpitis Different clinical & pathological classifications are artificial and confusing: 1) Acute or chronic The beginning of the lec wasn't so clear and not recorded from the first sentence but nothing important it's the difference between acute and chronic inflammation 2) Partial or total Dental pulp as small as it's it can be totally or partially inflamed . The best example is Molar teeth it has large pulp chamber so maybe in one area we have Pulpitis but in another area still healthy 3) Open or closed The pulp surrounded with a hard tissue which is the dentine . Close :: if we get pulpitis and the surrounding dentine is still there Open :: like when we have large carious cavity 4) Exudative or suppurative We can calcify it according to what material is included in the inflammation
Exudative : Exudate is derived from exude, "to ooze from the Latin exsdre, "to (ooze) out like sweat" Suppurative : pus formation , abscess >>> is a collection of pus (dead neutrophils) that has accumulated in a cavity formed by the tissue in which the pus resides on the basis of an infectious process >> Liquefactive necrosis

5) Reversible or irreversible >>> The most important clinical classification Irreversible :: we expect it will progress into pulp necroses >> root canal treatment .

Pulpitis is a dynamic process and presents a continuous spectrum of changes reflecting interplay between cause and host defense What defense mechanisms dose the pulp have ?? 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 Poor correlation between microscopic changes & clinical symptoms We could have really bad pulp and we can't see symptoms

Pulpitis Clinical Features Presents as pain which patient may have difficulty in localizing to a particular tooth.
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The pulp does not has proprioceptor ( it's a location receptors ) and this is a main difference between the pulp and the periodontal tissues in general . Now if u has an inflammation in the PDL once u touch the tooth u will know that this is the painful tooth but in pulpitis it's a different situation bcz one nerve branch feed number of teeth so the patient can't know exactly which tooth is the painful one SO pulpitis pain poorly localized but periodontal pain easily localized by the patient and this difference make us to differentiate between pulpitis and Periapical Periodontitis ( we will talk about it in the next lec )

Pain may radiate to adjacent jaw, face, ear, or neck. Dental pain can be felt in these areas .
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May be continuous for several days or may occur intermittently over a longer period ( and some times the patient may has chronic pulpitis large cavity and doesn't feel any pain or feel little pit pain and ignore it )
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Pulpitis is often described as acute or chronic based on duration and severity of symptoms a lot of pain >> acute
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Clinical Features Acute pulpitis: Severe throbbing, lancinating pain on thermal stimulation or lying down, keeps patient awake. Generally lasts 10-15 minutes but may be more or less continuous (reversible pulpitis). With progression, may become spontaneous & continuous (irreversible pulpitis). Clinical Features Chronic pulpitis: Bouts of dull aching which can last for an hour or more. Not easy to decide it's reversible or irreversible pulpitis so u have to open the tooth remove the caries and see if we have caries exposure . Pain on thermal stimulation or spontaneously.

Pulpitis Clinical Features

Pulpitis may be asymptomatic.

Most important decision clinically is whether pulpitis is reversible or irreversible. Bcz u want to know wither to restore this tooth or treat it .
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Decision is made based on many factors including:

1) Severity of symptoms. 2) Duration of symptoms. 3) Size of carious lesion. 4) Pulp tests >> server and electric 5) Direct observation during operative procedure. U have a patient with pulpitis u going to move the caries >> if the base of the cavity still clean and u don't have exposure u can depend on that in ur decision 6) Age of patient. Younger pulps are more likely to resolve and heal more than older pulps .

Pulpitis Etiology 1. Microbial: 1) Dental caries. 2) Traumatic exposure. >> if u are preparing a cavity and while that u expose part of the pulp this is called traumatic exposure sometimes we try something called direct pulp capping >> place the pulp capping agent directly on the pulp to allow pulp deposit tertiary dentine >> if there is still a thin layer and u can see the pulp through it might try indirect pulp capping 3) Marginal leakage When u have a restoration and there is a leakage ( defective margins ) 4) Cracked tooth 5) Coronal fracture 6) Attrition >> when it sever may cause pulpitis . 7) Abrasion 8) Traumatic restorative procedure 9) Invaginated odontome 10) Advanced periodontitis (periodontal-endodontic lesion) Periodontium consists of Alveolar bone , Cementum , Gingiva and Periodontal ligament Gingivitis which is an result for poor oral hygiene progresses slowly into periodontitis ( the rest of the previously mentioned tissue get inflamed ) >> we loose the attachment between the tooth and the gigiva create what we called periodontal cocatte ( 3'aleban alkelmeh 3'ala6 bas I tried my best to hear it and I can't srry for that :( ) >> still of the healthy gingival sulcus but we get separation between all the tissues and the tooth surface >> the tooth start to move from it's place >> now if we have bacteria and a latral root canal the bacteria access through this small foramina into the pulp and cause pulpitis

Side talking between two guys , the recorder mostly between them and the Dr talking without mice to a student the result >> I can't hear a single word :p ya36ekoum al3afyeh :P
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Pulpitis starts before leading organisms in carious dentin reach pulp

We don't need the bacteria to directly invade the pulp to cause pulpitis even at the beginning of the carious lesion the bacteria enters into the dentinal tubule and start release it's products that will cause pulpitis Pulpitis is not usually seen histologically until organisms are within 1mm of the pulp in permanent teeth, or 2mm in deciduous teeth.
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2 . Chemical and thermal injury:

During restorative procedures: frictional heat, irritant substances. May respond by reactionary dentin formation.

3. Barotrauma (aerodontalgia): Flying at high altitude in unpressurized aircraft, or rapid decompression in divers.
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Attributed to formation of nitrogen bubbles in pulp tissue or vessels.

Thought not to be a direct cause, but rather an exacerbating cause in presence of caries.
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Pulpitis Histopathology
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Poor correlation between microscopic changes & clinical symptoms. Inflammatory process may be modified by several factors: Nature, severity and duration of insult. Efficiency of host defenses. Efficiency of pulpo-dentinal complex defenses. Special anatomy of pulp: surrounded by hard tissue and cannot tolerate edema .

1. 2. 3. 4.

Reactionary dentin may continue to form after onset of pulpitis if odontoblasts and pulp have not been irreversibly damaged, and may protect pulp.
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Pulpitis caused by caries starts as a localized area, but extends throughout pulp if caries is not treated.
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If inflammation is severe, local microcirculation may be compromised, leading to local necrosis and suppuration of pulp (pulp abscess), or diffuse suppuration and necrosis.
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Immune reactions in inflamed tissue may contribute to tissue damage.

Rate of progression of pulpitis is variable, but end result of untreated pulpitis is total necrosis except in the case of pulp polyp formation.
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Closed pulpitis: whether acute or chronic, may progress to necrosis due to limited ability of pulp to withstand inflammatory edema since it is surrounded by hard tissues.
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Pulpitis Chronic Hyperplastic Pulpitis (Pulp Polyp)

Open pulpitis or chronic hyperplastic pulpitis (pulp polyp):

Large carious cavities. Young molar teeth with wide apices and good blood supply. Usually devoid of sensation on gentle probing.

Polyp consists of chronically inflamed hyperplastic granulation tissue protruding from pulp cavity.
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May become epithelialized by spontaneous grafting of desquamated oral epithelial cells from saliva.
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Pulpitis Chronic Hyperplastic Pulpitis (Pulp Polyp) Usually a molar tooth in young individual develop this type but it could happen in permanent tooth >> very large cavity >> the pulp is exposed >> undergo edema and inflammatory process >> still there is a good blood supply to the apical foramina bcz it still wide >> a pulp changes into a mass of granulated tissue >> call it Chronic Hyperplastic Pulpitis
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Large carious cavities. Young molar teeth with wide apices and good blood supply.

Usually devoid of sensation on gentle probing.

Polyp consists of chronically inflamed hyperplastic granulation tissue protruding from pulp cavity.
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May become epithelialized by spontaneous grafting of desquamated oral epithelial cells from saliva.
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Although the pulp doesn't have epithelium when we examine effected tooth we could see epithelium and they think that this is epithelium comes from oral mucosa that try to shedding the cells from the surface by covering them with epithelium Pulpitis Effects of Cavity Preparation & Restorative Materials Cavity preparation: speed, heat, pressure & coolant may all cause pulp irritation And actually we need this irritation to stimulate the formation of tertiary dentine
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Aspiration or displacement of odontoblasts into dentinal tubules, with reduction of numbers.

Effects of cavity preparation & restorative materials may further complicate pulpitis caused by caries or other causes.
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Thickness & nature of remaining dentine may affect pulp response to dental material.
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Healing of Pulp

Injured odontoblasts are replaced by new cells from pulp

U know the pulp has stem cells they migrate to the area where we have denteno pulpal junction and they differentiate into odontoblasts and start deposite tertiary dentine Now tertiary dentine not regular as secondary dentine bcz its usually deposit faster
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Pulpitis may resolve upon removal of irritant.

It may resolve due to reactionary dentin formation even without removal of caries.
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Pulp capping after traumatic pulp exposure or pulpotomy: Ca(OH)2 agents stimulate formation of a calcified barrier.
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Pulp Calcification

Pulp stones (denticles): developmental, known as true (tubular structure), or false (concentric calcifications).
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Dystrophic calcifications: amorphous calcified material, may obstruct endodontic treatment.

Pulp obliteration by irregular dentin upon injury not sufficient to cause necrosis.
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Pulp obliteration by a normally formed dentine in dentinogenesis imperfecta and dentinal dysplasia.
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Pulp Necrosis

If the pulpitis irreversible and we fail to save this pulp by pulp capping or by any other procedure then ::::
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May follow pulpitis or trauma to apical blood vessels. Coagulative necrosis after ischemia.

Bcz this necrotic debris start to go into the dentinal tubule Liquefactive necrosis after pulpitis may become gangrenous with foul odor upon infection by putrefactive bacteria from caries.
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Pulp necrosis in sickling crisis of sickle cell anemia. >> not common

Age Changes in the Pulp

We have primary dentine , secondary dentine and tertiary dentine Primary dentine >> the first dentine formed in the tooth before eruption . Secondary dentine >> the dentine formed normally after eruption . Tertiary dentine >> Reactionary to trauma and caries So with age we get increased of secondary dentine there for we get smaller pulp chamber
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Gradual decrease in volume due to secondary dentin formation. Decreased vascularity & cellularity. Increased collagen fiber content. Impaired response to injury and healing potential. Increase of pulp stones and diffuse calcification.

Done By ::: HaNaa JadAllah *__^