نسترن صباغ زاده

Endodontics Notes

*Cardial sign of inflammation & their causes:

Dolor = pain

Calor = heat

Tumor = swelling

Rabor = redness

Functionalsia = loss of function

*First is vasodilation followed by vasoconstriction (anterior constriction); the sequence:

↑ blood flow

↑ vascular permeability

Enema / Exaduation

Escape of Leukocytes of sites of injury

necrosis

*Types of inflammation:

1. Chronic : long - Macrophages

2. Acute : suddenly - Neutophils

*Causes of pulpal inflammation:

1.Bacterial (most common cause)

2.Physical

3.Chemical

4.Idiopathic

1. Bacterial (mostly streptococcus mutans)

At Coronal (crown) & Radical (root) cause caries which leads to :

Fracture (complete or incomplete)

Non-fracture trauma (weakness due to pathologic)

once there is caries or fracture on crown which provide an opening or passage for bacteria to reach the apex & by disturbuting of infection cause widdening of periodomtal space & breakage of lamina dure & formation of sinus tract & in advance result toinflammation at lymph nodes:

Parotid gland = stensen's duct

Sublingual gland = Bartholin's duct

Submandibular gland = Wharton's duct

At Anomalous tract :

Tubercle or protuberance from the involved surface thats shows extra bump or cusp.

originates from the central groove or lingual ridge.

Dens invaginatus : incisor, most common is max lateral.

Dens envaginatus : Premolars & molars, most common is mandibular premolars.

At Radiation

Retrogenic infection through:

Periodontal inflammtion & calcular deposite cause 1.periodontal disease(gum recession) 2.periodontal pocket 3.periodontal abscess

Blood cause hematogenic (pertaining to the formation of blood or blood cells).

Saliva cause periodontal cancer by radiotion therapy.

bacteria has 2 way to reach apex: 1.pulp 2.periodontal ligument

2. Physical

Acute:

Sudden Fracture by 1.coronal 2. radiation

Vascular stasis during correction of orthodontic problem by forces that apply to the tooth.

Luxation (labial/buccal or lingual movement) & Avulsion (tooth suddenly lock out of socket)

Chronic:

Adolescent

Female Bruxism that leads to 1.Abrasion 2.Malocclusion 3.TMJ problem 4.Truma to periodontium 5.Pulp exposure

Attrition (physiological) /Abrasion (mechanical)

Erosion (chemical)

3. Chemical

Filiing material

cement:

IRM (Internative & Restorative material; Disadvantages is Expensive)

GIC (Flouride release that stop formation of caries)

Zinc Oxide Eugenol (Temporary cement that Promote tertiary dentin)

Polycarboxylate (True adhesion to tooth structure as a base or lutting cement when the cavity preparation is close to the pulp;The powder is zinc oxide & liquid is polyacrylic acid or a copolymer of that acid; Disadvantages are low tensile strength & no fluoride release & intraoral solubility)

Zinc phosphate (Never use in vital teeth because it contain acid & can irrigant the pulp)

Plastic:

Polymeric resins (use in restoring & replacing tooth structure or missing teeth that can be bonded with other resins or directly to tooth structure or to other restorative materials such as amalgam; Polymer is the liquid & Monomer is powder. Examples: Self cure resin & Heat cure resin)

Composite resin resotorative fillings (Because of the resin mimics has the appearance of natural teeth that also known as “white fillings” or “tooth-colored fillings")

Etching agent:

Removes smear layer & wet of the enamel to promote adhesion. 35% phosphoric acid for 15 seconds & wash well the tooth with water & dry after use

Cavity liners:

Cavity warnish for Amg

Bonding agent for composite

curing times is 20 sec

Alcohol/ether:

Cavity base that provides protection

Calcium hydeoxide (Dycal)

GIC type I (Luting cement for cementation of crown & bridges), type II (Restorative)

Disinfectant

AgNo3 (silver nitrate)

Phenol (using during pulpotomy)

NaFl (sodium fluorescein)

4. Iatrogenic

Cause by dentist druring:

Cavity prepration by Expose the pulp.

Restoration by wrong pack (No space between filling material).

Intentional extripation (ریشه کنی و نابئدی عمدی) by Exposing pulp tissue.

Orthodontic movement by forces that apply to the tooth.

Periodontal curettage by Severe mobility of tooth

Electrosurgery by Laser burns

Periapical curettage

Osteotomy by Cutting the bone.

Intubation by strike the teeth as it's rapidly and forcefully passed through the mouth and cause chipped teeth.

*Idiopathic - None cause:

Aging

Internal resorption

External reorption

Hypophosphatasia

Effect bone formation & disturbe mineralization

Sickle cell anemia

Hematogenic disease that decrease RBC so ↑ risk of infection.

*Pathogenesis:

1st ↓dentin permeability that leads to dentin sclerosis (hardening of dentin)

2nd formation of new dentin (secondary dentin)

3rd inflammatory & immune reaction (hyperemia) that leads to pulpitis then necrosis.

*Disease of the pulp :

1. Hyperemia

Physiologic term for inflammation.

↑ blood flow of pulp tissue.

Different with pulpitis.

Significance is 1st sign of pulp in stress.

Because of presence of causes (bacteria, trauma,...) that leads to Hypercemia (vasodilation followed by vasoconstriction) which finally result to Pulpitis.

2. Pulpitis

inflammation of pulp can be:

Acute/Chronic

Partial(some part of pulp expose) / Total (all part of pulp expose)

Infected (pus/abscess) / Sterile (no pus)

*Types of Pulpitis:

Inflammatory (Reversible & Irreversible)

Pulp Degeneration (calcific & Atrophic & Fibrous & Pulpartifacts & Tumors)

Necrosis

Inflammatory

Reversible

Mild to moderate inflammation of pulp because of noxious stimuli.

Px complain of pain that produced by thermal (hot & cold) stimuli.

Capable to retaining to uninflamed state by removal of stimuli.

Pain of brief duration produced by thermal stimuli.

Pain subside as soon as stimuli removed.

Sharp pain for few second or moment. (dentinal tubules is exposed)

Symptomes by cold food or cold air.

No accur spontaneously, its reactive.

No continue to accour when cause removed.

Thernal response are momentary, quick, sharp, hypersensitive response, subsides as soon as stimulus removed.

Percussion & Palpation is Negative.

in X-ray :

Caries not reach the pulp. (only in enamel or dentin)

No radiolucency at apex.

No widdening of periodontal space

Lamina dura is intact - continious & radiopaque (lamina dura is thin bone occupize periodontal space but if there is break ,No contact)

Tx of reversible:

Early detectable & removal of cause.

Retreatment of cure.

prepare wet cavity & proper utilization chemical drug & restorative procedure.

Never desicate dentin during restorative procedure.

Outcome of treated reversible:

Favorable if irritant is removed early enough; if not detectable & treate on time, will continue & develop into irreversible.

Irreversible

Persistant inflammatory condition of pulp cause by Noxious stimulus.

Can be Symptomatic (pain) or Asymptomatic (no pain)

Can be Acute or Chronic.

Can be with Pus (infected) or No pus (sterile)

Progression of reversible pulpitis.

Pain caused by hot/cold stimulus.

Pain man accour spontaneously.

Pain persist for several min to hour.

Lingering after removal of thermal stimuli (Can ot go back to normal)

Hemorrhage & pain during probing.

In X-ray:

Deep cavity extending to pulp or decay under filling.

Caries exposed pulp or envolved surface of pulp.

Tx irreversible:

Emeregency tx is pulpectomy & placing material such as Formocresol (has too much formalin cause bone resoption)

Root canal tx

Extracted if its not restorable

Outcome of treated irreversible:

Favorable after proper endodontic procedure is done with proper restoration of tooth; if not detectable & treate on time, will continue & develop into necrosis.

Types of irreversible:

1. Acute

Short duration

Abnormally response tp cold/heat

Caries:

Smooth surface (labial, buccal, lingual, proximal)

Pit & Fissure&occlusal (lingual pit of max 1st molar, Buccal pit of mand molar, incisors)

Radiographic:

Deep caries with apparent pulpal exposure, extensive restoration

Theckening of periodontal space (advance stage)

Symptomatic:

Moderate-severe spomtaneous(accour naturally)

Inter mittent(on&off) or continous, sharp, dull

Radiating(not local,can go to neck) or Reffered(can not determined location), difficult to localize.

Intense pulsating type which becomes intermittent & throbbing

Contious for long period & worse when heat is applied

Pain relieved by application of heat/cold

Affect by postiral change(at night, sleep); Sleep with elevated head(seatin position)

Types of acute:

Suparative pulpitis presence of pus

Serous Pulpitis Extensive carise with No pulp expusure; Mild pain & increase sensivity during hot/cold test, sprecially hot test & negative to percussion

2. Chronic:

Asympotomatic

With pulp exposure

Hyperplastic pulpitis

Internal resorption

Types of chronic:

Chronic Close pulpitis No gross cavity & slowing advamcing caries

Chronic open pulpitis Big caries involvement

1. Ulcerative

expose the pulp & may favorable if symptomes relieved

2. Hyperplastic

Other name is pulp polyp

Chronic proliferative pulpitis, productive inflammation(hyperplasia) of pulp to extensive caries exposure of young pulp.

Characterized by development of granulation tissure that covered with epithelium; in otherword Granuloma with stratified squamous epithelium lined with polymorphous cell.

Clinical appearance is Fleshy reddish pulp that filled pulp chamber.

Resulting from long standing low grade irritation of pulp.

In young px & adult, no more above 50 y.o

Pain is not common unless disterbuted, painfull during presence of food & sensitive to hot/cold.

Tx is cut the pulp with spoonshape & excavation then RCT.

Outcome is favorable after endo tx or resto & can be unfavorable if left withouy tx.

X-ray of pulp polyp shows big radiolucency with direct access to pulp chamber.

*Pulp inflammation overview

1. pulp hyperemia

If does not treat will lead to Reveressible

2. Reversible pulpitis

If does not treat will lead to Irreveressible

3. Irreversible pulpitis

3.1. Actue Irreversible pulpitis

3.1.a. Acute Suparative pulpitis

3.1.b. Acute Serous pulpitis

3.2. Chronic Iireversible Pulpitis

3.2.a. Chronic Close pulpitis

3.2.a.b. Chronic Open Pulpitis

3.2.a.b.a. Chronic ulcerative Open Pulpitis

3.2.a.b.b. Chronic huperplastic Open Pulpitis

If does not treat will lead to Necrosis

4. Necrosis

4.1. Liquifactive necrotic pulp

4.2. Coagulative necrotic pulp

4.2.a. Caseation Coagulative necrotic pulp

Necrosis

Common condition affecting tooth which pulp killed by Acute or Chronic inflammation.

History of pain that disappear.

Pulp extripation on tooth extraction is necessary.

Pulp Death that cause reduction of pain of tooth because all the tooth's nerves are in pulp, by death of pulp the px can feel the pain any more

Death of pulp can be partial or total.

sequel of inflammation of pulp following a traumatic injury:

1. Pulp is destroyed before inflammatory reaction takes place.

2. Ischemic infarction causing Dry-gangreous necrotic pulp whicj is blackage or bluish discoloration is most common cause by trauma.

3. Liquifactive, proleolytic enzyme convert pulp tissue into softtened mass that results liquid amorphous debris.

3. Coagulative necrotic, soluble portion of tissue is precipitated or converted into solid material.

4. Caseation is form of Coagulative necrotic, tissue converted to chessy mass consisting chiefly of Coagulated protein, fat, water.

End product of pulp decomposition is Hydrogen sulfide, Ammunis, Fleshy substance, Indican, Ptomaines, water, carbon dioxide.

Intermediate products contribute to unpleasant odor emanting from root of canal.

*Periapical Abscess

Result of decay & infection extending into pulp of tooth.

Break in periodontal ligument provide passage of bacteria toward the apex.

pain is severe, persistant, throbbing.

Tooth is tender to touch if not treted pus.

Tx:

Incision-dranaige of pus & Antibiotic therapy (Amoxicillin 500mg, Dispence # of antibiotic with type of anitbiotic either capsule or tablet, instruction take one capsule 3 times aday)

Root canal therapy

Extraction

*Periapical Granuloma:

Other name is Acute Periodontitis.

One of the most common sequel of pulpitis

Localized mass of chronic granulation tissue formed due to infection.

Hyperemia, Edeme, Inflammation of apical periodontal ligument.

X-ray:

Thickening of periodontal space

Root canal at apex is circumscribed.

*Osteomyelitis:

Inflammation of bone & bone marrow

Result of Odontogenic infection that develops to the Jaw.

Reference:

Lecture of Dr annalie De Lemos at national university college of dentistry-manila philippines