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 Caries – most common form of injury that
DISEASES OF THE PULP causes pulpitis
1. Reversible pulpitis
2. Irreversible pulpitis: symptomatic,  Operative dental procedures – may also trigger
asymptomatic, chronic hyperplastic pulpitis an inflammatory response in the dental pulp
3. Pulp necrosis
 Heat, friction, chemical associated with
ABNORMALITIES OF THE PULP filling materials are potential irritants
1. Pulp calcification
2. Internal resorption  Reduce damage by: using cooling
3. External resorption water spray during tooth preparation
and using insulating baste to protect
DISEASES OF THE PERIAPICAL TISSUES pulp from irritating chemicals
1. Periapical abscess
2. Periapical granuloma  Trauma – those that results to a root or crown
3. Radicular cyst fracture
4. Phoenix abscess
5. Condensing osteotitis  Periodontitis – that has extended to an apical
or lateral root foramen
In the dental pulp, inflammation is the response to
injury, just as it is in any other organ.
The level of pulpal inflammation is determined through DIAGNOSIS SIGNS&SYMPTOMS RADIOGRAPH RESPONSE
a combination of clinical criteria. Results of electric, TESTS
Normal pulp None +
heat, cold and percussion tests must be added to the
Reversible May have sharp +
patient history, clinical examination and clinician pulpitis pain
experience to arrive at the most appropriate diagnosis Symptomatic Sharp pain, but Response
of for the correct tooth. irreversible may have deep, (may be
pulpitis dull, gnawing extreme
pain; and/or
Generally, the more intense the pain and the longer
spontaneous lingering)
the duration of symptoms, the greater the damage to pain; referred
the pulp. Sever symptoms usually indicate irreversible pain; or a past
damage history of pain
Asymptomatic; None, may have +
irreversible past history of
 Encased by hard tissue (dentin/enamel)
- Does not allow for the usual swelling CLASSIFICATION
associated with the exudate of the acute  Normal pulp
inflammatory process. - A clinical diagnostic category in which the
pulp is symptom free and normally
 No collateral circulation responsive to pulp testing.
- To maintain vitality when the primary
blood supply is compromised.  Reversible pulpitis
- A clinical diagnosis based on subjective and
 Biopsies and direct application of medications objective findings indicating that the
are impossible inflammation should resolve and the pulp
- Without causing necrosis of the entire pulp return to normal if the cause is removed.

 Pain or increasing levels of sensitivity are the  Mild to moderate pain, typically
only signs intermittent, provoked, disappears
- That can be used to determine the severity upon removal of stimulus.
of pulpal inflammation
 Histologic appearance: dilation and
engorgement of BV (hyperemia),
exudation of plasma proteins.
 Treatment: remove the irritant (caries,  CF: gradual onset, little to no
fracture, old restorations, etc) and discomfort, intermittent discharge of
restore. pus through an associated sinus tract.

 Chronic hyperplastic pulpitis  Rx appearance: periapical radiolucency

- Occurs in the molar teeth (both primary
and permanent) of children and young Acute apical abscess
adults.  An inflammatory reaction to pulpal infection
- Rather than undergoing necrosis, the pulp and necrosis characterized by gradual onset,
tissue reacts in a hyperplastic manner, little or no discomfort, and the intermittent
producing a red mass of reparative discharge of pus through an associated sinus
granulation tissue that extrudes through tract.
the pulp exposure.  A localized collection of pus at the root apex of
a tooth following death of the pulp
 Symptoms seldom occur:  Pulpal infection that extends to the periapical
- No exudate under pressure tissues through the apical foramen
- No nerve tissue that proliferates with the
granulation tissue  Clinically: patient often experiences
malaise, fever and lymphadenopathy
 Irreversible process
- Indicated for endodontic therapy or  Rx appearance:
extraction - No significant changes (may have widened
 Pulp necrosis - Periapical radiolucency
- A clinical diagnosis category indicating
death of the dental pulp. The pulp is  Treatment: either from the tooth or via
usually non responsive to pulp testing and soft tissues, followed by root canal
is asymptomatic. treatment.

Teeth don’t die a natural death. You kill them :(  If left untreated – body will try to
establish drainage intraorally via a
TREATMENT: sinus tract or extraorally
PERIAPICAL PATHOLOGIES - Ineffective drainage: spread of infection
Symptomatic apical periodontitis into facial spaces in head and neck.
 Inflammation of apical periodontium
 Clinical symptoms: painful response to biting  On Abx: prescribe only if there is
and/or percussion or palpation systemic symptoms
 May or may not show radiographic changes
(depending on the stage of disease)  DD: Periodontal abscess

Asymptomatic apical periodontitis

 Inflammation and destruction of the apical PERIAPICAL GRANULOMA
periodontium that is of pulpal origin  Focus of chronically inflamed granulation tissue
 Appears as an apical radiolucency located at the apex of non-vital tooth
 No clinical symptoms (-pain/percussion)  Initiated and maintained by the degradation
products of necrotic pulp tissue
 An inflammatory reaction to pulpal infection CYST
and necrosis characterized by rapid onset,  Most common cysts of the jaws, develops from
spontaneous pain, tenderness of the tooth to preexisting periapical granuloma
pressure, pus formation, and swelling of  Occurs as a result of epithelial proliferation which
associated tissues. helps to separate inflammatory stimulus (necrotic
 Inflammatory reaction to pulpal infection and pulp) from surrounding bone
necrosis  Usually asymptomatic and are often discovered
 Results from a long standing, low grade accidentally during routine radiographic
infection examination
 RCT only if periapical lesions resolve after removal  Resorption of dentin of pulpal wall
of the irritant (necrotic pulp)  May be seen as part of inflammatory response
 RCT + apicoectomy and direct curettage to pulpal injury
 Extraction and curettage of apical zone  May also be seen in cases in which no apparent
trigger can be identified
PHOENIX ABSCESS  Any tooth may be involved, usually, only a
 Acute exacerbation of a chronic lesion single tooth is affected
 An acute inflammatory reaction superimposed  In advanced cases, teeth may appear pink >
on an existing chronic lesion, such as cyst or proximity of pulp tissue to tooth surface
granuloma  Generally asymptomatic, unless root fracture
 Can occur after a failed or an unfinished or communication with periodontal pocket
endodontic treatment occurs
 COHEN: phoenix abscess is CAP that became
 Several causes: adjacent pathologic process
CONDENSING OSTEITIS such as orthodontic process reimplanted teeth,
 Osteosclerosis/condensing apical impacted teeth, or idiopathic
periodontitis/focal sclerosing osteomyelitis  May occur in one or more teeth, any tooth can
 Focal bony reactions due to a low grade, be involved, although molars are least likely to
chronic inflammation in response to a mild be affected
irritation through the root canal  No plausible or evident explanation for the
 Usually seen at the apex of tooth with long condition
standing pulpitis  No effective treatment
 Usually asymptomatic and are discovered in  Over an extended clinical course, resorption
routine radiographic examination eventually causes loss of the affected tooth.
 Only lesion with radiopacities in the periapical
 No treatment necessary

 Asymptomatic apical periodontitis
 Periapical granuloma
 Radicular cyst (periapical/apical periodontal
 Chronic apical abscess

 Rather common phenomenon, occurs with
increasing age for no apparent reason
 May be diffused (linear) – found in root canals
or nodular (pulp stones) – found in pulp
 No clinical significance and not associated with
any form of pulpitis
 Problematic during endodontic therapy of non-
vital teeth