1 Endodontics
The word endodontic comes from two Greek words meaning “inside” and “tooth.” Endodontics is the science of diagnosing and treating pulpal and periradicular disease. Endodontics is that branch of dentistry concerned with the morphology, physiology, and pathology of the human dental pulp and periradicular tissues. Its study and practice encompass the basic and clinical sciences, including the biology of the normal pulp, and the etiology, diagnosis, prevention, and treatment of diseases and injuries of the pulp and associated periradicular conditions.*
OUTLINE OF REVIEW
1.1 Pulpal Diseases
A. What is the pulp?
2. Several factors make it unique and thus alter its ability to respond to irritation:
a. The pulp is almost completely surrounded by hard tissue (dentin), which limits the available room for expansion and thus restricts the pulp’s ability to tolerate edema.
B. Physiology of pulpal pain
2. Dentinal pain
a. A-delta fibers are larger, myelinated nerves that enter the root canal and divide into smaller branches, coursing coronally through the pulp.
3. Pulpitis pain
a. In pulpal inflammation, the response is exaggerated and disproportionate to the challenging stimulus (hyperalgesia). This response is induced by the effects of inflammatory mediators that are released in the inflamed pulp.
b. Progression of pulpal inflammation can change the quality of the pain response. As the exaggerated A-delta fiber pain subsides, pain seemingly remains and is perceived as a dull, throbbing ache. This second pain symptom is from C nerve fibers.
d. Unlike A-delta fibers, C fibers are not directly involved with the pulpodentinal complex and are not easily provoked.
C. Clinical classification of pulpal diseases
1. Within normal limits
2. Reversible pulpitis
a. In reversible pulpitis, thermal stimuli (usually cold) cause a quick, sharp, hypersensitive response that subsides as soon as the stimulus is removed.
d. Reversible pulpitis can be clinically distinguished from a symptomatic irreversible pulpitis in two ways:
3. Irreversible pulpitis
a. By definition, the pulp has been damaged beyond repair, and even with removal of the irritant it will not heal.
b. Microscopically:
c. Following irreversible pulpitis, pulp death may occur quickly or may require years; it may be painful or, more frequently, asymptomatic. The end result is necrosis of the pulp.
d. Asymptomatic irreversible pulpitis (possible consequences)
(1) Hyperplastic pulpitis: a reddish, cauliflower-like growth of pulp tissue through and around a carious exposure. The proliferative nature of this type of pulp is attributed to a low-grade, chronic irritation of the pulp and the generous vascular supply characteristically found in young people.
e. Symptomatic irreversible pulpitis
(2) Sudden temperature changes (often to cold) elicit prolonged episodes of pain that lingers after the thermal stimulus is removed.
(3) Occasionally, patients may report that a postural change, such as lying down or bending over, induces pain.
4. Necrosis
b. Pulpal necrosis may be partial or total:
d. Protein breakdown products along with bacteria and their toxins will eventually spread beyond the apical foramen—which will lead to thickening of the periodontal ligament. The clinical manifestation presents as tenderness to percussion and chewing.
e. Microscopically:
(1) As inflammation progresses, tissue continues to disintegrate in the center of the pulp to form an increasing region of liquefaction necrosis.
(2) Because of the lack of collateral circulation and the unyielding walls of dentin, there is insufficient drainage of inflammatory fluids.
1.2 Periradicular Diseases
A. What is periradicular disease?
1. Periradicular lesions of pulpal origin are inflammatory responses to irritants from the root canal system.
3. The sign most indicative of a periradicular inflammatory lesion is radiographic bone resorption, but this is unpredictable. Periradicular lesions are frequently not visible on radiographs.
4. Periradicular lesions do not occur as individual entities; there are clinical and histologic crossovers in terminology regarding periradicular lesions because the terminology is based on both clinical signs and symptoms and on radiographic findings. There is no correlation between histologic findings and clinical signs, symptoms, and duration of the lesion. The terms acute and chronic apply only to clinical symptoms.
B. Classification of periradicular diseases
1. Acute periradicular periodontitis
a. Acute periradicular periodontitis means painful inflammation around the apex (localized inflammation of the periodontal ligament in the periradicular region). It can be the result of:
b. Because acute periradicular periodontitis may occur around vital and nonvital teeth, conducting pulp tests is the only way to confirm the need for endodontic treatment.
c. Even when present, the periradicular periodontal ligament may radiographically appear within normal limits or only slightly widened.
e. If the tooth is vital, a simple occlusal adjustment will often relieve the pain. If the pulp is necrotic and remains untreated, additional symptoms may appear as the disease advances to the next stage—acute apical abscess.
2. Acute periradicular abscess (acute apical abscess)
c. The periodontal ligament may radiographically appear within normal limits or only slightly thickened.
d. Radiographically, the periapical radiograph reveals a relatively normal or slightly thickened lamina dura (because the infection has rapidly spread beyond the confines of the cortical plate before demineralization can be detected radiographically).
f. The lesions can also result from infection and rapid tissue destruction arising from within chronic periradicular periodontitis—often referred to as a phoenix abscess. (The symptoms of the phoenix abscess and the acute apical abscess are identical; however, when a periapical radiolucency is evident, it is called a phoenix abscess.)
g. Histopathological findings:
3. Chronic periradicular periodontitis
a. Chronic periradicular periodontitis is a long-standing, asymptomatic, or mildly symptomatic lesion.
c. Bacteria and their endotoxins cascading out into the periradicular region from a necrotic pulp cause extensive demineralization of cancellous and cortical bone.
4. Suppurative periradicular periodontitis (chronic periradicular abscess)
a. It is associated with either a continuously or intermittently draining sinus tract without discomfort.
b. The exudate can also drain through the gingival sulcus, mimicking a periodontal lesion with a “pocket.”
1.3 Endodontic Diagnosis
A. Triage of the pain patient
1. Orofacial pain can be the clinical manifestation of a variety of diseases involving the head and neck region.
B. Medical history (developing data)
C. Dental history
2. Location
b. “Could you point to the tooth that hurts or swells?” (The patient is asked to indicate the location by pointing to it directly with one finger.)
c. The accuracy of the patient’s description of pain depends on whether the inflammatory state is limited to the pulp tissue only:
d. Referred pain: pain can also be referred to the adjacent teeth or in the opposing quadrant.
(2) Pain from posterior teeth may be referred to the preauricular area, down the neck, or up to the temple, on the ipsilateral side.
3. Chronology
b. Patient may be aware of the history of dental procedures or trauma, clinical course, and temporal pattern of the symptoms:
(1) Mode: Is the onset of symptoms spontaneous or provoked (i.e., sudden or gradual)? If symptoms can be stimulated, are they immediate or delayed?
4. Quality of pain
1.4 Endodontic Examination and Testing
Extraoral Exam
C. Occasionally, facial lesions (e.g., a sinus tract) can be traced to a tooth as the source. All sinus tracts should be traced with a gutta-percha point by radiograph (Fig. 1-1).
Intraoral Endodontic Examination
Intraoral diagnostic tests enable the practitioner to:
• The dentist should include adequate controls for test procedures. Several adjacent, opposing, and contralateral teeth should be tested before the tooth in question to establish the patient’s normal range of response.
A. Palpation
B. Percussion
1. Although the percussion test does not indicate the health of the pulp, the sensitivity of the proprioceptive fibers does reveal inflammation of the apical periodontal ligament.
2. A positive response to percussion indicates not only the presence of inflammation of the periodontal ligament, but also the extent of the inflammatory process. (The degree of response correlates with the degree of inflammation.)
3. Other factors may also inflame the periodontal ligament and yield a percussion positive test result:
C. Thermal tests (Table 1-1)
1. Cold test: cold testing can be done with cold water baths, sticks of ice, ethyl chloride (−5° C), dichlorodifluoromethane (DDM: Endo Ice −30° C, −21° F), and carbon dioxide ice sticks(−77.7° C,−108° F).
a. In the ethyl chloride or Endo Ice method, ethyl chloride is sprayed liberally onto a cotton pellet.
2. Heat test: these include warm sticks of temporary stopping, rotating a dry prophy cup to create frictional heat, and a hot water bath with rubber dam isolation. The hot water bath will yield the most accurate patient response.
3. Responses to thermal tests: the sensory fibers of the pulp transmit only pain, whether the pulp has been cooled or heated. There are four possible responses:
a. No response: a nonvital pulp is indicated; it can also indicate a false negative response because of excessive calcification, an immature apex, or recent trauma.
D. Electric pulp tests (see Table 1-1)
• Electric pulp testing does not suggest the health or integrity of the pulp; it simply indicates that there are vital sensory fibers present within the pulp.
• The electric pulp test does not provide any information about the vascular supply to the pulp, which is the true determinant of pulp vitality.
• Electric pulp test readings do not correlate with the relative histologic health or disease status of the pulp.
• Several conditions can cause false responses to electric pulp testing; therefore, it is essential that thermal tests be performed before a final diagnosis is made.
1. Electric pulp testing technique
c. The electrode should then be applied to the dry enamel on the middle third of the facial surface of the crown.
E. Periodontal examination
F. Mobility
1. Tooth mobility is directly proportional to the integrity of the attachment apparatus or to the extent of inflammation of the periodontal ligament.
2. The clinician should use two mouth mirror handles to apply alternating lateral forces in a facial-lingual direction.
I. Radiographic exam
1. What can I find on radiographic exam?
a. A radiolucency will not begin to manifest until demineralization of bone extends through the cortical plate of the bone. (Clinicians should not rely exclusively on radiographs in an attempt to arrive at a diagnosis.)
2. Radiographic interpretation
b. A sudden change in appearance of the canal from dark to light indicates that the canal has bifurcated or trifurcated.
c. A necrotic pulp will not cause radiographic changes until demineralization of the cortical plate. (Significant medullary bone destruction may occur before any radiographic signs start to appear.)
d. The attending dentist should be cautioned in accepting prior diagnostic radiographs from the patient or another dentist, no matter how recently they were made. Prior iatrogenic mishaps such as ledge formation, perforation, or instrument separation are critical for a newly treating dentist to uncover.
3. Buccal Object Rule (“SLOB” Rule): Same Lingual, Opposite Buccal
a. Principle: the object closest to the buccal surface appears to move in the direction opposite the movement of the tube head/cone up or down or side-to-side when compared with a second radiograph. Objects closest to the lingual surface appear to move in the same direction of the cone.
4. Radiographic differential diagnosis of periradicular radiolucencies (Table 1-2)
a. Vertical root fracture: a long-standing vertical root fracture may be viewed as a variant of apical periodontitis.
b. Lateral periodontal cyst: tracing of the lamina dura and normal responses to pulp vitality testing establishes the diagnosis.
c. Osteomyelitis: a highly variable radiographic appearance with sclerotizing and osteolytic processes sometimes occurs in the same patient.
d. Developmental cysts: the incisive canal cyst (nasopalatine duct cyst) may exhibit radiographic features similar to apical periodontitis. Tooth vitality responses become particularly important in differential diagnosis.
e. Traumatic bone cyst
g. Cemental dysplasia
h. Cementoblastoma
i. Central giant cell granuloma
j. Systemic disease
1.5 Cracked Tooth Syndrome
A. Clinical features
C. Incidence
A strong majority are lower molars, with a slight preference for the first molar over the second.
D. Diagnosis
E. Treatment
2. Irreversible pulpitis or necrosis with acute periradicular periodontitis
1.6 Vertical Root Fracture
A. Clinical findings
B. Etiologies
Predisposing factors are a weakening of the root structure by:
1.7 Endodontic–Periodontal Relationships
A. How do the pulp and periodontium communicate?
B. Types of endodontic and/or periodontal lesions
1. Primary endodontic lesions
2. Primary periodontal lesions
OUTLINE OF REVIEW
2.1 Nonsurgical Endodontics
A. Objectives
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