Endodontic History and Examination

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PATIENT MANAGEMENT

ANATOMY OF DENTAL PULP

Dental pulp contains nerve fibers, blood vessels and connective tissue, and is completely surrounded by dentin. The limited circulation and available room for expansion restricts the pulp’s ability to tolerate edema and inhibits a mature tooth’s ability to cope with any type of insult. In health the dental pulp contains fibroblasts, odontoblasts, histiocytes (macrophages) and lymphocytes. When pulp becomes inflamed/diseased, a cellular shift will see elevated numbers of polymorphonucleocytes, plasma cells, basophils, eosinophils, lymphocytes, and mast cells.

A-delta fibers are larger, myelinated nerves intimately associated with the odontoblastic cell layer and responsible for transmitting quick, sharp pain that dissipates quickly. These afferent nerve fibers enter at the apical foramen, following the blood vessels, and branch to form the plexus of Raschkow underneath the cell rich zone. Here they lose the myelin sheath and project through the subodontoblastic plexus into the odontoblastic layer and the predentin, forming the pulpo-dentinal complex.

C fibers are smaller, unmyelinated nerves that are not directly involved with the pulpo-dentinal complex and are normally not easily stimulated. C fibers respond to stimuli which have stronger intensities and cause lingering, throbbing/aching, poorly localized (radiating) pain. C fiber pain indicates significant irreversible local tissue damage. Proprioceptive nerve fibers are not found in the pulp.

PULPITIS AND PULPAL NECROSIS

Healthy pulp is vital and lacks symptoms or diagnostic test results associated with inflammation. A healthy pulp will be asymptomatic and will react favorably to vitality tests such as heat, carbon dioxide (CO2) snow, ice and/or electric pulp tester (EPT). With any of these tests there is usually a positive result that subsides very quickly (within a few seconds). With age comes increased amounts of secondary dentin deposition in the pulp chamber which usually diminishes test results.

Reversible pulpitis implies that the pulp is still vital but inflamed, and is expected to return to normal when the aetiological irritant has been removed. Reversible pulpitis is not a disease itself but a description of symptoms. A tooth with irreversible pulpitis may present with intense, sharp reactions to thermal stimuli. Most often pain is only associated with direct stimulation (e.g. exposure to cold), mediated by the A-delta pain fibers, and there is no spontaneous pain present. The response is exaggerated/disproportionate compared to the stimulus (hyperalgesia).

Irreversible pulpitis implies that the pulp is still vital but severely inflamed so that complete healing is an unlikely outcome. Pulpal necrosis and subsequent infection is the predicted outcome and the treatment options are set accordingly. The presenting symptoms associated with irreversible pulpitis can sometimes be misleading, and many teeth with irreversibly inflamed pulp may never present with symptoms (asymptomatic irreversible pulpitis). Teeth that present with symptomatic irreversible pulpitis can be very sensitive to thermal changes. When a long and intense enough stimulus is placed there is an initial sharp pain, mediated by the A-delta nerve fibers, followed by a poorly localized dull pain sensation mediated by centrally located C fibers. The pain sensation has the tendency to linger (for more than 10 seconds) as a dull ache after the stimulus has been removed.

A history of spontaneous pain is perhaps the clearest sign of irreversible pulpitis, especially if the pain has woken the patient up or interrupted sleep. A sensitivity to heat that is relieved by cold is a tell-tale sign of irreversible pulpitis. Occasionally patients may report that a postural change (lying down) leads to dental pain. The microscopic appearance of irreversibly inflamed pulp may include micro-abscesses, tiny zones of necrosis, and areas with dense inflammation and cellular degeneration. Thickening of the apical portion of the periodontal ligament may become radiographically evident in advanced-stage disease.

Hyperplastic pulpitis a variation of irreversible chronic pulpitis that occurs when the pulp of young teeth have been exposed by caries or trauma. Symptoms may vary, and often there is a lack of symptoms or pain from the area is mild. Thermal and electrical sensitivity tests may elicit normal responses. Teeth present with a reddish, cauliflower-like outgrowth of pulpal tissue often through a carious exposure. Microscopic examination may reveal a mass of inflamed granulation tissue (resembling a pyogenic granuloma) combined with a mixed inflammatory cell infiltrate containing neutrophils, plasma cells and lymphocytes. The surface of the polyp usually shows epithelization or even full keratinization. Pulpotomies have been suggested with the hope of keeping radicular pulp alive.

Necrotic pulp lacks all vitality, and vitality testing returns no response. Pain and sensitivity is likely associated with periapical pathology and not with the dead pulpal tissue. It is possible (and sometimes very frustrating) to find a tooth with partially necrotic pulp that presents with a confusing history and mixed clinical presentation. A molar tooth may contain necrotic pulp in the canals close to the origin of the trauma (e.g. carious lesion) and irreversibly inflamed pulp in a distant canal. Necrotic tissue and bacterial byproducts/toxins will eventually spread beyond the apical foramen leading to apical periodontitis and subsequent apical spread of pathology.

INTERNAL AND EXTERNAL ROOT RESORPTION

Internal root resorption may occur in response to chronic pulpal inflammation or trauma. It is seen as a radiolucency in the pulpal cavity, most frequently associated with incisors and mandibular molars. Advanced root resorption may be seen visually as a reddish/pink area due to the granulation tissue showing through the resorbed area (pink tooth). If the unmineralized predentin layer immediately adjacent to the odontoblast layer is lost or disrupted, it predisposes the dentine to internal resorption by odontoclasts. If internal resorption is detected, a pulpectomy should be performed immediately, and the tooth dressed with CaOH. A tooth with inflammatory resorption that has progressed to a perforation will have a poor long term prognosis. Recall the different layers of dentin:

Mantle dentin – the initial ~150 μm outer layer of dentin found in the periphery of the tooth in the coronal region. It is mainly atubular dentine laid down before odontoblast maturation. The collagen fibers are larger and less organized than those of the circumpulpal dentin.

Globular dentin – zone of disturbed dentin that sits between mantle dentin and circumpulpal dentin, believed to be a result of deficient mineralization seen during the maturation of odontoblasts.

Circumpulpal dentin – the majority of dentin found in the tooth, deposited by mature odontoblasts.

Primary dentin – most prominent dentin composed of mantle, globular and circumpulpal dentin.

Secondary dentin – normal circumpulpal dentin that forms after eruption, with a similar structure to primary dentine. It deposits slowly and is not formed in response to trauma.

Tertiary dentin – aka reactive, sclerotic or reparative dentin, this is an irregular and disorganized layer of dentine that is deposited directly in response to trauma or irritant (caries).

External root resorption involves cementum and dentine and is caused by injury to the PDL, damage to the root surface, or periradicular inflammation/infection. Resorption can also be triggered by aggressive orthodontic forces, or be an unfortunate outcome of internal bleaching. Surface resorption is very common and usually self limiting, sometimes only involving cementum and not even visible radiographically. Replacement resorption sees the root surface substituted with bone, resulting in ankylosis. If left unchecked, destruction can progress rapidly. It is possible to arrest external root resorption with root canal treatment. A calcium hydroxide medicament is used and replaced every 3 months for 1 year, all the while radiographically monitoring the tooth. If external resorption has stopped the tooth is cleaned and obturated.

PERIAPICAL DIAGNOSIS

The term apical periodontitis refers to inflammation in the periapical tissues. Like pulpal inflammation, the periapical inflammation can be symptom free and discovered radiographically. A periapical lesion is likely (but not necessarily) caused by an infection within the root canal system and will require definitive endodontic treatment to resolve. Normal apical tissues are not sensitive to percussion or palpation testing. Radiographically the lamina dura surrounding the root is intact and the periodontal ligament space is uniform and of average width (0.1-0.2mm).

Acute apical periodontitis refers to acute inflammation in the periodontal ligament space that can cause the tooth to be tender to touch, percussion and palpation. There are usually little to no radiographic changes associated with this diagnostic term. A tooth with acute apical periodontitis may have pulp that is vital (irreversibly inflamed) or non-vital. First line treatment for a tooth with acute apical periodontitis secondary to an endodontic infection is conventional root canal treatment. Early-stage apical pathology may be identified by possible radiographic changes to the periodontal ligament (PDL) space or lamina dura, seen as:

Widening of PDL space, especially around the apex.
Thickening of the lamina dura.
Periapical radiolucency.
Sclerosis around the apex (condensing apical periodontitis).

Vitality/viability testing is of utmost importance when confronted with a dental history and symptoms associated with apical periodontitis. Though endodontic inflammation/infection is the most likely source of apical periodontitis, inflammation of the periapical tissues can also be caused by other sources, like occlusal trauma.

Chronic apical periodontitis refers to a periapical lesion that is not known to be strongly associated with symptoms. Often a periradicular radiolucency is noted without clinical symptoms. A thorough clinical history, vitality testing, radiography and/or test cavity preparation will confirm a necrotic pulp. A tooth with chronic apical periodontitis is non-vital. First line treatment for a tooth with chronic apical periodontitis is conventional root canal treatment. Occasionally an acute flare up of a chronic lesion will cause purulent swelling and/or pain in the area. This is termed an acute exacerbation of chronic apical periodontitis, also known as a Phoenix abscess or recrudescent abscess.

Acute periapical abscesses is the usual result of a mature endodontic infection. Periapical inflammation causes the breakdown of tissue and the accumulation of pus around the tooth. An acute apical abscess may present with rapid onset, spontaneous pain, tenderness to percussion, pus formation, and swelling of associated tissues. A tooth with an associated periapical abscess is non-vital. First line treatment for a tooth with an apical abscess is conventional root canal treatment.

Apical periodontitis with sinus tract shares features with apical periodontitis with abscess, but the breakdown of bone results in a path for the purulent exudate to follow to the surface. A draining fistula is most commonly visible in the gingiva or mucosa adjacent to the offending tooth. If the origin of the sinus is not clear, a gutta percha cone (size 25 or 30) could be inserted into the fistula and a radiograph taken. Occasionally a sinus tract can appear on the surface of the skin. Because of the lack of pressure buildup there is usually little to no pain associated with a sinus tract and swelling will not occur. Once the source of the infection has been eliminated the sinus tract should heal within a few days without any other intervention.

A clinical description of an endodontically involved tooth will usually list both the endodontic and periapical diagnosis. For example, irreversible pulpitis with acute periapical periodontitis.

PERIAPCIAL PATHOLOGY

Osteomyelitis is an uncommon sequelae of infection of the bone that results in the diffuse spread of the infection throughout the medullary spaces. If untreated it can lead to serious subsequent necrosis of bone. Symptoms include severe pain with overlying inflammation, fever, and general malaise. Because of the rapid spread of infection there may be little radiographic evidence initially. Osteomyelitis has been seen in the maxilla and mandible. This is a serious medical emergency that requires immediate referral.

A granuloma is small benign growth of granulation tissue continuous with the periodontal ligament. It is composed of a pathological mass of lymphocytes, plasma cells, histiocytes and polymorphonuclear leukocytes that are surrounded by a fibrous capsule. Granulomas are often found incidentally because they are mostly painless. Radiographically they appear as a small round well-defined periapical radiolucency. A tooth with an associated granuloma is non-vital. The first line treatment is orthograde root canal treatment. Removing the source of the infection will likely result in complete resolution.

An apical scar is a dense band of collagenous connective tissue usually located at the apex of a tooth. Clinically viewable as a periapical radiolucency, it is generally found after a surgical procedure or endodontic treatment A tooth with an apical scar will be non-vital, and may require further treatment (retreatment, apicoectomy).

Recall a cyst is an epithelium-lined cavity filled with fluid (or air), surrounded by granulomatous tissue and a peripheral fibrous capsule. The cellular origin may vary, but cysts are usually triggered by some type of inflammatory response. They will appear as a radiolucency if located in bone. Cysts may become infected and the contents of the lumen may resemble that of an abscess.

A radicular cyst arises from epithelial cell remnants (cell rests of Malassez) in the periodontal ligament. These cysts are the most common odontogenic cystic lesions of inflammatory origin affecting the jaws, and are most commonly found associated with the apices of endodontically compromised teeth. They may, however, be found on the lateral aspects of the roots linked to lateral accessory canals. The iconic radiographic appearance of a radicular cyst is a round or oval, well-circumscribed radiolucency associated with the apex of the tooth.

Many are symptomless and are discovered during radiographic examination of teeth with non-vital pulps. The inflammation in a preexisting granuloma may trigger cyst formation. A tooth with an associated radicular cyst may respond favorably to non-surgical (conventional endodontic therapy) treatment. Some cysts will require surgical intervention, either marsupialization or enucleation.

A lateral periodontal cyst (LPC) is usually seen in an area other than the apex of the tooth, originating from epithelial rests in the periodontal ligament (dental lamina). LPC is generally asymptomatic and presents as a uniform round/oval radiolucency with well-defined borders. A tooth with an associated LPC is usually vital.

Condensing osteitis describes a diffuse radiopaque lesion created by excess bony deposits around the apex of a tooth. An endodontic infection by a less virulent organism that spreads to periapical tissues triggers a localized sclerotic bony reaction. There are usually no symptoms associated with this lesion. A tooth with associated condensing osteitis is usually non-vital. First line treatment is conventional root canal treatment.

A traumatic bone cyst is an uncommon non epithelial lined cavity of the jaws (not a true cyst). It is most commonly seen in young people between the mandibular canine and the third molar. Clinically, the lesion is asymptomatic and usually discovered during routine radiological examination. The unilocular radiolucency appears to scallop around the roots of the teeth.

An ameloblastoma is a benign odontogenic tumor derived from odontogenic ectoderm. It is more common in the lower jaw, and more common in the posterior mandible as compared to the anterior. Though benign, ameloblastomas can grow aggressively and can develop into a malignancy termed malignant ameloblastoma (ameloblastic carcinoma). Radiographically they appear as multilocular radiolucencies (“soap-bubble”) with associated bony expansion and tooth root resorption.

A cementoma (periapical cemental dysplasia) is an odontogenic tumor of cementum. Commonly found in the anterior region of the mandible, this spherical radiopaque calcification usually starts as a radiographic radiolucency. A tooth with an associated cementoma is usually vital.

A cementoblastoma is a rare benign odontogenic tumor characterized by the formation of a mass of cementum-like tissue derived from ectomesenchyme. Commonly found in the mandibular molar area, cementoblastomas appear as a radiopaque attachment to the roots of a tooth. Cementoblastoma are distinctive but relatively uncommon tumors.

The mental foramen is usually located close to the apex of the lower second premolars, and may be radiographically superimposed over the root, mimicking a pathological radiolucent change.

CLINICAL ASSESSMENT

Accurate pulpal diagnosis is the key to all predictable endodontic treatment. The diagnosis is based on presenting symptoms, history of symptoms, diagnostic tests and clinical findings. The clinical assessment should include:

Medical and dental history – including a description of the intensity, type, timing, location, duration of pain as well as modifying factors, e.g. exacerbated by temperature or pressure.

Clinical Exam:

- Extraoral exam – taking note of the patient’s general appearance, skin tone, facial asymmetry, obvious swelling, redness, sinus tracts, and the status of surrounding lymph nodes (tender, enlarged).

- Intraoral exam – thorough visual and digital examination of the mucosa and gingiva, noting any discoloration, inflammation, ulceration, swelling, or the presence of sinus tracts. An intraoral exam should also include oral cancer screening.

Dental exam – careful inspection of the dentition. Carious pulpal exposure means a high likelihood of irreversible pulpitis or pulpal necrosis. Severe periodontal disease can have deleterious effects on dental pulp. A tooth with a history of pulpal insult (deep restorations, possible incomplete caries removal, pulp capping etc.) is more likely to present with pulpal problems.

SOCRATES is a commonly used mnemonic acronym used to systematically evaluate pain. It stands for:

S (Site) – Where the majority of pain is located?

O (Onset) – When did the pain start? Was it sudden or gradual?

C (Character) – A description of the pain. A dull ache? Shooting/stabbing?

R (Radiation) – Is the pain localized or does it radiate?

A (Association) – Other signs or symptoms associated with the pain.

T (Time) – Any pattern to the pain?

E (Exacerbating) – Anything that makes the pain worse (or better)?

S (Severity) – How bad is the pain out of 10?

Pain can be a misleading, subjective clinical indicator that is not meant as a definitive measure. Odontogenic pain can be referred to another site innervated by the trigeminal nerve. For example, pain from a lower tooth may seem like it’s coming from an upper tooth, the maxillary sinus, TMJ etc. The pain is referred vertically (on the same side) and very rarely would cross the midline. Similarly, numerous orofacial diseases may mimic odontic pain. For example, acute maxillary sinusitis that presents as a toothache.

CLINICAL TESTS

Sensibility testing refers to tests like cold tests and electric pulp tests that are used to determine the health of the pulp. Sensibility testing assesses neural activity and not vascular supply. Pulse oximetry measures actual blood flow and has been shown to be a reliable, non-invasive and accurate way of confirming the presence of a blood supply (vitality) in the pulp. The terms “vitality testing” and “sensibility testing” have been known to be used interchangeably.

Electric pulp tester (EPT) uses electric current to stimulate the sensory nerves of the dental pulp, specifically the fast conducting myelinated A-Delta fibers. The incisal edge on anterior teeth and the mesio-buccal incisal edge on posterior teeth is the optimal placement site for the tester to determine the lowest response threshold. The bipolar stimulating mode is claimed to be more accurate because the current is confined to the coronal pulp, but most EPTs are still monopolar. A conductive medium like toothpaste/prophy paste is required. A positive response is an indication that the pulp is vital, but there is no clear correlation between the pain thresholds and the exact condition of the pulp. A negative result hints that the pulp is necrosed/partially necrosed. Electric pulp testers are not effective at determining the health of pulp in immature or deciduous teeth. An EPT test is not appropriate for patients with a cardiac pacemaker. Any of the following could interfere with the EPT measurement:

The width and density of enamel and dentin (electrical resistance).
Tooth being too dry.
Fractures or infractions.
Restorations, especially crowns or large insulating restorations.
Dental caries.
Pulp canal obliteration or pus-filled canals.
Immature tooth (open apex).
Recent trauma.
Analgesics, or a very nervous patient.

According to the hydrodynamic theory, thermal tests cause the sensation of pain by inducing hydrodynamic fluid flow through the dentinal tubules, which trigger the mechanoreceptors of myelinated nerves located in the pulp.

Cold test – the most effective tools are frozen sticks of carbon dioxide (-78°C) or a cotton pellet sprayed with a Tetrafluoroethane/Chlorodifluoromethane refrigerant (-50°C). Older techniques of using refrigerator ice or ethyl chloride (-4°C) are less reliable. The incisal edge on anterior teeth and the mesio-buccal incisal edge on posterior teeth is the optimal placement site for cold tests.

Heat test – can be a more difficult test to perform since too much heat can cause pulpal or soft tissue damage. Techniques include using a dry prophy cup on the tooth to create heat via friction, single tooth rubber dam isolation and warm water, or using a single cone of heated gutta percha.

Percussion and palpation are not true vitality tests but are indicative of periodontal ligament inflammation. Sensitivity to percussion and/or palpation in conjunction with a symptomatic vital pulp response suggests irreversible pulpitis. Percussion testing can be performed with digital pressure, or more commonly with the handle of a mouth mirror. Palpation aims to detect inflammation in the mucoperiosteum around the tooth root. Care is taken to note any tenderness, fluctuation, hardness, crepitus or swelling present.

Mobility is directly proportional to the integrity of the periodontal attachment apparatus and to the extent of inflammation of the periodontal ligament. However, care needs to be taken when differentiating pathological mobility with other causes of mobility, which include:

Periodontal disease.
Tooth fracture.
Recent trauma.
Bruxism or parafunctional habits.
Orthodontic treatment.
Bone disease (osteoporosis).
Pregnancy.

Periodontal probing can provide some information about the periapical and pulpal health as well as the structure of the tooth. A narrow localized pocket may indicate a vertical root fracture or pathosis of pulpal origin.

Selective anesthesia can be useful for locating an offending tooth. In the case of referred pain, a block or infiltration could narrow down the pain to a quadrant. An intraligamentary injection can sometimes be successful in isolating a single tooth. However, the normal diffusion of local anesthetic makes distinguishing between immediate neighbors difficult.

Test drilling (test cavity) can be used when other forms of testing is not possible, or as a final confirmation of a suspected diagnosis. But use this diagnostic test with care. You don’t want to introduce healthy pulp to a rotary bur!

Other possible pulp tests include:

Laser Doppler flowmetry – a light beam is scattered by moving red blood cells and undergoes a frequency shift that is picked up by photodetectors, producing a signal which is proportional to the red cell flux. Used to measure pulpal blood flow.

Ultrasonic pulse echo – uses the transmission and reflection of sound from the dental hard tissues.

Crown surface temperature – based on the hypothesis that teeth with vital pulp are warmer and will rewarm faster after cooling than non-vital teeth. Infrared thermographic cameras have been used.

Pulse oximetry – a modified probe produces two wavelengths which is used to provide a ratio of the absorption of wavelengths for oxygenated and deoxygenated blood.

Dual wavelength spectrophotometry – similar to pulse oximetry, spectrophotometry uses a dual wavelength light source (760 and 850 nm) to determine the oxygen saturation levels of the pulp.