Inspiring Dental Excellence

Anatomy of Root Canal Systems: Part 5

Pulp Degeneration and Periradicular Disease

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Inflamed pulp tissue is not inherently painful as I learned in the pediatric clinic at dental school. I was examining a child with gross carious destruction of the crown of a lower molar and I found a hypertrophied mass of tissue growing over the tooth. At first, I thought it was overgrown gingival tissues, but as I moved it around with an instrument I determined that the tissue was actually the pulp without hard tissue encasement. This kind of freaked me out because at that point in my education, all I knew about dental pulps was to avoid them at all costs. When I asked the kid whether it caused him pain, he said it only hurt when he nailed it with a tortilla chip. This was the first clue I had about the true etiology for pulpal pain.

Periradicular Disease

All endodontic pain is a pressure phenomena

That's why teeth with periapical lesions and a sinus tract are never painful pre-operatively or post-operatively unless the sinus tract closes up. In this vein, it is critical to success in endodontic diagnosis and pain management to understand how pulps degenerate in root canals and how that disease state extends out the portals of exit of the RCS and into the peri-radicular tissues. A few important things to keep in mind about pulp death and PR disease:

1.) Pulps die from coronal to apical because they are injured in the pulp chamber and because that is the region that is most distant from the rich PR blood supply and the immune response that depends on it. It is common to open a tooth that didn't respond to pulp tests, and find an apical pulp stump remaining. It is also common to see lateral root lesions of endodontic origin developing before a PA lesion can be seen (Fig. 1.66).

Fig. 1.66. Central incisor with a laterally-positioned LEO and no visible PA lucency. This is a common occurrence because pulp degenerate from coronal to apical.

2.) Lesions of endodontic origin tend to develop symmetrically about the portals of exit from the RCS, so by mapping LEO's in 3D CBCT space, clinicians can better locate obscure canals by beginning the search on the root surface in the center of the lucency (Fig. 1.67).

Fig. 1.67 (above). MB root of upper molar seen in a M view. The MB3 was not found in this volume until the PR lucency was identified, then by looking at the center of the lesion, the faint canal was found.


3.) No bone, no lucency. When the root apex projects into a maxillary sinus space or is outside the cortical plate, there will be no lucency seen on conventional radiographs. To see PR pathoses in these situations, it requires CBCT imaging, because volumetric imaging shows soft tissues, because the slice data doesn't display overlying anatomic artifacts, and because we can look at roots and bone from the mesial and distal view which displays the area of interest crystal clear and LEO's as obvious as night and day (Figs. 1.68 A, B.)

Fig. 1.68A. Central incisor as seen with conventional radiography-an apparently intact apical PDL is shown.

Fig. 1.68B (right). The same tooth and periapical region as seen in CBCT space. Note the root apex out of the cortical plate with an obvious PA lucency associated with it.

4.) LEO's can be seen periapically while pulps continue to respond to thermal pulp testing-usually in cases with partial necrosis of the pulp-because periradicular pathogens can move through vascular structures, then out of PEO's, and into periradicular tissues at the early stages of irreversible pulpitis (Fig. 1.69 A-C).

Fig. 1.69A. This mandibular molar has a pulp exposure, a PA lesion (lucency) associated with the mesial root apex, and a vital response from the thermal pulp tests.

Fig. 1.69B. A pulptomy is done and is finished with a bio-ceramic pulp cap.


Fig. 1.69C. 6 months later the PA lucency associated with the mesial root has resolved and densified.

5.) When pulp chambers calcify in multi-canalar teeth, formerly syncytial pulps can become dissevered into separate pulp spaces and separate pulps and each of those newly separate pulps can have a different pulpal condition (Figs. 1.70A-C).

Fig. 1.70A. Illustration of tooth with calcified pulp chamber resulting in three independent root canals and three different pulpal conditions. The DB canal has a vital/asymptomatic pulp and no PR lucencies.

Fig. 1.70B. The MB pulp is fully necrotic with LEO's seen at apical and lateral root surfaces.

Fig. 1.70C. The palatal canal has a partially necrotic pulp-the remaining vital segment in the apical third. This condition is etiology for the most painful of all pulp deaths.

6.) For the first ten years of practice I told patients who asked why their pulp died 3-5 years after a crown was placed, that the pulp had been injured, it had survived but slowly atrophied its threshold of vitality and it then croaked. After the advent of bonded resin cements, I came to realize that pulp death after crown prep and placement became rare in well-trained dentist's hands, and I finally understood that pulps die from bacterial invasion of the RCS, not from atrophy. The pulps that died 3-5 years after crown placement died because that is how long it takes for zinc phosphate cement to wash out from under the margins-opening a direct route of entry through the exposed dentinal tubules.


7.) Many lecturers and authors have decried the complexity of diagnosing endo/perio cases, but that is not the case; is it endodontic disease, is it periodontal disease, or is it both? Understanding this conundrum requires the clinician to first assess the pulpal health of the tooth in question with thermal testing, and then assess the patient's generalized periodontal condition. The best finding in these situations is that pulp disease is the etiology for an isolated periodontal pocket, as it is more predictable to treat endo disease than chronic periodontitis (Fig. 1.71). Perio defects of endodontic origin tend to be fairly narrow as they are simply pressure relief valves and they often heal between acute flareups of the endodontic infection. The diagnosis is definitive if the pulp tests vital/asymptomatic, the perio defect is several millimeters wide, and the patient has generalized periodontal disease. Perio defects of perio origin have a much lower prognosis for regeneration after treatment.

Fig. 1.71. Illustration of tooth with a necrotic pulp chamber, a lateral canal off the coronal third of the MB root, and a LEO emanating from the mesial furcation that has pushed through the attachment apparatus crating a narrow, deep perio pocket.




Ab                         Antibiotic

B                           Buccal

CDJ                     Cemento-Dentinal Junction

CEJ                       Cemento-Enamel Junction

D                           Distal

Dx                         Diagnosis

epi                         Epinephrine

FA                         Flute Angle

GGB                     Gates Glidden Burs

HERS                   Hertwig's Epithelial Root Sheath

KF                         K-file

L                           Lingual

LOC                     Law of Centrality

LEO                     Lesion of Endodontic Origin

NVB                     Neurovascular Bundle

M                         Mesial

MB2                     Mesio-palatal canal in the MB root of an upper molar

MD                       Maximum Diameter

MFD                     Maximum Flute Diameter

MIE                     Minimally Invasive Endodontics

NiTi                     Nickel Titanium Alloy

PAA                     Positive Apical Architecture

PC                         Pulp Chamber

POE                     Portal of Exit

RC                       Root Canal

RCS                     Root Canal System

RCT                     Root Canal Therapy

Rx                         Prescription

SOEA                   Student of Endodontic Anatomy

SS                         Stainless Steel

Sx                         Symptoms

Tx                         Treatment

VPFA                   Variable Pitch Flute Angle