Pocket Atlas of Endodontics (eBook)

Anatomy, and Types of Endodontic Pathology

Normal Endodontium

The endodontium consists of mineralized (dentin) and nonmineralized (pulp) portions, and encompasses the functional-anatomic relationships of the dentin-pulp system.

The dentin consists of:

• odontoblasts and their processes

• dentinal tubules

• peritubular dentin

• intertubular dentin

• mantle dentin.

The odontoblasts are densely aligned along the inner surface of the dentin. Their processes extend through the entire dentin layer to the dentinoenamel junction, and are up to 5mm long depending on the dentin thickness. The odontoblasts are interconnected through gap junctions as well as tight junctions. These cells synthesize the primary dentin, consisting of type I collagen, glycoproteins, and glycosaminoglycans. This organic precursor later becomes mineralized at some distance from the odontoblast layer.

The majority of the dentin is referred to circumpulpal dentin and is located between mantle dental and the pulp chamber. Mineralization begins only when the predentin has achieved a certain degree of histologic maturity.

The odontoblastic processes course within the dentinal tubules. Between the cytoplasmic membrane of the processes and the canal wall there is often a periodontoblastic space that contains tissue fluid and collagen fibrils, as well as dentin matrix.

The very densely mineralized peritubular dentin covers the dentin canal wall. It is not found in predentin. Its thickness depends on patient age, but it may also be laid down as a defense against external influences. Dentinal tubules with small lumens and thick peritubular walls appear as a translucent zone when viewed in ground sections under a light microscope; this zone is called sclerosed dentin.

The dentinal tubules are separated from each other by less densely mineralized intertubular dentin.

The peripheral layer of dentin exhibits highly branching odontoblastic processes referred to as mantle dentin. In contrast to the circumpulpal dentin, this layer is less densely mineralized. Dental enamel is attached to the mantle dentin. As demonstrated by R.M. Frank and coworkers, nerve fibers also extend to the dentinoenamel junction. Thus the vitality of dentin tissue is not the result of hydrodynamic transfer of irritation, as was long believed, but rather for the most part on direct nerve conduction, i.e., the nerve endings are directly stimulated.

The pulp consists of loose connective tissue. In addition to odontoblasts it contains fibroblasts, replacement cells, and defense cells. The fibroblasts represent the largest cell population, and appear as inactive and active cells, the latter producing the intercellular substance and collagen precursors. Replacement cells are undifferentiated mesenchymal cells that cannot be differentiated from fibroblasts by shape. These cells may replace odontoblasts as well as defense cells, and assume their functions.

Figures

A Structure of a secretory odontoblast.

B Formation of circumpulpal dentin: Predentin, secreted by odontoblasts, mineralizes at a distance ca. 20μm distal to the odontoblasts, emanating from focal centers that accumulate as calcium globules (circles). These aggregate in the subsequent mineralization process. At this time, the formation of peritubular dentin begins.

C The formation of secondary as well as intertubular dentin (dark) reduces the size of the pulp chamber as well as the dentinal tubules (right).

D Zone-like formation of the coronal pulp from the odontoblastic zone (middle), subodontoblastic, cell-poor zone, and cell-rich bipolar zone (below). The latter is characterized by fibroblasts, undifferentiated replacement cells, and the Raschkow nerve plexus.

E The Hertwig epithelial sheath induces the differentiation of ectomesenchymal cells of the tooth bud into odontoblasts.

Dental Caries

Enamel caries, clinically detectable as an opaque discoloration, is reversible. Initial caries is divided into three zones: On the advancing caries front, a translucent layer is visible; a dark zone is attached. The body of the lesion represents the third zone, suprajacent to the apparently intact enamel surface.

Dentin caries is differentiated into early and advanced lesions: In an early dentin carious lesion histologic changes occur without enamel cavitation, whereby plaque toxins diffuse through the enamel and cause secondary (reparative) dentin formation as well as early accumulations of inflammatory cells. If the cause is eliminated, partial regression of dentin caries can occur at this stage.

With advanced dentin caries, on the other hand, enamel cavitation has already occurred. The bacterial destruction expands along the mantle dentin. The lesion becomes more extensive, undermining the enamel. Initially, the advanced lesion is a combination of defense and destruction. Later in the process, there is unhindered penetration of bacteria. At this stage, six zones can be differentiated:

1 softening and liquefaction, with excavatable dentin

2 demineralization with multiple areas of destruction

3 advancing bacteria penetrate the dentinal tubuli

4 hypermineralization

5 the transparent zone is clinically hard

6 reparative (secondary) dentin forms on the pulpal wall.

Diagnosis

Clinical examination alone is not sufficient to determine the depth of the carious lesion in occlusal fissures. In a study by Tveit, teeth that were scored as noncarious clinically were examined histologically and only 10% were caries-free while 76% already exhibited enamel caries. Of 131 lesions with small occlusal cavitation, 41 already exhibited dentin caries, which had only been detected by clinical probing in 31 instances. In a study of the influence of clinical probing, in one group teeth were only examined visually, others with probing. One week later, the teeth were extracted. The histologic examination revealed only seven carious defects in the group without probing, but after clinical probing 60 defects of tooth hard structure were observed. In addition, in this group there was even evidence of tooth surface destruction into the dentin.

Radiographic diagnosis doubles the sensitivity for detection of fissure caries. However, more than half of even deeper dentin lesions remain undetected. The capability of detecting carious teeth (sensitivity) is 12% with visual diagnosis alone, 14% with probing, and 20% with the use of magnifying loupes. Only with the additional use of bitewing radiographs was it possible to increase the sensitivity to 49%.

In a study of proximal carious lesions, 66% exhibited opaque enamel discoloration, 32% of the teeth showed small lesions, and 1.3% pronounced cavitation. In teeth with a radiographic index of grade 1 (enamel), 13% exhibited clinical dentin caries, and with a radiographic index of 3, 58% exhibited cavitations. There was no direct correlation between radiographic findings and actual clinical observations. In the posterior arch segments, only 30% of carious lesions can be conclusively determined using bitewing radiographs. C4 lesions (deep dentin caries), however, can be precisely detected.

In almost every case, the histologic picture of caries is more advanced than what the radiograph shows. Experience and degree of training enhance caries diagnosis. Experienced practitioners interpret radiographs more cautiously. Dental students, on the other hand, too often diagnosis caries, with the danger of “overtreatment.”

Histology

A/B Penetrating advanced dentin caries, with carious opening into the pulpal tissue and adjacent necrosis.

C/D Dilation of the dentinal tubules as ampullae and garlands (zones 1–3).

E/F Bacterial expansion of dentinal tubules.

G   Bacteria can also penetrate into a tubular reparative dentin (zone 6).

Caries Detector

In the absence of any therapeutic measures, profound caries caused by infection will lead to an inflammatory host response within the pulp, and the ultimate consequence will be necrosis. The goal in tooth maintenance is therefore to completely remove all infected tooth substance. In this way, the further progress of toxins, antigens, and bacteria can be effectively inhibited. Use of special color indicators can significantly simplify such clinical treatment.

The cause of dental caries is bacterial infection. Since the spatial expanse of carious involvement cannot be absolutely determined, if any diseased tooth structure is left behind, more or less high concentrations of bacteria near the pulp can be expected. This sort of compromise during treatment does not provide true causal treatment of the infection.

Even if the number of remaining microorganisms can be significantly reduced following definitive treatment, there remains a long-term risk of remaining caries and the danger of pulpal involvement. Combating bacteria with topical medicaments (e.g., calcium hydroxide-based),...