4: Biologic Aspects

Biologic Aspects

Protection of the Pulp and Dentin Adhesion

Protection of the Pulp

The following characteristics make the dental pulp unique compared with any other body tissue:

Functions of the Dental Pulp

The dental pulp has four major functions: dentinogenic, defensive, sensory, and nutritive.

Figure 4-2 shows the radiographs of 8-, 25- and 79-year-old patients. These are sound teeth with healthy pulp that exhibit physiologic responses to pulp vitality and percussion tests and that radiographically do not show any sign of calcification or root resorption but a normal lamina dura and a periodontal space of normal width.

The incisor and the pulp of the 8-year-old are healthy, and the tooth has an immature apex housed within very thin walls of dentin. Likewise, the pulp of the incisor of the elderly patient (79 years old) is healthy, with severe reduction of the pulp chamber and the root canals owing to the continuous deposition of dentin by the odontoblasts over the years.


Figure 4-3 shows pulp that has aged prematurely, as it belongs to a young patient (tooth 9). The pulp chamber and root canal have clearly disappeared. This is a sign of pulp damage and can be observed as the result of trauma with injury of the neurovascular bundle. The crown is discolored as a result of degradation of hemoglobin released from the red blood cells that infiltrated the dentinal tubules.

This kind of aging is frequently asymptomatic, and often the patient comes to observation because of unsightly dental crown discoloration or the onset of periodontal symptoms caused by pulp necrosis; in some cases it is noted on x-ray images. The following clinical case (Figure 4-4) is the result of trauma. This young patient (21 years old) presents a buccal supracrestal and palatal subcrestal complete crown-tooth fracture complicated by pulp exposure (Ellis Class V fracture). Figures 4-5 and 4-6 also show the outcome of the trauma.

What the Pulp Should Be Protected From

In the early 1970s the pivotal studies of Brännström clarified that the greatest threat to pulp and dentin integrity is represented by bacteria and their metabolic products (Figures 4-7 and 4-8).

As early as 1927 Growell hypothesized that pulp inflammation was attributable to bacterial infection.

Restorative materials do not cause any significant pulp reactions, even when they are in contact with the pulp.


Microleakage is the clinically undetectable passage of bacteria, fluids, and molecules between the cavity wall and the restoration (Figures 4-9 to 4-11).

It is important to maintain the integrity of the marginal seal over time. According to Brännström (1984), when the bacteria nested in the dentin are deprived of nutrients, they probably die.

The evidence suggests that under restorations bacterial multiplication occurs only in the presence of microcracks and infiltration.

In restorative dentistry, the most important means of pulp protection—aside from prevention—is the removal of root caries.

According to Langeland (1987), pulp reactions caused by initial caries can be reversed by removing the carious dentin.

Recurrent caries with pulpal involvement are often the result of residual bacteria under restorations, which are able to proliferate thanks to the nutrients that reach them via microleakage or that spread from the pulp.

The key factors for a successful caries treatment are as follows:

Protection of the dentinal tubules exposed by cavities or prosthetic abutment preparation is crucial for the preservation of pulp vitality, in order to avoid the passage of bacteria and toxins into the pulp. This can be achieved with hermetically sealed restorations able to prevent marginal microleakage and bacterial invasion (Figure 4-13).

Defense Mechanisms

The pulp-dentin complex defends itself against bacterial invasion: 6 hours after cavity preparation, dentin permeability is reduced by approximately 75% (Pashley, 1983).

The reaction of the pulp depends essentially on the type and amount of bacterial metabolism products that reach the pulp chamber; the response of the pulp—that is, the ability of odontoblasts to produce irregular secondary dentin or tertiary dentin in the inner portion of the tissue and sclerotic dentin in proximity of the surface at an early stage; and the inflammatory reaction, which can cause pulpal necrosis if it is too strong.

The defenses of the pulp-dentin complex against bacterial invasion as well as natural and iatrogenic stimuli are:

Inner and Outer Dentin

Inner dentin is characterized by a high tubular density (45,000 to 65,000 tubules/mm2) with an average diameter of 2.5 to 3.0 microns, whereas the outer dentin exhibits fewer tubules (15,000 to 20,000/mm2) with a reduced diameter of 0.8 microns (the dentinal tubules are spaced farther apart, with as much as 96% intertubular dentin). This is important because dentin permeability is directly proportional to the number and diameter of the exposed tubules and inversely proportional to dentin thickness.

Dentin close to the pulp is eight times more permeable than the outer dentin. The preparation for a prosthetic crown on molars creates an area of 3 to 4 cm2 (potential opening of 6 to 12 million tubules) (Pashley, 1989).

During preparation of the abutment it is important to know the thickness of the residual dentin in order to protect the pulp, as the dentin near the pulp is about eight times more permeable than the outer dentin.

Protection of the Pulp

Another way to protect the pulp-dentin complex is by using a rubber dam.

The factors that affect the response of the pulp in restorative dentistry are:

The following three key considerations must be made:

Another important point is the lack of correlation between the histologic status of the pulp and its clinical aspect, as well as the complete lack of correlation between pain intensity and the extent of pulp involvement.

Pulp Damage

In restorative dentistry the pulp can sometimes get injured during cavity preparation, but in healthy pulps this damage is reversible.

In prosthetic dentistry, pulp damage can occur during preparation of the abutment, impression taking, or the phase of provisional restoration and its cementation.

Other factors that can damage the pulp are the effects of the periodontal disease and its treatment on the endodontium.

There is certainly a great need to protect the pulp-dentin complex, which is repeatedly traumatized by very invasive preparation with the exposure of millions of tubules and the amputation of millions of odontoblast processes (large wound). Therefore prompt disinfecting treatment and isolation from the oral environment is fundamental.

The pulp-dentin complex cannot use its natural defense mechanisms, such as formation of tertiary dentin or reactive sclerosis, because they need a certain amount of time to develop.

Temporary Restoration

It is essential to protect the pulp-dentin complex from bacterial, chemical, physical, and thermal insults in the period between tooth preparation and definitive cementation of the direct or indirect prosthetic restoration (Figure 4-15).

During prosthetic preparations of full crowns, removal of tooth structure exposes a large number of dentinal tubules.

Pulp Necrosis Caused by Periodontal-Prosthetic Treatments in Vital Teeth

A study conducted by Ferrara (1991) examined the frequency of periradicular lesions after pulp necrosis of vital teeth used as abutments in periodontal-prosthetic treatments. The teeth had been reduced at least 2 years before the beginning of the study, and at the time they were sound and had no history of trauma. Periradicular lesions were found in 22.6% of cases, and the percentage increased when periodontal involvement was more severe. A previous study by Bergenholtz and Nyman (1984) yielded similar results.

The purpose of temporary restorations is to prevent the cumulative effect of irritative, bacterial, chemical, and other kinds of stimuli on the pulp, the consequences of which can make root-canal treatment necessary. Therefore the pretreatment status of the pulp (which is unknown), together with removal of dentin around the perimeter of the tooth and possible bacterial colonization of the dentinal tubules in the event of lengthy prosthetic treatments, may cause secondary caries of the prosthetic abutment or at the interface with the restorative material.

Therefore precision of the margins as well as optimal internal adaptation of the provisional (relining) is very important. This prevents dissolution of the temporary cement owing to infiltration of saliva, imprecise margins, and/or excessive thickness of the cement (Fichera, 2004).

Natural Communication Routes between the Endodontium and the Periodontium

The pulp-dentin complex and the periodontium communicate with each other via major routes that form a direct bridge between the dental pulp and the periodontium and permit the mutual passage of inflammatory and degenerative insults.

The communication routes are represented by dentinal tubules, the apical foramen, and lateral channels (Figures 4-16 and 4-17).


Figure 4-16 First lower molar.


Figure 4-17 Dentinal tubules.

Dentinal Tubules and the Apical Foramen

The dentinal tubules run from the pulp to the amelo-dentinal junction and the cemento-dentinal junction, with a diameter of about 2.5 microns on the pulp side and about 1 micron at the opposite end (see Figure 4-17).

Under normal conditions, dentinal tubules do not communicate with the periodontium because of the presence of the radicular cement. Periodontal disease (with exposed root surface), congenital absence of cement, and root planing can create communication between the dentinal tubules and the oral environment.

The apical foramen is the main route of communication between the endodontium and the periodontium and represents the main exchange channel for diseases in both directions (Figures 4-18 to 4-21).

Lateral Canals

Lateral canals are quite common and can be found along the entire root surface and at the bifurcation of multiradicular teeth.

According to a study on the morphology of root canals conducted by Walter Hess (1925), the occurrence of lateral canals is estimated to be about 43.5%.

Some authors have suggested a correlation between lateral canals and periodontal disease and treatment.

Lateral canals unquestionably act as a point of exit of the disease toward the endodontium-periodontium; the hypothesis of the point of entry in the opposite direction is still being investigated. The larger lateral canals contain pulp and fibers that are closely connected with the main canal (Figure 4-22, A and B).

Influence of Periodontal Disease and Periodontal Treatment on the Endodontium

Some authors agree that the periodontal disease can cause pulp alterations (Craney, 1925; Cahn, 1927; Bauchwitz, 1932; Seltzer and colleagues, 1963; Rubach and colleagues, 1965; Staml, 1966; Bender and Seltzer, 1972; Seltzer, 1975), whereas others believe that periodontal disease cannot affect the pulp (Mazur and Massler, 1964; Smukler and Tagger, 1976; Bergenholtz and Lindhe, 1978; Czarnecki and Schilder, 1979; Torabinejad and colleagues, 1985).

Langeland and co-workers (1974) identified retrograde pulpitis caused by periodontal disease. Retrograde inflammation of the pulp can lead to pulp necrosis. Regarding the influence of the periodontal treatment on the endodontium, Schilder (1978) argued that retrograde pulpitis can be caused by periodontal treatment. For instance, sectioning a vascular pedicle of a large lateral channel with a curette can lead to pulp necrosis. The periodontal treatment can cause pulp necrosis when the blood supply to the pulp through an accessory canal is interrupted by a curette (periodontal curettage—sectioning of a lateral vessel—loss of blood supply resulting in ischemia and pulp necrosis) (Figures 4-24 to 4-26).

Regarding the possibility of pulp infection secondary to periodontal disease, this is a very rare finding and occurs only when the periodontal disease exposes the root apex, thus connecting the pulp with the oral environment. In this case the tissue can become infected and we may find retrograde inflammation of the pulp with subsequent retrograde pulpitis or necrosis caused by periodontal disease.

Protective Bases

Several materials can be used as protective bases for cavities, such as calcium hydroxide [Ca(OH)2], simple varnishes, cavity liners, Intermediate Restorative Material (IRM), and glass-ionomer cements (GICs) (Figures 4-27 and 4-28).

Jan 1, 2015 | Posted by in Dental Materials | Comments Off on 4: Biologic Aspects
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