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.

Figure 4-2 Radiographs of three patients aged 8 (A), 25 (B), and 79 (C).

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.

Trauma

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.

Figure 4-3 A, Radiograph of tooth 9 showing a prematurely aged pulp and disappearance of the pulp chamber and root canal. B, Upper left central incisor (9). Clinical appearance of the dental crown; note the change in color.

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.

Figure 4-4 A 21-year-old patient with a buccal supracrestal and palatal subcrestal complete crown-tooth fracture complicated by pulp exposure (Ellis Class V fracture). Unfortunately, this case required a root-canal treatment.

Figure 4-5 The coronal fragment was removed, and after detachment of a partial-thickness flap the patient underwent an osteotomy and osteoplasty. Later the operative site was isolated with a rubber dam, and after endodontic treatment the coronal fragment was bonded with the aid of a carbon-fiber post.

Figure 4-6 Checkups after 1 year (A and B) and after 2 years (C and D).

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).

Figure 4-7 A, Marginal deterioration and wear of composite Class II restoration. B, X-ray film of the right lower first molar (30). Wide radiolucent area under the composite restoration (secondary caries). The radiolucency around the mesial root also involves the bifurcation. The recurrent caries under the old restoration caused pulp necrosis.

Figure 4-8 First and second upper left premolars (12 and 13). Faulty, infiltrated, and anatomically incorrect restorations. The margins show the presence of secondary caries.

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

Marginal bacterial infiltration or microleakage: Infection of the microgap between the restoration material and cavity walls that inexorably leads to bacterial invasion along the dentinal tubules up to the pulp.

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

Microleakage

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

Figure 4-9 Amalgam restoration with serious margin flaws and fracture of the filling mass. Recurrent caries under the old restorations caused pulp necrosis.

Figure 4-10 First and second right lower molars (30 and 31). A, Preoperative image. Old composite restorations heavily worn with infiltration and secondary recurrent caries. B, Postoperative image. C, One-year checkup.

Figure 4-11 First and second right premolars (4 and 5). A, Composite restorations with serious marginal flaws and infiltration. B, Postoperative image. Gold-ceramic crown on tooth 4; composite restoration on tooth 5.

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:

• Complete removal of softened infected dentin

• Best possible fit between restorative material and the enamel-dentin substrate to prevent bacterial growth and reinfection of the dentin tubular system (Figure 4-12)

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).

Non–Hermetically Sealed Restorations

Figure 4-12 Pulp damage may be caused by a traumatic insult but also by tooth decay, erosion, and abrasion. The bacterial colonization of the pulp causes irreversible pulpitis, which over time will lead to pulp necrosis. A, First upper right molar (3). Old amalgam filling and severely infiltrated composite restoration. B, Preoperative radiograph with necrotic pulp and periradicular lesion. C, Recurrent caries under the old restoration (which caused pulp necrosis). D, Full occlusal coverage amalgam restoration. E, X-ray checkup after 1 year.

Figure 4-13 Lower first right molar (3). Full occlusal coverage amalgam restoration.

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.

Dentin

Primary dentin: Produced during odontogenesis until tooth eruption.

Secondary dentin: Deposited slowly for the life of the tooth on the pulp side and below the primary dentin, leading to gradual reduction of the pulp chamber.

Physiologic sclerotic dentin: Sealed peritubular dentin below the enamel layer; it is the result of natural aging.

Tertiary dentin: Secondary or reactive dentin or irregular or reparative dentin formed on the pulp side. It is produced when the pulp is subjected to irritant stimuli that can induce the reaction of the odontoblasts with the apposition of new tissue, in order to preserve pulp vitality.

Pathologic sclerotic dentin: This is apposed on the surface, just below the area of the lesion. High mineralization associated with progressive obliteration of the lumen of dentinal tubules. First biologic barrier capable of significantly reducing dentin permeability.

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

1. Dentinal pain

2. Inflammation of the pulp

3. Pathologic sclerotic dentin

4. Tertiary dentin (or reactive dentin)

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.

“I disinfect and protect the exposed dentin very easily by isolating the operative site with a rubber dam” (Monari, 2000).

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

• Preoperative conditions of the pulp

• Size of the preparation

• Method of cavity preparation and cleaning

• Tissue changes in dentin and permeability

• Amount and pathogenicity of bacteria at the tooth-restoration interface

Recommendations for Pulp Protection

• Completely remove carious tissue

• Use the instruments carefully

• Avoid overheating, dehydration, mechanical trauma

• Avoid excessive pressure and the use of worn rotary instruments

• Work under a constant jet of water (Fitzgerald and Heys, 1991)

The following three key considerations must be made:

• The real status (histology) of the pulp at the time of restoration cannot be ascertained.

• The effect of the iatrogenic trauma of preparation cannot be assessed. Excavation and drying can deal the final blow to the pulp, which is already damaged (even if asymptomatic).

• The countless variables related to materials, dentin substrate, and clinical procedures should be considered.

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.

Preparation of the Abutment for a Full Crown

Abutment preparation for a full crown affects all the dentinal tubules. This is an extreme case.

Increasing the depth of the preparation increases the risk of pulp damage owing to the higher number of dentinal tubules that are larger in diameter. According to Perrini (1985), 0.5 to 1 mm of dentin can safely be removed without damaging the pulp.

In the case of the first upper molar, which has a mesialized pulp chamber, removal of the mesial dentin wall should be performed very carefully (Figure 4-14).

Figure 4-14 Upper right first molar (3, section). Note the position of the mesialized pulp chamber.

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).

Figure 4-15 The tooth is protected during the period between preparation and final cementation of the crown.

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.

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).