Protection of the Pulp and Dentin Adhesion
Protection of the Pulp
• Vascularization is terminal arteriolar, which reduces the pulp’s ability to regenerate itself after an injury; one or more arterioles enter the tooth through the apical foramen, and smaller vessels can enter the pulp through lateral channels.
• It is composed almost entirely of specialized loose connective tissue and a highly sophisticated cell population: odontoblasts in the outer area near the dentin, and fibroblasts, lymphocytes, macrophages, and undifferentiated mesenchymal cells in the inner portion of the tissue.
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.
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 4-7 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 4-10 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.
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.
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).
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.
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.
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.
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.
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.
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.
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).
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).
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.
Figure 4-16 First lower molar.
Figure 4-17 Dentinal tubules.
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.
Figure 4-19 Lower diaphanized premolar.
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%.
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).
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).
Figure 4-24 Forty-five–year-old patient with an acute alveolar abscess. The preoperative radiographic examination showed substantial radiolucency at the apex and on the distal aspect of the root of the left upper incisor (10). The lesion was fistulized buccally and in the gingival sulcus. The tooth did not respond to vitality tests. There was no history of trauma, and no coronal caries was detected. Mild chronic adult periodontitis with slow progression. Vertical atrophy of the bony ridge was noted on the distal aspect of tooth 10; there was a limited bucco-distal pocket of 9 mm at the fistulous tract of the gingival sulcus (the endodontic drainage simulated a periodontal problem). The cavity was prepared without anesthesia, which confirmed the diagnosis of pulp necrosis and the periapical lesion of endodontic origin. The endodontic drainage was left in place until complete resolution of the acute symptoms.
Figure 4-25 The postoperative radiograph showed a significant lateral channel at the cervical third on the distal side of the root. The diagnosis was primary periodontal lesion with secondary endodontic involvement, pulpitis, and retrograde pulp necrosis because of periodontal treatment. The radiographic checkup a few months later confirmed the healing of the bone (with a residual probing depth of 5 mm) and the good conditions of the gum. Furthermore, the signs of the previous periradicular lesion were no longer detectable.
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.
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).
According to the study conducted by Piperno and Spiering (1982 to 1984), a 2-mm protective base (0.5 mm calcium hydroxide and 1.5 mm zinc oxyphosphate) results in a 20% reduction in a 60° C heat stimulus.