Diseases of the Pulp and Periapical Tissues
The dental pulp is a delicate connective tissue liberally interspersed with tiny blood vessels, lymphatics, nerves, and undifferentiated connective tissue cells. Like other connective tissues throughout the body, it reacts to bacterial infection or to other stimuli by an inflammatory response known as pulpitis, which is the most common cause of odontalgia or toothache. Certain anatomic features of this specialized connective tissue; however, tend to alter the nature and the course of this response. The enclosure of the pulp tissue within the rigid calcified walls of the dentin precludes the excessive swelling of tissue that occurs in the hyperemic phases of inflammation in other tissues. The fact that the blood vessels supplying the pulp tissue must enter the tooth through the tiny apical foramina precludes the development of an extensive collateral blood supply to the inflamed part.
The diseases of the dental pulp to be considered in this section are those occurring chiefly as sequelae of dental caries. Those reactions following various physical and chemical injuries are discussed in Chapter 12 on Physical and Chemical Injuries of the Oral Cavity. The sequential conditions are almost exclusively inflammatory and do not differ basically from inflammation elsewhere in the body.
Most cases of pulpitis are primarily a result of dental caries in which bacteria or their products invade the dentin and pulp tissue. Dental caries is usually obvious unless it extends under the edge of a restoration. Brannstrom and Lind, among others, have reported that changes in the pulp may occur even with very early dental caries represented by demineralization limited to the enamel alone, appearing as white spots without actual cavitations.
Occasionally, there is bacterial invasion in the absence of caries, as in cases of tooth fracture due to trauma or cracked tooth syndrome that expose the dental pulp to the oral environment. In cracked tooth syndrome, a tooth, usually a restored premolar may split under masticatory stress. These cracks are often minute and invisible clinically, and they allow the bacteria to enter into the pulp. Bacterial invasion may also occur as a result of a bacteremia and septicemia. Pulpitis may rarely follow chronic periodontal disease wherein the microorganisms enter through the accessory canals of the exposed root surface especially through lateral canals in furcation areas of molars.
The significance of microorganisms in the etiology of pulpitis has been confirmed by Kakehashi and his associates, who produced surgical pulp exposures in germ-free rats. It was found that no devitalized pulps or periapical infections developed even when gross food impactions existed. By contrast, conventional animals rapidly developed complete pulpal necrosis.
Pulpitis may also arise as a result of chemical irritation of the pulp caused by erosion or use of acidic restorative materials. This may occur not only in an exposed pulp to which some irritating medicament is applied but also in intact pulps beneath deep or moderately deep cavities into which some irritating filling material is inserted. This is undoubtedly a result of penetration of the irritating substances into the pulp via the dentinal tubules. In many instances; however, the pulp may respond to the irritation either by dentinal sclerosis or by forming reparative dentin rather than progressing to pulpitis.
Severe thermal change in a tooth may also produce pulpitis. Polishing procedures, tooth restored with exothermic restorative materials, or large metallic restorations, particularly, in which there is inadequate insulation between the restoration and the pulp are more prone to pulpal inflammation.
Heat produced by over-rapid tooth preparation or without sufficient coolant may also cause pulpal irritation. Heat and more particularly, cold are transmitted to the pulp, often producing pain, and if the stimulus is prolonged and severe, leading to actual pulpitis. Mild thermal changes are most apt to stimulate only the formation of reparative dentin, and this is a relatively common phenomenon.
When two dissimilar metallic restorations are present, the saliva acts as an electrolyte and there will be formation of a galvanic current. This may be transmitted to the pulp through metallic restoration and may thus initiate pulpitis.
It is apparent that pulpitis may be caused by a variety of circumstances and the nature of the etiologic agent or agents can usually be found through study of the clinical or microscopic features of the condition or both.
Pulpitis has been classified in a variety of ways, the simplest being a division into acute and chronic pulpitis. Furthermore, some investigators classify both acute and chronic pulpitis in several different ways. There may be a partial pulpitis or a subtotal pulpitis, depending upon the extent of involvement of the pulp. If the inflammatory process is confined to a portion of the pulp, usually a portion of the coronal pulp such as a pulp horn, the condition has been called partial or focal pulpitis. If most of the pulp is diseased, the term total or generalized pulpitis has been used. But this is of marginal clinical significance.
Another classification of both acute and chronic pulpitis is based upon the presence or absence of a direct communication between the dental pulp and the oral environment, usually through a large carious lesion. The term open pulpitis (pulpitis aperta) has been used to describe those cases of pulpitis in which the pulp obviously communicates with the oral cavity, whereas the cases in which no such communication exists are described as closed pulpitis (pulpitis clausa). In both the clinical and the histologic features of open and closed pulpitis, differences do exist that are referable to the presence or absence of drainage, which in turn determine the degree of pain present. The basic process is the same in each case, but the classification has been used as an aid in understanding the variations in clinical features that occur in different cases.
In this section, pulpitis will be discussed under the two chief types of the disease: acute and chronic. In addition, attention will be drawn to those differences in clinical and histologic features that are dependent upon the extent of the inflammation and upon whether drainage can occur.
One of the earliest forms of pulpitis is the condition known as focal reversible pulpitis. At one time, this was often referred to as pulp hyperemia. However, it is known that vascular dilatation can occur artefactually from the ‘pumping’ action during tooth extraction as well as pathologically as a result of dentinal and pulpal irritation. Therefore, this early mild transient pulpitis, localized chiefly to the pulpal ends of irritated dentinal tubules, is now known as focal reversible pulpitis.
A tooth with focal pulpitis is sensitive to thermal changes, particularly to cold. The application of ice or cold fluids to the tooth results in pain, but this disappears upon removal of the thermal stimuli or restoration of the normal temperature. It will be found also that such a tooth responds to stimulation by the electric pulp tester at a lower level of current, indicating a lower pain threshold (or a greater sensitivity) than that of adjacent normal teeth. Teeth in which this condition exists usually show deep carious lesions, large metallic restorations (particularly without adequate insulation), or restorations with defective margins.
Focal pulpitis is characterized microscopically by dilatation of the pulp vessels (Fig. 10-1). Edema fluid may collect because of damage to the capillary walls, allowing actual extravasation of red blood cells or some diapedesis of white blood cells. Slowing of the blood flow and hemoconcentration due to transudation of fluid from the vessels conceivably could cause thrombosis. The belief has prevailed also that self-strangulation of the pulp may occur as a result of increased arterial pressure occluding the vein at the apical foramen. Boling and Robinson argued that this belief is incorrect because the pulp may have several afferent and efferent vessels and several foramina, making self-strangulation unlikely.
Supporting this, in clinical practice, when a necrosed pulp chamber is opened, there may be vital tissue in the root canal of some teeth proving that total necrosis does not always occur. Reparative dentin may be noted in the adjacent dentinal wall.
Focal pulpitis is generally regarded as a reversible condition, provided the irritant is removed before the pulp is severely damaged. Thus, a carious lesion should be excavated and restored or a defective filling replaced as soon as it is discovered. If the primary cause is not corrected, extensive pulpitis eventually results, with subsequent ‘death’ of the pulp.
Extensive acute inflammation of the dental pulp is a frequent immediate sequela of focal reversible pulpitis, although it may also occur as an acute exacerbation of a chronic inflammatory process. Significant differences in both the clinical and microscopic features are found between acute and chronic pulpitis.
Acute pulpitis usually occurs in a tooth with a large carious lesion or restoration, commonly a defective one around which there has been ‘recurrent caries’. Even in its early stages when the inflammatory reaction involves only a portion of the pulp, usually in the area just beneath the carious lesion, relatively severe pain is elicited by thermal changes, particularly when taking ice or cold drinks. Characteristically, this pain persists even after the thermal stimulus has disappeared or been removed. However, a clinicopathologic study by Mitchell and Tarplee provided evidence that evaluation of the type or degree of pulpitis is present by sensitivity to either heat or cold is fallacious, since in their study most patients with any type of pulpitis exhibited increased sensitivity to both heat and cold. This has been confirmed by Seltzer and his associates, who have also shown that the severity of the pain is only partially related to the severity of the inflammatory response.
As a greater proportion of the pulp becomes involved with intrapulpal abscess formation, the pain may become even more severe and is often described as lancinating or throbbing type. The pain generally lasts for 10–15 minutes but may be more or less continuous, and its intensity may be increased when the patient lies down. The application of heat may cause an acute exacerbation of pain. The tooth reacts to the electric pulp vitality tester at a lower level of current than adjacent normal teeth, indicating increased sensitivity of the pulp. When necrosis of the pulp tissue occurs, this sensitivity is lost.
Severe pain is more likely to be present when the entrance to the diseased pulp is not wide open. The pulpal pain is not only caused by the pressure built-up due to lack of escape of inflammatory exudates but also by the pain producing substances released by the inflammatory reaction. Caviedes-Bucheli J and coworkers have demonstrated that, the receptors for substance P, a neurotransmitter in the pain fiber system, increases during inflammation of pulp. Soon there is rapid spread of inflammation throughout the pulp with pain and necrosis. Until this inflammation or necrosis extends beyond root apex, the tooth is not particularly sensitive to percussion. When a large open cavity is present, there is no opportunity for a build-up of pressure. Thus the inflammatory process does not tend to spread rapidly throughout the pulp. In such a case the pain experienced by the patient is a dull, throbbing ache, but the tooth is still sensitive to thermal changes. Mobility and sensitivity to percussion are usually absent.
Early in the course of the disease, the polymorphonuclear leukocytes are confined to a localized area, and the remainder of the pulp tissue appears relatively normal. The rise in pressure in the pulp associated with an inflammatory exudate causes local collapse of the venous part of the circulation. This leads to local tissue hypoxia and anoxia, which in turn may lead to localized destruction and the formation of a small abscess, known as a pulp abscess, which contains pus arising from breakdown of leukocytes and bacteria as well as from digestion of tissue (Figs. 10-2, 10-3). This necrotic zone contains polymorphonuclear leukocytes and histiocytes. Abscess formation is most likely to occur when the entrance to the pulp is a tiny one and there is lack of drainage. The chemical mediators released from the necrotic tissue lead to further inflammation and edema. Hepatocyte growth factor (HGF), a multifunctional cytokine mediates epithelial mesenchymal interaction, and is involved in the development and regeneration of various tissues including teeth. Ohnishi T et al, have reported the presence of HGF during acute inflammation of the pulp. Interleukin-8 level in the exudate of the acute pulpitis is higher than that in chronic pulpitis as shown by Guo X et al.
Figure 10-2 Acute pulpitis with pulp abscess formation.
There is diffuse inflammation of the pulp chamber in A beneath the carious lesion (1) with the formation of a circumscribed focus of suppuration, a pulp abscess (2). In B, the carious lesion (1) has evoked only a focal inflammation of the pulp with abscess formation (2).
Eventually, in some cases in only a few days, the acute inflammatory process spreads to involve most of the pulp so that neutrophilic leukocytes fill the pulp. The entire odontoblastic layer degenerates. If the pulp is closed to the outside, there is considerable pressure formed, and the entire pulp tissue undergoes rather rapid disintegration. Numerous small abscesses may form, and eventually the entire pulp undergoes liquefaction and necrosis. This is sometimes referred to as acute suppurative pulpitis (Fig. 10-4).
The pulp, especially in the later stages of pulpitis following carious invasion, contains large numbers of bacteria. These microorganisms are usually a mixed population and consist essentially of those found normally in the oral cavity.
There is no successful treatment of an acute pulpitis involving most of the pulp that is capable of preserving the pulp. Once this degree of pulpitis occurs, the damage is irreparable. Occasionally, acute pulpitis—especially with an open cavity—may become quiescent and enter a chronic state. This is unusual; however, and appears to occur most frequently in persons who have a high tissue resistance or in cases of infection with microorganisms of low virulence. In very early cases of acute pulpitis involving only a limited area of tissue, there is some evidence to indicate that pulpotomy (removal of the coronal pulp) and placing a bland material that favors calcification, such as calcium hydroxide, over the entrance to the root canals may result in survival of the tooth. This technique is also used in cases of mechanical pulp exposures without obvious infection (Fig. 10-5). Teeth involved with acute pulpitis may be treated by filling the root canals with an inert material, provided the pulp chamber and root canals can be sterilized.
Chronic pulpitis may arise on occasion through quiescence of a previous acute pulpitis, but more frequently it occurs as the chronic type of disease from the onset. As in most chronic inflammatory conditions, the signs and symptoms are considerably milder than those in the acute form of the disease. A special form of chronic pulpitis known as chronic hyperplastic pulpitis has characteristic features and will be described separately.
Pain is not a prominent feature of chronic pulpitis, although sometimes the patient complains of a mild, dull ache, which is more often intermittent than continuous. The reaction to thermal change is dramatically reduced in comparison to that in acute pulpitis. Because of the degeneration of nerve tissue in the affected pulp, the threshold for stimulation by the electric pulp vitality tester is often increased. The general features of chronic pulpitis are not distinctive, and serious involvement of the pulp may be present in the absence of significant symptoms. Even in cases of chronic pulpitis with wide-open carious lesions and with exposure of the pulp to the oral environment, there is relatively little pain. The exposed pulp tissue may be manipulated by a small instrument, but though bleeding may occur, pain is often absent. As Selzer and his associates have emphasized, pulps may become totally necrotic without pain.
Chronic pulpitis is characterized by infiltration of the pulp tissue by varying numbers of mono-nuclear cells, chiefly lymphocytes and plasma cells (Fig. 10-6) and more vigorous connective tissue reaction. Bacterial products may act as antigens and the dendritic cells of the pulp capture the antigens, migrate to lymph nodes and present them to lymphocytes. These activated T cells then leave the lymph nodes and reach the pulp. Capillaries are usually prominent; fibroblastic activity is evident; and collagen fibers are seen, often gathered in bundles. There is sometimes an attempt by the pulp to ward off the infection through deposition of collagen fibers around the inflamed area. The tissue reaction may resemble the formation of granulation tissue. When this occurs on the surface of the pulp tissue in a wide-open exposure, the term ulcerative pulpitis is applied. With bacterial stains, microorganisms may be found in the pulp tissue, especially in the area of a carious exposure. In some cases, the pulpal reaction vacillates between an acute and a chronic phase. This holds true not only for diffuse inflammation but also for that form of pulp disease characterized by pulp abscess formation. Thus a pulp abscess may become quiescent and be surrounded by a fibrous connective tissue wall, which is known as the pyogenic membrane.
Figure 10-6 Chronic pulpitis.
(A) The pulp of this tooth shows diffuse involvement by chronic inflammatory cells. The entrance to the pulp chamber is wide open (open pulpitis), but contains food debris (1). (B) In the high-power photomicrograph there is seen diffuse infiltration of lymphocytes and plasma cells with fibrosis and loss of the odontoblastic layer.
Chronic hyperplastic pulpitis is a unique form of pulpitis wherein the inflamed pulp, instead of perishing by continued suppuration, reacts by excessive and exuberant proliferation. It occurs either as a chronic lesion from the onset or as a chronic stage of a previously acute pulpitis.
Chronic hyperplastic pulpitis occurs almost exclusively in children and young adults who possess a high degree of tissue resistance and reactivity, and readily respond to proliferative lesions. It involves teeth with large, open carious lesions. A pulp so affected appears as a pinkishred globule of tissue protruding from the pulp chamber and not only fills the caries defect but also extends beyond (Fig. 10-7). Because the hyperplastic tissue contains few nerves, it is relatively insensitive to manipulation. However, Southam and Hodson have found that sometimes innervation of polyps may be quite rich and have stated that the number of nerve fibers in pulp polyps cannot be presumed to be directly related to the sensory acuity found on clinical examination. They have even noted innervation of the epithelium in epithelialized polyps in some instances. The lesion may or may not bleed readily, depending upon the degree of vascularity of the tissue and epithelialization.
Figure 10-7 Chronic hyperplastic pulpitis.
(A) There is a mass of tissue protruding from the pulp chamber into the carious lesion. (B) In the photomicrograph this is seen to be continuous with the pulp and covered by stratified squamous epithelium (A, Courtesy of Dr S Karthigakannan, Department of Oral Medicine, Sree Moogambica Dental College, Tamil Nadu).
The teeth most commonly involved by this phenomenon are the deciduous molars and the first permanent molars. These have an excellent blood supply because of the large root opening, and this coupled with the high tissue resistance and reactivity in young persons, accounts for the unusual proliferative property of the pulp tissue.
The hyperplastic tissue is basically granulation tissue made up of delicate connective tissue fibers interspersed with variable numbers of small capillaries (Fig. 10-7). Inflammatory cell infiltration, chiefly lymphocytes and plasma cells, sometimes admixed with polymorphonuclear leukocytes, is common. In some instances fibroblast and endothelial cells proliferation is prominent.
This granulation tissue commonly becomes epithelialized and the origin of these epithelial cells is a matter of controversy. The epithelium is stratified squamous in type and closely resembles the oral mucosa, even to the extent of developing well formed rete ridges. The grafted epithelial cells are thought to be normally desquamated cells carried to the surface of the pulp by the saliva. Most desquamated epithelial cells in the saliva are degenerated superficial squames, which have lost their dividing capacity. For the polyp to become epithelialized, the cells should have the capacity to divide and differentiate into stratified squamous epithelium. So, such cells must come from the region of the basal cell layer and might be released from trauma or from the gingival sulcus. In some instances, the buccal mucosa may rub against the hyperplastic tissue mass, and epithelial cells become transplanted directly. Southam and Hodson have reported that polyps from deciduous teeth were epithelialized far more frequently (82% of 56 polyps) than those of permanent teeth (44% of 77 polyps). It should be appreciated that the tissue reaction here is an inflammatory hyperplasia and does not differ from inflammatory hyperplasia occurring elsewhere in the oral cavity as well as in other parts of the body. In time, organization of the tissue leads to decreased vascularity and increased fibrosis. M Sattari, AK Haghighi, and HD Tamijani showed that presence and concentration of IgE, histamine and IL-4 were higher in pulp polyps than in normal pulps, and suggested that type I hypersensitivity reaction being involved in pulp polyp’s pathogenesis.
Once infection has become established in the dental pulp, spread of the process can be in only one direction—through the root canals and into the periapical region. Here a number of different tissue reactions may occur, depending upon a variety of circumstances.
It is important to realize that these periapical lesions do not represent individual and distinct entities, but rather that there is a subtle transformation from one type of lesion into another type in most cases. Furthermore, it should be appreciated that a certain degree of reversibility is possible in some lesions. The interrelations between the types of periapical infection must be clearly understood, and the schematic diagram shown in Figure 10-9 will aid in clarification of this.
Apical periodontitis is the inflammation of the periodontal ligament around the root apex. Though the inflammatory process here is similar to that occurring elsewhere, there may be resorption of the periapical bone and sometimes the root apex. This process may be acute or chronic depending upon the virulence of the microorganisms involved, the type and severity of the physical or chemical irritants, and host resistance. The common causes of apical periodontitis include spread of infection following pulp necrosis, occlusal trauma from a high restoration or biting suddenly on a hard object, inadvertent endodontic procedures such as over instrumentation, pushing the infected material into the apical portion or chemical irritation from root canal medicaments.
Patients suffering from acute apical periodontitis usually give the history of previous pulpitis. Thermal change does not induce pain as in pulpitis. Due to the collection of inflammatory edema in the periodontal ligament, the tooth is slightly elevated in its socket and causes tenderness while biting or even to mere touch. The external pressure on the tooth forces the edema fluid against already sensitized nerve endings and results in severe pain. Radiographic appearance is essentially normal at this stage except for a slight widening of periodontal ligament space.
The periodontal ligament shows signs of inflammation characterized by vascular dilatation and infiltration with polymorphonuclear leukocytes. Initially, these changes are localized around the root apex, as this area is richly vascular. The inflammation is transient if it is caused by acute trauma. If the irritant is not removed, it progresses with resorption of the surrounding bone. Abscess formation may occur if it is associated with bacterial infection and is known as acute periapical abscess or alveolar abscess.
Chronic apical periodontitis, also known as periapical granuloma, is a low-grade infection and one of the most common of all sequelae of pulpitis or acute periapical periodontitis. If the acute process is left untreated, it is incompletely resolved and becomes chronic. The acute inflammatory process is an exudative response whereas the chronic one is proliferative. Periapical granuloma is essentially a localized mass of chronic granulation tissue formed in response to the infection (Fig. 10-10). But the use of this term is not totally accurate since it does not shows true granulomatous inflammation microscopically.
It should be pointed out here that the spread of pulp infection is usually, but not always, in a periapical direction. The presence of lateral or accessory root canals opening on the lateral surface of the root at any level is a well-recognized anatomic deviation along which the infection may spread. This would give rise to a ‘lateral’ granuloma or related inflammatory lesion.
The involved tooth is usually nonvital and may be slightly tender to percussion, and percussion may produce a dull sound instead of a normal metallic sound because of the presence of granulation tissue around the root apex. Patients may complain of mild pain on biting or chewing on solid food. In some cases, the tooth feels slightly elongated in its socket and may actually be so. The sensitivity is due to hyperemia, edema, and inflammation of the apical periodontal ligament. The early or even the fully developed chronic periapical granuloma seldom presents any more severe clinical features than those just described.
Actually, many cases are entirely asymptomatic. There is usually no perforation of overlying bone and oral mucosa with the formation of a fistulous tract unless the lesion undergoes an acute exacerbation.
The earliest periapical change in the periodontal ligament appears as a thickening of the ligament at the root apex (Fig. 10-11). As proliferation of granulation tissue and concomitant resorption of bone continues, the periapical granuloma appears as a radiolucent area of variable size seemingly attached to the root apex (Fig. 10-12). In some cases, this radiolucency is a well-circumscribed, definitely demarcated from the surrounding bone. In these instances a thin radiopaque line representing a zone of sclerotic bone may sometimes be seen outlining the lesion. This indicates that the periapical lesion is a slowly progressive and long standing one that has probably not undergone an acute exacerbation.
Figure 10-12 Periapical granuloma.
The periapical radiolucencies signify destruction of bone and replacement by granulation tissue. The maxillary central incisor (A) has a carious lesion of the distal surface that involves the pulp. The mandibular incisors (B) have sustained traumatic injury with loss of pulp vitality and subsequent formation of diffuse periapical granulomata.