10: Diseases of the Pulp and Periapical Tissues

Diseases of the Pulp and Periapical Tissues

Diseases of Dental Pulp

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.

Etiologic Factors

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.

Bacteria circulating in the blood stream tend to settle out or accumulate at sites of pulpal inflammation, such as that which might follow some chemical or mechanical injury to the pulp and is known as ‘anachoretic pulpitis’. Anachoresis is a phenomenon by which blood borne bacteria, dyes, pigments, metallic substances, foreign proteins, and other materials are attracted to the site of inflammation. One probable cause of this phenomenon is increased capillary permeability in the particular area. Anachoretic pulpitis probably occurs in a clinically insignificant number compared with the number of cases occurring as a result of dental caries.

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.

A condition clinically simulating pulpitis by the occurrence of toothache was reported during World War II in flying personnel and has been called aerodontalgia. This has also been described in aircrew flying at high altitudes, astronauts, submarine crews, and in deep sea divers. This pain has been attributed to the formation of nitrogen bubbles in the pulp tissue or vessels. It is relatively uncommon and is associated particularly with recently filled teeth. The work of Orban and Ritchey suggests that the pain in decompression does not usually occur in normal pulps. Interestingly, aerodontalgia reportedly may be delayed for hours or even days after decompression or ascent to high altitudes. Some cases of pain localized to the dental area and resembling aerodontalgia have been reported to represent aerosinusitis and not to be related to the teeth.

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.

Classification of Pulpitis

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.

Focal Reversible Pulpitis

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.

Histologic Features

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.

Acute Pulpitis

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.

Clinical Features

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.

Other factors include establishment of drainage, the patient’s previous experiences, emotions, and so forth.

The pulpal pain is poorly localized and may be felt in any of the teeth of the upper or lower jaw of the affected side, since the pulp of the individual tooth is not represented precisely on the sensory cortex.

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.

The patient with a severe acute pulpitis is extremely uncomfortable and at least mildly ill. He/she is usually apprehensive and desirous of immediate attention from the dentist.

Histologic Features

Early acute pulpitis is characterized by the continued vascular dilatation seen in focal reversible pulpitis, accompanied by the accumulation of edema fluid in the connective tissue surrounding the tiny blood vessels. The pavementing of polymorphonuclear leukocytes becomes apparent along the walls of these vascular channels, and these leukocytes rapidly migrate through the endothelium-lined structures in increasing numbers. CD 44 is an adhesion molecule present in leukocytes, epithelial cells, endothelial cells, and smooth muscle cells. It has an important role in migration of leukocytes from the blood vessels to the area of inflammation. Pisterna GV and Siragusa M have demonstrated that CD 44 expression is higher during initiation and maintenance phase of pulp inflammation. As great collections of white blood are found in the inflamed region, especially beneath an area of carious penetration the odontoblasts in this area have usually been destroyed.

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.

image

Figure 10-3 Pulp abscess.
The high-power photomicrograph of Figure 10-2 A, shows the void caused by the loss of the suppurative contents of the abscess and the limiting band of leukocytes.

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.

Treatment and Prognosis

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

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.

Clinical Features

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.

Histologic Features

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.

In nearly all cases, the pulp is eventually involved in its entirety by the chronic inflammatory process, although this may take a long time to present few clinical symptoms.

Chronic Hyperplastic Pulpitis: (Pulp polyp)

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.

Clinical Features

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.

On occasion the gingival tissue adjacent to a broken carious tooth may proliferate into the carious lesion and superficially resemble an example of hyperplastic pulpitis. In such cases the distinction can be made by careful examination of the tissue mass to determine whether the connection is with pulp or gingiva (Fig. 10-8).

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.

Histologic Features

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.

Gangrenous necrosis of pulp

Untreated pulpitis, either acute or chronic, will ultimately result in complete necrosis of the pulp tissue. Since this is generally associated with bacterial infection, the term pulp gangrene has sometimes been applied to this condition, gangrene being defined as necrosis of tissue with superimposed bacterial infection. This gangrenous necrosis of the pulp is associated with a foul odor when such infected pulps are opened for endodontic treatment.

Pulp gangrene should not be considered a specific form of pulp disease but simply the most complete end result of pulpitis in which there is total necrosis of tissue. Necrosis of pulp has been reported in sickle cell anemia where there is blockage of pulp microcirculation by sickle erythrocytes. A type of gangrene known as dry gangrene sometimes occurs when the pulp dies for some unexplained reason. The nonvital pulp maintains its general histologic characteristics, being nonpurulent. This condition may be due to some traumatic injury or infarct.

Diseases of Periapical Tissues

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.

Acute Apical Periodontitis

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.

Chronic Apical Periodontitis

(Periapical granuloma)

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.

Clinical Features

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.

Radiographic Features

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.

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Related posts:

  1. 20: Diseases of the Nerves and Muscles
  2. 9: Dental Caries
  3. 4: Cysts and Tumors of Odontogenic Origin
  4. 6: Viral Infections of the Oral Cavity
  5. 12: Physical and Chemical Injuries of the Oral Cavity
  6. 1: Developmental Disturbances of Oral and Paraoral Structures

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Jan 12, 2015 | Posted by in Oral and Maxillofacial Pathology | Comments Off on 10: Diseases of the Pulp and Periapical Tissues

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