Conditions covered in this chapter
Inflammation of the dental pulp (pulpitis)
Unique characteristics of the pulp
Response of the pulp to dental caries
Internal resorption of dentin
Inflammatory lesions of the periapical tissues
Spread of inflammation from the pulp
Condensing osteitis (focal sclerosing osteomyelitis)
Acute pyogenic osteomyelitis of the jaws
Chronic osteomyelitis of the jaws
Acquired immunodeficiency syndrome (AIDS)
As a working image for this section, try thinking of the tooth as a castle under siege—a stone monolith perched on a rise above the misty moors with King Pulp residing inside (saliva-covered gingiva over the mandibular arch . . . get it?). Passageways and underground caves establish secret links to the outside to transport supplies back and forth. The enemy army attacks, tearing down walls and digging under the ramparts in an attempt to capture the king. The enemy’s most effective strategies are (1) cut off the supplies and (2) persist on a multitude of fronts. For the defenders, the most effective strategies are to (1) adjust to variable supplies, (2) repair the walls as quickly as possible, and (3) fend off the attacking troops. Now, let’s take a closer look at the “Assault on Castle Dentin.”
Inflammation of the tooth pulp (pulpitis)
Unique characteristics of the pulp
The pulp is unique in that it is housed within mineralized tissue; this places it in a low-compliance environment. In this regard, the pulp is similar to tissues such as the brain, bone marrow, and nail bed. Furthermore, the pulp lacks a collateral circulation and is therefore entirely dependent on the arterioles entering the apical foramen for its blood supply.
When edema fluid accumulates in a soft tissue, such as the skin, swelling can occur to accommodate the increase in extravascular fluid. Because the pulp is unable to swell, inflammation can produce a marked increase in intrapulpal pressure.
Does inflammation per se lead to pulp necrosis? According to the strangulation theory, the space for additional blood and tissue fluid resulting from inflammation is provided by compression of venules because pressure in the venules is lower than in the arterioles and capillaries. This theory holds that compression of venules produces increased vascular resistance, which results in passive congestion. This in turn would result in hypoxia and pulpal necrosis. Is this theory plausible? Not really.
First of all, it is unlikely that venules would be compressed to the point that passive congestion would develop. The pulp is rich in proteoglycans, and these molecules have the ability to bind water, thus making the pulp a resilient tissue. Consequently, pulpal venules are in a relatively compliant environment; this protects them from abrupt pressure changes. It has been demonstrated that pressure changes in one part of the pulp usually do not produce pressure changes in other parts.
There seems to be an effective mechanism for removing edema fluid from the pulp. Remember Starling’s Law? When interstitial tissue pressure exceeds intravascular pressure, fluid is forced back into the venules. Also, lymphatics are capable of removing excess fluid. In fact, research has shown that increased tissue pressure in the pulp may actually begin to decrease, while blood flow is still increasing.
If the strangulation theory were valid we would expect inflamed pulps to undergo infarction. An infarct is an area of ischemic necrosis produced either by occlusion of the arterial supply or its venous drainage. Pulpal infarcts are uncommon and usually due to trauma to the vessels entering the pulp rather than to inflammation.
How then does pulpal necrosis develop? As in any other tissue, necrosis develops when host defenses are unable to eliminate the irritant. Liquefactive necrosis is the most common form of pulpal necrosis, and this is generally due to the presence of pyogenic organisms. Infection due to dental caries or tooth fracture is the principal cause of pulp necrosis.
The neuropeptides CGRP and SP and their release from sensory nerve fibers were discussed in Chapter 2. (First reader to identify the page and paragraph in Chapter 2 will receive a lifetime supply of both CGRP and SP as a thoughtful gift from us.) In experimental animals, researchers have shown that release of these mediators produces vasodilation and increased vascular permeability. It is felt that neurogenic inflammation is important in the pulp because there are few mast cells to release histamine, at least in normal pulp tissue.
Following injury to the tooth pulp, there is extensive sprouting of unmyelinated nerve fibers that are immunoreactive for CGRP and SP. Sprouting is promoted by nerve growth factor (NGF), which is secreted by pulp fibroblasts. Receptors for NGF are located on the axoplasmic membrane of unmyelinated nerve cells and on Schwann cells with which the nerve fibers are associated. In laboratory studies it has been shown that nerve sprouting is extensive if an abscess forms and then subsides with the elaboration of reparative dentin.
Neuropeptide release can have a profound influence on pulpal inflammation. CGRP and SP are capable of stimulating mast cells, neutrophils, and monocytes, as well as fibroblasts and vascular endothelium.
The sprouting of sensory nerve fibers undoubtedly enhances the delivery of neuropeptides to pulp tissue.
Response of the pulp to dental caries
“Hey King A . . . the walls have been breached . . . all hands on deck (oops, wrong service) . . . whatever will we do now?” (that’s “soldier speak”). And the great king hollered from the parapet to his troops below:
“Dental caries is a localized, progressive destruction of tooth structure and the most common cause of pulp disease.”
For caries to develop, specific bacteria must become established on the tooth surface. Products of bacterial metabolism, notably organic acids and proteolytic enzymes, cause the destruction of enamel and dentin. Bacterial metabolites diffusing from the lesion to the pulp are capable of eliciting an inflammatory reaction. Eventually, extensive involvement of dentin results in bacterial infection of the pulp.
Nature of bacteria present in carious lesions
As compared with plaque on the tooth surface, conditions for growth and availability of nutrients are quite different in carious lesions. Streptococcus mutans colonizes the surface of enamel, whereas lactobacilli thrive in sites of cavitation. The low pH in dentinal lesions allows only aciduric organisms to flourish. Studies on the microbial flora in the dentin where demineralization is occurring have shown that bacterial involvement is rather nonspecific. No single species was found in more than 20% of the dentinal lesions. It appears that the environment for growth varies at different times and in different locations within the lesion. A number of proteolytic organisms have been identified. It appears they are capable of degrading collagen that has been denatured by acid, and utilizing it as a source of substrate.
Injury to odontoblasts
As bacteria penetrate the enamel and enter the dentin, the underlying odontoblasts are adversely affected. Initially, they are stimulated to produce collagen, and there is an accompanying increase in metabolic and enzymatic activity. Soon, however, even before inflammatory changes appear in the pulp, the size and number of odontoblasts is decreased (Fig 9-1). At the same time, their metabolic activity is reduced, and collagen synthesis is depressed. Although they are normally tall columnar cells, odontoblasts affected by caries are transformed into flat or cuboidal cells.
Eventually, the primary odontoblasts die as a result of injury. This usually evokes the formation of a dead tract. A dead tract is an area of dentin that is devoid of odontoblast processes because the odontoblasts have undergone necrosis. Primary odontoblasts that have died are replaced by cells derived from pulpal fibroblasts that migrate from the cell-rich zone of the pulp and differentiate into new odontoblasts. These “replacement” odontoblasts then deposit reparative dentin over the pulpal aspect of the dead tract.
Bacterial antigens diffusing through the dentinal tubules and into the pulp evoke an immune response. Eventually, bacteria proliferate deep into the dentinal tubules and infect the pulp.
Basic reactions that tend to protect the pulp against caries involve:
- A decrease in the permeability of the dentin (dentinal sclerosis)
- The formation of new dentin (reparative dentin)
- Inflammatory and immunologic reactions
Antigenic and other irritating substances reach the pulp by diffusing through the dentinal tubules. Therefore, the permeability of the tubules is of critical importance in determining the extent of pulpal injury. The most common response to caries is dentinal sclerosis. In this reaction the dentinal tubules become partly or completely filled with mineral deposits consisting of both carbonated apatite and whitlockite crystals.
Dentinal sclerosis develops at the periphery of almost all carious lesions. This response has the effect of decreasing the permeability of dentin, thus shielding the pulp from irritation. For sclerosis to occur, vital odontoblast processes must be present within the dentinal tubules. If the odontoblasts die as a result of injury, a dead tract is formed. The presence of a dead tract stimulates the pulp to produce reparative dentin in order to seal off the pulpal ends of the tubules.
The formation of reparative dentin limits the diffusion of toxic substances to the pulp. The rate of carious attack also seems to be a determining factor, as more dentin is formed in response to slowly progressing (chronic) caries than to rapidly advancing (acute) caries. For this reason, carious exposure of the pulp is likely to occur earlier in acute caries than in chronic caries.
The walls of dentinal tubules along the boundary line between primary and reparative dentin are thickened, and in most instances there is a barrier of atubular dentin situated between the primary and reparative dentin. This barrier is less permeable than ordinary dentin and may serve to block the ingress of bacteria and their products. (More on reparative dentin coming up!)
Inflammation evoked by caries
Clinically, diagnosis of the extent of pulpal inflammation beneath a carious lesion is difficult. Many factors play a role in determining the nature of the carious process; the individuality of each carious lesion should be recognized. The response of the pulp may vary depending on whether caries progresses rapidly, relatively slowly, or not at all (arrested caries). Moreover, caries tends to be an intermittent process, with periods of rapid activity alternating with periods of quiescence. The rate of carious attack can be influenced by any or all of the following:
- Age of the host (mature enamel is more highly calcified than immature enamel)
- Composition of the tooth, particularly fluoride content
- Nature of the bacterial flora in the lesion
- Rate of salivary flow (patients with xerostomia generally develop rampant caries)
- Antibacterial substances in the saliva (eg, IgA antibodies, lysozyme)
- Oral hygiene (plaque removal)
- Cariogenicity of the diet (refined fermentable carbohydrates) and the frequency with which acidogenic foods are ingested
- Caries-inhibiting factors in the diet (eg, phosphates, calcium-containing foods, chocolate perhaps?)
Dental caries is a protracted process, and lesions progress slowly over a period of years. Consequently, it is not surpris-ing that pulpal inflammation evoked by carious lesions begins insidiously as a low-grade, chronic response rather than an acute inflammatory reaction. The chronic response represents activation of the immune system by bacterial antigens reaching the pulp from the carious lesion.
Recently, dendritic cells have been identified in the odontoblast layer of the pulp. In a normal pulp, it is thought that these cells play a role in immunosurveillance. Presumably in caries they facilitate immunologic reactions by capturing and processing antigens entering the pulp from the carious lesion. From the pulp, the processed antigen is transported to lymph nodes and presented to T-helper cells. Pulpal macrophages are also able to process and present antigen.
The initial inflammatory cell infiltrate consists almost entirely of lymphocytes, plasma cells, and macrophages (Fig 9-2). Additionally, there is a proliferation of small blood vessels and fibroblasts, and the deposition of collagen fibers. This pattern of inflammation is generally regarded as a cellular immune response.
Remember that chronic inflammation does not necessarily result in permanent damage to tissue; it is similar in many respects to the process of repair. Thus, if the bacteria in the carious lesion are eliminated or inactivated before the pulp becomes infected, connective tissue repair will replace the chronic inflammatory elements. However, in a deep carious lesion, the removal of carious dentin may cause a pulp exposure and further traumatize the pulp. Proper management of a deep carious lesion requires sound clinical judgment and well-developed operative skills.
The severity of pulpal inflammation beneath a carious lesion depends to a great extent on two factors: (1) the depth of bacterial penetration, and (2) the degree to which dentin permeability has been reduced by dentinal sclerosis and/or reparative dentin formation. Usually, if the distance between the invading bacteria and the pulp (including the thickness of reparative dentin) is greater than 1 mm, the inflammatory response is mild. However, by the time the lesion is within 0.5 mm of the pulp, chronic inflammation generally progresses to acute inflammation. This invariably occurs once the reparative dentin beneath the lesion is invaded by bacteria. By this time, the layer of replacement odontoblasts has been destroyed and replaced by inflammatory cells (Fig 9-3).
With the onset of acute inflammation there is vasodilatation, increased vascular permeability, and the accumulation of neutrophils. Neutrophils migrate from blood vessels in response to chemotactic factors derived from the invading bacteria and complement activation. So avid is the neutrophil response that many neutrophils migrate up into the dentinal tubules (see Fig 9-3).
Carious exposure of the pulp results in massive mobilization of neutrophils, and eventually suppuration develops. Pus is formed when neutrophils release their proteolytic enzymes and the tissue is digested (liquefactive necrosis). The area where tissue digestion is occurring has a greater osmotic pressure than the surrounding tissue; this pressure differential increases the sensitivity of sensory nerve endings. This explains why pulpal abscesses are often painful and why drainage provides relief.
Now, here comes the really gruesome and dreaded part. The King is dead and the Evil Knight reigns supreme over the darkened land . . . forever!
As the size of the carious exposure enlarges and an ever-increasing number of bacteria enter the pulp, the host defenses are eventually overwhelmed. It must be remembered that the pulp has a limited blood supply (4–8 arterioles enter the apical foramen of each root). Therefore, when the demand for neutrophils and other inflammatory elements exceeds the ability of the vascular supply to transport them to the site of bacterial penetration, the inflammatory response can no longer be sustained. As a consequence, bacteria commence to colonize the pulp, and this ultimately leads to pulp necrosis. Some authorities believe that bacterial colonization of the pulp chamber marks the onset of irreversible pulpitis.
Chronic hyperplastic pulpitis (pulp polyp)
This condition occurs most often in primary and immature permanent teeth with incompletely formed roots. At this stage of development, numerous blood vessels supply the pulp through the wide apical foramen. Because of its rich blood supply and high degree of cellularity, the young pulp is better able to resist bacterial infection than an older pulp. When caries reaches the pulp and produces a pulp exposure, an acute inflammatory reaction ensues. As the pulp exposure increases in size, it may eventually produce a large open cavity. This opening provides a pathway for drainage of the inflammatory exudate. Once drainage is established, acute inflammation subsides and chronic inflammatory tissue proliferates up through the opening created by the exposure. This proliferation results in the formation of a pulp polyp (Fig 9-4). Eventually the polyp becomes epithelialized as desquamated epithelial cells from the oral mucosa are “grafted” onto the surface of the proliferating connective tissue.
Painful pulpitis associated with caries
During the progression of caries, the tooth may remain asymptomatic, even while the pulp is undergoing necrosis. Pain is the exception, not the rule. Occasionally, early in the carious attack, dentinal pain may be evoked by candy or other sweets, or by thermal stimuli. This involves activation of intradental myelinated fibers by hydrodynamic stimuli. Such pain is usually sharp and of short duration. Dull, throbbing, continuous pain is evidence that the pulp is severely inflamed and/or degenerating. The fact that there is no reliable correlation between the severity of pain and the extent of pulpal injury is consistent with what neurologists have observed in other damaged tissues.
Hyperalgesia is a condition in which the sensitivity of sensory nerves is increased (eg, the responsiveness of sunburned skin to mechanical pressure). For example, hyperalgesia causes a tooth to become more sensitive to hot and cold foods and beverages. Although a precise explanation of hyperalgesia is lacking, certain inflammatory mediators, such as bradykinin, serotonin, prostacyclin, and prostaglandin E2, are known to play a role.
The development of pain symptoms depends on changes in the local environment of sensory nerve fibers. Several local factors including release of inflammatory mediators, decrease in pH, variation in ionic milieu, alterations in blood flow, and changes in tissue pressure probably act in concert to cause pain in a diseased tooth.
Pain is an important symptom, but it may be misleading. While severe pain of pulpal origin is usually indicative of irreversible pulpitis, other diagnostic aids, such as vitality testing, radiographic examination, and palpation and percussion tests, must be employed to ensure a correct diagnosis. In addition, one must always consider the possibility that pain is referred from another tooth or from other structures, as referred pain is very common in and around the oral cavity.
Repair in the pulp
The inherent healing potential of the pulp is well recognized. As in all other connective tissues, repair of tissue injury commences with debridement by macrophages followed by proliferation of fibroblasts and capillary buds and by the production of collagen. Because of the open apex of a young tooth, the apical pulp is larger than that of a mature tooth. This allows more blood vessels to enter through the apical foramen. The highly cellular and vascular pulp of a young tooth should have a better healing potential than the pulp of an older tooth, but proof of this is lacking.
In pulpal injury the presence of bacteria severely hampers repair. In experiments on germ-free rats, mechanical exposure of the pulp was followed by complete healing and deposition of reparative dentin beneath the exposure site, whereas the same procedure in conventional animals (ie, not germ-free) generally resulted in total pulp necrosis.
Reparative dentin (RD)
Developmental (primary) dentin is formed during tooth development. When the tooth comes into functional occlusion, the rate of dentin formation is greatly reduced in the coronal portion of the tooth (the root is still forming). Dentin that forms following the completion of tooth formation is termed sec – ondary dentin. Secondary dentin continues to form at a slow rate throughout the life of the tooth, gradually reducing the size of the pulp chamber.
Reparative dentin differs from developmental and secondary dentin because it is produced only in response to specific stimuli. In the case of caries, it forms on the dentin wall beneath the carious lesion. Irritants include extensive wear of the tooth surface, erosion, cracks in the enamel and dentin, dental caries, loss of cementum from the root surface, and dental operative procedures. Thus, RD represents a defense mechanism against loss of enamel, dentin, or cementum.
RD is formed by cells that replace primary odontoblasts that have been destroyed. Morphologically, these cells are flat to cuboidal in shape, and the odontoblast layer they form has a lower density of cells than the original odontoblast layer (Fig 9-5).
Following the loss of primary odontoblasts, there is a time lag of about 20–40 days before RD formation commences. During this time the following events are taking place: (1) odontoprogenitor cells in the underlying pulp undergo mitosis; (2) the daughter cells migrate to the site where RD will be formed; (3) they differentiate into preodontoblasts and commence to secrete dentin matrix; and (4) the preodontoblasts further differentiate into odontoblasts.
As compared with primary dentin, RD is generally less tubular and less well calcified. In some cases no tubules are formed. The quality of RD (ie, the degree to which it resembles primary dentin) is highly variable. Factors influencing its formation include the nature and magnitude of the stimulus (injury or irritant) and the status of the pulp. If the pulp is healthy, the RD is of good quality. If the pulp is inflamed, the quality is poor. At times, RD is laid down so haphazardly that areas of soft tissue become entrapped within the developing matrix, thus producing a “Swiss cheese” pattern.
Is RD protective, or is it simply a form of scar tissue? Available evidence indicates that it actually does shield the pulp from injury. In the case of caries, RD often helps the pulp survive. It seems that operative procedures are better tolerated in teeth having a layer of preformed RD beneath the cavity preparation than in teeth without RD. However, it must be emphasized that poor-quality RD may not shield the pulp from injury.
Why can RD be protective? As pointed out earlier, there is often an atubular zone at the interface between primary and reparative dentin that presumably limits the diffusion of irritants through the dentin, thus blocking the inward diffusion of irritants.
Internal resorption of dentin
Two types of resorption affect teeth: internal and external. The former involves the pulp chamber and root canals, whereas the latter affects the external surface of the root. The etiology of internal resorption remains speculative. A few cases have been reported where internal resorption occurred in healthy teeth, even in unerupted teeth. Most often, resorption occurs in chronically inflamed pulps where lymphocytes are present and there is proliferation of small blood vessels. Resorption bays containing osteoclasts can be observed on the surface of the dentin (Fig 9-6).
Internal resorption appears to be an intermittent process with periods of active resorption alternating with periods of inactivity. During periods of remission, mineralized tissue is often deposited within the areas of resorption.
Which inflammatory stimuli initiate internal resorption? There are at least three possibilities: (1) cytokines such as IL-1 and TNF, (2) prostaglandin E2, and (3) increased tissue pressure.
Internal resorption is usually detected radiographically, although sometimes it manifests as a pinkish hue on the tooth surface (due to the underlying vascular tissue). The resorptive defect is always larger than it appears on radiographs. Once diagnosed, root canal treatment should be instituted, as resorption is usually progressive and the pulp must be removed to halt the process. Untreated, resorption may perforate the crown and provide a portal of entry for microorganisms.