Inflammatory Periapical Conditions

PTHL 312b: Oral and Maxillofacial Pathology

Dental Caries, Inflammatory Pulp, and Periapical Diseases

Topic 9:

Teeth and Jaws: Dental Caries, Inflammatory Pulp, and Inflammatory Periapical Conditions

Dental Caries Introduction Incidence of Dental Caries Etiology and Pathogenesis of Dental Caries Histopathology of Dental Caries

Inflammatory Pulp Diseases Introduction Inflammatory Diseases of the Pulp Pulp Hyperemia Acute Pulpitis Chronic Pulpitis Chronic Hyperplastic Pulpitis Pulp Necrosis

References Learning Guide Objectives Definitions Workbook

Web Site Images Study Questions Terms and Definitions “Flash Cards” Disease Features “Flash Cards” Web Reader with Images Reader and Learning Guides PDFs

Inflammatory Periapical Diseases General Features Acute Inflammatory Periapical Diseases Chronic Inflammatory Periapical Diseases

©2008 William H. Crawford, Jr., D.D.S., M.S. All rights reserved. Copying for commercial purposes is prohibited.

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Dental Caries Introduction Dental caries has afflicted humans longer than any other disease. Dental caries was not prominent in the earliest humans; it appeared around 12,000 B.C. or about 14,000 years ago. From that time to the present, dental caries has afflicted almost all human populations, all socioeconomic levels, and all ages. The pain and other suffering this disease has caused has been chronicled in literature, art, and movies. Understanding dental caries has stimulated much research. The first studies were published in the 1870’s and have continued uninterrupted to the present. As the result of these efforts, control of dental caries is more promising that at any time. Prevention of dental caries has spawned an industry with sales of over $20 billion each year. While this attention has decreased the incidence of this disease in United States’ young people, its incidence remains high in the 50% of the U.S. population and in most of the world’s under developed countries.

Incidence of Dental Caries The incidence of dental caries has been studied most in American white populations. The results show dental caries to be most prevalent chronic disease in this population. The disease affects all regardless of location, sex, age, or social stratum. The disease starts in young people just as soon as teeth erupt. About 90% of youngsters are affected by age 14. As mentioned earlier however, the incidence of caries is decreasing in this young population in the U.S. and in other Western countries. This downward trend is explained by increased fluoridation of community water supplies and by increased attention to regular care at dental offices and at home. Isolated populations who have not adopted eating habits of the West have long been known to decrease incidence of dental caries. Inuits, some African natives, and inhabitants of rural India are examples of such “immune” populations. Examination of teeth shows considerable abrasion of the occlusal surfaces indicating consumption of a coarse, abrasive diet. It is not uncommon to observe teeth abraded down to the contact points between adjacent teeth. This no doubt explains the fact that dental caries in these “primitive” populations is restricted to the interproximal areas below contact areas where food impaction may occur. While decreased incidence has been observed in the U.S. young, caries rates are increasing in Third World countries as they adopt Western diets. It is also increasing in the U.S. elderly. In this population, retention of teeth into old age with accompanying exposure of root surfaces, has led to an increase in “cemental caries.”

Etiology and Pathogenesis of Dental Caries From the earliest days of dental caries research, the role of acids and microorganisms in its development was appreciated. Carious lesions were produced in extracted teeth by exposing their crowns to acid. The microbial source of acid soon followed. A quotation from a past standard pathology text said it all when dental caries was described as “…a microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth.” While this description accurately summarizes the etiology of dental caries, the emergence of two theories led to this unified concept. Acidogenic Theory In 1882, a pioneer in caries research, Willoughby Miller promulgated the acidogenic theory of dental caries, a theory that has survived pretty much unchanged until today. In it Miller, recognized two stages in the carious process: decalcification of enamel and dissolution of protein interrod substances. Decalcification of enamel, the first step in the process, was, Miller believed, caused by metabolism of carbohydrate food residues by microorganisms. In the early days, Lactobacillus acidophilus was thought to be the prime culprit. More recently, Streptococcus mutans and other microorganisms have been implicated as well. Whatever organisms are involved, the calcified portion of enamel is dissolved exposing the protein rod sheaths to degradation as well.

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Acid-producing bacteria are attached to teeth by plaque proteins that protect them. Carrying Miller’s theory forward to modern times, scientists have found that microorganisms become attached to tooth surfaces by adhesive proteins in dental plaque where they are protected from the immunologic properties of saliva. Thus, if plaque is allowed to form, microorganisms attach and metabolize food debris forming decalcifying acids. Placed in the modern context, Miller’s acidogenic theory explains the development of smooth surface caries in which plaque becomes attached to the labial, lingual, mesial, or distal tooth surfaces. The Proteolytic Theory Another theory was developed presumably to explain the origin of caries of the occlusal surfaces (pit and fissure caries). The idea here is that bacteria first invade malformations commonly found in enamel. The most common of these are incompletely calcified occlusal grooves and protein lamellae that extend through enamel. As bacterial acids accumulate in these sites, surrounding protein is destroyed exposing calcified enamel to bacterial acids. Combination Theory While bacterial acids are the initiating agent in both theories, the proteolytic theory starts with destruction of protein rather then calcified enamel. Actually both may be correct. Perhaps the acidogenic theory operates in the etiology of smooth surface caries while the proteolytic theory better explains pit and fissure caries.

Histopathology of Dental Caries Enamel Caries Except in old people and those suffering from periodontal disease, the exposed surfaces of teeth are covered with enamel. As a consequence of this anatomic fact, most carious lesions must start by attacking the body’s hardest tissue—enamel. Smooth Surface Enamel Caries On smooth surfaces, enamel decalcification produces cone-shaped lesions, the tips pointing at the dentinoenamel junction (DEJ) and the wide ends facing the external surface. Since most enamel rods are oriented perpendicular to the external surface and since destruction of rods follows them, the carious lesion’s long axis is also perpendicular to the tooth surface. Eventually, the cone-shaped lesion contacts dentin along the DEJ. At first only a small spot of dentin is exposed to the action of carious microorganisms. At this early stage, before dentin caries is far along, removal of the lesion and restoration of the tooth can be accomplished with minimal tooth structure sacrifice. Microscopically, several zones have been identified. It is not important to recount them except to state that in the early stages of enamel caries, while enamel is still intact, the lesion is darker than surrounding unaffected enamel. The lines of Retzius, are much more conspicuous here than in surrounding enamel. Incremental lines on individual enamel rods are also affected, a change indicating that rod dissolution is not far away. There is an important clinical principle that is based on the microscopic changes summarized above: early enamel caries usually cannot be detected upon clinical examination; however, the disease can be detected on radiographs. Pit and Fissure Enamel Caries While the process is the same, the effect of pit and fissure caries is significantly different from that of smooth surface caries. Because enamel rods diverge at the base of occlusal pits and fissures, a carious lesion will, when it reaches the DEJ, infect a large area of dentin. In pit and fissure caries, the small end of the infecting cone is located at the occlusal surface while its broad end is located at the DEJ. Removal of these lesions and subsequent restoration of the tooth requires sacrifice of considerable tooth structure.

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Dentin Caries Sooner than later, the carious process will reach the DEJ. Because dentin is less calcified than enamel (70% vs. 96%) and is perforated by innumerable channels (dentinal tubules), dentin caries progress more rapidly than enamel caries. In the earliest stages of exposure to microorganisms, there is an effort to seal the tubules. This is accomplished by increased calcification. The result is a visible change known as “transparent dentin” or, better, “dentinal sclerosis.” In addition, pulpal odontoblasts, stimulated by the advancing carious lesion, will rapidly deposit dentin. The dentinal tubules in this new dentin are irregular, making them less permeable. Histologists cannot seem to decide what to call this newly formed dentin; the terms “irregular dentin,” “reparative dentin,” “secondary dentin,” and “tertiary dentin” all have been used. Dentinal sclerosis and reparative dentin may be successful deterrents if the carious lesion progresses slowly. As microbial invasion progresses along dentinal tubules, acid production decalcifies surrounding dentin. As decalcification continues, clefts oriented perpendicular to dentinal tubules appears. This carious dentin is loaded with microorganisms; when the pulp chamber is finally breached, bacterial invasion of the dental pulp will ensue. Cementum Caries In older people, gingival recession exposes root surfaces to oral fluids. If plaque is allowed to form on these exposed surfaces, bacterial invasion of cementum will occur. Microorganisms will inhabit holes left by the detachment of periodontal ligament fibers (Sharpey’s fibers). Soon after, cementum is decalcified. Because cementum is deposited concentrically around the root, bacterial invasion tends to follow this concentric pattern. As a consequence, cemental caries proceeds on a very broad front: “circumferential invasion.” Repair of cemental caries is technically demanding and often unsuccessful. Prevention of plaque deposition in older people and prevention of cemental caries is a better approach to this difficult aging problem.

Inflammatory Pulp Disease Introduction Bacteria and/or their related products will invariably enter the dental pulp soon after caries extends into dentin. You will remember that odontoblast processes extend from the dentino-enamel junction to the pulp. As the processes retreat from dentin caries, bacteria can make their way to the pulp along empty dentinal tubules. Bacterial products stimulate an inflammatory reaction within the pulp. Therefore, inflammation is the prominent pathologic feature of infected pulps. Depending on the types of microorganisms and the capability of host defenses, the inflammatory process may be acute or chronic. These responses produce a variety of signs and symptoms that clinicians call “pulpal diseases.” Whatever the inflammatory response, pain is the predominant symptom.

Inflammatory Diseases of the Pulp While inflammation of the dental pulp has a similar pathogenesis to inflammation elsewhere, the pulp’s unique anatomic features cause a discrepancy between clinical and histologic features. Acute inflammation is accompanied by classic signs/symptoms of heat, redness, pain, and swelling; these are muted or absent in chronic inflammation. Since the pulp is hidden from view clinical signs of heat, redness, and swelling are not features of pulpal inflammation. The symptom of pain is the only clinical manifestation of inflammation that accompanies pulpal inflammation whether acute or chronic. There is, therefore, little correlation between the clinical and histologic features of pulpal inflammation. Because pathologists think in histologic terms, what follows, then, is a histologic classification of pulpal inflammatory disease. Anatomic Features Affecting Inflammation of the Dental Pulp There are three basic features about the location of the dental pulp that profoundly affect an inflammatory response. First, unyielding calcified walls surround the dental pulp; the pulp cannot swell. Capillary dilation and the transudation of fluids increase the volume of tissue. Swelling causes increased pressure stimulating

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pulpal nerves to register pain. Second, pulpal blood vessels, while numerous, are supplied by small feeder vessels entering through, usually, a single narrow channel—the apical foramen. Again, there is usually, no secondary blood supply. This constricted blood source makes the pulp less capable of carrying out an inflammatory response. Also, as the pulp swells, the blood supply is cut off. As a consequence of these features, the dental pulp may undergo necrosis in the face of an inflammatory response that would cause no lasting damage elsewhere. Third, because the tooth is embedded in the jaws, products of inflammation, pulp necrosis, and microorganisms will exit the apical foramina and invariably enter into the surrounding bone—causing “periapical” inflammation. Table 1: Anatomic Features Unique to the Dental Pulp Anatomic Feature

Unfavorable Result

•

Unyielding walls

•

Limits pulp swelling

•

Constricted Blood Source

• •

Limits blood supply Subject to “strangulation” by pulp swelling

•

Tooth surrounded by bone

•

Bone inflammation invariably results

Etiology of Pulp Inflammation The bacterial infection caused by dental caries is the most common cause of pulpal disease. However, there are ways bacteria can infect the pulp in the absence of dental caries. Cracked teeth are one example. It is not uncommon for teeth, particularly restored teeth in the elderly, to have a hairline cracks extending through the crown traversing the pulp chamber. If that occurs, bacteria in saliva enter the dental pulp through the crack. It is conceivable, but rare, for a bacteria in an infection elsewhere, like the kidney, to be carried by blood to the dental pulp. The reverse of this, infected teeth causing infections elsewhere, was once thought by physicians to be a common source of systemic infections: they called them “focal infections.” Such focal infections are now known be exceedingly rare. It is possible for pulpal inflammation to be caused by chemicals used in cavity preparation. The cutting of dentin in routine cavity preparation cut across odontoblastic processes causing, in many cases, odontoblast death and subsequent inflammation. Not too long ago, cavity preparation was performed without cooling water sprays. Such “dry cutting” elevated the temperature of dentin causing pulpal inflammation. Now, cooling water sprays reduce dentin temperature and reduce inflammation. Finally, trauma to teeth (without fractures) can cause pulpal trauma leading to pulpal death and subsequent inflammation. Table 2: Causes of Pulpal Inflammation Etiologic Agent Microbial infection

Irritation

Source • •

Dental caries Cracked teeth

• • • •

Chemicals (e.g., used in cavity preparation) Trauma (e.g., blows to the face) Heat (e.g., dry tooth cutting) Electrical stimulation (e.g., pulp testing)

Pulp Hyperemia (Focal Reversible Pulpitis) A common condition affecting a tooth accompanied by short-lived pain following application of heat or cold; the pulp usually recovers. It is a common observation after placement of a dental restoration the restored tooth becomes sensitive to hot and cold. This commonly observed syndrome is known as “pulp hyperemia” or “focal reversible pulpitis.” The affected tooth does not hurt all the time; pain is elicited with thermal stimulation, particularly application of cold. When pulp vitality tests are employed, the tooth over-reacts (reacts quicker than adjacent normal teeth).

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While dental pulps are submitted for microscopic examination only rarely, researchers have determined that the symptoms described above seem to be associated with dilated blood vessels and transudation of fluids, hence the common name “pulp hyperemia.” It is the absence of continual pain and the relationship of intermittent pain to thermal stimulation that brings the clinician to a diagnosis of pulp hyperemia. Over the years clinicians have learned to prevent pulpal irritation during placement of dental restorations. They cool their cutting instruments with water sprays and place insulating material underneath metallic restorations. If these preventive measures do not suffice, the patient is advised to avoid extremes in temperature (overly hot and overly cold beverages). In most cases teeth with pulp hyperemia will become asymptomatic in time. Acute Pulpitis A common condition affecting a tooth accompanied by severe, relentless pain; the acute inflammation associated with it invariably causes pulp death requiring pulp extirpation or tooth extraction. A “toothache” is one of the most exquisitely intense pains that can be suffered. Only kidney stones or earaches are in the same pain league with toothaches. To dentists, the presence of this pain signifies acute pulpitis, a condition from which the pulp will not recover. Severe relentless pain is the predominant feature of acute pulpitis. It usually arises spontaneously but may be initiated by thermal stimulation. Once it starts, the pain persists until treatment is performed. Sometimes patients report that their pain can be alleviated by application of cold (ice water). The usual explanation for this is that application of cold reduces intrapulpal swelling for a while. The affected tooth usually has a deep carious lesion or extensive restoration. However, sometimes acute pulpitis is not associated with dental caries bacterial infection but with a cracked tooth or trauma. If examined microscopically, pulps affected with acute pulpitis show features of acute inflammation including neutrophils and suppuration. Pulps with acute pulpitis will not recover. Given that reality, there are only two ways to treat it: tooth or pulp removal. In former days, tooth removal (extraction) was the treatment of choice. Extraction may be performed from time to time if the dentist determines that restoration of the tooth is impossible or beyond the patient’s financial means. More commonly the offending pulp is removed (pulp extirpation). This procedure removes the infection and establishes a pathway for the acute inflammatory response to drain (like incision and drainage). Cleansing and filling the root canals (i.e., endodontic therapy) as well as restoration of the crown follows pulp extirpation. Chronic Pulpitis A common condition affecting a tooth accompanied by dull, bearable pain; the chronic inflammation associated with it usually causes pulp death requiring pulp extirpation or tooth extraction. Not all toothaches have sharp, unbearable, relentless pain. Often, patients describe their pain as dull, throbbing, and intermittent. Such toothaches are usually diagnosed as “chronic pulpitis.” The overwhelming pain of acute pulpitis may replace sometimes-dull pain; that is, chronic pulpitis may become acute pulpitis. Usually, there is no event or circumstance that precipitates it, and the patient is able to cope with the pain for several days. It is not uncommon, however, for the pain to be more severe at night (when the patient lies down) an event that may precipitate a midnight call to the dentist. The offending tooth, like acute pulpitis, has a deep carious lesion or extensive restoration. Chronic inflammation associated with chronic pulpitis produces irreversible changes; it does not resolve. As a consequence, endodontic therapy or extraction is the only recourse. If endodontic therapy is pursued, it is usually not necessary to establish drainage before finishing the root canal filling (because there is no suppuration). Pulp Polyp (Chronic Hyperplastic Pulpitis) An uncommon condition affecting a carious tooth in a youngster in which a soft-tissue mass grows out of the affected pulp; there is usually little or no pain; often “pulp capping” successfully treats the tooth. Both acute and chronic pulpitis are irreversible—the pulp will not return to normal but, instead, dies. This vulnerability is caused by the limited blood supply to the pulp and the inability of the pulp to accommodate swelling. Root development isn’t completed, however, until some years after eruption. Therefore, the apical foramen is not constricted in youngster’s permanent teeth. The pulps of these incompletely formed teeth are large and are supplied with blood by a number of vessels entering it through a wide apical foramen

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(clinicians call this a “wide-open apical foramen” or “blunderbuss canal”). These young incompletely formed permanent teeth can withstand inflammation better than older fully formed ones. Pulps of young teeth can recover where pulps of older teeth die. Sometimes when dental caries extends into the pulp of a child’s permanent tooth, rather than causing acute or chronic pulpitis and subsequent pulp death, the pulp responds by undergoing hyperplasia instead—“chronic hyperplastic pulpitis.” Because of the extensive unconstricted blood supply afforded these young pulps, the ensuing inflammatory reaction causes no particular harm. A stratified squamous epithelial membrane covers the exposed pulp. The exposed covered pulp may grow out (hyperplasia) of the carious lesion into the oral cavity forming a “pulp polyp.” The source of the epithelial covering is debated. Some suggest that oral epithelial cells are “transplanted” on the exposed while others maintain that they arise by differentiation within the pulp. There is granulation tissue and chronic inflammatory cells (lymphocytes) in the underlying pulp. If the tooth is salvageable, removal of caries and the polyp followed by capping the exposed pulp with some nonirritating material will usually be successful. Endodontic therapy usually is not attempted because the apical foramen is too large for proper condensation of the endodontic filling material and complete pulp removal will destroy odontoblasts and stop root formation. If, on the other hand, the tooth is not salvageable, extraction is the usual alternative. Pulp Necrosis A common condition affecting a tooth in which the pulp has been killed by acute or chronic inflammation; usually there is a history of pain that has disappeared; because the pulp is dead, pulp extirpation or tooth extraction is necessary. Inflammation of fully formed “adult” teeth usually results in pulp death (pulp necrosis). Clinicians use the term “pulp necrosis” in reference to a tooth that once caused a toothache but subsequently became “asymptomatic.” This sequence is most commonly observed in patients who have coped with chronic pulpitis pain that subsides never to return. The affected tooth will have a large carious lesion or extensive restoration. The tooth will have no response to pulp testing. Microscopic examination of the pulp will reveal necrosis. Extraction or endodontic therapy is the two treatment procedures appropriate to pulp necrosis.

Periapical Inflammatory Diseases General Features of Periapical Diseases Dental caries first infects enamel, then dentin, and then the pulp. When dentin is invaded, bacteria and/or bacterial products can enter the pulp through empty dentinal tubules. Upon entering the pulp, an inflammatory reaction results that, in fully-formed teeth, causes pulpal death. From the pulp, inflammatory, necrotic, and bacterial products can enter the surrounding bone through the apical foramen. Structures surrounding the apex of tooth roots are known collectively as “periapical tissues” (peri- = around; -apical = the apex). These periapical tissues are comprised of periodontal ligaments and alveolar bone. Lesions produced by periapical infection are in close proximity to the apices of the teeth. Because periapical tissues are not visible they are recognized by their radiographic appearance and by their symptoms. Definition of Periapical Disease Periapical diseases are “inflammatory conditions occurring around the apex of a tooth caused by a necrotic pulp.” All of the lesions covered in this topic are inflammatory in origin and all are caused by necrotic pulps. The nomenclature of periapical diseases used to be hopelessly idiosyncratic. John Ingle, the author of a well known endodontic textbook, introduced designations used here. Ingle reasoned that because periapical inflammation involves two important components of the periodontium (periodontal ligament and alveolar process), the term “periodontitis” (peri- = around, -dont- = tooth, -itis = inflammation of) was appropriate. To differentiate this “periodontitis” from gingival periodontitis, Ingle proposed that periapical inflammation be called “apical periodontitis.”

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Etiology of Periapical Disease Most, but not all, pulpal diseases are caused by bacterial invasion from dental caries or, less commonly, cracked teeth. The remaining ones are caused by non-bacterial pulpal deaths caused, for example, by trauma. In these cases pulp necrosis itself causes an inflammatory response. Most, but not all periapical diseases, are caused by bacterial invasion of the periapical tissues. The remaining ones are caused pulp necrosis products not related to bacterial action. Clinical Features of Periapical Disease Being inflammatory in origin, periapical diseases manifest with the signs and symptoms of acute or chronic inflammation. However, there is no consistent relationship between patient’s symptoms (e.g., pain) and histologic findings. In the discussion that follows, it will be assumed the correlation is higher that is actually the case. Radiographic Features of Periapical Disease Most, but not all, periapical lesions destroy bone around the tooth apex resulting in radiolucent defects on radiographic examination of the area. Because it takes several days for enough bone destruction to produce a radiolucent lesion, the earliest periapical lesions may not be detected in a radiograph. The more long-lived ones will cause enough bone destruction to produce a radiolucency that can be easily detected in a radiograph. As will be seen, most periapical lesions are small (< 1.0 cm. in diameter) and wellcircumscribed. It is uncommon for these lesions to become large, to spread, or to break through the surrounding cortical bony plates.

Acute Inflammatory Periapical Diseases Acute Apical Periodontitis A common condition accompanied by excruciating pain, a necrotic pulp, and radiographic thickening of the apical periodontal ligament space; treatment requires pulp extirpation or tooth extraction. Excruciating pain is associated with acute pulpitis; it is also associated with extension of the acute inflammatory process into the periapical tissues creating “acute apical periodontitis.” While bacterial infection and necrotic pulps are responsible for the onset of most cases of acute apical periodontitis, it may also be a complication of initial endodontic therapy. In these cases, mechanical cleansing of the root canals force irritating debris into the periapical tissues initiating an acute inflammatory response there. Sudden onset and excruciating pain are the hallmarks of acute apical periodontitis. The patient may also sense that the affected tooth is higher than nearby ones. Often the pain is so diffuse that the patient cannot localize it. The dentist can usually locate the offending tooth by the crude but effective technique of tapping (percussion) on one tooth after another until the patient experiences pain. Extension of the acute inflammatory response into the periodontal ligament explains both tooth elevation and tapping-induced pain. Acute apical periodontitis arises so quickly, probably within an hour or two, that bone destruction and its resulting radiographic changes may not be evident. Sometimes, however, widened periodontal ligament around the apex may produce a radiolucent thickening there. Microscopic features include a localized acute inflammatory exudate with dilated capillaries, and neutrophils. Since the source of acute apical periodontitis is a necrotic pulp, it follows that pulp extirpation or extraction is the appropriate therapy for it. If the lesion resulted from endodontic therapy, the endodontist will usually re-open the canal to allow drainage or, if the canal filling has been completed, enter the periapical area surgically to debride the region. Antibiotics are commonly prescribed to reduce microbial activity. Apical Abscess A collection of purulent exudate at the apex of a nonvital tooth accompanied by pain and fever with potential discharge into the mouth; usually there is no periapical radiolucency; the condition requires pulp extirpation or tooth extraction, incision and drainage, and antibiotic therapy. Pain associated with acute apical periodontitis is sufficient to require the patient to seek dental care. It is also usually the case that the patient’s defenses are capable of localizing the infection to the periapical region.

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Occasionally, however, a particularly virulent microorganism is involved and/or the patient’s defenses are weak. In these cases the acute inflammatory reaction may form an abscess. The term “apical abscess” is used here; “dento-alveolar abscess” is a more common, but older, term. Necrotic pulps cause apical abscesses. Abscess formation suggests that the microorganisms responsible are virulent or the patient’s immunologic defenses are impaired. Apical abscesses are painful; however, they may not cause as much pain as acute pulpitis or acute apical periodontitis. Fever, leukocytosis1, and neutrophilia2, are commonly present. As the lesion enlarges, it may encounter and penetrate the buccal or lingual cortical plates expanding into the surrounding soft tissues. Such extension may include the floor of the mouth, the palate, the face, and the neck. Soft tissue extension will show the usual features of acute inflammation: redness, swelling, and warmth. Unless a dentist intervenes, the abscess will drain spontaneously exuding a purulent exudate. Apical abscesses, like acute apical periodontitis, arise so suddenly that there is little radiographic change. If the lesion has been present long enough, however, a faint, diffuse radiolucency may be evident. Abscesses are composed of an intense acute inflammatory reaction. In addition to the usual features of acute inflammation, immature neutrophils (“band cells”) are likely to be seen; dead and dying neutrophils and necrotic debris (i.e., suppuration) are also prominent. In the absence of significant radiographic changes, the dentist must rely on clinical features to arrive at a proper diagnosis (e.g., pain, systemic features, suppuration). Once the presence of an apical abscess is suspected, vigorous treatment must be pursued. First, the source of the acute inflammatory response is identified and eliminated. Second, a bacterial culture of the exudate is obtained and submitted to a laboratory to identify the offending microorganism and determine the antibiotic most effective in killing it (culture and sensitivity test). Finally, the dentist prescribes an antibiotic in sufficient dosage to kill the organism. If the abscess has spread into the surrounding soft tissues, an incision and drainage (I & D) should be performed. This procedure provides a source of exudate for culture and sensitivity testing, and removes suppuration so that repair will follow unhindered. Acute Osteomyelitis A microbial infection of bone marrow of the mandible (usually) accompanied by pain, fever, potential drainage of suppuration into the mouth, ill-defined radiolucencies and, sometimes, ill-defined radiopacities; treatment includes removal of cause, debridement, and vigorous antibiotic therapy. The main reason for treating apical abscesses with vigor is to prevent spread along the bone marrow spaces causing a condition known as osteomyelitis (osteo- = bone; -myel- = marrow, -itis = inflammation of). Osteomyelitis is a very serious condition that can cause destruction of large sections of the jaw and be difficult to manage. Osteomyelitis may be the inevitable result of untreated pulpal and/or periapical infection. Almost always, bacterial infection is involved. The offending microorganism may be a particularly virulent one that can cause an infection in a normal individual. More often these days, an impaired immunologic defense is responsible. Patients who have impaired immunologic defenses are said to be “immunocompromised.” There are a number of situations that produce immunocompromised patients. Some diseases (e.g., HIV infection) and some treatments (e.g., cancer chemotherapy) may produce immunocompromised patients. Osteomyelitis more commonly affects the mandible rather than the maxilla. Probably the maxilla’s excellent blood supply is the difference. There is usually malaise (discomfort), pain, fever, and leukocytosis. There may be swelling of the mandible and purulent drainage into the oral cavity. Because osteomyelitis takes longer to develop than other acute inflammatory lesions, usually there are significant and specific radiographic changes. These include involvement of bone away from the periapical region, indistinct outline (diffuse growth pattern) and combination of radiolucencies and radiopacities (mottled radiographic appearance). Microscopically in addition to acute inflammation, osteomyelitis shows bone destruction (osteoclasts) and bone deposition (osteoblasts) proceeding side-by-side. In fibrous connective tissue, inflammation and repair commonly occur simultaneously. So it is in bone: inflammation-induced bone 1. Increased numbers of white blood cells; increased wbc count. 2. Increased numbers of neutrophils; increased neutrophil count.

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resorption and bone repair (deposition) may proceed simultaneously. It is this reaction that produces the mottled radiographic features of osteomyelitis. Osteomyelitis is difficult to cure. It is for this reason, among others, that acute apical periodontitis and apical abscesses must be treated vigorously lest these common conditions progress to osteomyelitis. The offending microorganism must be identified, and antibiotic therapy instituted. Sometimes it may be necessary to remove segments of dead bone (sequestrum) in order to speed repair. It even may be necessary to place the patient in an oxygen-rich environment within a hyperbaric chamber to enhance antibiotic effectiveness and encourage repair. There are two reasons for the difficulty in treating osteomyelitis. First, the blood supply to the mandible is not as extensive as in other bones, a situation that reduces the effectiveness of antibiotic therapy. Second, osteomyelitis more commonly affects immunocompromised patients who are least capable of mounting an effective immunologic response to the infection.

Chronic Inflammatory Periapical Diseases The patient’s defenses usually are able to cope with an irritant by confining it to the periapical regions. If the source of the irritants is not removed, there will be continued exposure of the periapical tissues to it. If the initial inflammation was acute, as time goes by, it will become chronic. If the inflammation was chronic to begin with (i.e., chronic pulpitis), it will remain chronic. Occasionally, however, an area within a chronic inflammatory reaction will exacerbate (flare up) producing a focus of acute inflammation. So, because periapical chronic inflammation is long-lasting and because it is stimulated by continual irritation, there is more than one possible outcome. Chronic Apical Periodontitis A common condition usually without severe signs or symptoms recognized by a well-defined radiolucency at the apex of a nonvital tooth; its treatment requires endodontic therapy or tooth extraction. The fundamental lesion of chronic periapical inflammation is known as “chronic apical periodontitis.” While this designation is the preferred one, most dentists know it by the term “dental granuloma;” recently the term “periapical granuloma” has come into vogue. The lesion is not a granuloma at all because it is not composed of granulomatous chronic inflammation. Whatever it is called, the lesion is very common—at least it is commonly submitted to oral pathologists for microscopic examination. Endodontists remove these lesions by the thousands; most are submitted for microscopic examination. Chronic apical periodontitis (CAP) is caused by irritants entering periapical tissues from necrotic pulps. Sometimes the condition may arise from constant irritation from a faulty root canal filling. Whatever the source, the body is able to cope by localizing it in the periapical tissues. Being chronic inflammation, there are few signs or symptoms. There may be mild intermittent pain but there is no swelling or suppuration. The offending tooth will have a large carious lesion, a deep restoration, or a root canal filling and will be nonresponsive to pulp tests (is non-vital). On radiographic examination, there is a well-circumscribed radiolucency at the apex of the effected tooth. The radiolucent lesion is small (usually < 1.0 cm. in diameter). On microscopic examination, CAP is composed of chronic inflammatory cells: lymphocytes, plasma cells, macrophages, and fibroblasts/collagen. Sometimes the macrophages are the predominant cells, a feature that no doubt led to calling the lesion a “granuloma” (because macrophages are prominent in chronic granulomatous chronic inflammation). In addition to a chronic inflammatory exudate there may be epithelial cells as well. These are remnants of Hertwig’s epithelial root sheath which are found in virtually all periodontal ligaments. These epithelial remnants are known as the “epithelial rests of Malassez.” A few clumps of epithelial cells are often found amidst the chronic inflammatory exudate in CAP. Being the product of a necrotic pulp in a non-vital tooth, CAP must be treated by endodontic therapy or by tooth extraction. Condensing Osteitis (Chronic Focal Osteomyelitis) A fairly common condition usually without severe signs or symptoms recognized by a well-defined radiopacity at the apex of a nonvital tooth; therapy requires endodontic therapy or tooth extraction. Most of the time, periapical inflammatory lesions will result in localized bone destruction and its replacement with inflammatory tissue. In some individuals, however, these inflammatory lesions will result

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in bone deposition. When this happens a radiopacity appears on radiographic examination, a condition once called “condensing osteitis.” Some recent textbook authors reason that since this condition, after all, is an infection of bone, it qualifies as “chronic focal osteomyelitis.” Condensing osteitis is caused by the same irritants associated with other types of periapical inflammatory disease (e.g., necrotic pulps). The condition is observed more often in children and teenagers than in adults. Increased resistance and more abundant blood supply are the usual explanations of this distribution. There are no features that suggest condensing osteitis on intraoral examination. The tooth producing the lesion is non-vital and has deep caries, a deep restoration, or an inadequate root canal filling. The patient may have experienced pain in the past and may have some vague discomfort now; there are, however, no overt symptoms. The radiographic features are the most characteristic feature of condensing osteitis. The lesion is marked by a periapical radiopacity. The radiopacity is usually well circumscribed; it may be demarcated from the surrounding bone by a narrow radiolucent border. As might be expected, microscopic examination of this lesion reveals the presence of new bone intermixed with a fibrous connective tissue stroma in which chronic inflammatory cells reside. The treatment of condensing osteitis is the same as recommended for other inflammatory periapical lesions: extraction, or endodontic therapy. Once the associated non-vital tooth is removed or treated, the radiopaque lesion often remains behind. Since these remaining opacities are no longer infected, they can be left alone. Other Lesions Associated with Chronic Apical Periodontitis CAP is the basic manifestation of periapical chronic inflammation. This lesion is generally successful in isolating the causative agent to the periapical region. There are, however, circumstances where changes occur altering CAP’s clinical and/or microscopic appearance. Suppurative Apical Periodontitis A situation in which suppuration developing within chronic apical periodontitis (CAP) drains into the oral cavity. The apices of many teeth are very close (< 1 mm.) to the buccal and lingual cortical plates. The incisors and the cuspids are teeth with such relationships. Sometimes a small pocket of acute inflammation will arise within CAP that does not become an acute abscess. Because this pocket of acute inflammation produces a purulent exudate it is known as “suppurative apical periodontitis.” The transformation is recognized by drainage of a purulent exudate from tissues overlying the apex of a tooth. The exudate is transported through a channel lined by fibrous connective tissue and chronic inflammation, a passage known as a “fistula” or “fistulous track.” The surface drainage site is marked by a mound of granulation tissue known as a “parulis” or, as the public calls it, a “gum boil.” Management of this lesion is identical to other periapical inflammatory lesions. Apical Cyst A common lesion in which epithelial cells within chronic apical periodontitis are stimulated to line a central cavity forming a cyst. Islands of epithelial cells, the epithelial rests of Malassez, are found in many CAP lesions. If these are activated causing them to proliferate, an “apical cyst” develops. This transformation is important because cysts can become quite large, much larger than the basic lesion of CAP. The story of jaw cysts, including apical cysts, will be told in the next topic. Apical Scar A cicatrix forming in the periapical regions following removal of chronic apical periodontitis. It is recognized by the persistence of a well-defined radiolucency. It is common practice for endodontists treating non-vital teeth with radiolucent periapical lesions to perform a procedure that includes removal of the necrotic pulp, cleansing and enlarging the pulp canals, obliterating the canals with a filling material, and removing the periapical lesion. In the large majority of patients, the void created by lesion-removal will soon be filled with normal bone. In the remainder, the void fills with fibrous connective tissue producing a cicatrix (“apical scar”). There is no real problem with this except that a cicatrix within bone is radiolucent on radiographic examination. When this happens, the endodontist has a dilemma: Does the radiolucency indicate that a cicatrix has formed, or has the periapical chronic

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inflammatory lesion recurred due to failure of the root canal filling? There are two ways of proceeding: observe the lesion for signs of enlargement indicating that CAP has recurred or re-enter the periapical region removing the lesion and filling the apical foramen with amalgam (performing a “retrofill”).

References Kronfeld, Rudolph & Boyle, Paul: Histopathology of the Teeth and Their Surrounding Structures. Lea & Febiger, 1955. Shafer, W. G.: Textbook of Oral Pathology. W. B. Saunders, Fourth Edition, 1983.

Learning Guide 1.

After completion of this topic, the student should be able to • • • • • • • • • • • • • •

2.

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write and identify the terms listed in items 2 and 3 below. write and identify the differences in the lesions of smooth-surface and pit-and-fissure caries. write and identify the relationship between cemental caries and age. write and identify three factors that predispose dental pulps to necrosis. write and identify the two common ways nonvital teeth are treated. write and identify the relationship of acute pulpitis, chronic pulpitis, pulp hyperemia, and pulp polyp to the vitality of adjacent teeth. write and identify the differences in signs/symptoms between acute and chronic pulpitis. write and identify the most common cause of periapical diseases. write and identify the etiologic similarities and radiographic differences between chronic apical periodontitis and condensing osteitis. compare and identify the clinical appearance and sign/symptoms of chronic apical abscess and suppurative apical periodontitis. write and identify the radiographic features and patient susceptibility to osteomyelitis. compare and identify the sign/symptoms and radiographic features of acute apical periodontitis and chronic apical periodontitis compare and identify histologic features of apical abscess, chronic apical periodontitis, and condensing osteitis. write and identify the vitality of pulps in apical abscesses, suppurative apical periodontitis, condensing osteitis, and acute apical periodontitis.

Associate (by identifying them) the following prefixes/suffixes and their meanings. In other words, when confronted with these prefixes/suffixes, be able to pick the correct term/definition from a list (multiple choice or matching).

endo

within

retro

backward

myelo

bone marrow

scler

hard

peri

around

PTHL 312b: Oral and Maxillofacial Pathology

3.

Dental Caries, Inflammatory Pulp, and Periapical Diseases

Associate (by writing them) the following terms with their definitions or with clinical examples of them. In other words, when confronted with the definition or example of the following, be able to write, and correctly spell, the defined term. In addition, be able to recognize the context in which each exists. In addition be able to pick the correct term/definition from a list (multiple choice or matching).

Abscess

A localized collection of pus.

Cemental Caries

Caries affecting cementum exposed by gingival recession; usually occurs in the aged.

Culture and Sensitivity

Common laboratory test involving identification of microorganisms and determining the antibiotic most effective against it

Endodontic Therapy

Series of procedures including a) pulp removal, b) cleansing and enlargement of root canal, and c) obliteration of root canals with a filling material.

Gum Boil

The name by which the public knows a parulis.

Non-Vital

Absence of life; dead. A designation given a tooth that does not respond to pulp tests.

Parulis

A raised suppurating mucosal lesion through which a fistula ends.

Pit and Fissure Caries

Caries occurring in the grooves on the occlusal surfaces of teeth.

Smooth Surface Caries

Caries that occurs in the buccal, lingual, mesial, or distal surfaces of teeth

4.

Associate (by identifying them) the following terms and their definitions. In other words, when confronted with the term or definition of the following, be able to pick the correct term/definition from a list (multiple choice or matching).

Acidogenic Theory

A theory of caries pathogenesis suggesting that enamel calcification is caused by acid-producing bacteria.

Acute Apical Periodontitis

An acute inflammatory periapical condition characterized by excruciating pain.

Acute Pulpitis

A reaction to some injury resulting in acute pulpal inflammation and excruciating pain.

Apical Abscess

An abscess forming in the periapical tissues; characterized by acute inflammation and suppuration.

Apical Scar

A fibrous c.t. cicatrix within bone resulting from periapical surgery

Chronic Apical Periodontitis

A common periapical condition composed of chronic inflammation that is associated with a non-vital tooth

Chronic Hyperplastic Pulpitis

A reaction to deep caries in a young tooth in which an inflamed pulp extends through a large carious lesion.

Chronic Pulpitis

A reaction to some injury in which chronic inflammation appears in the pulp resulting in dull, intermittent pain.

Condensing Osteitis

A periapical lesion resulting from a necrotic tooth in which bone deposition, not bone resorption, results.

Dental Granuloma

Another name for chronic apical periodontitis

Dental Sclerosis

Another name for obliteration of dentinal tubules in the face of bacterial invasion.

Epithelial Rests of Malassez

Remnants of Hertwig’s sheath located in the periodontal ligament

Extraction

Removal of a tooth.

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Fistula

A connection between two surfaces; in the oral cavity, a pathway conducting pus to the mucosal surface.

Focal Reversible Pulpitis

Another, more scientific, name for pulp hyperemia.

Immunocompromised

A condition in which a patient’s defense against infection is compromised.

Irregular Dentin

Dentin rapidly produced by pulp against encroaching bacterial invasion; composed of irregularly-arranged dentinal tubules.

Leukocytosis

Elevation in the number of circulating white blood cells.

Mottled Radiographic Appearance

An appearance of a lesion on a radiograph that is composed of a mixture of radiolucencies and radiopacities

Neutrophilia

Elevation in the number of circulating neutrophils

Non-Vital

Absence of life; dead. A designation given a tooth that does not respond to pulp tests.

Osteomyelitis

A serious infection of bone marrow

Percussion

The act of tapping as an aid in diagnosis of hidden lesions.

Periapical Diseases

A group of inflammatory conditions that involve periapical tissues

Periapical Tissues

Tissues located around tooth apices: periodontal ligament + alveolar bone.

Proteolytic Theory

A theory of caries pathogenesis suggesting that enamel breakdown is initiated by destruction of protein found between enamel rods.

Pulp Extirpation

Removal of a pulp.

Pulp Hyperemia

A reaction to some irritant in which pulp blood vessels dilate increasing pressure in the pulp resulting in pain.

Pulp Polyp

Another, more common, name for chronic hyperplastic pulpitis; emphasizes the appearance of the pulp extending through the carious lesion.

Secondary Dentin

Another name for reparative dentin; also references normal deposition of dentin after root formation.

Suppurative Apical Periodontitis

A small suppurative acute inflammatory reaction arising in chronic apical periodontitis that drains onto the mucosal surface.

5.

Identify three anatomic features of the dental pulp that predisposes it to necrosis. 1.

Predispose pulps to necrosis

2. 3.

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Proteolytic Theory

By placing “Xs” in the empty cells, match the theories with the printed statements.: Acidogenic Theory

6.

Dental Caries, Inflammatory Pulp, and Periapical Diseases

Statements

Decalcification of enamel is first Enamel lamellae Willoughby Miller Plaque Pit and fissure caries Smooth surface caries 7.

What are two basic ways non-vital teeth are treated.

Non-vital teeth are treated by 8.

1. 2.

What is the most common cause of periapical diseases?.

Most periapical diseases are caused by:

Cemental caries

Smooth surface caries

By placing “Xs” in the empty cells, match the terms with the population that is most at risk.: Pit and fissure caries

9.

Statements

Elderly dentulous people Young Americans without fluoridation “Immune” populations Small area of dentin initially infected Large area of dentin initially infected Infected dentin rings the tooth

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Cemental Caries

Dentin Caries

Enamel Caries

10. By placing “Xs” in the empty cells, match the terms with the printed features.:

Statements

Circumferential invasion Accentuated lines of Retzius Rod dissolution Proceeds slowly Proceeds rapidly Bacteria inhabit detached Sharpey’s fiber “holes” Usually not detected on clinical examination Dentinal sclerosis and reparative dentin may slow down invasion

Chronic Pulpitis

Acute Pulpitis

Pulp Hyperemia

11. By placing “Xs” in the empty cells, match the terms with the printed features.:

Features

Dull pain intensifying at night Excruciating continual pain Transient pain to cold Lymphocytes Dilated blood vessels Neutrophils

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Dental Caries, Inflammatory Pulp, and Periapical Diseases

Periapical Diseases

Chronic Apical Periodontitis

Periapical Tissues

12. By placing “Xs” in the empty cells, match the terms with the printed features.:

Features

Infected pulps often the etiology Name given periapical inflammation Periodontal ligament + alveolar bone Cracked teeth may be a cause 13. What are the etiologic similarities and radiographic differences between chronic apical periodontitis and condensing osteitis?. Condition

Etiologic Similarities

Radiographic Differences

Chronic apical periodontitis Condensing osteitis

Non-Vital Tooth

Vital Tooth

14. By placing “Xs” in the empty cells, match the terms with the printed conditions.:

Condition

Acute apical periodontitis Apical abscess Suppurative apical periodontitis Condensing osteitis Chronic apical periodontitis Apical scar

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Condensing Osteitis

Suppurative Apical Periodontitis

Chronic Apical Periodontitis

Osteomyelitis

Apical Abscess

Acute Apical Periodontitis

15. By placing “Xs” in the empty cells, match the conditions with the printed features.:

Features

Localized collection of pus Mottled radiographic appearance Radiopacity at the apex of a non-vital tooth Also known as a “dental granuloma” Pain on percussion a common feature Pus conducted to surface through a fistulous tract Affected patients often immunocompromised Often associated with fever, leukocytosis, neutrophils Culture/sensitivity and I&D often performed Well-defined radiolucency at apex of a non-vital tooth Serious infection of the jaws A parulis (“gum boil” is present Widened pdl may be the only radiographic feature Proliferation of bone is a feature

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Condensing Osteitis

Apical Scar

Suppurative Apical Periodontitis

Chronic Apical Periodontitis

Osteomyelitis

Apical Abscess

Acute Apical Periodontitis

16. By placing “Xs” in the empty cells, match the conditions with the printed histologic features.:

Histologic Features

Acute inflammation Chronic inflammation Dead and dying neutrophils and necrotic debris Lymphocytes and new bone formation Dead bone is often present Macrophges often prominent Composed of dense fibrous c.t.

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Condensing Osteitis

Apical Abscess

Chronic Apical Periodontitis

Purulent Exudate

Chronic Inflammation

Acute Inflammation

17. By placing “Xs” in the empty cells, match the conditions with the printed fictitious histories.:

History

A 10 year-old female was brought to a dental office because she suddenly complained of severe pain. Examination revealed a carious maxillary central incisor and a nearby soft tissue swelling in the labial vestibule. Examination elicited severe pain, but soft pressure on the swelling produced a bad-smelling yellow fluid. A 53 year-old male came to his dentist with increasing pain in the mandibular molar region. Clinical examination revealed that the mandibular second molar had been restored with a full gold crown. Tapping on that tooth elicited pain. Radiographic examination revealed a radiolucent area around the apices of the mandibular second molar. Vitality testing proved the tooth to be nonvital. The lesion was surgically removed; the biopsy report stated that the lesion was “composed mainly of lymphocytes and macrophages. When viewing a routine panoramic radiograph of a 35 year-old female, her dentist noted a well-defined radiopacity near the apex of a mandibular first molar tooth that had undergone endodontic therapy some years before. The tooth was asymptomatic and root canal filling appeared to be adequate.

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