Classification of Pulpal and Periradicular Pathoses
Diagnosis is defined as the “art of distinguishing one disease from another.” Diagnostic procedures in endodontics encompass a review of the medical and dental histories, clinical and radiographic examinations, and a battery of diagnostic tests. In order to interrelate the findings of these diagnostic procedures with an appropriate treatment modality, a classification system, which allows for the systematic grouping of endodontic pathoses on the basis of the diagnostic findings must be established. In addition, this classification system should use clinical terms that are suggestive of the disease process and serve as a means of communication between dental practitioners.
A tooth with a noninflamed pulp is asymptomatic and gives a positive response when stimulated with the electric pulp tester (EPT). This normal tooth will also respond positively when thermal tested with heat or cold. However, the response is mild and goes away immediately after the stimulus is removed. In addition, percussion will cause no discomfort and the radiograph will reveal no pulpal or periradicular pathosis. As a result of caries, restorative procedures, or trauma, the normal pulp may become inflamed and present itself clinically as either a reversible or irreversible pulpitis.
A review of the dental history reveals that the patient is experiencing an intermittent, exaggerated response to a stimulus such as cold or hot. However, the discomfort does not linger after the stimulus is removed. The following diagnostic findings are present: clinical and radiographic exams – restoration and/or caries associated with the involved tooth and the periodontal ligament (PDL) space is WNL; EPT – positive response; thermal tests – nonlingering, exaggerated response to cold and/or hot; percussion – no unusual sensitivity. If the etiology of the inflammation is identified and corrected, the pulp will return to a normal state and the symptoms will disappear. However, if the inflammation continues, localized areas of tissue necrosis will occur which can progress to an irreversible pulpitis.
Irreversible pulpitis may be either symptomatic or asymptomatic. With symptomatic irreversible pulpitis, the patient presents with spontaneous pain and/or an exaggerated response to hot or cold, which lingers when the stimulus is removed. Because the pulp does not contain proprioceptive nerve fibers, patients will have a difficult time localizing the origin of their pain. Thus, referred pain should be considered during the diagnostic workup. The following diagnostic findings are present: clinical and radiographic exams – extensive restoration and/or caries may be associated with the involved tooth, and the PDL space may/may not be widened; EPT – positive response; thermal tests – exaggerated response which lingers after the stimulus is removed; percussion – may/may not elicit a painful response. In some cases of irreversible pulpitis, cold actually alleviates the pain, and the patient might present with a glass of ice water. This finding should then be used as a diagnostic test to determine the etiology of the pain. If the inflammatory exudate causing the increase intrapulpal pressure and resultant moderate to severe pain escapes from the surrounding dentin via a carious exposure or loss of restoration, the irreversible pulpitis may become asymptomatic. In addition, internal resportion and hyperplastic pulpitis (pulp polyp) are examples of asymptomatic irreversible pulpitis.
A circumferential spread of the inflammation will eventually result in either partial or total necrosis of the pulp tissue. If it is partial, the tooth may exhibit some of the signs and symptoms of irreversible pulpitis. Teeth with total pulpal necrosis are usually asymptomatic unless the periradicular area is involved.
Eventually, the pulpal inflammation will spread through the apical foramen into the periradicular tissue. In fact, periradicular inflammation usually occurs before total necrosis of the pulp has taken place. The response in the periradicular area may be symptomatic (acute) or asymptomatic (chronic).
Acute Periradicular Periodontitis (APP)
Acute periradicular periodontitis may be either primary or secondary. Primary APP is due to an extension of the pulpal disease into the periradicular area or occlusal trauma, while secondary APP is iatrogenic in origin; e.g. overextension of endodontic instruments or obturating materials. In either case, the patient presents with a tooth, which is extremely tender to occlusion or pressure. If resulting from an extension of the pulpal lesion, the tooth may also exhibit the signs and symptoms of irreversible pulpitis. The one diagnostic sign, which is pathognomonic of a tooth with APP, is an extreme response to percussion. In addition, the periradicular area may be tender to palpation.
Acute Periradicular Abscess (APA)
If large numbers of bacteria from the infected pulp tissue gain entry into the periradicular tissue and the patient’s immune system is not able to combat the invasion, the patient will present with the signs and symptoms of an acute periradicular abscess. Clinically, the patient presents with swelling and mild to severe pain. Depending on the relationship of the apices of the involved tooth to the muscular attachments, the swelling may be localized to the vestibule or extend into a facial space. In addition, the patient may exhibit systemic manifestations such as fever, chills, lymphadenopathy, headache and nausea. Since the reaction to the infection occurs very quickly, the involved tooth may/may not show radiographic evidence of a widened PDL space. However, in most cases, the tooth will elicit a positive response to percussion, and the periradicular area will be tender to palpation.
Chronic Periradicular Periodontitis (CPP)
If the immune system is able to combat the influx o bacteria, a low-grade long-standing lesion forms in the periradicular area. As long as the irritants keep emanating from the root canal system, the soft tissue lesion keeps expanding at the expense of the surrounding bone. Clinically, the CPP is asymptomatic and is detected only radiographically by a small or large periradicular radiolucency, which is either well circumscribed or diffuse. Thus, this lesion is often detected during a routine examination, and the patient is surprised that it is present. Histologically, a CPP takes the form of a granuloma or cyst; a diagnosis which can be made only microscopically not radiographically.
Chronic Suppurative Periodontitis (CSP)
If the periradicular lesion establishes drainage by breaking through the cortical plate into the oral cavity, a diagnosis of chronic suppurative periodontitis is made. Clinically, the patient presents with a sinus tract, which can be traced with a gutta-percha point to determine its source radiographically. The patient is usually asymptomatic because the sinus tract allows for drainage of any purulent exudate forming in the periradicular area. The radiographic exam usually reveals a periradicular radiolucency associated with the involved tooth, while the”vitality”, percussion and palpation tests render no response.
A phoenix abscess is an acute exacerbation of a chronic periradicular periodontitis resulting from an increase in the virulence of the bacteria in the lesion and/or a decrease in the patient’s resistance. The patient exhibits the same signs and symptoms of an acute periradicular abscess except the radiographic exam reveals a periradicular radiolucency associated with the involved tooth.
Chronic Periradicular Periodontitis with Symptoms
Radiographically, this pathosis is the same as CPP; a radiolucent lesion is present. However, instead of being asymptomatic, the patient presents with symptoms such as pain to biting or pressure. It is imperative that these cases receive timely endodontic therapy because they have the potential of evolving into a phoenix abscess.
Before initiating endodontic therapy, it is imperative that the clinician determines the etiology of the patient’s chief complaint. In order to do this, a thorough diagnostic workup must be performed and both a pulpal and periradicular diagnosis made and entered into the patient’s treatment record. This clinical update presented a classification system of these diagnoses.
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