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Figure 1-10 A, Extraoral sinus tract opening on the skin in the central chin area. B, Radiograph of mandibular incisors and canine after root canal therapy.
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As with any dental examination, there should be a routine evaluation of the intraoral soft tissues. The gingiva and mucosa should be dried, either with an air syringe or a 2 × 2-in. gauze. By retracting the tongue and cheek, all of the soft tissue should be examined for any abnormalities in color or texture. Any raised lesions or ulcerations should be documented and, when necessary, evaluated with a biopsy or referral.52
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Intraoral swellings should be visualized and palpated to determine if they are diffuse or localized and if they are firm or fluctuant. These swellings may be present in the attached gingivae, alveolar mucosa, mucobuccal fold, palate, or sublingual. Other testing methods are required to determine if the etiology is endodontic, periodontic, or a combination of these two or is of nonodontogenic origin.
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Figure 1-11 ^ The healed opening of the extraoral sinus tract one month after root canal therapy was completed. Note the slight concavity of the skin in the area of the healed extraoral opening.
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Figure 1-12 Fluctuant swelling in anterior palate associated with periradicular disease from the lingual root of maxillary first premolar.
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Swelling in the anterior part of the palate (Fig. 1-12) is most frequently associated with an infection present at the apex of the maxillary lateral incisor or the palatal root of the maxillary first premolar. More than 50% of the maxillary lateral incisor root apices deviate toward the distal or palate. A swelling in the posterior palate (Fig. 1-13) is most likely associated with the palatal root of one of the maxillary molars.50,84
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Figure 1-13 Fluctuant swelling in posterior palate associated with periradicular disease from the lingual root of the maxillary first molar.
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Figure 1-14 Fluctuant swelling in mucobuccal fold associated with periradicular disease from the maxillary central incisor.
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Intraoral swelling present in the mucobuccal fold (Fig. 1-14) can result from an infection associated with the apex of the root of any maxillary tooth that exits the alveolar bone on the facial and is inferior to the muscle attachment present in that area of the maxilla. The same is true with the mandibular teeth if the root apices are superior to the level of the muscle attachments and the infection exits the bone on the facial. Intraoral swelling can also occur in the sublingual space if the infection from the root apex spreads to the lingual and exits the alveolar bone superior to the attachment for the mylohyoid muscle. The tongue will be elevated and the swelling will be bilateral because the sublingual space is contiguous with no midline separation. Severe infections involving the maxillary and mandibular molars can extend into the parapharyngeal space, resulting in intraoral swelling of the tonsillar and pharyngeal areas. This can be life threatening if the patient's airway becomes obstructed.50,84
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Occasionally a chronic endodontic infection will drain through an intraoral communication to the gingival surface known as a sinus tract. This pathway,6 which is sometimes lined with epithelium, extends directly from the source of the infection to a surface opening, or stoma, on the attached gingival surface. As previously described, it can also extend extraorally. The term fistula is often inappropriately used to describe this type of drainage. The fistula by definition is actually an abnormal communication between two internal organs or a pathway between two epithelium-lined surfaces.1
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Histologic studies have found that most sinus tracts are not lined with epithelium throughout their entire length. Harrison and Larson35 found only 1 of the 10 sinus tracts they studied were lined with epithelium. The other nine specimens were lined with granulation tissue. In a study with a larger sample size, Baumgartner et al6 found 20 of 30 specimens did not have epithelium that extended beyond the level of the surface mucosa rete ridges. The remaining ten specimens had some epithelium that extended from the oral mucosa surface to the periradicular lesion. The presence or absence of an epithelial lining does not seem to prevent closure of the tract as long as the source of the problem is properly diagnosed and adequately treated and the endodontic lesion has healed. Failure of a sinus tract to heal will necessitate further diagnostic procedures to determine if other etiologic factors are present or if a misdiagnosis occurred.
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Figure 1-15 A, To locate the source of an infection, the sinus tract can be traced by threading the stoma with a gutta percha point. B, The radiograph of the area shows an old root canal in the tooth #4, and a questionable radiolucent area associated with tooth #5, with no indication as of the etiology of the sinus tract. C, After tracing the sinus tract, the gutta percha is seen to be directed to the source of pathosis, the apex of tooth #5.
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Generally, a periapical infection that has an associated sinus tract is not painful, although often there is pain of varying magnitude prior to the sinus tract development. Besides providing a conduit for the release of infectious exudate and the subsequent relief of pain, the sinus tract can also provide a useful aid in determining the source of a given infection. Sometimes objective evidence as to the origin of an odontogenic infection is lacking. The stoma of the sinus tract may be located directly adjacent to or at a distant site from the infection. Tracing the sinus tract will provide objectivity in diagnosing the location of the problematic tooth. To trace the sinus tract, a size #25 gutta percha cone is threaded into the opening of the sinus tract. Although this may be slightly uncomfortable to the patient, the cone should be inserted until resistance is felt. After a periapical radiograph is exposed, the termination of the sinus tract is determined by following the path taken by the gutta percha cone (Fig 1-15). This will direct the clinician to which tooth is involved, and more specifically, which root of that tooth is the source of the pathosis. Once the causative factor of the sinus tract is removed, the stoma and the sinus tract will close within a few days.
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The stoma of intraoral sinus tracts may open in the alveolar mucosa, in the attached gingiva, or through the furcation or gingival crevice. They may exit through either the facial or lingual tissues depending upon the proximity of the root apices to the cortical bone. If the opening is in the gingival crevice, it is normally present as a very narrow defect in one or two isolated areas along the root surface. When a narrow defect is present, the differential diagnosis must include the opening of a periradicular endodontic lesion, a vertical root fracture, or the presence of a developmental groove on the root surface. This type of sinus tract can be differentiated from a primary periodontal lesion because the latter generally presents as a pocket with a very broad coronal opening and more generalized alveolar bone loss around the root. Other pulp testing methods will assist in verifying the etiology.34,83
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In the course of the soft tissue examination, the alveolar hard tissues should also be palpated. Emphasis should be placed on detecting any soft tissue swelling or boney expansion, especially noting how it compares with and relates to the adjacent and contralateral tissues. In addition to objective findings, the clinician should question the patient on any areas that feel unusually sensitive during this palpation part of the examination.
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Figure 1-16 Percussion testing of a tooth, using the back end of a mirror handle.
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Referring back to the patient's chief complaint may indicate how essential percussion testing can be. If the patient is experiencing acute sensitivity or pain upon mastication, this response can typically be duplicated by individually percussing the teeth, which often isolates the symptoms to a particular tooth. Pain to percussion does not indicate that the tooth is vital or nonvital, but is rather an indication of inflammation in the periodontal ligament (i.e., an acute periradicular periodontitis). This inflammation may be secondary to physical trauma, occlusal prematurities, periodontal disease, or the extension of pulpal disease into the periodontal ligament space. The indication of where the pain is coming from is interpreted by the mesencephalic nucleus, receiving its information from proprioceptive nerve receptors. Although subject to debate, the general belief is that there are few, if any, proprioceptors in the dental pulp; however, they are prevalent in the periodontal ligament spaces.15 This is why it may be difficult for the patient to discriminate the location of dental pain in the earlier stages of pathosis, when only the C-fibers are stimulated. Once the disease state extends into the periodontal ligament space, the pain may become more localized for the patient; therefore the affected tooth will be more identifiable with percussion and mastication testing.
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Before percussing any teeth, the clinician should tell the patient what will transpire during this test. Because the presence of acute symptoms may create anxiety and possibly alter the patient's response, properly preparing the patient will give more accurate results. The contralateral tooth should first be tested as a control, as well as several adjacent teeth that are certain to respond normally. The clinician should advise the patient that the sensation from this tooth is normal and ask to be advised of any tenderness or pain from subsequent teeth. The testing should initially be done gently, with light pressure being applied digitally with a gloved finger-tapping. If the patient cannot detect any significant difference between any of the teeth, the test should be repeated using the blunt end of an instrument, like the back end of a mirror handle (Fig. 1-16). The teeth should first be percussed occlusally, and if the patient discerns no difference, the test should be repeated, percussing the buccal and lingual aspects of the teeth. For any heightened responses, the test should be repeated as necessary to determine that it is accurate and reproducible, and the information should be documented.
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Figure 1-17 Mobility testing of a tooth, using the back ends of two mirror handles.
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Like percussion testing, an increase in tooth mobility is not an indication of pulp vitality. It is merely an indication of a compromise to the periodontal attachment apparatus. This compromise could be the result of acute or chronic physical trauma, occlusal trauma, parafunctional habits, periodontal disease, root fractures, rapid orthodontic movement, or the extension of pulpal disease, specifically an infection, into the periodontal ligament space. Often the mobility reverses to normal after the initiating factors are repaired or eliminated. Because determining mobility by simple finger pressure can be visually subjective, the back ends of two mirror handles should be used, one on the buccal aspect of the tooth, and one on the lingual aspect of the tooth (Fig. 1-17). The degree to which the tooth moves should be recorded as follows:
+1 mobility: the first distinguishable sign of movement greater than normal
+2 mobility: horizontal tooth movement no greater than 1 mm
+3 mobility: horizontal tooth movement greater than 1 mm, with or without the visualization of rotation or vertical depressability
Any mobility over +1 mobility should be considered abnormal. However, the teeth should be evaluated on the basis of how mobile they are relative to the adjacent and contralateral teeth.
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Periodontal probing is an important part of any intraoral diagnosis. The measurement of periodontal pocket depth is an indication of the depth of the gingival sulcus, which corresponds to the distance between the height of the free gingival margin and the height of the attachment apparatus below. Deep pocket depths indicate pathologic horizontal or vertical bone loss. Using a calibrated periodontal probe, the clinician should record the periodontal pocket depths on the mesial, middle, and distal aspects of both the buccal and lingual of the tooth, noting the depths in millimeters. The periodontal probe is "stepped" around the long axis of the tooth, progressing in 1-mm increments. Periodontal bone loss that is wide, as determined by a wide span of deep periodontal probings, is generally considered to be of periodontal etiology and is typically more generalized in other areas of the mouth. However, isolated areas of vertical bone loss may be of an endodontic etiology, specifically from a nonvital tooth whose infection has extended from the periapex to the gingival sulcus. Again, proper pulp testing is imperative, not just for the determination of a diagnosis but also for the development of an accurate prognosis assessment. For example, a periodontal pocket of endodontic origin may resolve after endodontic treatment, but if the tooth was originally vital with an associated deep periodontal pocket, endodontic treatment will not improve the periodontal condition. Additionally, as discussed elsewhere in this chapter, a vertical root fracture may often cause a localized narrow periodontal pocket that extends deep down the root surface. Characteristically, the adjacent periodontium is usually within normal limits.
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