Chapter 4
Problem Solving in the Differential Diagnosis of Bony Defects Resulting from Pulpal and Periodontal Pathosis Problem-Solving List Problem-solving challenges and dilemmas that deal with the differential diagnosis of bone defects resulting from pulpal and periodontal pathosis addressed in this chapter: Controversies and Highlights of Disease Interactions An Endodontic Perspective on Chronic Periodontitis Periodontal Lesions of Bone that Can Be Confused With Pulpally Induced Bony Lesions
I have never found a pulp removed from a pyorrhetic tooth to be normal . . . where a pathologic pulp is present, a pyorrhetic condition cannot be cured by treatment applied exclusively to the external surface of the root, with no treatment of the pulp itself.12 L.R. Cahn, 1927
Acute periodontal abscess Lesions of chronic periodontitis Periodontal lesions involving the furcation Lesions associated with aggressive forms of periodontitis External root resorption Cemental tears Pulpally Induced Lesions that Can Be Confused With Periodontal Lesions Furcation or lateral lesions without loss of attachment Acute periapical abscess
Interradicular periodontal lesions can be initiated and perpetuated by inflamed or necrotic pulps. Extension of the inflammatory lesions from the dental pulp apparently occurs through accessory or lateral canals situated in the furcation regions of premolars and molars.45 S. Seltzer, I.B. Bender, H. Nazimov, 1967
Chronic sinus tracts of pulpal origin with drainage through the gingival sulcus Chronic sinus tracts of pulpal origin with permanent periodontal attachment loss Response of the periodontium to mechanical root perforations Bony Lesions of the Periodontium that Do Not Originate from Either Periodontal or Pulpal Pathosis Deep coronal fractures Vertical root fractures Developmental lingual groove on maxillary lateral incisors and similar lesions Other possible rare lesions
The relationship of disease processes coming from the pulp of the tooth to the supporting periodontium is a subject that has received much attention in endodontic literature for almost 90 years.10,12,18 The reverse situation has also been controversial: the impact of periodontal pathosis on the dental pulp.* Clinically, two important issues must be kept in focus. Pulpal pathosis and its extension into the periodontium causes a localized periodontitis with the potential for further extension into the oral cavity.26 Periodontal pathosis and its extension have little short-term effect on the dental pulp.26 However, the long-term effect of periodontal *References 15, 21, 28, 37, 46, 60, and 63.
70
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 71
pathosis, especially in conjunction with concomitant restorative procedures, must be considered in all diagnostic and treatment planning considerations.
Controversies and Highlights of Disease Interactions Pulp tissue degenerates after a multitude of insults—caries, restorative procedures, chemical and thermal insults, trauma, and some periodontal treatment. When products from pulp degeneration, in particular inflammatory exudates and bacteria, reach the supporting periodontium, many changes may occur, including a rapid onset of inflammation, lateral or furcation bone loss, tooth mobility, and sinus tract formation through the buccal mucosa or gingival sulcus. If this occurs in the apical region, a periapical lesion forms (see Chapter 3). If this occurs with crestal extension of the inflammation, a periodontitis of pulpal origin is formed.49 However, the lesion formed has little anatomic similarity to a defect of periodontal pathosis. Periodontal disease is generally a slow-developing process that may have a gradual atrophic effect on the dental pulp. Complete pulpal necrosis caused by periodontal pathosis, however, is uncommon. Changes in the pulp include chronic inflammation, localized tissue death (infarction), fibrosis, decrease in cellular populations, resorptions, local coagulation necrosis, or dystrophic calcification.32,43,46,50 Periodontal procedures such as deep scaling and curettage54 (with the use of localized medicaments) and gingival injury or wounding53 may enhance further pulpal inflammation and perpetuate the interrelated disease process in a small number of cases. The most intimate and demonstrable relationship of the communication of inflammation between the two tissues is via the vascular system,9,20,31,54 as demonstrated anatomically at the apical foramen and adjacent to aberrant accessory communications.11,18,25,36,43 These channels, when patent, may serve as potential routes of inflammatory interchange. Still other channels, covered by cementum, may be exposed during scaling or other periodontal therapeutic procedures.54 To what extent these vascular communications must be disrupted to cause a resultant overwhelming inflammatory process is unknown and a major concern.32 The main anatomic pathways must be considered as potential pathways in the exchange of inflammatory products and bacteria between the pulp and the periodontium (and vice versa) and include lateral/accessory canals that branch off the main root canal, open dentinal tubules (sometimes due to cemental agenesis), the presence of lingual grooves, removal of cementum during periodontal or restorative procedures or loss due to resorptive defects, and root or tooth fractures. For intact teeth, the principle avenues of communication would be the main foramen, lateral/accessory canals, and dentinal tubules. In the clinical setting, however, there are few means to determine that these particular avenues of communication are actively involved in the exchange of
inflammatory substances and/or bacteria. For our purposes, the pathophysiologic relationships that exist between the pulp and periodontium are less important than an accurate diagnosis or one based on the best clinical evidence available on clinical problems and lesions that present on a daily basis. In general, inflammation or bone loss in the periodontium caused by lesions of pulpal origin will heal following a wide range of endodontic treatments. These types of cases are seen as a radiolucent lesion around the root apex, in an isolated furcation that has no other etiology, or on the lateral surface of a root. Specific periodontal treatment in these cases is rarely if ever warranted. The vast majority of lesions of the periodontium do not affect the dental pulp. The incidence of cases in which a connection between a lesion of pulpal origin and one of periodontal pathosis is even suspected is small.27,42 This chapter has three objectives: (1) to clarify the most important diagnostic characteristics of lesions of the periodontium, with emphasis on those that resemble the extension of pulpal pathosis to the supporting root tissues; (2) to clarify the distinguishing diagnostic characteristics of periradicular lesions of pulpal origin that resemble or are mistaken for periodontal defects; and (3) to discuss the characteristics of lesions that are the result of neither inflammation/ infection of the pulp or periodontium, yet may share characteristics of both. Treatment suggestions will accompany the lesions described.
An Endodontic Perspective on Chronic Periodontitis The etiology and pathophysiology of chronic periodontitis is extremely complex. Briefly summarized, lesions of the disease are the result of microbiologic and immunologic effects of a biofilm that forms on the surfaces of roots.4,35,62 Fortunately, an accurate clinical diagnosis of periodontitis can usually be made on the basis of physical examination35 and radiographic findings of bone destruction.39 The clinical characteristic of this disease may be summarized as a “top-down” process, meaning simply that it begins with inflammation of the marginal periodontium and progresses apically with the gradual destruction of the crestal supporting bone (Fig. 4-1, A and B). For the dentist/endodontist, the periodontal probe is absolutely indispensable to clinical diagnosis. During assessment of the periodontium, measurement of attachment loss is the standard by which progression or remission of the disease is assessed.62 Within the discipline of endodontics, the discrimination between periodontal lesions and those originating from the dental pulp can usually be made by identifying the physical characteristics of the lesion itself.27,28 The technique of diagnostic periodontal probing should be done using a relatively small-diameter instrument (0.05 mm at the tip) with standard markings (Fig. 4-2).62 Probing should be done with as uniform a pressure as possible, slightly angling the tip of the probe toward the surface of the root.30
72 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
A
B
FIGURE 4-1 A, Typical radiographic presentation of periodontal bone loss on mesial of mandibular first molar. B, 5 years later, bone loss has progressed to a deeper level.
FIGURE 4-2 Periodontal probes with small-diameter tips are preferable.
FIGURE 4-3 Surgical exposure of advanced lesion of chronic
The normal periodontium is known to have fairly predictable dimensions.23 The average distance from the gingival margin to crestal bone has been found to be approximately 2.5 mm. Increased probing depths represent the loss of periodontal attachment to the tooth and crestal bone. Since chronic periodontitis is usually generalized, osseous defects are typically found in multiple areas of the dentition, particularly in the posterior sextants. This can be an important finding in the diagnosis of potential endodontic problems. In the diagnosis of a localized defect of unknown origin, begin the diagnostic examination by probing multiple random locations throughout the dentition.27 Findings of osseous defects in several locations well apart from the area of chief concern would tend to support a tentative diagnosis of periodontitis for the area in question. In contrast, random probings that reveal no indication of periodontal bone loss in any other area would suggest a possible nonperiodontal etiology for the localized defect being evaluated. Traditionally in routine periodontal examinations, probing depths have been recorded in six locations for each tooth: the mesial, midsurface, and distal of both the buccal and lingual surfaces.4 For the purposes of endodontic diagnoses and the
differentiation of lesions of pulpal origin from periodontal lesions, probings in the area of principle concern should be performed circumferentially on each tooth in small (1-mm) increments. The intent is to explore the physical morphology or bony architecture of a lesion. There is a distinction between “probing” the attachment levels and “sounding” the location of the crestal bone.27 In the technique of sounding, the probe is inserted past the level of attachment directly to bone. This is a more accurate method of assessment but will usually require some level of local anesthesia. Generally, probing will yield adequate diagnostic information, especially in combination with radiographs. Osseous defects resulting from chronic periodontitis are routinely found to be of varying depth but similar in form. Probing circumferentially across a broad root surface will usually indicate a gradual increase in depth until the deepest area of the defect is reached. Continuing past this point, the probing depths will then gradually decrease. The typical contours of crestal bone found in bony lesions of advanced periodontitis are illustrated in Fig. 4-3. Note the general increase in root exposure from mesial to distal, which would be reflected as a gradually increasing probing depth on a clinical examination.
periodontitis. Note altered contours of the crestal bone.
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 73
Periodontal Lesions of Bone that Can Be Confused With Pulpally Induced Bony Lesions Bony lesions of periodontal disease are usually not difficult to distinguish from bony lesions of pulpal origin. Periodontal defects begin in the marginal periodontium, and even deep periodontal pockets are usually far removed from the root apex (Fig. 4-4). Confusion in diagnosis usually arises in cases of acute periodontal abscess, periodontal infection causing chronic sinus tracts in the mucosa, or localized periodontal bony lesions extending deep enough to involve the apex of a tooth. The severity of periodontal bone destruction, however, varies in the same dentition. At times it may be quite localized and extend to the root apices. The following discussion of pathologic entities will include diagnostic procedures necessary to (1) arrive at the best diagnosis based on the gathered information and (2) determine the appropriate treatment plan.
is immediately apparent: there is loss of crestal bone interproximally, indicating a lesion of periodontitis as opposed to one of pulpal origin. There is no radiolucency at the apices. Since it is possible to have an acute periapical abscess without obvious or significant radiographic evidence of a periapical
A
Acute Periodontal Abscess An acute periodontal abscess is clinically identical to many acute periapical abscesses of pulpal origin. The patient may experience severe swelling (Fig. 4-5, A) along with the usual symptoms of acute infection such as pain, fever, and malaise. The location of swelling near the gingival margin is common to both types (see Fig. 4-5, B). Diagnostic procedures usually begin with a good radiograph. In this case (see Fig. 4-5, C ), significant information B
FIGURE 4-4 Lesions of advanced chronic periodontitis with
severe bone loss do not generally involve the apex, as seen on the second molar. Lesion on first molar is endodontic, with a drainage tract coursing coronal and exiting near the furcation. Circumferential probings of first molar reflect a level of attachment consistent with bone levels seen on radiograph and do not involve the furcation. Prognosis for root canal treatment of first molar and long-term tooth retention is good. Second molar is hopeless periodontally, regardless of pulpal status.
C
FIGURE 4-5 A, Acute facial swelling associated with periodontal abscess is identical to the swelling of acute periapical abscess. B, Clinical view of same acute periodontal abscess. C, Radiograph of periodontally involved teeth. Note bone loss between molars and lack of periapical involvement.
74 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
or lateral lesion, the next step in diagnosis is sensibility testing. In this case, all of the maxillary right posterior teeth respond normally to thermal and electrical sensibility tests. This finding eliminates the possibility of a pulpal etiology. The diagnosis of acute periodontal abscess is confirmed by signs, symptoms, and periodontal probings. Treatment planning will be based on probing depths. Probings that are found to confirm attachment loss to the level of the apical third would support tooth extraction as the treatment of choice. Probings to the level of the midroot might favor periodontal surgery to reduce or eliminate pocket depth.
Lesions of Chronic Periodontitis Bony lesions of chronic periodontitis are sometimes confused with lesions of pulpal origin because of a draining sinus tract. In Fig. 4-6, the patient was referred for endodontic evaluation because of the drainage tract in the attached gingiva over the left central incisor (arrow). In a similar case (Fig. 4-7), probings are consistent with a deep periodontal lesion. The radiograph clearly shows no apical rarefaction on either of the central incisors (see Fig. 4-7, D), and sensibility tests elicit normal responses. Surgical exposure illustrates the morphology of the defect (see Fig. 4-7, E). Contrast these cases with the endodontic case presented in Fig. 4-8. Clinically, the sinus tracts appear nearly identical (see Fig. 4-8, A; also see Fig. 4-6), but surgical exposure of the tooth reveals not only the periapical lesion but also intact crestal bone (see Fig. 4-8, B).
CLINICAL PROBLEM Problem: A 52-year-old male was seen for recurrent local swelling and drainage in the area of the maxillary right second premolar. Clinical examination revealed a draining sinus tract in the attached gingiva near the second premolar. A radiograph indicated that there was a widened apical periodontal ligament space consistent with a developing periapical lesion in addition to a deep periodontal defect interproximally on the distal (Fig. 4-9, A). At this point, the origin of the sinus tract was unknown.
Solution: Sensibility testing was performed. No responses were obtained from the second premolar, and the first molar previously had root canal treatment. A sinus tract exploration was done by placing a gutta-percha cone in the tract and exposing an additional radiograph (see Fig. 4-9, B). This examination indicated that the drainage was of periodontal origin. No communication between the two lesions was evident on the film, and none was found during probing. The diagnosis was concomitant periodontal and periapical lesions.6 Both root canal treatment and periodontal treatment will be required to resolve the infections in this case (see Fig. 4-9, C).
Although there may be ample evidence of a general chronic periodontitis in the oral cavity, some localized areas may have developed extremely severe bone destruction. If periodontal defects extend to the apex, the radiographic lesion present
FIGURE 4-6 Sinus tract of periodontal etiology found in attached gingiva over maxillary left central incisor.
may be confused with a periapical lesion of pulpal origin. The patient in Fig. 4-10 was sent for completion of root canal treatment on a second premolar. Note the endodontic access cavity in the crown of this tooth. The loss of bone radiographically correlated with the loss of attachment circumferentially by clinical probing. The extreme mobility of this tooth was another consequence of bone loss. A root canal procedure would have no effect on this condition, so the tooth was extracted.
CLINICAL PROBLEM Problem: A 57-year-old male with a history of recurrent swelling on the palatal aspect of the maxillary left first molar was referred for root canal treatment. The referring dentist noted a large periapical lesion encompassing the apex of the palatal root (Fig. 4-11, A). The radiograph also shows evidence of severe bone loss around the buccal roots that was not noted by the dentist. The molar had no restorations, and there was no evidence of a fracture in the crown.
Solution: Sensibility tests should be performed early in the examination. In this case, results were normal—in fact, the tooth was hypersensitive to a cold stimulus. Periodontal probings indicated that there was bone loss to the apex of the palatal root and confirmed severe attachment loss around the other two roots. As in the previous case, root canal treatment would have no effect on this problem, so the tooth was extracted. In these cases, calculus deposits are commonly seen covering the entire root surface (see Fig. 4-11, B).
Occasionally a periodontal bone lesion may resemble a periapical lesion and, at least radiographically, lack other obvious signs of generalized periodontitis.26 At the close of Chapter 3, an excellent example was depicted in Fig. 3-60. What appears to be a typical periapical lesion of pulpal origin is in reality a lesion of severe periodontitis. Once again, root canal treatment would have been of no benefit in this case.
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 75
A
B
C
D
E
FIGURE 4-7 A, Periodontal probing depth normal interproximally. B, Probing depth normal in midlabial area. C, Deep probing pattern associated with periodontal bone loss. D, Radiograph of same lesion. Note absence of periapical involvement. E, Surgical exposure of periodontal lesion.
CLINICAL PROBLEM Problem: A 38-year-old male presented with a history of recurrent acute abscesses in the buccal vestibule adjacent to the maxillary left first molar. The radiograph showed a “classic” periapical lesion on the apex of the mesial buccal root (Fig. 4-12, A). The lesion was noted to extend coronally along both the mesial and distal surfaces of the root. Solution: Sensibility tests indicated normal responses on this tooth, confirming that this is not a pulpal problem. Periodontal
Periodontal Lesions Involving the Furcation Loss of bone in the furcation of a molar due to periodontal disease is sometimes difficult to distinguish from bone loss
probing revealed complete loss of attachment over the entire buccal surface of the root (see Fig. 4-12, B). Large deposits of calculus were seen and felt on the root surface with the probe. The diagnosis of periodontal abscess was made. Since there was minimal periodontal involvement of the other two roots, the optimal treatment plan was to resect (amputate) the mesial buccal root; pulp exposure resulting from the amputation would necessitate root canal treatment on the remaining roots.
due to a necrotic pulp (communication via furcation canals)25 or a sinus tract that is traced to the furcation. As cited earlier, the periodontal probe may reveal a sometimes subtle distinguishing difference. Periodontal defects tend to affect the space in the furcation more or less symmetrically, whereas
76 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
A
B
FIGURE 4-8 A, Sinus tract similar to Fig. 4-6 but of pulpal etiology. B, Surgical exposure of apical lesion. Note normal crestal bone contours.
A
B
C
FIGURE 4-9 A, Maxillary right premolar area with history of recurrent drainage suspected to be of pulpal origin. There is both apical and periodontal pathosis evident on the second premolar. B, Sinus tract exploration with gutta-percha cone, revealing source of drainage is the periodontal lesion. C, Completed root canal treatment will only resolve the periapical lesion. Periodontal surgery is also indicated to eliminate the pocket. This will resolve both associated infection and the drainage tract.
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 77
A
FIGURE 4-10 Localized lesion of advanced chronic periodontitis. Note tooth has been opened for root canal treatment that will have no effect on this lesion.
B
FIGURE 4-12 A, Maxillary left first molar with a “classic” periapical lesion on mesial buccal root. B, Clinical examination reveals periodontal etiology. Sensibility test results are normal. A
B
FIGURE 4-11 A, Radiograph of maxillary left first molar area with apical lesion of chronic periodontitis. Pulp test results are completely normal. B, Following extraction. Note calculus deposits covering entire palatal root.
sinus tracts tend to align with one root and more directly with a lesion at the apex. Therefore periodontal defects will tend to probe both vertically (parallel to the root) and horizontally (buccal-lingually, parallel to the occlusal plane). Sinus tracts of pulp origin tend to probe in a vertical direction only, but in some cases the tract may take a tortuous path, depending on the nature of the bone around the tooth, so straight probes will be of less value in the differential
diagnosis of a lesion of this type. This emphasizes the need to have both straight and curved probes (Nabers or Cattoni probes, Hu-Friedy Co., Chicago, IL, USA). The furcation defect in Fig. 4-13, A was suspected to be the result of inadequate root canal treatment of the mesial buccal root. Periodontal probings indicated there were deep vertical and horizontal components to the defect. Surgical exploration showed the extent of the bone loss (see Fig. 4-13, B). The entire furcation was devoid of bone in addition to loss of the buccal plate covering the buccal roots, which accounted for the preoperative probing patterns. The diagnosis of advanced periodontitis was confirmed, and the tooth was extracted.
Lesions Associated With Aggressive Forms of Periodontitis Aggressive periodontitis in young people, once known as juvenile periodontitis, affects less than 1% of the population.4 This disease process is now associated with a specific pathogen, Aggregatibacter actinomycetemcomitans (formerly Actinobacillus).24 This pathogen has also been found to be dominant in some global environments,19 and therefore may be used as a specific diagnostic marker for the disease. However, studies have also indicated that other global populations may have different markers, such as Treponema lecithinolyticum40 or inflammatory cells and serum globulins that may be associated with the degree of periodontal destruction.47
78 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
A
B
FIGURE 4-13 A, Furcation lesion in bone, suspected to be the
result of extension of pulp pathosis into periodontium. B, Surgical exposure confirms the diagnosis of chronic periodontitis.
Owing to the diagnostic confusion with an acute periapical abscess and the rarity of periodontal pathosis in children, a necrotic pulp with a periapical lesion is sometimes suspected as the cause of this disease. The case depicted in Fig. 4-14 illustrates a bony lesion in a 12-year-old female who was referred for root canal treatment of the maxillary right first molar. After confirming the presence of a normal pulp with sensibility tests, the patient was referred for a periodontal consultation.
External Root Resorption External root resorption that occurs in the marginal periodontium is often confused with internal resorption of the root. Internal resorption is a pathologic process of pulpal origin.22,44,58,61 External resorption infrequently involves pulp.22 Root canal treatment may or may not affect this problem but is often necessary because of pulp exposure or near exposure during repair of the defect (Fig. 4-15).22 A more detailed discussion of resorption is found in Chapters 3, 13, 18, and 19.
Cemental Tears A cemental tear is a rare periodontal condition often associated with a root-treated tooth.57,59 This condition appears
A
B
FIGURE 4-14 A, Deep periodontal defect discovered on a 12-year-old patient. B, Radiograph of same lesion. Diagnosis is aggressive periodontitis.
CLINICAL PROBLEM Problem: A 64-year-old male was referred for evaluation of the maxillary left central incisor. His chief complaint was recurrent swelling and drainage in the roof of his mouth adjacent to the tooth. The periapical film showed previous root canal treatment and a periapical lesion (Fig. 4-16, A). The patient related that the treatment was done at least 35 years ago. A small radiolucency was also apparent in the coronal half of the root. Clinical examination confirmed tenderness to palpation in the midapical region on the facial aspect of the tooth. Circumferential probing indicated no bony defects, but a subgingival defect on the mesial palatal aspect of the root was identified.
Solution: Treatment options included periradicular surgery (see Chapter 18) with repair of the resorption defect or extraction. Removal of the sectional silver cone in the root canal was judged to be impossible. In evaluating the tooth for surgery, the size of the silver cone suggested that apical removal would also be impossible without severe reduction in the length of the root. At the same time, preparation of the resected root apex for a root-end filling would also be difficult with the silver cone in place. The lingual angulation of the long axis of the tooth placed the resorption defect in a very difficult location for repair. Extraction was elected as the treatment of choice (see Fig. 4-16, B).
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 79
A
B
C
FIGURE 4-15 A, Lesion of external resorption in marginal periodontium, resembling internal resorption. B, Probings suggest a periodontal defect. C, Surgical exposure confirms diagnosis of external resorption that arises in the periodontium.
A
B
FIGURE 4-16 A, Maxillary left central incisor with recurrent periapical pathosis and a palatal draining tract. B, Following extraction, external resorption lesion is seen on the palatal surface.
80 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
clinically as a periodontal infection with rapid loss of attachment. Although the etiology is unknown, there is a higher incidence in the elderly.59 At time of surgery, small segments of the cementum are often observed to have fractured away from the surface of the root. The literature has a number of case reports with some success in treatment outcomes, but
the level of evidence for the best way to manage these cases is less than ideal.57,59
CLINICAL PROBLEM Problem: Root canal treatment was completed on a mandibular right lateral incisor for an 85-year-old male. There was no indication of periodontal pathosis at the time of treatment. The patient was seen 18 months later for evaluation of a local swelling associated with the same tooth. Periodontal probings revealed a 7-mm localized periodontal defect on the distal aspect of the tooth; all other probing depths were within normal limits. The presumptive diagnosis was a recurrent periapical lesion due to inadequate root canal treatment or a vertical root fracture. A periapical radiograph showed a radiolucency on the distal aspect of the root, extending from the apex to crestal bone level (Fig. 4-17, A).
A
Solution: Exploratory surgery revealed a cemental tear on the labial surface of the root (see Fig. 4-17, B). Fragments of separated cementum were found attached to the elevated tissue and removed. The area of cemental separation was lightly recontoured with a composite finishing bur to remove the irregular margins of the tear, and the root surface was treated with citric acid for 30 seconds to enhance reattachment of the periodontal ligament fibers. After rinsing, the tissue was repositioned and sutured. Reevaluation at 6 months (see Fig. 4-17, C) indicated that probing depth had returned to normal.
Pulpally Induced Lesions that Can Be Confused With Periodontal Lesions B
There are also periapical lesions of pulpal origin that share clinical and radiographic features with lesions of periodontal origin. Most periapical lesions arise in the bone adjacent to the apical foramen, and there is usually no radiographic confusion with lesions of periodontitis (Fig. 4-18). Diagnosis on the basis of radiographic findings alone can be misleading, however, if a periapical lesion or evidence of a sinus tract should extend to the alveolar crest (Fig. 4-19; see Chapters 2 and 3).
Furcation or Lateral Lesions Without Loss of Attachment C
FIGURE 4-17 A, Radiograph of a mandibular right lateral
incisor 1 1 2 years after root canal treatment. Clinically there was local swelling and a periodontal defect in this location. Preoperatively, there had been no evidence of periodontal pathosis. B, Surgical exposure of defect, revealing cemental tear. Note margins of cemental defect on root surface. C, Six months post treatment, indicating normal probings.
Periapical (periradicular) lesions can become quite large and approach crestal bone. Radiographically, the appearance is similar to periodontal lesions with advanced bone loss, particularly because of the loss of crestal or furcation bone (Fig. 4-20, A). Careful circumferential probing will often indicate that there is no loss of attachment in the sulcus. Clearly, a normal probing pattern rules out a periodontal etiology for the lesion. Root canal treatment alone is usually effective to bring about resolution of the radiolucency (see Fig. 4-20, B).
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 81
FIGURE 4-18 Typical periapical lesion of pulpal etiology.
A
FIGURE 4-19 Typical periapical lesion of pulpal etiology with a draining sinus tract along the distal root surface. There was no periodontal disease.
B
FIGURE 4-20 A, Mandibular right first molar with large radiolucent lesion. Bone loss appears to extend from distal interproximal
crest to apex, but clinically there was no break in the sulcular attachment. B, Reevaluation at 15 months, indicating healing of periapical lesion and restoration of interproximal bony architecture.
A
B
FIGURE 4-21 A, Mandibular left first molar with radiographic evidence of furcation and lateral bone loss. There were two draining tracts in the attached gingiva but probings were normal. B, One year reevaluation, indicating complete healing. Some teeth with periodontal attachment and bone loss will develop large periapical lesions that may appear radiographically to merge with the periodontal bone loss (Fig. 4-21, A). These lesions have been identified by many as perio-endo lesions.6,48,63 Once again, however, periodontal
probing is the key to diagnosis. In this case, there is definite loss of bone from periodontitis. Nevertheless, circumferential probings identified a normal sulcus depth in the interproximal space, with no break in the attachment. This cannot be a so-called perio-endo lesion in the absence of the
82 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
periodontal disease component communicating with a lesion of pulpal origin. Root canal treatment was completed and a 1-year reexamination demonstrates healing of the interproximal crest of bone as well as the periapical lesion itself (see Fig. 4-21, B).
Acute Periapical Abscess Some acute periapical abscesses of pulpal origin will cause localized swelling of the marginal gingiva (Fig. 4-22, A). Additionally, probings may reveal a break in the attachment, and it is not unusual to observe purulent drainage around the probe tip during oral examination. Probings will also quickly rule out a periodontal etiology if no other defects are found. Routine endodontic examination should include sensibility tests. In the case of acutely abscessed teeth, the pulp is invariably necrotic, as was explained in Chapter 1. A radiograph most often will indicate the presence of a periapical radiolucency. Once the diagnosis is established, the tooth is customarily opened for root canal treatment (see Chapter 15), although in some cases an incision and drainage may also be indicated. The most important difference between acute periapical and periodontal abscesses is that attachment loss in the endodontic cases will be recovered, often within 1 week (see Fig. 4-22, B). Probings will return to normal in
the affected site once the infection heals and the drainage ceases. There are rarely any residual defects.
Chronic Sinus Tracts of Pulpal Origin With Drainage Through the Gingival Sulcus Seldom are sinus tracts of pulpal origin mistaken for periodontal lesions when they appear on the surface of the mucosa.27,28 Confusion arises most often when the tract exits through the gingival sulcus. Fig. 4-23, A illustrates a maxillary left first molar with an acute swelling on the mesial palatal surface. Probings identified a possible periodontal etiology, and the patient was referred to a periodontist for
A
A B
B
FIGURE 4-22 A, Local swelling secondary to acute periapical abscess. A narrow defect into the furcation was probed. B, One week following routine endodontic emergency procedures, swelling had subsided, and reattachment in the furcation had occurred.
C
FIGURE 4-23 A, Local swelling on mesial palatal surface of maxillary left first molar, which was presumed to be periodontal. B, Sectioned periodontal probe in the defect. C, Surgical exposure confirms diagnosis of a sinus tract of pulpal origin.
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 83
evaluation. Probings were essentially normal except for a narrow tract in the area of the swelling. The periodontist did a sinus tract exploration using a sectioned periodontal probe (see Fig. 4-23, B). The tissue was reflected in the area, and a sinus tract was observed to be a small defect without a change in the general contour of the bone (see Fig. 4-23, C ). This image illustrates the bone contours that characterize a “sinus tract–type probing” pattern.27,28 The probing depths along root surfaces with these defects are usually within normal limits until the defect is encountered. The probing depth at this point will precipitously become very deep as the probe enters the tract. Continuing circumferentially, the probing depth will just as precipitously return to normal. Root canal treatment of the molar was subsequently completed and the sinus tract healed uneventfully.
A
CLINICAL PROBLEM Problem: An 18-year-old female college student presented for evaluation of the maxillary right molar area. She related a history of recurrent soreness, local swelling, and a foul taste in the area between the first and second molars. Her family dentist had placed a large temporary restoration in the second molar just before she left for school (Fig. 4-24, A). Probings in the area identified a narrow sinus tract–type probing interproximally on the palatal side. A periapical film with a periodontal probe in the tract indicated the source of the drainage was a large periradicular lesion encompassing the apices of both the first and second molars (see Fig. 4-24, B). Sensibility testing showed that the pulp in the second molar was necrotic, but the first molar responded normally.
B
FIGURE 4-24 A, Maxillary right molar area with a history of symptoms. Probing indicates a narrow sinus tract on the distal-palatal surface. The sulcus depth was normal in all other areas. B, Radiograph indicating probe extending to the large periapical lesion through a sulcular drainage tract.
Solution: Evaluation of the periodontal status revealed a normal, healthy periodontium throughout the dentition. This was consistent with the crestal bone levels on the periapical film. Furthermore, osseous defects of advanced periodontitis would be extremely rare in an 18-year-old individual, so a periodontal etiology was ruled out. The periapical lesion was large and draining through the gingival sulcus. Root canal treatment of the second molar resulted in closure of the sinus tract in 2 weeks.
Chronic Sinus Tracts of Pulpal Origin with Permanent Periodontal Attachment Loss Some periapical lesions that drain through the sulcus can become periodontal lesions as well. In addition to bacteria, biofilm and calculus can form on the root surfaces,1 within sinus tracts, and even on the apices of roots in chronically draining periapical lesions (Fig. 4-25). Fig. 4-26 illustrates the case of a 24-year-old male with no clinical signs of periodontal pathosis. His chief complaint was a local swelling on the vestibular side of the mandibular right first molar
FIGURE 4-25 Calculus on apex of a root with history of chronic drainage from a periapical lesion of pulpal origin.
84 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
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FIGURE 4-26 A, Radiograph indicating furcation bone loss. Normal bone levels around adjacent teeth. There was no evidence of
chronic periodontitis. B, Probing indicating horizontal bone loss. Even though the defect is due to chronic drainage from a periapical lesion of pulpal origin, the prognosis for healing in the furcation is guarded.
that had been present for several months. The periapical radiograph showed no evidence of infrabony defects from periodontitis, but a large periapical radiolucency was present on the first molar and extended into the furcation (see Fig. 4-26, A). Clinically, probings confirmed both vertical and horizontal bone loss in the furcation (see Fig. 4-26, B). The outcome of root canal treatment in these cases is uncertain. Many cases will regain attachment after débridement of the root canal, but some will not. See Chapter 1, Fig. 1-13 for review of a case that healed satisfactorily in less than 1 month. If reattachment has not occurred approximately 1 month after treatment, it is not likely to occur at all. The prognosis for such a tooth is poor, so complete root canal treatment is not advisable until a prognosis has been established. The treatment of choice would be access to the chamber, canal débridement, and closure with calcium
CLINICAL PROBLEM Problem: A 70-year-old male was seen for a chief complaint of recurrent swelling and drainage on the buccal of the mandibular left lateral incisor The periapical film made at the examination showed a periapical radiolucency on the apex of the lateral incisor (Fig. 4-27, A). Sensibility tests indicated a nonvital lateral incisor. Periodontal probings indicated that there was a narrow drainage tract on the labial surface of the root (see Fig. 4-27, B). Root canal treatment was started and the canal was sealed with calcium hydroxide. One month later, the tooth was reevaluated. The patient felt better and was optimistic about retaining the tooth. The tissue color had improved, but probings revealed no change in the sinus tract.
Solution: The chance for reattachment after 1 month in treatment is very poor. The prognosis was hopeless, so the tooth was recommended for extraction.
hydroxide.34,38,51 Some authors and investigators would recommend using a combination of 2% chlorhexidine along with the calcium hydroxide for better bacterial control.5 The completion of root canal procedures would be indicated as soon as reattachment is observed, which can occur in as few as 10 days.
Response of the Periodontium to Mechanical Root Perforations Mechanical perforations into the periodontium that may occur during root canal procedures result in one of two types of periodontal lesions. Those found below the level of the attachment have characteristics similar to radicular abscesses that occur adjacent to a lateral canal in the presence of necrotic pulp abscesses. Those that occur in the marginal periodontium have characteristics of periodontal pockets. The prognosis of treatment for each is comparable; lesions have a much better prognosis for complete healing if the attachment is not involved.2 As a general rule, if a perforation occurs during root canal procedures, immediate repair is very important to prevent contamination of the periradicular tissues by bacteria or materials/solutions used in root canal treatment.3 Many materials have been used for sealing a perforation, with mineral trioxide aggregate (MTA) the most contemporary and possibly the most favorable for healing.13,41 Zinc oxide eugenol has also been used with some degree of success, but materials will be of no value if the site becomes infected. The case presented in Fig. 4-28 illustrates that if the periodontal attachment is normal preoperatively, attachment will most likely return following surgical repair. During surgery, the attachment area of the root surface should not be curetted. This case also illustrates the general observation that small perforations have a better outcome than large ones. Location is also important in assessing prognosis. Lateral perforations on broad accessible root surfaces have a better
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 85
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FIGURE 4-27 A, Periapical lesion of pulpal etiology. Pulp tests indicated pulpal necrosis. B, Probings confirm chronic draining tract through gingival sulcus. Root canal débridement was performed and the tooth closed with calcium hydroxide for monitoring. One month later, probings were unchanged. If healing has not occurred in this time interval, it is unlikely to occur at all. Extraction was recomended.
CLINICAL PROBLEM Problem: A 40-year-old female requested endodontic consultation for a local swelling in the gingiva over the maxillary right canine (Fig. 4-28, A). She related a history of a recent emergency visit to a dentist while on vacation in a distant city. The tooth felt better after the emergency treatment, but upon returning from the trip, the labial gingiva over the tooth became very sore to touch. In the last 3 days, the swelling appeared. Clinical examination confirmed that an endodontic access was made on the palatal aspect of the crown and was sealed with a temporary restoration. A periapical film showed a very generous access cavity. Periodontal probing depths were normal, so a diagnosis of perforation during access to the root canal was considered the most likely problem.
Solution: The mucoperiosteal tissues were elevated, and a small perforation was located. Without enlarging the orifice of the perforation, the defect was cleaned with an ultrasonic endodontic file and sealed with MTA (see Fig. 4-28, B). The elevated tissue was repositioned and stabilized with a sling suture. The root canal treatment was completed (see Fig. 4-28, C), and a photograph was made at an 8-month (see Fig. 4-28, D) reexamination appointment, at which time periodontal probings were normal.
prognosis for healing after repair than those on inaccessible surfaces or in the furcations (Fig. 4-29). Perforations can occur below the periodontal attachment. Strip-type perforations may occur during intracanal cleaning and shaping and during post space preparation (Figs. 4-30 and 4-31). Especially with misdirected post preparations,
severe defects in both tooth and bone can occur (Fig. 4-32). These types of perforations are very difficult to manage successfully because of inaccessibility and the presence of metal in the perforation defect. If repair is attempted, it is usually best if the post can be removed first to avoid the necessity of trying to cut back the metal during surgery in preparation for the repair material. Perforations into the periodontal attachment are disastrous events which cause irreversible damage to the crestal bone (Fig. 4-33). Regardless of the repair material, recovery of a more coronal attachment level is highly unlikely. In this sense, the lesion must be treatment planned for pocket elimination or extraction. Aesthetics will also be a major factor in the anterior teeth.
CLINICAL PROBLEM Problem: A 70-year-old male was examined for a complaint of chronic soreness in the facial gingiva of the maxillary left lateral incisor. The periapical image confirmed that a perforation during post space preparation had occurred (Fig. 4-34).
Solution: The mucoperiosteal tissues were elevated over the area, revealing a large perforation and severe localized interproximal bone loss. The perforation was repaired, and the tissue was positioned apically to eliminate the pocket as much as possible. The patient was advised that the area is likely to heal with a large space between the incisors due to lack of crestal bone support for the papilla.
86 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
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FIGURE 4-28 A, Localized swelling in attached gingiva over maxillary right canine which had been opened for endodontic treatment one month earlier. B, Surgical exposure of perforation. Note interruption of crestal bone, yet preoperative probings were normal. Surgical repair was completed with mineral trioxide aggregate (MTA without enlargement of perforation defect). C, Root canal treatment completed after surgical repair. D, Eight-month reexamination, indicating complete healing.
FIGURE 4-29 Perforation during access cavity preparation into the furcation with associated periodontal breakdown.
FIGURE 4-30 Strip perforation in the course of canal shaping.
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 87
FIGURE 4-31 Strip perforation resulting from intraradicular post placement.
FIGURE 4-34 Radiograph of lateral perforation into marginal periodontium post space preparation. The post was not protruding through the perforation defect. Surgical repair of perforation defect was possible but periodontal defect was irreparable.
FIGURE 4-32 Misdirected post preparation resulting in extension of post into lateral periodontium.
Bony Lesions of the Peridontium that Do Not Originate from Either Periodontal or Pulpal Pathosis The following lesions have similarities to pulpal and periodontal lesions described in the two previous sections but have entirely unrelated etiologies.
Deep Coronal Fractures
FIGURE 4-33 Access perforation into marginal periodontium. Without realizing the error, the clinician completed root canal treatment; result was acute periodontal abscess. Remedial root canal and periodontal treatment failed to improve severe periodontal defect, and tooth was extracted.
The subject of coronal fractures is discussed as an etiology of pulpal pathosis in Chapter 1. Most coronal fractures in teeth with pulpal symptoms are found to extend to the level of the pulp chamber and no farther. Root canal treatment followed by full coronal coverage provides an excellent long-term prognosis, the latter treatment depending on the age of the patient. Unfortunately at present, technology does not exist to measure the depth of a coronal fracture preoperatively. Since most fractures develop in a mesial-distal plane, they are not evident on two-dimensional radiographs. Cone-beam computed tomography (CBCT) may serve as an excellent tool in these situations (see Chapter 3). Clinically, fractures can usually be confirmed by visual examination (Fig. 4-35) and transillumination (Fig. 4-36), but the depth and direction cannot be determined with any reliability. If the fracture is
88 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
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FIGURE 4-35 Clinical examination of fracture line with an explorer.
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FIGURE 4-36 Transillumination of fractured tooth. The transmission of light stops at the fracture line. relatively new and deep enough to extend into the periodontal attachment, there may be slight to no initial changes in the probing depth. One useful early indication is increased tenderness to probing in the location of the fracture compared to other areas around the tooth. In some cases, coronal fractures are often deep enough to result in mobility of the coronal segments. Mobility is a good clue to the severity of depth and also the likely direction of the fracture line. If a fractured cusp is highly mobile while the remainder of the tooth is firm, the fracture is likely to be oblique with respect to the long axis of the tooth and not extend very far below the free gingival margin. These fractured segments are held only by gingival attachment. Crown lengthening can often make such teeth restorable (Fig. 4-37; see Chapter 17). A fractured molar is seen in Fig. 4-38. Separation in the fracture line is possible with an instrument, but neither segment is very mobile. This is a grave sign in terms of prognosis. The fracture most likely extends deep and parallel to
C
FIGURE 4-37 A, Oblique coronal fracture of maxillary left
canine. B, Fractured crown showing angle and extent of fracture. C, Following crown lengthening, tooth is again restorable.
the long axis of the tooth. Severe periodontal destruction is inevitable along the fracture lines. Fig. 4-39 illustrates a case of a tooth with a deep cuspal fracture that presents as an acute periodontal abscess. The swelling on the buccal is an extension of the infection that originated in the periodontium along the fracture line. Periodontal complications can present a serious diagnostic dilemma with recent fractures, because signs and symptoms of periodontal involvement are often lacking. As a consequence, some teeth are restored but later develop the periodontal sequelae, and extraction is the unfortunate outcome. Deep coronal fractures in maxillary molars may follow a different course and extend into the furcation. Clinical examination will usually identify the fracture, but there are seldom any significant radiographic changes. The effect is to divide
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 89
A
FIGURE 4-38 Mandibular left first molar with deep, unrestorable coronal fracture. Both coronal halves exhibit only slight mobility. B
CLINICAL PROBLEM Problem: A 50-year-old male complained of acute cold sensitivity in the maxillary right premolar area. He could not chew comfortably, and clinical examination revealed a mesial-distal fracture line through the crown of the second premolar. There was no mobility of either half of the crown. Sensibility tests confirmed the presence of an irreversible pulpitis. Root canal treatment was completed, followed by placement of a full crown. Five months later, the patient returned with the complaint of drainage around the tooth and occasional episodes of swelling in the area. Clinical examination showed draining tracts on both vestibular and palatal surfaces but probings on these surfaces were normal. Interproximal probings, however, identified deep narrow defects on both the mesial and the distal surfaces (Fig. 4-40, A), The periapical radiograph confirmed deep periodontal defects interproximally (see Fig 4-40, B).
Solution: The diagnosis of deep coronal fracture was made, and the tooth was extracted. Postoperative examination confirmed the presence of fracture lines on both mesial and distal surfaces (see Fig. 4-40, C and D). These locations were consistent with a coronal fracture rather than a vertical root fracture (discussed in the following section). A possible treatment plan for coronal fractures without periodontal signs of deep extension would be placement of circumferential protection (e.g., an orthodontic band), removal of occlusal contact, and observing for 1 to 2 months. If no signs of periodontal destruction appear, the tooth could be assumed to be restorable. When multiple sinus tracts are present on an individual tooth, there is a high likelihood of the tooth being fractured, whether a deep coronal fracture or a vertical root fracture.52, As this case illustrates, placement of a full crown over a tooth with a deep coronal fracture will not prevent periodontal deterioration and eventual extraction.
C
FIGURE 4-39 A, Mandibular right first molar presenting with acute periodontal abscess. B, Occlusal view. Note fracture lines on distal and lingual. C, Fracture of distal-lingual cusp was quite mobile, indicating that fracture may not be very deep.
the tooth in half buccal-lingually (Fig. 4-41). The patient will typically present with an acute abscess in the furcation that will probe normally on the buccal and palatal surfaces. Interproximal probings will reveal a loss of attachment and bone in the furcation.
Vertical Root Fractures A vertical fracture of the root is a much different entity than vertical fracture of the crown, though the etiology of both may be the same.7,8,17 Generally, vertical root fractures tend to develop from the apex and extend coronally (Fig. 4-42). The clinical presentation is a sinus tract–type periodontal probing pattern that surfaces in the specific areas where the fractures occur, namely the midbuccal or midlingual/palatal
90 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
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FIGURE 4-40 A, Probing on the mesial demonstrates deep, narrow defect, indicating periodontal defect. Distal has similar defect but probings on the buccal and palatal surfaces were normal. B, Radiograph indicating periodontal bone loss on mesial and distal surfaces, extending to midroot level. C, Mesial view of extracted tooth, showing fracture line extending from crown to midroot level. D, Distal view of tooth, showing fracture line to same level.
A
B
FIGURE 4-41 A, Clinical view of maxillary right second molar with obvious mesial-distal fracture. B, Extracted tooth, demonstrating that fracture extended directly into furcation and divided tooth in half.
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 91
FIGURE 4-42 Surgical exposure of typical vertical root
FIGURE 4-44 Unusual vertical root fracture on endodontically untreated tooth.
fracture.
in a study of Chinese teeth,14 the occurrence of such fractures generally is rare (Fig. 4-44).7
CLINICAL PROBLEM Problem: A 72-year-old male presented with low-grade
FIGURE 4-43 Vertical root fractures can be caused by excessive spreader pressures during lateral compaction. Extrusion of sealer and gutta-percha document that this occurred during this procedure.
surfaces of teeth or individual roots. Signs and symptoms include percussion tenderness and local palpation tenderness or swelling of the overlying soft tissues similar to a periodontal abscess.17 In contrast to deep coronal fractures, vertical root fractures tend to occur in the buccal-lingual plane.17 Most are found to involve only one surface of the root, but if the fracture extends completely through the root, fracture lines will be found on both buccal and lingual. When this occurs, two sinus tracts may be noted.56 Fractures of this type can be induced by excessive pressures with a spreader during lateral compaction of gutta-percha (Fig. 4-43; see Chapter 12).26 However, with present-day shaping techniques that have better divergent canal preparations, this occurrence is minimal. The etiology of the majority of vertical root fractures is not well understood, but two of the most common denominators seem apparent: previous root canal treatment and evidence of heavy occlusal forces. Except for a reported high incidence of vertical root fractures in untreated teeth found
discomfort in a mandibular central incisor. The discomfort had been vague for 2 or 3 months but now was more focused on this particular tooth. He reports having seen pus coming from around the tooth when he pushed on the gum tissue. Clinical examination revealed a small sinus tract at the mucogingival junction overlying the severely worn mandibular right central incisor. The tooth was slightly tender to percussion and definitely tender to palpation. A radiograph revealed a previously root-treated tooth with a large radiolucency (Fig. 4-45, A). Two canals were obturated in the tooth, and the quality of the root canal treatment appeared adequate. The initial impression gave a tentative diagnosis of endodontic failure.
Solution: A tentative diagnosis of subacute suppurative periapical periodontitis was appropriate, since the tooth had an apical lesion following root canal treatment, and purulence was present. Incremental circumferential probing was performed and normal sulcus depths found on the mesial and distal line angles (see Fig. 4-45, B and C). Probing between these points indicated a deep, narrow sinus tract–type defect that was pathognomonic of a vertical fracture (see Fig. 4-45, D), and extraction was the treatment of choice. This case emphasizes the use of probing to assess teeth that appear to have failed root canal treatment.
It is uncommon for vertical root fractures to be visible on radiographs. Many fractured roots have no radiographic signs of pathosis at all (Fig. 4-46). This is not surprising, considering the minimal osseous breakdown of a narrow drainage tract as compared to a typical periodontal defect. Since most fractures occur on the buccal or lingual surfaces, bone loss would also be obscured by the root itself. Infrequently, the fractured segments may separate, and the fracture may become radiographically apparent (Fig. 4-47).
92 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
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FIGURE 4-45 A, Radiograph indicating previous root canal treatment and periapical lesion on a mandibular central incisor. B, Normal probing depth on mesial-labial line angle. C, Normal probing on distal-labial line angle. D, Sinus tract–type probing diagnostic for vertical root fracture in this location.
As described in the preceding chapter, the most common diagnostic radiographic finding is a widened periodontal ligament space extending from the apex of the fractured root to crestal bone (Fig. 4-48, A).17 The dimension or actual radiographic width may vary and it may be observed on one proximal surface or both (see Fig. 4-48, B ). Chronic lesions in the periodontium from root fractures can reach significant dimensions and resemble primary periodontal lesions (Fig. 4-49). The diagnostic distinctions will be in the results of probings. Periodontal lesions will tend to probe deeply with a wide base in a circumferential pattern, whereas bone loss associated with vertical fractures will probe deeply on buccal and/or lingual surfaces only. Unfortunately, there is no remedy for a vertical root fracture. On single-rooted teeth, extraction is indicated. On multirooted teeth, root resection (amputation) is a possibility (see Chapter 18).
Developmental Lingual Groove on Maxillary Lateral Incisors and Similar Lesions The maxillary lateral incisor will occasionally develop with a groove on the lingual surface of the root.32,33 Although the periodontal status may remain normal for many years, the groove appears susceptible to periodontal breakdown.29 Patients eventually experience signs and symptoms of either acute or chronic periodontal abscess (Fig. 4-50, A), and the defect probes much like a sinus tract (see Fig. 4-50, B). The periapical film in this case demonstrates the groove (see Fig. 4-50, C and D). There is no treatment; extraction is indicated. The same phenomenon can occur on molars with fused roots.16,55 The most typical presentation is on the buccal surface of mandibular second molars, but the phenomenon
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 93
A
FIGURE 4-47 Vertical fracture line at apex of maxillary canine. Visible fractures on radiographs are unusual. B
C
FIGURE 4-46 A, Fracture of mesial buccal root without typical radiographic signs of pathosis. B, Probings reveal fracture defect. C, Surgical exposure of defect.
is possible on any multirooted tooth with this anatomic variation. Fusion of the roots sometimes creates a groove similar to the lingual developmental groove of the lateral incisor.16 Once again, a deep, narrow periodontal defect will be found on the midbuccal surface. Most teeth with these defects will respond normally to pulp tests. Prognosis is poor and dependent on the success of any possible periodontal treatment. When these fusions occur in mandibular molars or premolars, usually a C-shaped canal is present internally.16,55
Other Possible Rare Lesions After traumatic injury, some maxillary incisors will be found to have a deep probing defect in the palatal sulcus. This is
A
B
FIGURE 4-48 A, A widened periodontal ligament space
identifying vertical root fracture. In this case the radiographic sign may be slight but extends the full length of the root. B, Widened periodontal ligament space occasionally seen on both sides of root.
94 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects
FIGURE 4-49 Mandibular left molar with severe bone loss related to longstanding vertical root fracture.
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FIGURE 4-50 A, Sinus tract on labial surface of maxillary lateral incisor. B, Circumferential probings are normal except in the
location of the lingual developmental groove. C, Groove evident on radiographic image of tooth. D, Lingual groove demonstrated on an extracted tooth (arrows).
chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 95
the direct result of luxation and will generally close spontaneously without treatment. Periodontal defects associated with enamel pearls are generally found in the furcation areas of molars. Rarely they will cause periodontal breakdown but could present as an acute abscess. Probings are similar to periodontal pockets. Once again, prognosis for the tooth will depend on the possibility of periodontal treatment. References 1. Adriaens PA, De Boever JA, Loesche WJ: Bacterial invasion in root cementum and radicular dentin of periodontally diseased teeth in humans. A reservoir of periodontopathogenic bacteria, J Periodontol 59:222-230, 1988. 2. Albaricci MF, de Toldeo BE, Zuza EP, et al: Prevalence and features of palate-radicular grooves: an in vitro study, J Int Acad Periodontol 10:2-5, 2008. 3. Alhadainy HA: Root perforations. A review of the literature, Oral Surg Oral Med Oral Pathol 78:368-374, 1994. 4. Axelsson P: Diagnosis and risk prediction of periodontal diseases, Chicago, 2002, Quintessence Pub Co. 5. Basrani B, Ghanem A, Tjäderhane L: Physical and chemical properties of chlorhexidine and calcium hydroxide-containing medications, J Endod 30:413-417, 2004. 6. Belk CE, Gutmann JL: Perspectives, controversies and directives on pulpal-periodontal relationships, Can Dent J Assoc 56:10131017, 1990. 7. Bender IB, Freedland JB: Adult root fracture, J Am Dent Assoc 107:413-419, 1983. 8. Bender IB, Freedland JB: Clinical considerations in the diagnosis and treatment of intra-alveolar root fractures, J Am Dent Assoc 107:595-600, 1983. 9. Bender IB, Seltzer S: The effect of periodontal disease on the pulp, Oral Surg Oral Med Oral Pathol 33:458-474, 1972. 10. Black GV: Amputation of the roots of teeth. In Litch WF, editor: The American system of dentistry, Philadelphia, 1886, Lea Brothers. 11. Burch JG, Hulen S: A study of the presence of accessory foramina and the topography of molar furcations, Oral Surg Oral Med Oral Pathol 38:451-455, 1974. 12. Cahn LR: The pathology of pulps found in pyorrhetic teeth, Dent Item Int 49:598-617, 1927. 13. Casella G, Ferlito S: The use of mineral trioxide in endodontics, Minerva Stomatol 55(3):123-143, 2006. 14. Chan CP, Tseng SC, Lin CP, et al: Vertical root fractures in nonendodontically treated teeth—a clinical report of 64 cases in Chinese patients, J Endod 24:678-681, 1998. 15. Chen S-Y, Wang H-L, Glickman GN: The influence of endodontic treatment on periodontal wound healing, J Clin Periodontol 24:449-456, 1997. 16. Cleghorn BM, Christie WH, Dong CC: Root and root canal morphology of the human permanent maxillary first molar: a literature review, J Endod 32:813-821, 2006. 17. Cohen S, Blanco L, Berman L: Vertical root fractures: clinical and radiographic diagnosis, J Am Dent Assoc 134:434-441, 2003. 18. Coolidge ED: Anatomy of the root apex in relation to treatment problems, J Am Dent Assoc 16:1456-1465, 1929. 19. Cortelli JR, Cortelli SC, Jordan S, et al: Prevalence of periodontal pathogens in Brazilians with aggressive or chronic periodontitis, J Clin Periodontol 32:860-866, 2005.
20. Cutright DE, Bhaskar SN: Pulpal vasculature as demonstrated by a new method, Oral Surg Oral Med Oral Pathol 27:678-683, 1969. 21. Czarnecki RT, Schilder H: A histological evaluation of the human pulp in teeth with varying degrees of periodontal disease, J Endod 5:242-253, 1979. 22. Fuss Z, Tsesis I, Lin S: Root resorption—diagnosis, classification and treatment choices based on stimulation factors, Dent Traumatol 19:175-182, 2003. 23. Gargiulo AW, Wentz FM, Orban B: Dimensions and relations of the dentinogingival junction in humans, J Periodontol 32:261267, 1961. 24. Guentsch A, Puklo M, Preshaw PM, et al: Neutrophils in chronic and aggressive periodontitis in interaction with Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, J Periodontol Res 44:368-377, 2009. 25. Gutmann JL: Prevalence, location, and patency of accessory canals in the furcation region of permanent molars, J Periodontol 49:2126, 1978. 26. Gutmann JL, Dumsha TC, Lovdahl PE: Problem solving in endodontics, ed 4, St Louis, 2006, Mosby Elsevier. 27. Harrington GW: The perio-endo question: differential diagnosis, Dent Clin North Am 23:673-690, 1979. 28. Harrington GW, Steiner DR, Ammons WF, Jr: The periodontalendodontic controversy, Periodontol 2000 30:123-130, 2002. 29. Hou GL, Tsai CC: Relationship between palate-radicular grooves and localized periodontitis, J Clin Periodontol 20:678-682, 1993. 30. Kahn S, Cabanilla LL: Periodontal probing depth measurement: a review, Compend Contin Educ Dent 30:12-21, 2009. 31. Kramer IHR: The vascular architecture of the human dental pulp, Arch Oral Biol 2:177-189, 1960. 32. Langeland K, Rodrigues H, Dowden W: Periodontal disease, bacteria, and pulpal histopathology, Oral Surg Oral Med Oral Pathol 37:257-270, 1974. 33. Lara VS, Consolaro A, Bruce RS: Macroscopic and microscopic analysis of the palate-gingival groove, J Endod 26:345-350, 2000. 34. Law A, Messer H: An evidence-based analysis of the antibacterial effectiveness of intracanal medicaments, J Endod 30:689-694, 2004. 35. Lindhe J, Lang NP, Karring T: Clinical periodontology and implant dentistry, ed 5, Oxford, 2008, Blackwell Munksgaard. 36. Lowman JV, Burke RS, Pelleu GB: Patent accessory canals: incidence in molar furcation region, Oral Surg Oral Med Oral Pathol 36:580-584, 1973. 37. Mazur B, Massler M: Influence of periodontal disease on the dental pulp, Oral Surg Oral Med Oral Pathol 17:592-603, 1964. 38. Peters LB, et al: Effects of instrumentation, irrigation and dressing with calcium hydroxide on infection in pulpless teeth with periradicular bone lesions, Int Endod J 35:13-21, 2002. 39. Pitiphat W, Crohin C, Williams P, et al: Use of preexisting radiographs for assessing periodontal disease in epidemiologic studies, J Public Health Dent 64:223-230, 2004. 40. Riep B, Edesi-Neuss L, Claessen F, et al: Are putative periodontal pathogens reliable diagnostic markers? J Clin Microbiol 47:17051711, 2009. 41. Roberts HW, Toth JM, Berzins DW, et al: Mineral trioxide aggregate use in endodontic treatment: a review of the literature, Dent Mater 24(2):149-164, 2008. 42. Rotstein I, Simon JH: The endo-perio lesion: a critical appraisal of the disease condition, Endod Topics 13:34-56, 2006. 43. Rubach WC, Mitchell DF: Periodontal disease, accessory canals, and pulp pathosis, J Periodontol 36:34-38, 1965. 44. Seltzer S, Bender IB: The dental pulp, ed 3, Philadelphia, 1984, JB Lippincott.
96 chapter 4 | Problem Solving in the Differential Diagnosis of Bony Defects 45. Seltzer S, Bender IB, Nazimov H: Pulpitis-induced interradicular periodontal changes in experimental animals, J Periodontol 38: 124-129, 1967. 46. Seltzer S, Bender IB, Ziontz M: The inter-relationship of pulp and periodontal disease, Oral Surg Oral Med Oral Pathol 16:14741490, 1963. 47. Shi D, Meng H, Xu L, et al: Systemic inflammation markers in patients with aggressive periodontitis: a pilot study, J Periodontol 79:2340-2346, 2008. 48. Simon JHS, Glick DH, Frank AL: The relationship of endodonticperiodontic lesions, J Periodontol 43:202-208, 1972. 49. Simring M, Goldberg M: Pulpal pocket approach: retrograde periodontitis, J Periodontol 35:22-48, 1964. 50. Sinai I, Soltanoff W: The transmission of pathologic changes between the pulp and the periodontal structures, Oral Surg Oral Med Oral Pathol 36:558-568, 1973. 51. Siqueira JF, Jr, de Uzeda M: Disinfection by calcium hydroxide pastes of dentinal tubules infected with two obligate and one facultative anaerobic bacteria, J Endod 22:674-676, 1996. 52. Slutzky-Goldberg I, Tsesis I, Slutzky H, et al: Odontogenic sinus tracts: a cohort study, Quintessence Int 40:13-18, 2009. 53. Stahl SS: Pathogenesis of inflammatory lesions in pulp and periodontal tissues, Periodontics 4:190-195, 1966. 54. Stallard RE: Periodontic-endodontic relationships, Oral Surg Oral Med Oral Pathol 34:314-326, 1972.
55. Sutalo J, Simeon P, Tarle Z, et al: “C”-shaped canal configuration of mandibular second permanent molars, Coll Antropol 22:179186, 1998. 56. Tamse A, Fuss Z, Lustig J, et al: An evaluation of endodontically treated vertically fractured teeth, J Endod 25:506-508, 1999. 57. Tai T-F, Chiang C-P, Lin C-P, et al: Complex cementodentinal tears in a maxillary central incisor—a case report, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 103:e55-60, 2007. 58. Tronstad L: Pulp reactions in traumatized teeth. In Gutmann JL, Harrison JW, editors: Proceedings of an international conference on oral trauma, Chicago, 1986, American Association of Endodontists. 59. Tulkki MJ, Baisden MK, McClanahan SB: Cemental tear: a case report of a rare root fracture, J Endod 32:1005-1007, 2006. 60. Wang H-L, Glickman GN: Endodontic and periodontic interrelationships. In Cohen S, Burns RC, editors: Pathways of the pulp, ed 8, St Louis, 2002, Mosby. 61. Wedenberg C, Linkdskög S: Experimental internal resorption in monkey teeth, Endod Dent Traumatol 1:221-227, 1985. 62. Wilson GW, Kornman KS: Fundamentals of periodontics, Chicago, 1996, Quintessence Pub Co. 63. Zehnder M, Gold SI, Hasselgren G: Pathologic interactions in pulpal and periodontal tissues, J Clin Periodontol 29:663-671, 2002.