Dynamics of Bone Loss in Cases with Acute or Chronic Apical Abscess

Dynamics of Bone Loss in Cases with Acute or Chronic Apical Abscess

Introduction: Acute and chronic apical abscesses are two dramatic ways that periradicular tissues may react to pulpal infection and necrosis. Although both of these clinical states are the response to pulpal infection, their clinical manifestations are significantly different. It is not clear why the body responds to root canal infection in one way or another. The objective of this study was to evaluate the size and pattern of bone loss in patients with acute apical abscess (AAA) and chronic apical abscess (CAA) using cone beam computed tomography (CBCT) images. Methods: 23 CBCT images of cases with AAA and 25 cases with CAA were selected and evaluated. Presence and location of fenestration; and volume and pattern of the periradicular lesions were recorded and compared between the two groups using Fisher’s exact and Mann-Whitney U tests. Results: 100% of cases with CAA had cortical fenestration, but only 47% of cases with AAA had cortical fenestration (p < 0.05). The median volume of the lesions was 233 mm3 in CAA group and 109 mm3 in AAA group (P > 0.05). CAA cases, in comparison to AAA group, had relatively larger cortical disruptions. Conclusions: Cortical fenestration is fundamental for the development of chronic apical abscess. However, periradicular lesions without evident cortical fenestration can still cause acute apical abscess and fascial space involvement.

Introduction

The spectrum of endodontic infections ranges from complete absence of any clinical signs or symptoms to severe local or systemic manifestations of infection characterized by pain and swelling. Acute and chronic apical abscess are two dramatic ways that periradicular tissues may react to pulpal infection and necrosis. In a chronic apical abscess, the abscess gradually drains to the surface with the patient having minimal or no discomfort and is typically characterized by evidence of rarefying osteitis in a conventional periapical radiograph (Hasselgren, Glickman 2013). On the other hand, acute apical abscess is portrayed by rapid progression of infection; severe pain and discomfort; and swelling with possible systemic and fascial space involvement. However, there may be no evidence of osseous destruction in a periapical radiograph (Glickman 2013). Although both of these clinical states are the response to pulpal infection, their clinical manifestations are significantly different. It is not clear why the immune system responds to root canal infection in one way or another. The differences in the patterns of osseous destruction in these two conditions may offer some insights into the mechanisms of the host response to endodontic infection.

Cone beam computed tomography (CBCT) is an accurate and reliable tool for detection, 3-dimensional evaluation, and volume measurement of periradicular lesions (Barnett 2018, Liang 2014). CBCT technology together with image segmentation software have provided a unique opportunity to explore the dynamics of endodontic infections in more detail. The objective of this study was to evaluate the size and pattern of bone loss in patients with acute apical abscess (AAA) or chronic apical abscess (CAA), using CBCT images.

Materials and Methods

This study was approved by the Institutional Review Board of the Texas A&M College of Dentistry, Dallas, TX (#2018-1377-CD-EXP). To determine the sample size, two previous studies were used (Gupta 2003, Pak 2012). A power analysis was completed according to the method described by Naing et al (Naing 2006), which indicated that at least 19 cases were needed to achieve both 80% power and to control for type 1 error <.05.

48 limited field of view CBCT studies of cases with AAA or CAA were randomly selected from an existing database. The clinical diagnoses were made using the criteria established by the American Association of Endodontists (Glickman 2013). Inclusion criteria were as follows: patients with periradicular diagnosis of AAA or CAA; patients at least 18 years old; and patients with limited field of view CBCT studies obtained before initiation of treatment. CBCT studies in which the entire volume of the periapical lesion and/or the associated tooth was not captured were excluded from the study. All the images were small field of view (FOV) CBCT studies that were taken between January 1, 2016, and June 1, 2018, as part of an endodontic examination for diagnosis and treatment planning purposes. The CBCT unit used in this study was the CS 9000 3D (Carestream Health, Inc, Rochester, NY) with an isotropic voxel size of 76 mm and FOV of 50 X 37 mm. Exposure parameters were 60–90 kVp and 6–15 mA.

The CBCT images were viewed with InvivoDental Imaging Software version 6.0.02 (Anatomage, San Jose, CA) on a Dell Professional P2213 workstation (Dell, Round Rock, TX) with a 22-inch Dell light-emitting diode monitor with a resolution of 1680 X 1050 pixels in a dimly lit room. The window/level of the images was adjusted using the image processing tool in the software to ensure optimal visualization. Two observers, a board-certified oral and maxillofacial radiologist and a board-certified endodontist, were calibrated based on the criteria and variants established before the evaluation session. All images were analyzed simultaneously to reach a consensus for the interpretation of the radiographic findings. Multiplanar images were interactively examined in a sequential fashion in all 3 dimensions, and findings were correlated across these images to arrive at a conclusion.

During evaluation of the CBCT studies the following data were recorded:

1. Volume of the periradicular lesions
2. Presence of cortication (a uniform, high attenuation line at the periphery of the lesion)
3. Presence or absence of cortical fenestration
4. Buccal or palatal location of the fenestration
5. Location of the cortical fenestration relative to the associated root (coronal 3^rd, middle 3^rd, apical 3^rd, or subapical)
6. Vertical extension of the cortical fenestration relative to the associated root (extension to one location or more than one location)
7. Distance of the involved apex to the buccal and lingual/palatal surface of the cortical bone

Volume of the periradicular lesions were measured using Mimics Innovation Suite software version 19 (Materialise NV, Belgian). Masks were created from thresholding and the lesions were segmented using 3D Live Wire tool (Figure 1). Then the masks of the periradicular lesions were converted to a 3-D model and the volume was recorded.

For multirooted teeth with multiple distinct lesions, the pattern of the lesion with cortical fenestration was recorded as the primary lesion. If no cortical fenestration was present, the lesion with the larger size was considered as the principal lesion. For multirooted teeth with a single lesion associated with multiple roots, the entire lesion was considered as the principal lesion.

After data collection, data entry was performed in Excel (Micro- soft, Redmond, WA), and data analysis was performed with Statistical Package for Social Sciences version 22 (SPSS Inc, Chicago, IL). Differences between the groups were compared using the chi-squared, Fisher’s exact, and Mann Whitney tests. Using Shapiro-Wilk test, it was determined that the data for the volume of the lesions was not normally distributed, and therefore it was expressed as median and interquartile range (IQR). The level of significance was set at p < 0.05.

Results

23 cases with AAA and 25 cases with CAA were included in the study. As summarized in Table 1, for age, gender, tooth location and pulpal diagnosis, there was no statistically significant difference between AAA and CAA groups (Table 1). The median volume was 109 mm3 for AAA and 233 mm3 for CAA (Table 2), but there was no statistically significant difference between the groups (P > 0.05). All the cases with CAA had cortical fenestration, but only 47.8% of cases with AAA had cortical fenestration (P < 0.05). 5 of the AAA cases had fascial space involvement with 3 of them not having any evident cortical fenestration. For all cases combined, the median of the distance from the involved apex to the surface of buccal cortex was 3.2 mm (IQR=3.0) and it was 8.1 mm (IQR=5.6) to the lingual/palatal cortex (P < 0.05). Combined data showed that 91.6% of the fenestrations occurred in the buccal cortex (P < 0.05).

For both AAA and CAA groups, the differences between the vertical location of fenestration was not statistically significant (P > 0.05), and the most common location for cortical fenestration was at the apical 3^rd (Table 3). CAA cases, had relatively larger cortical disruptions than AAA cases, and 48% of them had fenestrations extending to more than one location of the root (e.g. apical 3^rd to middle 3^rd). Only 4.3% of AAA cases had similar extensive fenestrations.

8% of cases with AAA and 13% of cases with CAA showed a corticated border (P > 0.05).

Discussion

In contrast to cases with CAA which all had cortical disruptions, more than half of the cases with AAA did not show any radiographic evidence of cortical fenestration. Transmission of the inflammation in cases with intact cortical bone was most likely through the path of blood vessels and lymphatics (Bauer 1943), which resulted in soft tissue swelling or fascial space involvement (Figure 2). Another possible pathway for the spread of inflammation from the confined lesions to the peripheral soft tissue could be via bone marrow and cortical microchannels that were not detectable with CBCT studies. A study by Simon et al. using high quality computed tomography showed the presence of cortical microchannels in metacarpal bones in healthy subjects (Simon 2014). Therefore, absence of radiographic evidence of cortical disruption does not necessarily mean that no pathway exists through the bone, and the cortical plate may not serve as an impenetrable shell enclosing the cancellous bone.

In the majority of AAA cases, cortical fenestration was either absent or smaller in size than seen in CAA cases. This could partly explain the differences between the signs and symptoms of the two conditions. In CAA cases, the presence of these pressure relief valves could prevent emergence of swelling and severe discomfort. However, this was not a factor exclusive to CAA cases, as there are a few cases with AAA that had large cortical disruptions similar to that of CAA cases. In addition, although it appears that in the majority of cases with CAA the lesion followed the least resistant path by establishing a bony tract through the cancellous bone (Figure 3), in some cases the lesions apparently exited through unexpected pathways (Figure 4). It is worth noting that cone beam computed tomographic appearance of the two conditions may be very similar, and one cannot anticipate the existence of either of these conditions by just examining their CBCT imaging.

On average, size of the lesions in the AAA group were smaller than in the CAA group. However, there was no statistically significant difference between the two groups. In CAA cases, the smallest lesion had a volume of 34 mm3. However, two of the lesions in AAA group had PDL widening only (volume of less than 10 mm3), without a distinct periapical lesion. It can be speculated that in those AAA cases with very small lesions, inflammation spread so quickly that there was inadequate opportunity for osseous destruction to occur. This also explains why a case with AAA may not show evidence of a lesion in a periapical radiograph (Glickman 2013).

The apices of the involved roots were closer to the buccal cortex than the lingual cortex in both groups. Perhaps consistent with this is that more than 90% of the fenestrations were found in the buccal cortex. In addition, the overall incidence of fenestrations was the lowest at a location beyond the apex of the involved root. The thickness of the cortical bone decreases as one moves coronally from the location of tooth apices. As lesions tend to grow through the path of least resistance, the location of the fenestrations is understandable.

It has been suggested that a corticated border is indicative of a lesion with chronic nature, and sclerotic boundary is commonly seen with cysts and slow-growing lesions (White and Faroah chapter 26). Based on this notion, one may expect a higher incidence of corticated border in CAA cases compared to AAA cases. However, in this study only 8% of cases in CAA group and 13% of cases in AAA group showed a corticated margin, and there was no statistically significant difference between the two groups (p=0.567). This finding questions the reliability of radiographs in determining the chronicity or acuteness of a lesion.

There are many elements (e.g. different components of immune system and species of bacteria) involved in emergence of endodontic signs and symptoms as a reaction to root canal infection, and a large number of states may be expected as a consequence. However, by self-organization, the immune system usually reduces the possible inflammatory reactions to only a few number of states, such as a draining sinus tract or an acute cellulitis (Jalali 2015).

Although there are differences between these inflammatory scenarios, one should not forget that these conditions are part of a continuum of inflammatory responses. Categorization of these conditions may be necessary for proper treatment planning and decision making, but it should not prevent the clinicians from considering the fuzziness of their boundaries. For example, a case with an endodontic sinus tract, if left untreated, can simply transform into an acute apical abscess or vice versa.

Notwithstanding the results of this study suggested the absence of fenestration as a possible contributing factor for emergence of acute symptoms, the other variables in the system should not be neglected. Presence of an infinite number of variables and their interactions make the inflammatory response to endodontic infection a complex nonlinear dynamic system (Jalali 2015, Seely 2000). Therefore, it may not be wise to pinpoint one element as the causative factor for the development of these inflammatory states. Studies focusing on this aspect of endodontic infection are needed.

This study showed that cortical fenestration is fundamental for the development of chronic apical abscess. However, periradicular lesions without evident cortical fenestration can still cause acute apical abscess and fascial space involvement.

References:

1. Gupta R, Hasselgren G. Prevalence of odontogenic sinus tracts in patients referred for endodontic therapy. J Endod 2003;29:798-800.
2. Glickman G, Schweitzer J. Endodontic Diagnosis. In: Colleagues for Excellence. Chicago: American Association of Endodontists; 2013.
3. Barnett CW, Glickman GN, Umorin M, Jalali P. Interobserver and Intraobserver Reliability of Cone-beam Computed Tomography in Identification of Apical Periodontitis. J Endod 2018;44:938-40.
4. Pak JG, Fayazi S, White SN. Prevalence of periapical radiolucency and root canal treatment: a systematic review of cross-sectional studies. J Endod 2012;38:1170-6.
5. Liang YH, Jiang L, Gao XJ, Shemesh H, Wesselink PR, Wu MK. Detection and measurement of artificial periapical lesions by cone‐beam computed tomography. Int Endod J 2014;47:332-8.
6. Naing L, Winn T, Rusli BN. Practical issues in calculating the sample size for prevalence studies. Arch Orofac Sci 2006;1:9-14.
7. Bauer WH. Maxillary sinusitis of dental origin. Am J Orthod Dentofac. 1943 1;29:B133-51.
8. Simon D, Faustini F, Kleyer A, Haschka J, Werner D, Hueber AJ, Sticherling M, Schett G, Rech J. in Vivo Visualization of Cortical Microchannels in Metacarpal Bones in Patients with Cutaneous Psoriasis By High Resolution Peripheral Computed tomography-Detecting Cortical Pathologies before the Clinical Onset of Psoriatic-arthritis.: 1892. Arthritis Rheumatol 2014;66:S832-3.
9. White SC, Pharoah MJ. Oral Radiology Principles and Interpretation, 7^th ed. Missouri. Elsevier; 2014.
10. Jalali P, Hasselgren G. Endodontic inter-appointment flare-ups: An example of chaos? Dent Hypotheses 2015;6:44–8.
11. Seely AJ, Christou NV. Multiple organ dysfunction syndrome: exploring the paradigm of complex nonlinear systems. Crit Care Med 2000;28:2193–200.