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Current Oral Health Reports

, Volume 4, Issue 4, pp 278–285 | Cite as

Definitions and Epidemiology of Endodontic Infections

  • I. F. Persoon
  • A. R. ÖzokEmail author
Open Access
Epidemiology (M Laine, Section Editor)
Part of the following topical collections:
  1. Topical Collection on Epidemiology

Abstract

Purpose of Review

This review describes the recent findings from epidemiological studies on endodontic infections. The recent literature was screened for studies on the prevalence of primary apical periodontitis and posttreatment apical periodontitis in various populations.

Recent Findings

Twenty-nine articles reporting data on the prevalence of primary or posttreatment apical periodontitis from all over the world were included. The prevalence of apical periodontitis varied between 7 and 86%, while that of posttreatment apical periodontitis varied between 10 and 62%. The quality of the coronal restoration and the root filling appears to be the major predictors of apical periodontitis.

Summary

The recent findings from epidemiological studies on the prevalence of primary and posttreatment apical periodontitis in various populations are not substantially different from those from earlier years. It appears that the health of periapical tissues has not majorly improved in the general population.

Keywords

Endodontic infections Epidemiology Primary apical periodontitis Posttreatment apical periodontitis Prevalence 

Introduction

Definition of Endodontic Infections

The root canal system is, in its healthy and intact state, free from infection. Unlike the oral cavity, the root canal system has no commensal microbiota, and any microorganism detected here can be regarded as a potential pathogen. Once microorganisms find their way into the root canal system, the consequences may vary from a simple reversible pulpitis to the necrosis of the pulpal tissue and eventually formation of a periapical lesion: apical periodontitis. Pulpal necrosis on its own, when no microorganisms are involved, does not necessarily lead to apical periodontitis [1]. Nevertheless, a necrotic pulp, following for example a mechanical or thermal trauma, can hardly maintain its ‘sterile’ status due to the lack of blood circulation and defense mechanisms that could eliminate intruding microorganisms. An infected root canal system is a prerequisite for the formation of apical periodontitis [2]. Apical periodontitis is an inflammatory response of the periapical periodontal tissues to the infected root canal system. A bony lesion is formed as calcified periapical tissues erode, caused by the toxic irritation deriving from the infected root canal and the immune response of the host.

The microorganisms identified within endodontic infections are a selection from the commensal microbiota of the oral cavity. The ecological conditions select for a certain microbiota. In a healthy oral ecosystem, microbiota live in homeostasis with the host. When the conditions change, for example by a diet rich in carbohydrates, certain microorganisms can dominate and cause disease. Dental decay may create access to a new niche: the root canal system. Since the ecological conditions are different from the oral cavity, microorganisms will be selected and establish a new microbial community. Although advancing analytical techniques have uncovered an immense diversity and variance of the microbiota within infections, a pattern according to the disease activity can be drawn: symptomatic versus asymptomatic [3]. The microorganisms that contribute the most to endodontic infections are bacteria, both in biomass and diversity [4]. Although Lactobacillus, Actinomyces, and Streptococcus are among the most abundant genera detected in root canals associated with apical periodontitis [5], regarding the aseptic nature of the root canal system in its healthy and intact state, any bacteria present can be regarded as an endodontic pathogen. Still, fungi [4], viruses [6], and archaea [7] can be detected within root canal infections and periapical lesions. Despite their low numbers, they might contribute significantly to the composition and virulence of the overall microbiota and to the host response. Such influence could lead to persistence and symptomology of the apical periodontitis.

Possible Effect on Epidemiological Studies of the Diagnosis of Apical Periodontitis and the Definition of Its Severity

Symptomatic apical periodontitis is characterized by the inflammation of the periapical tissues, generating clinical symptoms including a painful response to biting or percussion or tenderness with palpation. Depending on the phase of the disease, radiographic changes may or may not be detectable [1]. Asymptomatic apical periodontitis can, however, be solely diagnosed by the presence of radiographic changes, namely a periapical radiolucency created by the bony lesion on the radiograph.

The most commonly used radiographic detection methods for a periapical lesion are conventional or digital periapical radiography, panoramic radiography or, most recently, cone-beam computed tomography (CBCT). Various degrees of diagnostic accuracy for each one of the abovementioned methods have been reported. In the premolar and mandibular molar regions, significantly more periapical lesions can be detected on conventional periapical radiographs than on panoramic radiographs [8].

Due to its three-dimensional nature, the CBCT stands out from the rest [9, 10]. The diagnostic accuracy of CBCT in detecting apical periodontitis is significantly higher compared to digital periapical radiography [10] or panoramic radiography [11]. The possibility of false-negative diagnosis is, therefore, much higher when conventional two-dimensional radiography is used. This may pose a challenge for the diagnosis of the disease, which subsequently may have an impact on the findings of the studies on its prevalence leading to an underestimation. CBCT, on the other hand, has its own limitations with regard to epidemiological studies. Concerning the relatively high effective dose for CBCT and the as low as reasonably achievable (ALARA) principle, when a CBCT scan is made to diagnose apical periodontitis, it is recommended to use limited volume CBCT, in which the field of view (FOV) is limited to a volume smaller than the jaws and suitable for imaging only a few teeth [12]. This may negatively impact studies on the prevalence of apical periodontitis. When a small FOV is used, only a limited part of the dentition is evaluated, and the information about the prevalence of the disease in the rest of the dentition remains censored. From an epidemiological point of view, data collection only on the tooth level, instead of on a subject level, seems less relevant.

Not only the detection of periapical disease is challenging but also the definition of its severity. There seems to be little consensus on the degree of bone destruction at which a bony lesion can be defined as apical periodontitis. Several indexing methods have been introduced for the assessment of the severity of apical periodontitis, each with its limitations. The most commonly used method is the periapical index (PAI) [13], and it is reported to have excellent observer agreement [14]. The PAI scoring system aims to assess the severity of apical periodontitis on dental radiographs with the use of a 5-score scale, where score 1 represents healthy periodontium and scores 2 to 5, respectively, represent periapical disease increasing in severity [13]. This scoring system, however, is not based on direct histopathological examination, but on a simplified modification of the radiographic method of interpretation based on the histopathological examination executed by Brynolf [15]. Since Brynolf used only upper incisors in her study [15], the reliability of the PAI system in premolar or molar regions is unclear.

Another limitation of the PAI system and any other scoring system based on conventional or digital radiographs is related to the two-dimensional nature of these radiographs. While it is, to a certain extent, possible to measure the diameter of the lesion in the mesial-distal direction on a two-dimensional radiograph, its diameter in the buccal-lingual direction remains unmeasurable. The surrounding anatomical structures and the thickness of the bone can further obscure the lesion on the radiograph. This is an even greater problem for multirooted teeth.

There is no clear consensus on the description of apical periodontitis in epidemiological studies using the PAI system screened in this review. While some studies accepted only a PAI score of 1 as healthy apical periodontium [16, 17], many others included a PAI score of 2 in the healthy category as well [18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31•] or even a PAI score of 3 [32].

The Incidence and Prevalence of Apical Periodontitis

Unfortunately, studies into new diagnoses of endodontic infections per time period, the incidence, are not feasible, since the detection of the onset of the periapical disease is nearly impossible. The time needed for apical periodontitis to become visible on the radiograph is relatively long and depends on several factors. A substantial amount of trabecular bone mineral loss or the erosion of the cortical bone is needed for the lesion to become radiographically visible [33]. Therefore, most studies on the epidemiology of endodontic infections focus on their prevalence, where the proportion of a population with apical periodontitis is estimated based on examination of a sample of the population of interest.

Recent Findings on the Prevalence of Apical Periodontitis

This review identified relevant studies using a search of the MEDLINE electronic database via PubMed and from the reference list of relevant articles. The search strategy, limited to a period from January 2014 to May 2017, identified the terms ‘apical periodontitis’ and ‘epidemiology’ or ‘prevalence’ and generated 103 hits. Only 51 of these titles were actually related to the search terms. After screening these abstracts, 45 relevant articles were selected for full-text reading. Twenty-nine articles reporting cross-sectional data of epidemiological studies met the inclusion criteria (Table 1). Studies using tooth as the unit of estimation were included only if the data were applicable to subject level or the general population. Outcome studies were excluded, since these only assess the targeted root-filled teeth. Review articles where the abovementioned criteria were not met or if it was not possible to extract this information were excluded as well. The current review defines teeth associated with apical periodontitis and without a root filling as teeth with primary apical periodontitis, and root-filled teeth associated with apical periodontitis as teeth with posttreatment apical periodontitis. Since not every study reported data on the prevalence of primary or posttreatment apical periodontitis separately, in the following part of the text, the term ‘apical periodontitis’ refers to a total of primary and posttreatment apical periodontitis.
Table 1

Characteristics and findings of epidemiological studies on apical periodontitis (AP)

           

Patient level

Tooth level

 
           

Root-filled teeth

AP

Primary AP

Post-treatment AP

All teeth

Root-filled teeth

AP

Primary AP

Post-treatment AP

 

Publication date

Study date

Country of study

Type of study

Detection method

Index

Systemic condition

Patients (N)

Men (N)

Women (N)

Age range (years)

N

(%)

N

(%)

N

(%)

N

(%)

N

N

(%)

N

(%)

N

(%)

N

(%)

Reference

2014

2007-2008

Sweden

CS

OPT, CE

NR

NR

440

NR

NR

20-89

  

186

(42)

108

(25)

  

11876

678

(6)

  

140

(1)

  

[34]

2014

2009-2012

UK

CS

CBCT

De Moor [35]

NR

245a

128

117

18-86

        

3595

171

(5)

209

(6)

128

(4)

81

(47)

[36]

2014

2012

UK

CS

OPT

De Moor [35]

NR

136

63

73

16-65+

  

67

(49)

    

3396

115

(3)

138

(4)

94

(3)

44

(38)

[37]

2014

NR

Brazil

CS

PR

PAI

Institutionalized elderly

98

41

57

60-94

48

(49)

42

(43)

    

942

126

(13)

114

(12)

32

(4)

82

(65)

[22]

2014

NR

Serbia

CS

OPT

PAI

NR

153

64

89

18-60

120

(78)

      

3526

438

(12)

    

227

(52)

[21]

2014

2008-2009

Denmark

LONG

PR

PAI

NR

327

NR

NR

20-63 at start

         

350

     

147

(42)

[24]

2014

2009-2011

Turkey

CS

CBCT

 

NR

276

142

134

15-72

         

522

     

238

(46)

[38]

2014

2009-2010

Brazil

CS

PR

PAI

Coronary artery disease

67

38

29

mean 64

  

34

(51)

             

[29]

      

Healthy

36

14

22

mean 57

  

9

(25)

              

2014

2004-2012

South Korea

CS

PR

Strindberg [39]

NR

590

265

325

NR

         

1030

     

421

(41)

[40]

2015

2013

India

CS

OPT

PAI

NR

1340

NR

NR

18+

  

865

(65)

    

30098

1234

(4)

1759

(6)

1297

(4)

462

(37)

[30]

2015

1983-2003

Sweden

RCS

PR, OPT

PAI

NR

788

417

371

20-70

         

2634

     

594

(23)

[20]

2015

2012-2013

France

CS

CBCT

CBCTPAI

NR

100a

47

53

18-88

        

2368

431

(18)

204

(9)

28

(1)

176

(41)

[41]

2015

NR

Spain

CS

OPT

Halse and Molven [42]

Post-menopausal osteoporosis

48

none

48

59-68

  

12

(25)

             

[43]

      

Healthy

27

none

27

59-68

  

2

(7)

              

2015

2009-2011

Nigeria

CS

PR

PAI

NR

285

133

152

18-60

  

212

(74)

    

8094

287

(4)

586

(7)

475

(6)

111

(39)

[19]

2015

2009-2011

Nigeria

CS

PR

PAI

NR

756

414

342

20-60+

463

(61)

508

(67)

    

21468

2625

(12)

3083

(14)

2015

(11)

1068

(41)

[18]

2015

2011-2013

Spain

CS

OPT

PAI

Diabetes mellitus

83

41

42

18+

27

(33)

52

(63)

44

(53)

8

(10)

         

[23]

2016

2012

Saudi Arabia

CS

OPT

PAI

NR

193

81

112

18-65+

         

324

     

190

(59)

[16]

2016

2008-2009

Turkey

CS

CBCT

PAI

NR

748

336

412

15-65

         

147

     

93

(63)

[17]

2016

2013-2015

Denmark

CS

OPT

De Moor [35]

Liver cirrhosis

110

71

39

39-82

  

51

(46)

        

(4)

    

[44]

2016

2006-2008

Finland

 

OPT, CE

PAI

Coronary artery disease

467

254

254

NR

316

(68)

342

(73)

    

10163

1026

(10)

172

(2)b

84

(1)b

88

(9)b

[32]

2016

2013

Croatia

CS

PR, OPT

PAI

Smoking

108

82

177

mean 40

89

(82)

93

(86)

26

(24)

67

(62)

         

[25]

      

Non-smoking

151

   

119

(79)

118

(76)

25

(17)

93

(62)

          

2017

2010-2012

Saudi Arabia

CS

OPT

Other

Mixed

926

540

386

16-55+

        

25028

1541

(6)

1559

(6)

942

(4)

617

(40)

[45]

2017

2000-2001

Finland

CS

OPT

Other

NR

5335

47%

53%

30-95

3095

(58)

 

(27)

 

(10)

 

(39)

120635

7986

(7)

      

[46]

2017

NR

USA

CS

PR, OPT

PAI

Rheumatoid arthritis

131

19

112

22-83

82

(63)

65

(50)

    

3260

203

(6)

129

(4)

80

(3)

49

(24)

[27]

      

Healthy

131

19

112

 

77

(59)

71

(54)

    

3395

192

(6)

120

(4)

61

(2)

59

(30)

 

2017

2013-2014

Austria

CS

OPT

PAI

NR

1000

430

570

19-91

  

605

(61)

    

22586

2504

(11)

1454

(6)

388

(2)

1066

(43)

[28]

2017

2012-2015

Italy

CS

PR, OPT, CE

PAI

Inflammatory bowel diseases

110

49

61

mean 46

   

(64)

             

[47]

      

Healthy

110

53

57

mean 41

   

(59)

              

2017

2015

Jordan

CS

OPT

PAI

Diabetes mellitus

145

71

74

         

3111

130

(4)

409

(13)

373

(13)

36

(28)

[26]

      

Healthy

146

75

71

         

3127

57

(2)

372

(12)

361

(12)

11

(20)

 

2017

2008

Australia

CS

OPT

PAI

NR

695

292

403

10-88

138

(20)

179

(26)

88

(13)

91

(13)

16936

284

(2)

325

(2)

207

(1)

118

(42)

[31]

2017

2013

Belgium

CS

CBCT

De Moor [35]

NR

631a

267

364

mean 45

        

11117

1357

(12)

656

(6)

212

(2)

444

(33)

[48]

Percentages on patient level were calculated by dividing the number of individuals with one or more AP by the total number of participants. Percentages on tooth level were calculated for root-filled teeth by dividing the number of root-filled teeth by the total number of teeth, for AP by dividing the number of teeth with AP by the total number of teeth, for primary AP by dividing number of teeth with primary AP by the total number of non-root-filled teeth, for post-treatment AP by dividing the number of teeth with post-treatment AP by the total number of root-filled teeth

NR: not reported; CS: cross-sectional; LONG: longitudinal; RCS: repeated cross-sectional; OPT: orthopantomography; CE: clinical examination; CBCT: cone-beam computed tomography; PR: periapical radiography; PAI: periapical index;

ascans; b PAI 1+2+3 =healthy

Based on the included articles, the lowest prevalence of apical periodontitis on a patient level, meaning one or more periapical lesions per patient, was 7% in an otherwise healthy Spanish population [43], and the highest was 86% in a Croatian population of smokers [25] with a median of 52.5%. The corresponding percentages for the prevalence of primary apical periodontitis, respectively, were 10% in a Finnish population [46] and 53% in a Spanish population [23] with a median of 20.5%. The lowest prevalence of root-filled teeth on a patient level was 20% in an Australian population [31•], and the highest was 82% in a Croatian population of smokers [25] with a median of 61%. The lowest prevalence of posttreatment apical periodontitis on a patient level was 10% in a Spanish population [23] and 62% in a Croatian population [25] with a median of 39%.

The prevalence rates on tooth level were lower for each condition. The prevalence of apical periodontitis ranged from 2% in a Finnish population [32] to 14% in a Nigerian population [18]. The median was 6% on a total of 304,721 teeth, which compares well to the 5% found in a previous systematic review and meta-analysis [49••]. This review was on studies from 1987 till 2009 on a total of 300,861 teeth. The prevalence of primary apical periodontitis ranged from 1% in Finnish [32], French [41•], Swedish [34], and Australian [31•] populations to 13% in a Jordanian population of diabetics [26]. The median was 3.5%, which is similar to the 2% from the previously mentioned meta-analysis [49••]. The slightly lower rate might be caused by a more systematic inclusion and also inclusion of studies from mainly well-developed countries. The prevalence of root-filled teeth ranged from 2% in an Australian population [31•] to 18% in a French population [41•]. The median was 6%, which is in the same range as the 10% from the previously mentioned meta-analysis [49••]. The lower prevalence of root-filled teeth in the more recently published studies (published from 2014) might indicate a limited access to oral healthcare, which is likely when studies are done in less-developed countries [30]. The prevalence of posttreatment apical periodontitis ranged from 20% in an otherwise healthy Jordanian population [26] to 65% in a Brazilian population [22]. The median was 41%, which is similar to the 36% found in the previously mentioned meta-analysis [49••]. Overall, the prevalence rates seem similar to rates in not so recent studies (published prior to 2014), even though more recent studies (published from 2014) are done on samples from less-developed countries or individuals with access to newer treatment techniques.

Gender

The effect of gender on apical periodontitis remains ambiguous. Studies on Swedish [20], Nigerian [19], Danish [44], or Belgian [48] populations reported no significant difference in the prevalence of apical periodontitis between men and women. However, a significantly higher prevalence of apical periodontitis in men than in women was revealed in Turkish [38], Finnish [46], or Austrian [28] populations, while in Scottish [36], Jordanian [47], or Saudi Arabian [45] populations, the prevalence of apical periodontitis was higher in women than in men. It is quite challenging to explain the difference between the outcome of these studies. Research suggests that women perceive more pain [50] and are more likely to seek treatment for orofacial pain [51], possibly at an earlier, more treatable stage of the disease. Also, cultural characteristics of a population may affect the frequency a man or a woman seeks dental care. Since the results are ambiguous, the effect of gender on apical periodontitis remains unresolved.

Quality of the Root Filling or the Coronal Restoration

Both the quality of the coronal restoration and the quality (length or the density) of the root filling are reported to be major predictors of posttreatment apical periodontitis. There is a negative correlation between the quality of the coronal restoration and the prevalence of posttreatment apical periodontitis [16, 17, 20, 28, 30, 40]. Similarly, when the root canal is filled too short of the root apex, the root filling is extruded into the periapex, or the root filling contains voids, the prevalence of posttreatment apical periodontitis increases [16, 17, 20, 21, 22, 24, 28, 30, 37, 40, 48].

Systemic Conditions

An increasing number of studies are conducted to reveal a possible bidirectional association between the apical periodontitis and the systemic health. This means that a systemic condition can be aggravated by apical periodontitis and, vice versa, that systemically affected individuals are more prone to apical periodontitis. Thus far, limited studies are available on the effect of systemic disease on endodontic outcome [52••, 53, 54, 55]. Besides, the evidence is of limited quality and indefinite, which demands that the found associations are to be interpreted with caution [52••]. In order to detect indisputable bidirectional associations between oral disease and the systemic conditions, there is an urgent need for the application of stringent criteria on research reporting [56].

Individuals with uncontrolled diabetes mellitus are reported to have significantly more periapical lesions in comparison to controls with well-controlled diabetes mellitus (23 vs. 49% [23], 9 vs. 18% [26]). Also, individuals with diabetes mellitus are 1.4 times more likely to have root-filled teeth with apical periodontitis than healthy controls [53]. Apical periodontitis might decrease glycemic control, aggravating diabetes. In turn, diabetes might limit the host’s inflammatory response to combat the endodontic infection. In women suffering from postmenopausal osteoporosis, low bone density is reported to be associated with a higher prevalence of apical periodontitis [43]. An association between the prevalence of apical periodontitis and coronary artery disease is reported, where the inflammatory burden of the endodontic infection might be contributing to the systemic condition [29, 32]. Individuals with liver cirrhosis and periapical lesions also had higher C-reactive protein levels and a higher prevalence of cirrhosis-related complications such as ascites, hepatic encephalopathy, and variceal bleeding [44]. Women suffering from inflammatory bowel disease are reported to have more teeth with apical periodontitis and with more severe bone destruction. The prevalence of apical periodontitis was even higher when these women were treated with immunomodulators [47]. Regarding the prevalence of apical periodontitis, there was no significant difference between individuals with rheumatoid arthritis [27] and their healthy counterparts.

Smoking

Smoking is reported to be one of the strongest predictors of apical periodontitis in a Danish [44] and in a Nigerian population [19]. A Croatian population of smokers had two times more apical periodontitis than the never-smokers did [25]. Smoking might negatively affect the periodontal bone and is associated with dental caries, one of the main causes of apical periodontitis.

Age

Several studies described age as a predictor for apical periodontitis [19, 44]. The findings of a systematic review and meta-analysis of cross-sectional studies on the prevalence of apical periodontitis and root-filled teeth in persons 65 years of age or older conducted in 2016 do not deviate substantially from the findings of the studies included in this review [57••]. That review confirmed that the prevalence of both apical periodontitis and root-filled teeth increases with age. With aging, not only the comorbidity increases but also the immune system deteriorates. Additionally, oral disease experience in the elderly is higher than younger adults [58]. This might be an important confounder when considering age as a predictor for apical periodontitis.

Conclusions

Although there seems to be an increase in recent years in studies from less-developed countries and newer detection techniques for periapical disease, such as CBCT, are introduced, the findings from epidemiological studies on the prevalence of primary and posttreatment apical periodontitis in various populations are not substantially different from those from earlier years. It appears that the health of periapical tissues has not majorly improved in the general population, despite technological progress of endodontic treatment and increasing access to healthcare worldwide.

Of all the studied possible predictors, the quality of the coronal restoration and the root filling are the most consistently reported risk factors for apical periodontitis. To identify all possible risk factors efficiently, the design and reporting of epidemiological studies on apical periodontitis should be standardized and improved.

Notes

Compliance with Ethical Standards

Conflict of Interest

Rifat Özok and Ilona Persoon declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

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Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Authors and Affiliations

  1. 1.Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA)University of Amsterdam and Vrije Universiteit AmsterdamAmsterdamThe Netherlands
  2. 2.Department of Endodontology, Academic Centre for Dentistry Amsterdam (ACTA)University of Amsterdam and Vrije Universiteit AmsterdamAmsterdamThe Netherlands

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