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 Table of Contents  
Year : 2022  |  Volume : 19  |  Issue : 1  |  Page : 25

Clinical, radiological, and histological correlation in diagnosis of pulpitis

1 Endodontology Research Center, Kerman University of Medical Sciences, Kerman, Iran; Department of Orofacial Pain and Dysfunction, Academic Center for Dentistry of Amsterdam, University of Amsterdam and Vrije Universities Amsterdam, Amsterdam, The Netherlands
2 Department of Oral and Maxillofacial Medicine, Faculty of Dentistry, Mashhad Univercity of Medical Science, Mashhad, Iran
3 Oral and Dental Diseases Research Center, Kerman University of Medical Sciences, Kerman, Iran
4 Endodontology Research Center, Kerman University of Medical Sciences, Kerman, Iran
5 Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran

Date of Submission04-Dec-2020
Date of Acceptance30-Sep-2021
Date of Web Publication21-Mar-2022

Correspondence Address:
Dr. Elahe Vazavandi
Department of Oral and Maxillofacial Medicine, Faculty of Dentistry, Mashhad Univercity of Medical Science, Mashhad
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1735-3327.340110

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Background: To establish an endodontic diagnosis, a clinician should consider a variety of factors. Various studies have failed to demonstrate a strong correlation between histological findings with clinical and radiographic assessments. This study sought to evaluate the histopathological features of reversible and irreversible pulpitis diseases and their correlation with clinical diagnosis in extracted human molar teeth.
Materials and Methods: In this experimental ex vivo study, 75 molars with caries and three intact molars were used. According to the radiographic findings and clinical criteria and the need for root canal therapy, samples were categorized as having normal/reversible pulpitis and irreversible pulpitis. Immediately after extraction, an exposure was made at 2 mm below the cementoenamel junction. Formalin-fixed specimens were decalcified, sectioned and stained with hematoxylin and eosin for histological examinations using light microscopy. Variables including the type and severity of the inflammation, hyperemia, necrosis, fibrosis and the existence of an odontoblastic layer and dentin bridge were evaluated. The Fisher's exact test and the Chi-squared test were used for statistical analysis. P <0.05 was considered as significant.
Results: Acute inflammation, hyperemia and pulp exposure were significantly more common among subjects with irreversible pulpitis (P < 0/005). However, fibrosis was significantly higher in the reversible group (P < 0/005). There were no statistically significant differences between the groups regarding the other variables.
Conclusion: Some discrepancies between clinical, radiographic and histological findings were observed in our experimental study. Indeed, effective clinical practice requires consideration of all discrepancies found.

Keywords: Diagnosis, histology, pulpitis, root canal therapy, signs and symptoms

How to cite this article:
Raoof M, Vazavandi E, Parizi MT, Hatami N, Mohammadalizadeh S, Amanpour S, Haghani J. Clinical, radiological, and histological correlation in diagnosis of pulpitis. Dent Res J 2022;19:25

How to cite this URL:
Raoof M, Vazavandi E, Parizi MT, Hatami N, Mohammadalizadeh S, Amanpour S, Haghani J. Clinical, radiological, and histological correlation in diagnosis of pulpitis. Dent Res J [serial online] 2022 [cited 2023 Oct 4];19:25. Available from: https://www.drjjournal.net/text.asp?2022/19/1/25/340110

  Introduction Top

Dental caries is one of the most common infectious diseases found in humans. Providing a proper treatment plan for dental caries, especially at a young age, is a great asset to any practitioner. There are various therapeutic strategies along with a wide range of restorative materials for tooth decays.[1] Vital pulp therapy, as a biologic and conservative treatment modality, is one of the most effective treatments and is increasingly seen in permanent immature teeth and in teeth with closed apex.[2] Vital pulp therapy offers several further advantages over nonvital pulp therapies, including the maintenance of the tooth structure that contributes to increased mechanical resistance, as well as maintenance of defensive mechanisms provided by the vital pulp such as proprioception and tooth sensitivity.[3],[4]

On the other hand, producing successful therapeutic outcomes in vital pulp therapies mainly depends on the accurate assessment of pulp status. Unfortunately, the diagnosis of pulpal pathology appears to be very complicated. There is no clear correlation among clinical signs and symptoms, pulpal sensibility tests, radiographic features, and the histological analysis of dental pulp.[5],[6] To date, very few studies have directly investigated any correlations.[5],[6],[7],[8],[9],[10],[11],[12] Therefore, the present study has been conducted to investigate the relationship between the histopathological status of the dental pulp tissues in carious teeth, with the clinical and radiographic features.

  Materials And Methods Top

The present experimental study was approved by the Ethics Committee of Kerman University of Medical Sciences, Kerman, Iran (code: IR. KMU. REC1394.730). For the present study, seventy-five extracted mature carious molars, along with 3 intact ones, were used. The teeth were extracted from 83 patients ranging in age from 21 to 64 years old with an average age of 35.7 ± 10.88. Teeth were extracted from patients who refused to accept available treatment options, instead insisting on extraction for differing reasons such as financial constraints and dental fear. Teeth with calcified roots, resorption, previous root canal treatment, extensive restorations, crown, or severe periodontal problems were excluded. The practitioner provided periapical and bitewing radiographs prior to the extraction. It is not appropriate to have an interval <6 months between radiographs.[13] However, we did not have access to some previous radiographs and in some cases the quality of radiographs were not acceptable. Hence, to avoid unnecessary radiation, patients who had radiographic examinations within the previous 6 months were excluded from the study. Patients who had radiographic examinations within the previous 6 months were also excluded from the study. According to the clinical criteria, the radiographic feature and the need for root canal treatment; and similar to the study by Ricucci et al., samples were categorized as having normal/reversible pulpitis and irreversible pulpitis. Normal pulp was classified in the reversible pulpitis group because the pulp of both groups can be preserved.[9]

Patients in the normal/reversible pulpitis group did not have any history of overnight, throbbing, persistent, or prolonged pain, while they mostly reported a mild sensitivity to stimuli including cold, sweets or biting pressure. Moreover, pain from cold tests was not severe and did not linger more than 30 s. Percussion and palpation tests also proved negative. Radiographic examinations showed no pulp exposure and no periradicular destruction. A total of 27 teeth were placed in this group. In addition, 3 intact third molars were included in this group.

The group of patients with irreversible pulpitis reported severe pain to temperature changes that may or may not linger, spontaneous pain, referred pain and throbbing pains that resulted in patients waking up while proving difficult to control with painkillers. Eight teeth were tender to percussion. Moreover, palpation testing produced a sensitive response for 5 teeth. No periradicular changes were observed in radiographs, even though a few cases of periodontal ligament widening were found. Cases with radiographic exposure of the pulp were also included. A total of 48 teeth were placed in this group.

This study excluded cases other than those caused by dental caries. Cases in which clinical and radiographical factors were associated with pulp necrosis were also excluded from the study.

After recording the pulp response to the cold test by using a refrigerant spray (Denronic, Germany), a general practitioner performed all tooth extractions. The teeth were immediately cleaned with a flow amount of normal saline. To increase the penetration rate of the fixing agent and deceased risk of distortion and cell lysis, pulp exposure was accomplished by use of a diamond fissure bur No. 012 L/837 (Tizkavan, Tehran, Iran) just beneath the cementoenamel junction of an intact side of the teeth. Following fixation of the teeth in 10% buffered formalin for 24 h, all samples were decalcified in 15% nitric acid solution for 4–8 weeks (Merck/Germany). Subsequently, samples were washed in running tap water for 24 h and then dehydrated, embedded in paraffin and cut into serial sections of 3–5 microns.[14],[15],[16] Hematoxylin and eosin-stained slides were examined under a light microscope (Olympus, Tokyo, Japan) with ×10 and ×40 magnifications. The pathologist scanned different areas of the pulpal tissue and the worst pattern was recorded for each sample.[17] The following features were assessed: The type and severity of inflammation, hyperemia, necrosis, fibrosis and the presence of an odontoblastic layer and dentin bridge. The histological sections were given scores as previously described with minor modifications [Table 1].[15],[18] Reproducibility was determined using the Kappa (K) coefficient. K coefficients were ≤0.76 for all items.
Table 1: Scoring system used for histopathologic evaluation of the pulp

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The X-ray diagnosis was performed by an endodontist under ×2.5 magnification on a negatoscope. The occurrence of pulp exposure was recorded. The kappa value for the intra-examiner reliability was 0.82, indicating almost perfect agreement between the two measurements.

Statistical analysis included measures of central tendency and dispersion. Data were also analyzed by Chi square and Fisher's exact test using the SPSS software, version 16 (SPSS, Inc., Chicago, IL, USA).

  Results Top

[Table 1] represents the histopathological scoring system used for the present study.

The type of inflammation, hyperemia and fibrosis were significantly different between the two comparison groups [Table 2]. 20.8% of the teeth with irreversible pulpitis showed acute inflammation. However, 43.3% of the specimens with reversible pulpitis showed no inflammation (Fisher exact test, P = 0.005). In the reversible pulpitis group, 13.3% of the samples exhibited severe hyperemia, whereas 47.9% of the teeth with irreversible pulpitis showed severe hyperemia (Chi-square test, P = 0.006). Moreover, 63.3% of teeth diagnosed with reversible pulpitis presented fibrosis, while in the irreversible group, only 27.1% of the samples had fibrosis (Chi-square test, P = 0.002). In 58.3% of the cases in the irreversible group, pulp exposure could be detected on radiographs, while none of the specimen in the reversible pulpitis group exhibited pulp exposure (Chi-square test, P = 0.0001).
Table 2: The variables with significant differences in scores between the groups

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There were no significant differences between the two groups with respect to the severity of inflammation, necrosis, and presence of an adjacent odontoblastic layer [Table 3]. Most of the cases in both groups showed mild inflammation. In the reversible pulpitis group focal necrosis was observed in one case, while in the irreversible group, 14.6% showed focal necrosis (P > 0.05). An odontoblastic cell layer was present in 96.7% of the teeth diagnosed with reversible pulpitis and in 87.5% of the samples of irreversible pulpitis group (P > 0.05) [Figure 1]. Moreover, we didn't observe dentin bridge formation adjacent to the carious lesion in any of the samples examined.
Table 3: The variables with no significant differences in scores between the groups

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Figure 1: Hematoxylin and eosin stained demineralized sections of extracted carious molars. (a) Normal dentine-pulp showing: D: Dentine; P: Predentin layer; O: Odontoblast cell layer; (×40). (b) Histological features of reversible pulpitis in the area adjacent the caries site: D: Dentine; O: Odontoblast cell layer; F: Fibrosis. (c). Histological features near the carious lesion in tooth section with irreversible pulpitis: D: Dentine; H: Severe hyperemia

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There were significant differences between reversible and irreversible pulpitis groups regarding the responses to the cold test (P < 0.001). In the irreversible pulpitis group, 64.6% of the patients experienced pain for <10 s. While, 29.2% of the cases felt a pain lasting more than 10s by the cold stimulation. Among the samples of this group, 6.3% reported no pain following the cold test. In the reversible pulpitis group, 96.7% of the cases had 1–10s pain sensation due to the cold stimulation of the teeth. Notably, there were no cases of having pain for more than 10s. In 3.3% of the cases cold stimulation didn't elicit dental pain.

Histological examination of intact pulps revealed uninflamed connective tissues, with abundant cells, neurovascular bundles, and cell layer of odontoblasts.

  Discussion Top

In the present study, the number of noninflamed samples was significantly higher in the reversible pulpitis group than the irreversible one. Moreover, acute inflammation was more frequent in irreversible pulpitis compared to the other group. Irreversible pulpitis is characterized by the presence of bacteria or their by-products in dental tubules and the pulp tissue adjacent to deep caries;[19] as well as through an acute-inflammatory reaction predominantly characterized by the presence of neutrophils in the tissue beneath a lesion, suggesting neutrophil-chemotactic activity.[20]

Nonetheless, no significant difference was observed between the two study groups regarding the severity of inflammation. Mejare et al., in a systematic review, stated that there is not enough evidence to determine an association between the presence, nature and duration of clinical symptoms, with pulp inflammation severity.[21] The presence of inflammatory cells in a reversible pulpitis condition is not a strange finding. The inflammatory mechanisms help with pathogen elimination and repair stimulation. IL-10 is an immunosuppressive cytokine produced by many immune and non-immune cells, acting to suppress inflammation-associated immune responses, thus limiting damage to the host.[22] Moreover, within an inflammatory process, TNF-α may activate the p38 mitogen-activated protein kinase pathway, and induce odontoblast-like cell differentiation into dental pulp stem cells by increasing dentin sialoprotein, as well as dentin phosphoprotein expression, in turn forming tertiary dentin.[23] The accurate measurement of these cytokines may help predict the long-term prognosis of direct pulp capping. Besides, some molecular markers of inflammation from the dentinal fluids may also prove indicative of pulpal inflammation.[24]

Varying degrees of pulp inflammation have been found when caries extend through dentin, and more than half the distance to the pulp. Interestingly, in the cases where caries involve more than 50% of the dentin thickness, the severity of pulpal inflammation in primary molars is less in occlusal decays than in proximal ones.[16],[25] Further investigation into the assessment of pulpal inflammatory changes in permanent teeth, in conjunction with the location of carious lesions, is recommended.

Here, the presence of severe hyperemia was significantly more likely in the irreversible pulpitis group than in the reversible pulpitis one. However, in a pulp hyperemic condition, only some slight changes in an odontoblastic layer without inflammatory cells are typically observed.[17] Within the present study, in accordance with some previous studies,[26],[27] hyperemia was assessed based on the number of blood vessels. Nevertheless, we contend that immunohistochemical staining based on the vascular markers would be a more accurate method for assessment of vascular changes.

One of the interesting findings in our study was the high incidence of fibrosis in the reversible pulpitis group. Different inflammatory cytokines including interleukin-10 (IL-10) were detected in the dental pulp beneath both deep and shallow carious lesions.[28],[29] Elsalhi et al. showed significantly higher levels of IL-10 in the pulps of asymptomatic deep carious teeth as compared to the samples with irreversible pulpitis.[30] The role of IL-10 in contributing to the pathophysiologic development of fibrosis has been already suggested. Sun et al., indicated that IL-10-induced fibrocyte recruitment is likely mediated by the CCL2-CCR2 axis.[31] Moreover, dental pulp undergoes numerous regressive and reactive changes as individual ages. Increased fibrosis is one of the microscopically evident alterations.[32]

In the irreversible pulpitis group, 41.7% of the samples showed pulp exposure. In the study by Hasler and Mitchell, the rate of inflammation in nonexposed samples was significantly less than that of the exposed ones. However, it's an old study with wide confidence intervals and small sample size.[33]

In the present study, one case of the reversible pulpitis group exhibited localized necrosis. In a recent study, Zanini et al. also mentioned that pulp necrosis may be seen in asymptomatic patients whose disease could be wrongly diagnosed as reversible inflammation.[11] Decision making for a treatment plan would be even more complicated when we see good treatment outcomes resulting from vital pulp therapy techniques on symptomatic permanent teeth.[4]

If the carious process is controlled or arrested, stem/progenitor cells within the pulp congregate at the site of injury and to differentiate into odontoblast-like cells. These cells deposit a tertiary reparative dentin matrix, which clinically results in dentin bridge formation.[22] In the present study, probably due to the presence of active carious lesions, we didn't observe dentin bridge formation adjacent to the lesion in any of the samples examined. However, a dentin bridge is not necessarily a criterion for the healing of the pulp.[34]

Here, there was only 1 case of the reversible pulpitis group in which odontoblast layer could not be identified. However, the patient was 62 years old and thus we believe this finding may be attributable to the age of the patient. Beneath the carious lesion, primary odontoblasts would be exposed to bacteria, and their by-products which negatively affect them.[35] Cellular senescence may also occur in dental pulp tissue by different cell death pathways including necrosis, apoptosis or nonapoptotic pathways such as necroptosis, pyroptosis, or nemosis.[36],[37]

In this study, 29.2% of the samples in the irreversible pulpitis group had a reaction longer than 10 s following a cold testing, while none of the cases with reversible pulpitis had lingering pain. Hyman and Cohen stated that endodontic diagnostic tests could adequately identify cases which were free of disease, but were less effective in identifying disease-positive persons. The authors therefore suggested that practitioners should be prudent in their diagnosis of irreversible pulpal disease.[38] Interestingly, Ricucci et al. concluded that there is a good correlation between clinical and histological findings, especially in cases of normal pulp/reversible pulpitis.[9] In a systematic review, Mejare et al. found that the overall evidence was insufficient to assess the value of pulp testing, with reference to heat/cold stimulation in identifying the pulp condition.[21] Molecular-based strategies hold significant promise and may end up proving relevant in making the best treatment plan based on the pulp conditions.[11]

Among the limitations of this study, the followings is worthy of note. For histological studies, teeth should be extracted. Because most patients who are referred for tooth extraction have advanced carious lesions, the number of irreversible pulpitis samples in this study was therefore more than the samples with reversible pulpitis. Moreover, pulp inflammation involves several biological processes that can be evaluated at the macroscopic, microscopic, and molecular levels, and it is therefore imprecise to over-speculate on the nature of the cells, as well as the conditions of pulp tissue, when considering solely a morphological observation at the level of light microscopy.


The authors wish to thank the Research Committee of Kerman University of Medical Sciences for financial support. Thanks to the help of Mr. Vahid Bijari for English editing.

Financial support and sponsorship


Conflicts of interest

The authors of this manuscript declare that they have no conflicts of interest, real or perceived, financial or nonfinancial in this article.

  References Top

Rodd HD, Waterhouse PJ, Fuks AB, Fayle SA, Moffat MA; British Society of Paediatric Dentistry. Pulp therapy for primary molars. Int J Paediatr Dent 2006;16 Suppl 1:15-23.  Back to cited text no. 1
Trope M. Regenerative potential of dental pulp. Pediatr Dent 2008;30:206-10.  Back to cited text no. 2
Ou KL, Chang CC, Chang WJ, Lin CT, Chang KJ, Huang HM. Effect of damping properties on fracture resistance of root filled premolar teeth: A dynamic finite element analysis. Int Endod J 2009;42:694-704.  Back to cited text no. 3
Asgary S, Fazlyab M, Sabbagh S, Eghbal MJ. Outcomes of different vital pulp therapy techniques on symptomatic permanent teeth: A case series. Iran Endod J 2014;9:295-300.  Back to cited text no. 4
Seltzer S, Bender I, Ziontz M. The dynamics of pulp inflammation: Correlations between diagnostic data and actual histologic findings in the pulp. Oral Surg Oral Med Oral Pathol 1963;16:846-71.  Back to cited text no. 5
Schröder U. Agreement between clinical and histologic findings in chronic coronal pulpitis in primary teeth. Eur J Oral Sci 1977;85:583-7.  Back to cited text no. 6
Fox AG, Heeley JD. Histological study of pulps of human primary teeth. Arch Oral Biol 1980;25:103-10.  Back to cited text no. 7
Rayner JA, Southam JC. Pulp changes in deciduous teeth associated with deep carious dentine. J Dent 1979;7:39-42.  Back to cited text no. 8
Ricucci D, Loghin S, Siqueira JF Jr. Correlation between clinical and histologic pulp diagnoses. J Endod 2014;40:1932-9.  Back to cited text no. 9
Johnson RH, Dachi SF, Haley JV. Pulpal hyperemia – A correlation of clinical and histologic data from 706 teeth. J Am Dent Assoc 1970;81:108-17.  Back to cited text no. 10
Zanini M, Meyer E, Simon S. Pulp inflammation diagnosis from clinical to inflammatory mediators: A systematic review. J Endod 2017;43:1033-51.  Back to cited text no. 11
Garfunkel A, Sela J, Ulmansky M. Dental pulp pathosis. Clinicopathologic correlations based on 109 cases. Oral Surg Oral Med Oral Pathol 1973;35:110-7.  Back to cited text no. 12
Goodwin TL, Devlin H, Glenny AM, O'Malley L, Horner K. Guidelines on the timing and frequency of bitewing radiography: A systematic review. Br Dent J 2017;222:519-26.  Back to cited text no. 13
Parthasarathy A, Kamat SB, Kamat M, Kidiyoor KH. Histological response of human pulps capped with calcium hydroxide and a self-etch adhesive containing an antibacterial component. J Conserv Dent 2016;19:274-9.  Back to cited text no. 14
[PUBMED]  [Full text]  
Madani Z, Seyedmajidi M, Moghadamnia A, Bijani A, Zahed Pasha A. Histopathological evaluation of capsaicin on cat dental pulp. J Babol Univ Med Sci 2011;13:7-14.  Back to cited text no. 15
Kassa D, Day P, High A, Duggal M. Histological comparison of pulpal inflammation in primary teeth with occlusal or proximal caries. Int J Paediatr Dent 2009;19:26-33.  Back to cited text no. 16
Naseri M, Khayat A, Zamaheni S, Shojaeian S. Correlation between histological status of the pulp and its response to sensibility tests. Iran Endod J 2017;12:20-4.  Back to cited text no. 17
Nowicka A, Łagocka R, Lipski M, Parafiniuk M, Grocholewicz K, Sobolewska E, et al. Clinical and histological evaluation of direct pulp capping on human pulp tissue using a dentin adhesive system. Biomed Res Int 2016;2016:2591273.  Back to cited text no. 18
Love RM, Jenkinson HF. Invasion of dentinal tubules by oral bacteria. Crit Rev Oral Biol Med 2002;13:171-83.  Back to cited text no. 19
Rechenberg DK, Galicia JC, Peters OA. Biological markers for pulpal inflammation: A systematic review. PLoS One 2016;11:e0167289.  Back to cited text no. 20
Mejàre IA, Axelsson S, Davidson T, Frisk F, Hakeberg M, Kvist T, et al. Diagnosis of the condition of the dental pulp: A systematic review. Int Endod J 2012;45:597-613.  Back to cited text no. 21
Farges JC, Alliot-Licht B, Renard E, Ducret M, Gaudin A, Smith AJ, et al. Dental pulp defence and repair mechanisms in dental caries. Mediators Inflamm 2015;2015:230251.  Back to cited text no. 22
Paula-Silva FW, Ghosh A, Silva LA, Kapila YL. TNF-alpha promotes an odontoblastic phenotype in dental pulp cells. J Dent Res 2009;88:339-44.  Back to cited text no. 23
Zehnder M, Wegehaupt FJ, Attin T. A first study on the usefulness of matrix metalloproteinase 9 from dentinal fluid to indicate pulp inflammation. J Endod 2011;37:17-20.  Back to cited text no. 24
Duggal MS, Nooh A, High A. Response of the primary pulp to inflammation: A review of the Leeds studies and challenges for the future. Eur J Paediatr Dent 2002;3:111-4.  Back to cited text no. 25
Madani Z, Seyedmajidi M, Moghadamnia A, Bijani A, Zahedpasha A. Histologic evaluation of pulpal response to MTA and capsaicin in cats. Caspian J Dent Res 2012;1:8-13.  Back to cited text no. 26
Fachin EV, Scarparo RK, Pezzi AP, Luisi SB, Sant'ana Filho M. Effect of betamethasone on the pulp after topical application to the dentin of rat teeth: Vascular aspects of the inflammation. J Appl Oral Sci 2009;17:335-9.  Back to cited text no. 27
Hahn CL, Best AM, Tew JG. Cytokine induction by Streptococcus mutans and pulpal pathogenesis. Infect Immun 2000;68:6785-9.  Back to cited text no. 28
Elsalhy M, Azizieh F, Raghupathy R. Cytokines as diagnostic markers of pulpal inflammation. Int Endod J 2013;46:573-80.  Back to cited text no. 29
Elsalhy MM. Immunological Analysis of Dental Pulp Inflammation: Kuwait University; 2011.  Back to cited text no. 30
Sun L, Louie MC, Vannella KM, Wilke CA, LeVine AM, Moore BB, et al. New concepts of IL-10-induced lung fibrosis: Fibrocyte recruitment and M2 activation in a CCL2/CCR2 axis. Am J Physiol Lung Cell Mol Physiol 2011;300:L341-53.  Back to cited text no. 31
Baker A, Karpagaselvi K, Kumaraswamy J, Ranjini MR, Gowher J. Role of dental pulp in age estimation: A quantitative and morphometric study. J Forensic Dent Sci 2019;11:95-102.  Back to cited text no. 32
[PUBMED]  [Full text]  
Hasler JE, Mitchell DF. Painless pulpitis. J Am Dent Assoc 1970;81:671-7.  Back to cited text no. 33
Tronstad L, Mjör IA. Capping of the inflamed pulp. Oral Surg Oral Med Oral Pathol 1972;34:477-85.  Back to cited text no. 34
Yumoto H, Hirao K, Hosokawa Y, Kuramoto H, Takegawa D, Nakanishi T, et al. The roles of odontoblasts in dental pulp innate immunity. Jpn Dent Sci Rev 2018;54:105-17.  Back to cited text no. 35
Vanden Berghe T, Linkermann A, Jouan-Lanhouet S, Walczak H, Vandenabeele P. Regulated necrosis: The expanding network of non-apoptotic cell death pathways. Nat Rev Mol Cell Biol 2014;15:135-47.  Back to cited text no. 36
Man SM, Karki R, Kanneganti TD. Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases. Immunol Rev 2017;277:61-75.  Back to cited text no. 37
Hyman JJ, Cohen ME. The predictive value of endodontic diagnostic tests. Oral Surg Oral Med Oral Pathol 1984;58:343-6.  Back to cited text no. 38


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  [Table 1], [Table 2], [Table 3]


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