|Year : 2014 | Volume
| Issue : 2 | Page : 107-111
The effect of chronic periodontitis on dental pulp: A clinical and histopathological study
Surekha Ramrao Rathod1, Prajakta Fande (Zade)2, Trupti Satish Sarda1
1 Departments of Periodontics and Implantology, VSPM Dental College and Research Centre, Nagpur, Maharashtra, India
2 Department of Oral Pathology, VSPM Dental College and Research Centre, Nagpur, Maharashtra, India
|Date of Web Publication||28-Oct-2014|
Surekha Ramrao Rathod
Department of Periodontics and Implantology, VSPM Dental College and Research Centre, Mahalgi Nagar, Ring Road, Nagpur - 440 034, Maharashtra
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: This human study was carried out to evaluate the possible effects of severe chronic periodontal disease on the different aspect of dental pulp structure. Materials and Methods: A total of 20 permanent teeth with a hopeless prognosis due to severe chronic periodontitis were extracted from systemically healthy adults, with a pocket probing depth of ≥8 mm and a mobility of grade 3. After extraction, the apical 2-3 mm of the roots were immediately sectioned with a fissure bur. Results: Inflammation was usual finding in the samples, however, only 15% of the teeth showed no inflammation. Pulpal necrosis (partial or complete) was seen in different sections, and it was observed that 50% sections had no necrosis. Partial necrosis was a common finding seen when compared to complete necrosis (6.7%). About 60% of samples showed edematous pulp. Only 6.7% of samples showed absence of fibrosis. Pulp with moderate fibrosis was seen commonly seen in many sections. A majority of teeth (70%) also displayed a loss of odontoblastic integrity. In only 25% of samples, pulp stones were detected. Conclusion: Our results revealed that severe chronic periodontitis can affect dental pulp. The cumulative effect of the periodontal disease, as indicated by the factors of calcifications, apposition of calcified tissue, resorption or inflammation from the root caries or from the involved lateral canals, is damaged pulp tissue, but total disintegration is a certainty only when all main apical foramina are involved by bacterial plaque. Proper evaluation and treatment of periodontal-endodontic involvement is recommended.
Keywords: Chronic periodontitis, dental pulp, fibrosis, inflammation, necrosis
|How to cite this article:|
Rathod SR, Fande (Zade) P, Sarda TS. The effect of chronic periodontitis on dental pulp: A clinical and histopathological study
. J Int Clin Dent Res Organ 2014;6:107-11
|How to cite this URL:|
Rathod SR, Fande (Zade) P, Sarda TS. The effect of chronic periodontitis on dental pulp: A clinical and histopathological study
. J Int Clin Dent Res Organ [serial online] 2014 [cited 2020 May 31];6:107-11. Available from: http://www.jicdro.org/text.asp?2014/6/2/107/143494
| Introduction|| |
Apical, lateral or accessory canals provide intimate anatomical relation of the pulp to periodontal tissues. Colyer and Cahn reported the possibility that periodontal disease might be related to or cause pulpal disease and described structures that are currently termed lateral canals. Since then, several researchers have focused on this subject in clinical and histopathological investigations. The presence of lateral canals has been reported beyond doubt. ,
Studies in human beings and experimental animal models have shown that varying degrees of periodontal changes can be caused by pulpal pathosis. Moreover, it was concluded that, following routine endodontic therapy these regions of rarefaction become resolved with complete bone regeneration without periodontal therapy. However, controversy exists between the interrelationship of periodontal disease and pulpal pathosis with several opposing and apparently irreconcilable line of evidence being supported in the literature. ,,
The histological changes in the pulp tissue of periodontally involved teeth can vary from normal to necrotic. The reasons for such a melange in their respective findings may include lack of uniform documentation of case histories, lack of definitive criteria for selection of cases and their descriptive histological observations. 
The aim of the present study was to address the controversy surrounding the relationship between periodontal disease and pulpal tissue changes. To determine the degree to which pulpal pathosis is associated with periodontal disease, pulp of teeth affected by severe chronic periodontitis were evaluated. Cases with a history of periodontal therapy were excluded to eliminate causation by other complications such as decay, operative procedures or periodontal manipulation.
| Materials and methods|| |
Study sample consisted of 20 human teeth with chronic periodontitis that were extracted from patients with a mean age of 48.1 years visiting the Department of Periodontics and Implantology. The study was conducted after the approval from institution's Ethics Committee. Consent forms were signed from the patients who participated in this study. The diagnosis of chronic periodontitis was established based on the criteria of the American Academy of Periodontology (1999). Pulp tissue samples were obtained from 20 single rooted teeth that were extracted. Only caries free intact teeth were included in the study. Periodontally, each tooth was assessed by measuring periodontal pocket depth, soft tissue recession, and grade of mobility of each tooth. The extracted teeth exhibited probing pocket depth ≥8 mm and a mobility of grade 3, crown to root ratio >1:1, no caries or fillings, and no history of operative manipulation, trauma or bruxism. Systemically healthy patients who were not on any medication and did not show gingival recession were included. If tooth was diagnosed as hopeless, the treatment of choice to be carried out was extraction with either a bridge or ridge augmentation and an implant. All samples used in this study had natural periodontal involvement.
After injecting local anesthesia, the teeth were extracted as nontraumatically as possible to avoid the histological sequel of traumatic extraction. Immediately following extraction, the apical 2-3 mm of roots were sectioned with a fissure bur using a high-speed hand piece under a constant flow of cool water. This was done so that the formalin could enter the pulp chamber and therefore 7 days of fixation was sufficient. Decalcifying agents do have an effect on pulp and that is it little bit affects the staining quality of pulp tissue. It does not take up the hematoxylin stain properly. However, there is no way we can protect the pulp tissue while decalcification. Some changes do occur in pulp.
If apical root sectioning would not have been done and the tooth would have been placed directly in formalin then some changes would have been observed in the pulp tissue as it would take time for formalin to penetrate into the pulp chamber. Furthermore, exposing the coronal portion of the pulp would have produced more pulpal changes due to the heat liberated from the bur as a larger part of the crown would have to be sectioned. And so apical root sectioning was done.
Teeth were then placed in 10% neutral buffered formalin for 7 days. Then teeth were placed in 10% nitric acid for 10-15 days for decalcification. The specimens were histologically processed, embedded in paraffin and serially sectioned using a microtome at 3 μm thickness. The roots were arbitrarily divided into the coronal third, middle third and apical third zones. About 4-5 sections were mounted on each slide, and every third slide was stained with hematoxylin and eosin, the sections were later examined by the authors and oral pathologist. Experienced oral pathologists reviewed the slides. 
Microscopic examination of each section was made and then pulp was assessed based on the following parameters: Relative degree of inflammation, amount of fibrosis, presence of pulp stones, presence of edema and condition of pulpal vessels, and odontoblastic integrity. The criterion for grading the inflammation was: No inflammation (0-2 infiltrating cells), light inflammation (2-5 infiltrating cells), moderate inflammation (5-10 infiltrating cells), and severe inflammation (>10 infiltrating cells).
The criteria for grading fibrosis were as follows: Light fibrosis (3-10 fibroblast cells), moderate fibrosis (11-30 fibroblast cells), and severe fibrosis (≥31 fibroblast cells). Necrotic specimens were categorized into three groups (no necrosis, partial necrosis or complete necrosis). Necrosis in nearly one-third part of the pulp chamber was considered as partial and necrosis in entire pulp as complete. Nonnecrotic pulp is included while considering necrosis as shown in the table.
Vessels were divided into three groups (normal, atrophied, or dilated) according to the size. The vessels with very small lumen were considered as atrophied and with large lumen with or without red blood cells (RBCs) were considered as dilated. The vessels in between these two were considered normal which has an acceptable lumen with or without RBCs. After viewing multiple slides, obvious distinction can be made between normal, atrophied, and dilated blood vessels.
Edema was defined as the accumulation of the interstitial fluid in pulp. Each tooth was examined at coronal, mid-root and apical areas, and the cumulative results were considered [Table 1].
|Table 1: Histologic evaluation of teeth with chronic periodontitis under various parameters|
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| Results|| |
Histological sections were evaluated by microscopy, regardless of clinical results. Several microscopic sections indicate that the condition of the pulp in periodontally affected teeth can range from intact to necrotic in different sections of the same tooth. The mean age of participants in the study was 48.1 years, and pulp tissue samples were obtained from 20 single rooted teeth extracted due to hopeless prognosis. Inflammation was a common finding in the samples, however, only 15% of the teeth showed no inflammation. In most (41.7%) cases inflammation was mild. Pulpal necrosis (partial or complete) was seen in different sections, and it was found that 50% sections had no necrosis. Partial necrosis was more commonly seen as compared to complete necrosis (6.7%). About 60% of samples showed edematous pulp [Figure 1]. Only 6.7% of samples showed absence of fibrosis. Pulp with moderate fibrosis was seen in many sections [Figure 2] and [Figure 3]. A majority of teeth (70%) also displayed a loss of odontoblastic integrity. Pulp stones were present in only 25% of samples [Figure 4]. Finally, intact vessels were seen in most teeth but dilated, and atrophic changes (21.7%) were also seen.
|Figure 1: Severe pulpal fi brosis is seen along with edema at place (H and E, ×400)|
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|Figure 3: Presence of diffuse calcification is evident along with pulp fibrosis (H and E, ×400)|
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| Discussion|| |
In our study, we established interrelationship of periodontal disease and pulpal pathosis. Pulpal pathosis considered in the present study were inflammation, fibrosis, edema, necrosis, loss of odontoblastic integrity, pulp stones, and alteration in the state of blood vessels. The interrelationship between periodontal and pulpal diseases is based on anatomic and circulatory relationship which is a cost effect relationship.
Inflammatory lesions are produced in both the apical and radicular areas of the pulp by periodontal diseases. The latter is commonly associated with the periodontal lesion. Periodontal lesion can lead to secondary pulpitis.  More recently, while studying the vascular architecture of the human dental pulp, Russell and Kramer, Kramer, and Saunders established the intricate relationship of pulpal and periodontal tissues by utilizing perfusion techniques. A micro-radiographic technique was used by Saunders. Their investigations revealed that particularly in the bifurcation or trifurcation area large vessels may be found running through the radicular dentine. These large vessels supply one root canal, sometimes appearing to contribute more to the root canal vascular system than the vessels entering the apical foramen. Smaller vessels running between the root canal and the periodontal membrane are commonly found. These findings accredited to the fact that interradicular canals do exist and unite the pulp and periodontium in an intimate relationship. ,, In some text, there is no mention of lateral cannals, most often lateral canals are referred to as apical ramifications, this omission may occur if the teeth were not sectioned serially and thus the ubiquitous distribution of the lateral canals was not recognized. 
Pulp with partial or complete necrosis was seen in various sections, although several sections displayed no necrosis. The scientific thinking for development of necrosis was pressure from the mobility of the periodontally involved teeth. Another mechanism that could be considered for the production of atrophic changes, inflammation, and necrosis of the pulp was the interference of some of the blood supply through the lateral canals within the furcation region and along the side of the roots. The blood vessels supplying small areas of the pulp through the lateral canals may become involved as a result of the periodontal lesion. A pain spasm can be initiated by loss of blood supply to a small region of the pulp. Further, this can lead to subsequent death of the pulp cells supplied by the affected capillaries. A small area of infarction develops, followed by coagulation necrosis. The death of the cells with subsequent calcification is a usual sequence of blood deprivation.
Another cause of interferences with the blood supply to the pulp includes periodontal treatment necessitating curettage of pockets and planning of the root surfaces. 
Slight amount of pulpal inflammation was a usual finding in most of the teeth. These lateral canals could be avenues through which the toxic products and/or inflammatory extensions can affect the surrounding periodontal tissue. Similarly, literature from previous studies conducted on periodontally involved teeth manifested that all pulpal sections displayed a generalized infiltration of inflammatory cells including frequent lymphocytes, plasma cells, macrophages with a few polymorphonuclear leukocytes. 
Moderate fibrosis of the pulp was encountered commonly. Fibrosis is, usually, seen with aging and chronic irritation of the pulp. However, studies have showed that, after the age of 39 years, there is no increase in the collagen amount in radicular pulp. The justification for age not being consistently linked to pulpal calcification is that pulpal changes found in older patients are not further advanced than those seen in young patients. Hence, we can conclude that age per se cannot be regarded as a causative factor for fibrosis. 
In this study, no pulp stones were observed in most teeth, similar to other studies. Rubach and Mitchell in their study mentioned that denticles, ranging from diffuse to concentric laminated bodies, were most common in coronal pulp. Serial sections were taken, and it was found that these pulp stones were actually projection of primary or more often secondary dentin from the internal pulpal wall. The presence of surrounding odontoblast indicated that such structures were dentin. 
The vessels varied in diameter. Dilated pulpal vessels were commonly seen, although in other teeth intact vessels and atrophic changes were also seen. Even though, the blood vessels were dilated, nonedematous pulp was seen in most teeth. Ekblom and Hansson marked fenestrated capillaries frequently in odontoblastic region. Also, most of the teeth displayed no odontoblastic integrity. 
The concept of "retrograde pulpitis" was instigated in 1963 by Seltzer and others. Periodontal lesion routinely produced atrophic and degenerative changes in the pulp of involved teeth due to interference of nutritional supply.  Many pulp stones in several human cases of periodontal disease were found by Grajewska.  Nemec et al. showed that findings related to periodontally affected teeth included acute and chronic pulpitis, vascular congestion and pulp necrosis. 
In a contradictory to this study and several studies, many other studies have reported conflicting results. In a study by Mazur and Massler, they disagree that a periodontal disease has any effect on the pulp. It is their belief that the changes that were present in the pulps were due to systemic disease of the patient. However, they failed to mention what type of systemic diseases were encountered, if any.  Our findings were contradictory to those of Czarnecki and Schilder, who recommended no cause and effect relationship between the presence of periodontal disease and pulpal changes.  Also, Sauerwein in his study found no adverse effects on the pulpal tissues of the teeth with periodontal disease. 
This literature review had showed that the influence of the periodontal disease on the dental pulp has been approached from various angles. It seems likely that pulp tissue can be affected by periodontal disease, but we cannot consider that, just because periodontal disease exists, the pulp can become involved. It was demonstrated by Langeland et al. that although pulpal inflammation can occur in the presence of periodontal disease from involved accessory canals, total pulpal disintegration apparently occurs only when all main apical foramina are involved by bacterial plaque. Equally important from a periodontal standpoint of view is the fact that necrotic tissue and bacterial plaque housed in these canals, although not severely affecting the pulp, may tend to perpetuate periodontal furcation lesions making successful therapy nearly impossible. 
It is indeed, difficult to prepare a control group in human studies of periodontal disease and ideally, control and test teeth should be extracted from one person. Hence, it is unclear whether changes observed were limited to diseased teeth or whether they would also be observed in other teeth from the same patient. Discrepancies between previous results and those seen in this study can be because of the use of different criteria for histological and clinical evaluation of the pulp tissue or lack of similar documentation of the periodontal disease parameters. Some limitations need to be acknowledged. In our study, we did not use scanning electron microscope (SEM). SEM studies are difficult to perform as it is not easily available and is expensive.
| Conclusion|| |
Our results revealed that severe chronic periodontitis can affect dental pulp. The cumulative effect of the periodontal disease, as indicated by the factors of calcifications, apposition of calcified tissue, resorption or inflammation from the root caries or from the involved lateral canals, is damaged pulp tissue, but total disintegration is a certainty only when all main apical foramina are involved by bacterial plaque. Proper evaluation and treatment of periodontal-endodontic involvement is mandatory.
| References|| |
Colyer F. Bacteriological infection in pulps of pyorrhectic teeth. Br Dent J 1924;45:558.
Altman M, Guttuso J, Seidberg BH, Langeland K. Apical root canal anatomy of human maxillary central incisors. Oral Surg Oral Med Oral Pathol 1970;30:694-9.
Bender IB, Seltzer S. The effect of periodontal disease on the pulp. Oral Surg Oral Med Oral Pathol 1972;33:458-74.
Simon JH, Glick DH, Frank AL. The relationship of endodontic-periodontic lesions. J Periodontol 1972;43:202-8.
Stallard RE. Periodontic-endodontic relationships. Oral Surg Oral Med Oral Pathol 1972;34:314-26.
Torabinejad M, Kiger RD. A histologic evaluation of dental pulp tissue of a patient with periodontal disease. Oral Surg Oral Med Oral Pathol 1985;59:198-200.
Fatemi K, Disfani R, Zare R, Moeintaghavi A, Ali SA, Boostani HR. Influence of moderate to severe chronic periodontitis on dental pulp. J Indian Soc Periodontol 2012;16:558-61.
Russell LH, Kramer IR. Observations of the vascular architecture of the dental pulp. J Dent Res 1956;35:957.
Kramer IR. The vascular architecture of the human dental pulp. Arch Oral Biol 1960;2:177-89.
Saunders RL. X-ray microscopy of the periodontal and dental pulp vessels in the monkey and in man. Oral Surg Oral Med Oral Pathol 1966;22:503-18.
Second International Conference on Endodontics. Oral Surg Oral Med Oral Pathol 1960;13:990-3.
Ghoddusi J. Ultrastructural changes in feline dental pulp with periodontal disease. Microsc Res Tech 2003;61:423-7.
Rubach WC, Mitchell DF. Periodontal disease, age, and pulp status. Oral Surg Oral Med Oral Pathol 1965;19:482-93.
Ekblom A, Hansson P. A thin-section and freeze-fracture study of the pulp blood vessels in feline and human teeth. Arch Oral Biol 1984;29:413-24.
Grajewska I. Ultrastructural study of the dental pulp in patients with adult periodontitis. Ann Univ Mariae Curie Sklodowska Med 1997;52:23-8.
Nemec A, Pavlica Z, Stiblar-Martincic D, Petelin M, Erzen D, Crossley D. Histological evaluation of the pulp in teeth from dogs with naturally occurring periodontal disease. J Vet Dent 2007;24:212-23.
Mazur B, Massler M. Influence of periodontal disease of the dental pulp. Oral Surg Oral Med Oral Pathol 1964;17:592-603.
Czarnecki RT, Schilder H. A histological evaluation of the human pulp in teeth with varying degrees of periodontal disease. J Endod 1979;5:242-53.
Sauerwein E. Histopathology of the pulp in instances of periodontal disease. Dentabs 1956;1:467-8.
Langeland K, Rodrigues H, Dowden W. Periodontal disease, bacteria, and pulpal histopathology. Oral Surg Oral Med Oral Pathol 1974;37:257-70.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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