Effect of Dentin Thickness on the Pulp of Single Rooted Teeth in Severe Chronic Periodontitis: Histological Study

Introduction

Periodontium and pulpal spaces communicate through various portals, such as root canal foramina, dentinal tubules, and even crack lines, through which bacteria and microbial irritants may trigger inflammatory responses in the surrounding tissues.¹

There is evidence that pulp disease can initiate or spread as periodontal disease through the apical foramen. It has been shown by various studies that pulpal changes such as inflammation, necrosis, calcification, and fibrosis can be influenced by the presence of periodontal disease and its severity.^{2, 3}

Structural and ultrastructural changes observed in the radicular cementum and dentin of teeth which were periodontally affected, observed bacterial invasion. Bacteria were found to adhere to Sharpey’s fibers, radicular cementum, and odontoblastic processes.^{3, 4}

Bacterial invasion was also found in the dentinal tubules, especially in areas where attachment loss had occurred. Outer 3^rd of radicular dentin showed maximum accumulation.⁵

Studies have demonstrated that bacterial invasion can occur in the root cementum and radicular dentin of those teeth with periodontal involvement, and bacteria were detected on the pulpal wall and in the dental pulp of those teeth, which shows the influence of periodontitis upon pulpal tissues.⁶

In a study done to measure the radicular dentin thickness of both anterior and premolar teeth, it was found that the radicular dentine thickness mainly varies depending on location and section factors rather than tooth type. Larger values of dentine thickness were detected near the lingual and buccal surfaces with reduced thicknesses near the mesial and distal surfaces.⁷

Although there are many studies demonstrating the influence of severe periodontitis on the pulp, the issues of dentine thickness on the influence of pulpal changes in teeth with deep periodontal pockets has not been assessed. There is a lack of compelling data to establish its clear association. So, the present study evaluates the effect of dentin thickness on the pulp in severe chronic periodontitis.

Materials and Methods

From patients meeting the inclusion and exclusion criteria, 50 teeth with severe periodontitis were extracted and collected.

Inclusion criteria included: Age 18-65yrs, Grade III mobility, probing pocket depth ≥ 8 mm in single-rooted teeth, no caries or filling, no history of operative manipulation, trauma, or bruxism, and patients willing to give informed consent.

Teeth with carious involvement extracted for orthodontic treatment, patients with endodontic treatment history, and patients not willing to give informed consent were not included in the study.

Post-extraction, immediate access opening was done for each sample and placed in 10% formalin solution to ensure pulp fixation. After 7 days of pulp fixation, the samples were decalcified in 10% nitric acid for 12-15 days.The specimens were embedded in paraffin and serially sectioned using a microtome at 3μm thickness and staining with hematoxylin and eosin was done to assess the pulpal changes (Figure 1).

The histological parameters observed were inflammation, fibrosis, edema, necrosis, presence of pulp stones, odontoblastic integrity, and pulp vessels. A photomicrograph was taken and radicular dentin thickness was measured using GIMP software at three reference points on each specimen, i.e., coronal, middle, and apical third, and the mean radicular dentin thickness for each sample was calculated. (Figure 2). The obtained values were compared with the histological pulpal changes and analyzed.

Statistical analysis

Descriptive analysis of all explanatory and outcome parameters was done using mean and standard deviation for quantitative variables, frequency, and proportions for categorical variables. Inferential statistics Pearson Correlation test was used to evaluate the correlation between radicular dentin thickness and periodontal pocket depth. Chi Square Goodness of Fit test was used to compare the distribution of relative degree of inflammation, amount of fibrosis, presence of pulp stones, presence of edema, and condition of pulpal vessels, and odontoblastic integrity. The level of significance was set at P <0.05

Results

Fifty samples from 23 patients were included in the study; out of which 9 were males and 14 females. The mean age of the male and females patients, 45 and 46 years, respectively. There were no significant differences in age and gender distribution between the patients included in the study.

Histological studies on pulp changes in patients with chronic periodontitis revealed a variety of histological aspects that may correlate with the severity of periodontal lesions. (Figure 3)

Figure 3: Histological parameters (Hematoxylin & Eosin stain)

a) Inflammation

b) Presence of Edema

c) Fibrosis

d) Odontoblastic integrity

e) Pulp stone

f) Blood vessels

Inflammation was a common finding in the samples, with only 4% of the teeth showing no inflammation. Among the samples showing inflammation, 46% was mild, moderate in 18%, and severe in 32%. There was the presence of numerous mononuclear round lymphocytic, plasma cell and macrophage-type cells, and fewer granulocytic cells.

Fibrosis is defined as an increased concentration of fibroblasts and collagen fibers. Severe fibrosis was seen in 64% of the samples. Rest of the samples showed 18% each of mild and moderate fibrosis. Fibrosis, calcification, and collagen resorption have been reported in the pulps of teeth with long-standing periodontal disease.

Among the samples studied, 24% of the cases showed pulp calcification. The shape and sizes of these “dystrophic calcifications” varied from one patient to another.

Pulpal edema was seen in 46% of the cases and 54% of the samples showed no signs of edema in the pulp. Dental pulp tissue changes were accompanied by vascular changes. Pulp vessels were normal in 66% of the cases, dilated in 32%, and atrophied in 2% of the cases.

54% of the samples had complete odontoblast layers, and vacuolar degeneration of the odontoblastic layer was demonstrated by 46%. None of the samples showed pulpal necrosis.

Relations between radicular dentin thickness with pulpal changes were assessed (Table 1). In cases of mild inflammation, the mean dentin thickness was 183.38, and in moderate and severe inflammation the mean dentin thickness was 208.87 and 195.53, respectively, (p value of 0.71) which showed no statistically significant difference.

In case of mild, moderate, and severe fibrosis, the thickness of radicular dentin was 223.87, 208.75, and 181.46, respectively (p value 0.31). Although fibrosis was severe with reduced thickness of root dentin, it was not statistically significant.

Pulp stone, its presence or absence, when compared with the mean radicular dentin thickness, showed no statistically significant difference (p value 0.11). The mean thickness was 162.07 in the samples where pulp stones were present, whereas in samples where it was absent, the mean thickness was 204.09.

When the presence of edema with mean dentin thickness 195.44 or its absence (mean dentin thickness,192.78) was compared with root dentin thickness (p value 0.91), there was not a statistically significant difference.

Specimens which showed normal pulp vessels had a mean dentin thickness of 199.11, whereas dilated vessels showed a thickness of 184.66mm and in case of atrophied, it was 175 mm. No statistically significant difference was noticed. (p value 0.81)

The mean radicular dentin thickness was observed to be 185.73mm in cases where the odontoblastic integrity was lost while it was 201.06 mm in the specimens showing the presence of odontoblastic integrity. P value was 0.49 which was statistically insignificant. Necrosis was not seen in any of the collected samples.

Discussion

There is a general agreement that pulpal disease can initiate and/or perpetuate periodontal disease. Periodontal disease could cause pulpal inflammation, fibrosis, calcification, degenerative changes and necrosis, and root surface resorption has been suggested by several investigators.⁸ As teeth age, there is a general tendency for narrowing of the pulp cavity, a reduction in cellularity, vascularity, and increase in fibrosis of the pulp. Periodontitis and endodontic infections have been found to be linked to each other in several studies. Apical, lateral, or accessory canals provide an intimate anatomical relation of the pulp to periodontal tissues.^{8, 9}

Inflamed or necrotic pulps, produced from periodontal lesions, are instrumental in perpetuating the periodontal lesion by allowing these toxic products into the periodontal tissues through the lateral canals or other means of ingress.¹⁰

Studies have shown a greater incidence of pulpal inflammation and degeneration in periodontally involved teeth anda significant increase in dentin formation in teeth which are periodontally involved when compared to healthy teeth.¹¹

This study evaluated the pulpal tissue changes in teeth suffering from severe periodontitis and evaluated their influence on the pulp by comparing it with radicular dentin thickness.

Among the 96% of the samples showing inflammation, mild inflammation was seen in 46%, whereas moderate and severe inflammation was seen in 18% and 32% of the samples, respectively. The mechanism of inflammation in dental pulp is the same as that of other tissues. Pulp responds differently to different stimuli, based on the duration and intensity of it, ranging from mild inflammation to complete necrosis. In addition, irritation can cause degenerative changes in the pulp, including fibrosis and calcification. As a result of diverse stimuli, such as injury and bacterial contamination, various types of nonspecific inflammatory mediators, including serotonin, histamine, arachidonic acid metabolites (prostaglandin E2) , bradykinin, and various interleukins, are released in this process causing inflammation.¹²

The present study shows a positive correlation with the severity of periodontitis. It confirmed earlier study findings that the most frequent effects of periodontal disease on pulpal tissue are inflammation and degenerative pulpal alterations, such as fibrosis.¹⁰

Forty samples were used in the study to examine the pulpal alterations linked to advanced periodontitis, and it was discovered that fibrosis and pulpal edema were present in 36.84% of cases.¹³ In our study, 64% of the samples showed fibrosis which may be due to the initial effect of periodontal inflammation on the pulp which is degenerative. This adds up evidence to the existing literature that fibrosis is a common pulpal change in periodontitis affecting teeth. The study also investigated the pulpal calcifications and found that 52.62% of the samples showed pulp stones, whereas our study showed pulp stones in 76% of the samples.

These findings are compatible with the degenerative changes in the pulp consequently of pulp aging, which is well documented in the literature.¹⁴ Edema was defined as the accumulation of the interstitial fluid in pulp. Vasodilatation and increased vascular permeability were the result of secretion of various mediators. Increased serum protein filtration from the blood vessels leads to pulpal edema. This might be the possible mechanism of edema in 46% of the cases in the present study.¹²

Various nonspecific inflammatory mediators, including histamine, bradykinin, serotonin, arachidonic acid metabolites (prostaglandin E2), and various interleukins, are released leading to vasodilatation and increased vascular permeability. In the current study, 32% of the specimens showed dilatation of pulpal vessels. Although the blood vessels were dilated, most teeth showed non-edematous pulp. Present study did not show any pulpal necrosis.

Radicular dentin thickness

The mean radicular dentin thickness was highest with 208.87 mm in moderate inflammation cases, whereas in mild and severe cases it was 183.38 and 195.53 mm, respectively. The diversity of the results could be due to the influence of other parameters such as age. It is wildly reported that the young pulp has numerous vascular anastomoses to ensure favorable pulpal vascularization and sufficient defense potential. It also depends on dentin permeability.

When pulp stones were present, the mean thickness seemed to be reduced unlike in its absence. Teeth with the presence of absence of pulp stones, did not show any statistically significant difference when root dentin thickness was compared between the two. Although the thickness of root dentin was less in teeth with pulp stones, the p value was 0.11. This may be because there are no direct relationships between pulp stones and radicular dentin thickness, and the presence of pulp stones may change internal anatomy.¹⁵

Presence of edema showed similar results, with 194.44 mm in the presence of edema while the absence resulted in 192.78 mm of radicular dentin thickness.

When pulp vessels were compared with root dentin thickness, it was observed that in normal vessels the dentin thickness was 199.11. In vessel dilatation, the thickness was reduced and the thickness was least in case of atrophy. This again showed a positive co-relation between the root dentin thickness and pulpal changes, although statistically insignificant.

Odontoblastic integrity complied with other histological parameters. Teeth which showed loss of odontoblastic integrity had a mean thickness of 185.73mm while other samples with the presence of odontoblastic integrity had a thickness of 201.06 mm. Except inflammation and edema, all other parameters were positively correlated with radicular dentin thickness. This may suggest a connection between the pulpal alterations and the thickness of the radicular dentin.

All procedures involving the tooth‘s root must be guided by knowledge of the radicular dentine thickness. Biomechanical studies suggest that 1 mm or more of root dentine should remain to avoid the risk of root fracture.⁷

Periodontal procedures like root planing have a risk of removal of radicular dentin and thereby increase the risk of pulpal changes.

Although it has been proven by various studies that the entry of infection or microorganisms and mediation have been associated with lateral canals, accessory canals, and apical foramen, the thickness of root dentin can also affect the health of the pulp. Results revealed no statistically significant differences, thus a relationship between the pulpal of inflammation and radicular dentin thickness could not be established.

From the study, it can be proposed that radicular dentin thickness reduction can have a positive correlation with pulpal changes. This in turn may suggest the teeth with reduced root dentin thickness are at risk of developing pulpal changes.

Although the study did not show any statistically significant difference for the association of pulpal changes with the root dentin thickness, increasing the size of the sample and considering the presence of accessory canals and lateral canals could influence the outcome of the study. Moreover considering the normal anatomy of root dentin, the thickness of root dentin is less in the mesio-distal direction with added attachment loss in the interproximal area. This could also have a considerable variation in the study‘s results. The pulpal response is also related to the thickness and degree of calcification of the remaining dentin. Therefore, dentin permeability can be reduced by dentinal sclerosis and reparative dentin formation. Such conditions may also predispose the pulp to changes.

Within the constraints of the present investigation, we can say that root dentin thickness can have an influence on the health of the dental pulp in periodontitis patients, which requires further validation.

Conclusion

It can be inferred from the study that teeth with periodontal disease exhibit changes in the dental pulp. The changes seen may be predominantly inflammation, edema, presence of pulp stones, fibrosis, loss of odontoblastic integrity, and changes in pulp vessels. Although a statistically significant difference was not observed in the root dentin thickness changes in pulpal histology, there is a definitive increase in the severity of pulpal changes associated with inflammation. The fact that the study’s end point of decalcification varied despite the use of standard techniques was one of its limitations. Radicular dentin thickness may be an important parameter to be taken into account while performing any treatment involving the tooth root. Thus, it may be concluded that proper evaluation and treatment of periodontal -endodontic involvement is mandatory.

Source(s) of Support

Nil

Conflicts of interest

Nil