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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 4  |  Issue : 4  |  Page : 101-103

Comparative evaluation of alkaline phosphatase levels in dental pulp of diabetic and nondiabetic individuals


Department of Conservative and Endodontic Dentistry, Dr. D Y Patil Vidyapeeth, Dr. D Y Patil Dental College and Hospital, Pune, Maharashtra, India

Date of Web Publication15-Feb-2018

Correspondence Address:
Dr. Pradeep Shetty
Department of Conservative and Endodontic Dentistry, Dr. D Y Patil Vidyapeeth, Dr. D Y Patil Dental College and Hospital, Pimpri, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdrr.jdrr_2_18

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  Abstract 

Objective: The objective of this study was to evaluate changes in inflammatory components of alkaline phosphatase in dental pulp of patients with Type II diabetes mellitus and nondiabetic patients. Methodology: The study was carried out among 135 participants of the age group between 45 and 65 years, and participants were divided into three groups (n = 45 in each group) – a control group, diabetic with good glycemic control, and diabetic with poor glycemic contro l. After clinical examination with Russell's Periodontal Index, teeth indicated for extraction were extracted, and dental pulp was extirpated. Levels of alkaline phosphatase were assessed by p-nitro-phenylphosphate-2-amino-2-methyl-1-propanol (IFCC) and kinetic assay method. Results: Mean levels of the inflammatory component of alkaline phosphatase level were more in poorly controlled glycemic level group as compared to other two groups, and the difference between the groups was statistically significant (P < 0.001). Conclusion: Inflammatory mediators may have an impact on the pulpal treatment procedures. The results imply that diabetes is a critical factor that has profound effects upon oral tissues, resulting in expression of inflammatory mediators and modifications of structural components of dental pulp.

Keywords: Dental care, diabetes, inflammatory mediators, pulp, teeth


How to cite this article:
Shetty P, Mulay S, Chawala M, Shaikh M, Sawant S. Comparative evaluation of alkaline phosphatase levels in dental pulp of diabetic and nondiabetic individuals. J Dent Res Rev 2017;4:101-3

How to cite this URL:
Shetty P, Mulay S, Chawala M, Shaikh M, Sawant S. Comparative evaluation of alkaline phosphatase levels in dental pulp of diabetic and nondiabetic individuals. J Dent Res Rev [serial online] 2017 [cited 2021 May 5];4:101-3. Available from: https://www.jdrr.org/text.asp?2017/4/4/101/225629


  Introduction Top


Diabetes mellitus (DM) is nowadays a common but a complex metabolic disorder which is characterized by abnormal metabolism that results either from profound or absolute deficiency of insulin or from target tissue resistance to its cellular metabolic effects. The prevalence of diabetes is rapidly rising all over the globe at alarming rate. India currently faces an uncertain future in relation to the potential burden that diabetes may impose upon the country. Diabetes currently affects more than 62 million Indians, which is more than 7.1% of the adult population.[1],[2],[3],[4]

The metabolic consequences of the DM are hyperglycemia with widespread complications and damage. It particularly includes microangiopathy, macroangiopathy swith accelerated arteriosclerosis, neuropathy involving neuromuscular dysfunction, and decreased resistance to infection. However, in case of poorly controlled diabetics, the inflammatory reaction is more acute because of vascular leakage and cell dehiscence.[3],[5],[6]

Dental pulp is a unique connective tissue as it has a specific microcirculatory system with no lateral blood vessel branches. Along with it, dental pulp is located within solid dentinal walls that cannot accept any significant change of its volume, making it very prone to irreversible inflammatory changes shortly after the impact of noxious stimuli.[5] This can be significantly intensified in persons with DM known for their tissue vulnerability caused by macro- and micro-circulatory disorders.

The individuals suffering from diabetes are more prone to bacterial or opportunistic infections due to a generalized circulatory disorder where blood vessels are damaged by accumulation of atheromatous deposits in the tissues of the blood vessel lumen. In addition, blood vessels, particularly capillaries, develop a thickened basement membrane that impairs the leukotactic response, and there is a decrease in leukocyte microbicidal ability and failure to deliver the humoral and cellular components of the immune system. Long-standing diabetes also results in thickened basement membrane in dental pulp vessels which affects the pulpal blood flow.[7]

The literature regarding studies on the effects of diabetes on dental pulp, the effects of short and long-standing diabetes on dental pulp components such as nitrites, kallikrein, alkaline phosphatase, myeloperoxidase, and collagen are pretty scarce. For planning an appropriate endodontic treatment plan and predicting its outcome, it is very essential to know the basic changes occurring in the pulp. Knowledge of the inflammatory changes is a prerequisite to understand the reasons for exaggeration of symptoms and healing of pulpal and periapical diseases. Hence, the study was carried out with the objective to evaluate changes in inflammatory components of alkaline phosphatase in dental pulp of patients with DM (Type II) and nondiabetic patients.


  Methodology Top


The study was initiated after approval from scientific committee and institutional ethics committee. The study comprised of screening the patients visiting the outpatient department of the college, and a total of 135 individuals of the age group between 45 and 65 years who met the inclusion criteria and provided written informed consent to participate in the study were included. Sociodemographic variables along with appropriate medical and dental history of the study participants were recorded. Patients with known diabetes (Type I), not of the above-mentioned age groups, and having nonvital teeth on examination were excluded from the study. A total of three groups were formed out of which one was control group – Group 1 (glycated hemoglobin: 4%–6%) whereas the other two were of diabetic individuals with poor (Group 2) and better (Group 3) glycemic control. Diabetic status was determined with the help of blood tests (fasting blood sugar and postprandial blood sugar), and glycemic control was further assessed to divide the study participants into groups accordingly. The tests were carried out in the general pathology and biochemistry department of the institute under supervision of expert professionals.

The periodontal status of all the study participants was assessed with Russell's Periodontal Index. Pulpal status of teeth was recorded by electrical pulp vitality test. Teeth with Periodontal Index score of 6 and 8 were indicated for extraction and these teeth after extraction were immediately split into two with the help of mallet, and pulp was extirpated and subjected to biochemical analysis. Alkaline phosphatase was measured using p-nitro-phenylphosphate-2-amino-2-methyl-1-propanol and kinetic assay (with appropriate kit reagent and the reaction was read at 490 nm).[8]

Statistical analysis

Data collected were tabulated into Microsoft Excel sheet and were analyzed with the help of statistical software IBM SPSS v. 18. Results were expressed as mean and standard deviation. Inferential statistics were applied with use of one-way analysis of variance followed by Tukey's post hoc test (P < 0.05 – statistically significant at 95% confidence interval).


  Results Top


The mean values for levels of alkaline phosphatase in pulp in different groups are shown in [Table 1]. There was statistical significant difference between all the groups (P < 0.001), and post hoc test showed that there was intergroup significant difference between all the three groups (P < 0.001) as shown in [Table 2].
Table 1: Comparison of alkaline phosphatase level among the three study groups

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Table 2: Post hoc Tukey's test

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  Discussion Top


It is well established and a known fact that DM is associated with oral complications and with depression of natural defenses against infection. Patients with uncontrolled glycemic level are prone to gingival and dental injuries. Pulps of patients who suffer from diabetes tend to age more readily because of obliterative endarteritis and because the dental pulp has limited or no collateral circulation in the fully developed tooth.[3],[6] The impaired collateral circulation and the poor microvasculature with inhibition of microbicidal polymorphonuclear activity in diabetics are considered to result in an increased risk for infection or pulp necrosis. This complication of infection occurs by the process of anachoresis. The impaired vasculature also interferes with tissue nutrition and pulpal repair and creates a microaerophilic state for anaerobic development.[8]

There are numerous reports documenting, quite convincingly, that DM, especially when poorly controlled, is associated with significant periodontal disease and tooth loss due to periodontal disease.[6] The presence of periodontal disease worsens glycemic control. Hence, it can be hypothesized that periapical lesions being similar to periodontal disease can lead to increase insulin resistance and poor glycemic control.[9],[10] Greater inflammatory reactions in diabetic states cause an increase in blood glucose level, leading to an uncontrolled diabetic condition. This often requires therapeutic adjustment or increase in the dosage of insulin. Treating infections of pulp and periodontium will improve glycemic control and help in healing of lesions similar to nondiabetics. However, in patients with diabetes, very little data are available on the pathophysiology and clinical progression of pulpal lesions or the prognosis of endodontic treatment.[9],[10],[11]

However, Bender et al. reported that, in cases of poorly controlled diabetes, periapical radiolucencies tend to develop during treatment, but if diabetes is under therapeutic control, periapical lesions heal as readily as in nondiabetics.[12] In another study, Cheraskin and Ringsdorf monitored radiographically the healing of periradicular lesions following root canal treatment in 12 patients with low plasma glucose and 13 patients with high glucose, and after 30 weeks, the periradicular radiolucencies in the low glucose groups were reduced by an average of 74% compared with a reduction of only 48% for the high glucose group.[13] The results, obtained in our study also show increased level of inflammatory components in poorly controlled glycemic level group as compared to that of participants with good control of their glycemic level.[8],[9]

Since diabetes is the one of the most prevalent condition in medically compromised patients seeking dental treatment; the dental professionals should be aware of the possible relationship between endodontic infections and diabetes and take it into account the above consideration during the course of treatment for better prognosis.

Extensive investigation should be conducted to reveal and describe cellular and molecular mechanisms of recognized changes in pulp reparative response during diabetes. Although these mechanisms are still insufficiently known, therapeutic procedures to preserve the pulp vitality in diabetes patients should be realized with caution.


  Conclusion Top


The information available on pathogenesis, progression, and healing of pulpal disease in diabetic patients remains in its infancy. A number of important unanswered questions should be addressed in future research in this area. Ultimately, these should determine effective antimicrobial agents and treatment strategies for diabetic patients and help them to preserve a functional and healthy dentition throughout the life.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Hegde MN, Tahiliani D, Shetty S, Devadiga D. Salivary alkaline phosphatase and calcium in caries-active type II diabetes mellitus patients: An in vivo study. ContempClin Dent 2014;5:440-4.  Back to cited text no. 1
    
2.
Garber AJ. Diabetes mellitus. In Internal medicine, Stein JH ed, Mosby, St Louis, 1998. p. 1850-4.  Back to cited text no. 2
    
3.
Vemilllo AT. Dental considerations for treatment of patients with diabetes. J Am Dent Assoc 2003;134:24-33s.  Back to cited text no. 3
    
4.
Mohan V, Sandeep S, Deepa R, Shah B, Varghese C. Epidemiology of type 2 Diabetes: Indian scenario. Indian J Med Res 2007;125:217-30.  Back to cited text no. 4
[PUBMED]  [Full text]  
5.
Stratton IM, Adler AI, Neil HAW, Matthews DR, Manley SE, Cull CA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000;12;321(7258):405-12.  Back to cited text no. 5
    
6.
Loe H. The sixth complication of diabetes mellitus. J Diabetes Care 1993;16:476-80.  Back to cited text no. 6
    
7.
Russell BG. The dental pulp in diabetes mellitus. Acta Pathol Microbiol Scand 70:319-20.  Back to cited text no. 7
    
8.
Catanzaro O, Dziubecki D, Lauria LC, et al. Diabetes and its effects on dental pulp. J Oral Sci 2006;48:195-9.  Back to cited text no. 8
    
9.
Lamster IB, Borgnakke WS, Taylor GW. The relationship between oral health & Diabetes mellitus. J Am Dent Assoc 2008;139:19s-24.  Back to cited text no. 9
    
10.
Soskolne WA, Klinger A. The relationship between periodontal diseases and diabetes: An overview. Ann Periodontol 2001;6:91-8.  Back to cited text no. 10
    
11.
Seppala B, Seppala M, Ainamo J. A longitudinal study on insulin dependent diabetes mellitus & periodontal disease. J Clin Periodontal 1993;20:161-5.  Back to cited text no. 11
    
12.
Bender IB, Seltzer S, Freedland J. The relationship of systemic diseases to endodontic failures and treatment procedures. Oral Surg Oral Med Oral Pathol 1963;16:1102-15.  Back to cited text no. 12
    
13.
Cheraskin E, Ringsdorf WM Jr. The biology of the endodontic patient: Variability in periapical healing and blood glucose. J Oral Med 1968;23:87-90.  Back to cited text no. 13
    



 
 
    Tables

  [Table 1], [Table 2]


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