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Research Topic:


Effects of Diabetes Mellitus (DM) on Root Canal Treatments (RCT) conducted in the Griffith University Dental Clinics: A Clinical Audit.



1) Abstract:




Amy



Introduction:

Diabetes Mellitus (DM) is a chronic endocrine disease, that is multifactorial and affects immune function. Various literature has investigated whether DM can affect the treatment outcome of Root Canal Treatment (RCT) however discrepancy in the results of these studies exist. Further investigation is required to enhance the understanding on this topic. The following study aims to investigate the effect that diabetes mellitus has on endodontic treatment outcome by means of a clinical audit.


Methods:

A case-control, retrospective study design was conducted through reviewing patient charts, medical history and clinical records at Griffith University Dental Clinic (GUDC). The endodontic treatment outcome (successful or unsuccessful) for 100 diabetic and 100 matched non-diabetic patients were recorded as part of data collection. Data and statistical analysis was conducted using SPSS to investigate for an association between diabetic and non-diabetic patients in healing outcomes post-endodontic treatment.


Results:

Data and statistical analysis found similar rates of success for both diabetic and non-diabetic groups. No significant differences were seen between the success rates of the diabetic and non-diabetic groups (p>0.05).


Conclusion:

There is no clinically significant difference in the endodontic treatment outcome of diabetic and non-diabetic patients treated at Griffith University Dental Clinic.


2) Background: (Amy)


2a) Introduction and literature review:

Non-surgical root canal treatment (RCT) is a procedure indicated for the treatment of necrotic or irreversibly inflamed dental pulp caused from either trauma or bacterial infection of the dental pulp (Arya et al., 2017). Apical periodontitis is a condition that presents as a chronic or acute inflammatory lesion present around the root apex of a tooth and is caused by polymicrobial irritants originating from the infected root canal system (Segura-Egea et al., 2012). The primary objectives of RCT involve preventing and treating peri-radicular lesions through facilitating the healing of the periapical tissues (Fouad & Burleson, 2003). This is attained through the removal of dental pulp, disinfection of the root canal system and sealing of the root canal system via obturation (Fouad & Burleson, 2003).

Evaluation of root canal treatment outcome is conducted through monitoring the tooth for cessation of signs and symptoms of both pulpal and periapical pathosis (Fouad & Burleson, 2003). For accuracy of determining endodontic treatment outcome, the RCT should be assessed for a minimum of two years post-operatively to monitor the resolution of pre-existing periapical lesions and to ensure no development of new periapical lesions (Fouad & Burleson, 2003). Root canal treated teeth that upon post-operative assessment present signs and symptoms of endodontic treatment failure will be required to either undergo endodontic re-treatment, extraction or periapical surgery (Olcay, Ataoglu, & Belli, 2018). Endodontic treatment outcome may depend on various other factors including the periodontal disease status of the tooth, restorability of the tooth, presence of decay and the occurrence of tooth fracture (Olcay et al., 2018) Furthermore, healing and resolution of periapical lesions subsequent to RCT can be dependent on systemic factors including that of the individual’s immune defences (Holland, Gomes Filho, Cintra, Queiroz, & Estrela, 2017). Numerous studies have investigated various systemic diseases suspected of affecting RCT outcome. Included in these systemic diseases is that of Diabetes Mellitus.

In Australia, currently over 1.2 million adults (6% of the population), suffer from Diabetes Mellitus (ABS, 2018). Diabetes Mellitus (DM) is a chronic endocrine disease, that is multifactorial and affects immune function (Arya et al., 2017; Mohiuddin, 2018). DM has a high morbidity rate among affected individuals, with potential for mortality as well (Fouad & Burleson, 2003). The main feature of DM is hyperglycemia, which is due to the impaired chemotaxis of neutrophils, and the affected metabolism of carbohydrates, proteins and lipids (Arya et al., 2017; Leandro et al., 2003). Overall, hyperglycemia causes a state of inflammation, which impairs the cellular proliferations of the host (Arya et al., 2017). Type I diabetics experience complete loss of insulin secretion, due to autoimmune and cellular-mediated destruction of beta cells in the pancreas (Segura-Egea et al., 2012). Type II diabetes results from resistance to insulin, in combination with failure producing an adequate amount of insulin for compensating this resistance (Segura-Egea et al., 2012). Poorly controlled diabetes results in delayed healing, tissue breakdown and reduced capacity of tissues to repair (Leandro et al., 2003; Rudranaik, Nayak & Babshet, 2016). Oral complications such as periodontal disease and apical periodontitis, are associated with DM (Arya et al., 2017), with a disproportionately large percentage of severe periodontal and pulpal infections reported in diabetics (Segura-Egea et al., 2012). DM has been shown to cause varying alterations in periapical tissues and pulp, through augmented bone resorption and impaired collateral circulation (Segura-Egea et al., 2012). More specifically, the periapical tissues in diabetic patients, is associated with a heightened risk for ill-response to odontogenic pathogens; meaning, residual infection is not eliminated effectively by the host after root canal treatment (Leandro et al., 2003).

DM is known to impair the body’s healing and immune response, thereby making the body more susceptible to systemic infection (Arya et al., 2017). Healing is affected by DM through advanced breakdown of tissues and via a decrease in the capacity of the tissues ability to repair (Arya et al., 2017; Segura-Egea et al., 2012). Numerous studies have found an association between the presence of DM and the outcome of endodontic treatment. One of these studies reported that DM may increase the individual’s susceptibility to severe endodontic infections (Fouad & Burleson, 2003). This may be due to the presence of different endodontic microbial flora in diabetic patients when compared to non-diabetic patients (Fouad & Burleson, 2003). This difference in microbial flora may increase the susceptibility of patients with DM to peri-radicular disease (Fouad & Burleson, 2003). This is supported by a study by Fouad et al., that reported the presence of an increased pathogenic microbial profile within the necrotic dental pulps of teeth in patients with DM when compared with non-diabetic patients (2002). This difference in pathogenic microbial profile may account for the greater incidence of painful apical periodontitis and flare-ups during endodontic treatment amongst diabetic patient’s when compared to non-diabetic patients (Fouad et al., 2002). Furthermore, a study by Bender, Seltzer and Freedland (1963) explored the effects of controlled and uncontrolled diabetes on endodontic treatment, reporting that endodontic lesions will only heal if diabetes is controlled and that endodontic lesions may even increase in size despite endodontic treatment if diabetes is not controlled (Fouad & Burleson, 2003).


Gaps in current research

Currently, the prevalence of apical periodontitis and periapical radiolucencies in DM patients has been widely explored, however the association of Diabetes Mellitus with endodontic success remain as a gap in knowledge (Arya et al., 2017; Moazami, 2011). Only a few studies have explored the effect of increased inflammatory response in diabetes, on the ability of apical tissues to overcome infections (Moazami, 2011; Olcay et al., 2018). The current animal and clinical studies available, suggest a compromised peri-radicular immune response, which may result in increased root canal treatment failure (Lopez at al., 2011); however, very limited long-term prospective data on humans is available (Olcay et al., 2018).

In comparison to the association between diabetes and periodontitis, the association between DM and pulpally-originating dental infections has been scarcely investigated (Lopez et al., 2011). It has been established that apical periodontitis shares similar gram-negative microbiota as periodontitis, which in turn increases the levels of systemic inflammatory mediators (Holland et al., 2017). However, the effect of these inflammatory reactions on the success of root canal treatment, have not been explored (Holland et al., 2017). It is currently hypothesised that liposaccharides in gram-negative bacteria cause an inflammatory response in the innate immune system (Moazami, 2011). When this innate immune system is weakened, there may be a heightened risk for compromised peri-radicular immune response (Marending, Peters & Zehnder, 2005).

Although it has been established that controlling diabetes is beneficial for the outcome of endodontic treatment, methods for improving NSRCT in DM patients has not been explored (Olcay et al., 2018). In addition, the overall immune system of each individual with diabetes is variant, and will contribute to their likelihood for positive response to root canal therapy (Marending, Peters & Zehnder, 2005; Moazami, 2011; Oginni, 2010).


Limitations of current research

















Amongst the current literature available exploring the effects of DM on endodontic treatment outcome, a variety of limitations were identified.

The study by Wang et al., focusing on investigating the impact of DM on extraction of non-surgical root canal treated teeth entailed the limitation of not being a case-controlled study (2011). The results of this study found that DM was a significant risk factor for tooth extraction after non-surgical RCT after univariate analyses (Wang et al., 2011). However, additional clinical studies focusing on case-control need to be carried out in order to further support the hypothesis that DM results in a significantly increased risk of tooth extraction subsequent to non-surgical RCT compared to patients without DM (Wang et al., 2011).

Furthermore, an alternate study investigating the prevalence of peri-radicular radiolucencies in root canal treated teeth in patients with DM presented with multiple limitations (Britto, Katz, Guelmann, & Heft, 2003). Although this study focuses on investigating the effect of DM on endodontic treatment outcome, one limitation involves the inability to completely exclude clinical cases where endodontic treatment failure was due to poor treatment rather than the effects of DM (Britto et al., 2003). A second limitation of this study was instigated through the assessment of radiographs to determine endodontic treatment outcome. Britto et al., reported that it is impossible to accurately ascertain through radiographic assessment alone whether peri-radicular radiolucency’s seen on x-rays subsequent to RCT are a residual healing lesion or an endodontic treatment failure (2003).

In addition, a limitation was identified in the paper by Segura-Egea et al., which examines DM, periapical inflammation and endodontic treatment outcome (2012). This research follows the assumption that the link between periodontitis and DM is similar to the link between apical periodontitis and DM (Segura-Egea et al., 2012). It is well known in research that diabetes has a significant effect on periodontal disease. However, limited studies have been conducted to explore its effect on endodontic treatment outcome.

A significant limitation was highlighted in the 2003 study by Fouad and Burleson that focused on investigating the effect of DM on endodontic treatment outcome via identifying diabetic and non-diabetic patients who received RCT and assessing the data through an electronic record system. A limitation of this study was the limited number of cases that provided follow-up data for a minimum of two years subsequent to RCT (Fouad & Burleson, 2003). Out of 5494 cases of RCT only 540 of these had adequate follow-up data (Fouad & Burleson, 2003).

In conclusion, an association between Diabetes Mellitus and endodontic treatment outcome for non-surgical RCT has been investigated in recent research. These studies are suggestive that DM has a negative association with NSRCT outcome, however a consensus regarding this correlation has not been established in current research. This is mostly attributed to the limitations in current research on this topic, including limited follow-up data over a short period of time, lack of case-control studies, and minimal human studies. A significant limitation in the current human studies has been small sample sizes, thus presenting difficulty extrapolating the data found. Further exploration is required to determine the effect of increased inflammatory response in DM, on the ability of apical tissues to overcome infections.


2b) Aims and Objectives:

–          Aims: The aim of the study is to investigate the effect that diabetes mellitus has on endodontic treatment outcome. To determine if a clinically significant difference exists between the failure rates of endodontic treatment in diabetic and non-diabetic patients. To determine the distribution of anterior/posterior teeth and hand file/rotary RCT amongst the successful and unsuccessful RCT from our sample population.

–          Objectives:

o   Randomised sampling will be used to select a sample population of diabetic and non-diabetic patients from the patient management system ‘Titanium’ used at Griffith University Gold Coast Dental Clinic.

o   Data on endodontic treatment outcome will be collected from the diabetic patient sample

o   Data on endodontic treatment outcome will be collected from the non-diabetic patient sample (control group)

o   The data collected will be synthesised to determine the effect that the medical condition diabetes mellitus has on endodontic treatment outcome.


3) Materials and Methods: (Rochella)

A case-control, retrospective study design was conducted through reviewing patient charts, medical history and clinical records at the School of Dentistry and Oral Health Clinic, at Griffith University. This study has been approved by Griffith University Ethics Committee (HREC GU Ref No: 2019/119). 100 diabetic patients (study group) were matched with 100 non-diabetic controls, based on age, gender, tooth number, and time of endodontic treatment. These matched patient factors, were chosen to control non-diabetes related treatment variables. This comparative study design, is in-line with the study aims of assessing the difference in endodontic treatment success in diabetic versus non-diabetic patients. The selection criteria for patients to be included in the study consisted of those with: patient consent signed, non-surgical RCT started in the undergraduate dental clinic at Griffith University (with student dentists), patient completed their root canal treatment (obturation finished), and root canal completed over 6 months ago. For the diabetic patient selection, patients with gestational diabetes or family history of diabetes were excluded from the study. A successful root canal treatment was defined as one where: the patient did not have any continuing pain, the tooth did not receive nor require further endodontic retreatment and was not extracted due to endodontic causes.


(a) Patient data:


To retrieve patient data, the dental software system ‘Titanium’ at Griffith University was used. Firstly, appropriate diabetic patients were found, using the following searched terms on Titanium: “diabetes mellitus”, “DM” , “diabetes”, “type I DM” and “type II DM”. To ensure root canal treatments were completed, the ADA item code 419 (extirpation), 415 or 416 (chemo-mechanical preparation) , 417 or 418 (root canal obturation) were searched for each tooth. In order to reach the largest sample size possible, all patient data entries found on Titanium that fit the inclusion criteria, were included in the data collection. The initial search returned with 202 diabetic patients. Once this data was retrieved, patients who did not give consent for research and duplicate entries were deleted. Additionally, specialty medical tabs and patient medical history forms were read for each patient, to ensure they had diabetes mellitus. Once these diabetes participants were finalised, a matched non-diabetic patient was found for each on Titanium, and non-consented and duplicated patients were again deleted. The total sample size achieved was 200 participants: 100 diabetic, and 100 non-diabetic.


(b) Statistical analysis:


Each root canal treated tooth was categorised as: successful or unsuccessful. The RCT was also sub-categorised into anterior or posterior cases, and hand-file or rotary. All incomplete RCT teeth were deleted (extirpation or CMP only). The retreatment codes that were assessed for each of the unsuccessful RCT’s included: extraction (311, 314, 322, 323 and 324), re-extirpation (419, 419R), re-treatment (451, 451R, 452, 452R). Additionally, all patient files following the RCT were read, to include any required re-treatment that had not yet been completed (and thus not entered as an item code). All RCT treatment outcomes were coded, ready for SPSS analysis. Data cleaning and data analysis was done. The Chi-squared test and Wilcoxon test were carried out for statistical analysis.

The statistical analysis was compared to current literature. An electronic search was conducted on PubMed, ClinicalKey, Google Scholar, ScienceDirect and ProQuest with the key terms of “Diabetes Mellitus”, “Endodontic treatment outcomes”, “Apical Periodontitis” and “Non-surgical Root Canal Treatment”. The search was limited to English articles written in the past 16 years. In addition to the electronic search, references of journal articles were manually searched to discover other relevant journal articles.


3) Results: Maddy and Eileen

Table 1. Descriptive statistics table.































N (%)

Health Status

Diabetic 100 (50.0)

Non-diabetic 100 (50.0)

Position of teeth

Anterior 62 (31.0)

Posterior 138 (69.0)

RCT technique

Hand filing 99 (49.5)

Rotary 101 (50.5)

Success Rates

Successful 186 (93.0)

Unsuccessful 14 (7.00)

How long did the RCT last if it was unsuccessful

0-3 years 13 (92.9)

4-6 years 1 (7.10)

Treatment after RCT failure

Retreatment 2 (14.3)

Extraction 12 (85.7)

Table 2. Chi square test.


Variable

Endodontic Outcome



X^2

P value



Successful



N (%)


Unsuccessful



N (%)


Health status

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