The present study was conducted for the better understanding of the relationship between type 2 diabetes mellitus and chronic periodontitis as well as to investigate the effect of periodontal therapy in subjects with type 2 diabetes mellitus with chronic periodontitis in the absence of any changes in the medical therapy during the study period. At baseline, both the treatment and the control group showed similar levels of plaque accumulation, gingival and periodontal inflammation, as well as of periodontal breakdown (PPD, CAL).

The results of the present study demonstrated a significant improvement of metabolic control in the subjects of treatment group (Group A) at 3 months post therapy. A statistically significant decrease in HbA1c level (0.82%) was observed in the treatment group. Similar observations were made by Kiran et al.; they examined the effect of periodontal therapy with systemic doxycycline on periodontal health and glycemic control of individual type 2 DM subjects.

They had a control group of patients with diabetes whose periodontal status was similar and received no treatment as seen in the present study. Improvement of glycemic control with a reduction in mean HbA1c value (0.8%) was reported to be statistically significant. Control group of subjects in the present study showed negligible increase in HbA1c value after 3 months while in Kiran’s Study, there was no change.

Iwamoto et al. reported a slight reduction in plasma HbA1c level (0.8%) in a group of 13 Japanese subjects with type 2 DM. Grossi et al. conducted a research involving type 2 DM subjects with severe periodontitis and treated them with SRP , subgingival irrigation (H₂O, Chlorhexidine, povidone I₂ plus placebo or doxycycline- 100mg daily for 14 days). They reported significant reduction in HbA1c levels in subjects receiving doxycycline compared to placebo treated group which did not reach significance. Similar results were obtained by Stewart et al.These observations were in accordance with the present study.

Rodrigues et al. also reported similar statistically significant reduction in HbA1c level after periodontal therapy in type 2 DM patients with chronic periodontitis, but instead of doxycycline, they used amoxicillin/clavulanic acid-875mg as an adjunct to mechanical debridement. Similar observations were made by Singh et al. but they used systemic doxycycline as an adjunct to mechanical debridement. We used adjunctive systemic doxycycline 100mg for 14 days in our study along with scaling and root planing based on the study by Grossi et al. and its usage can be justified by the following:

First, it is a broad spectrum antibiotic that is effective against most of the periodontal pathogens and it reaches higher concentration in GCF than in serum, providing an important adjunct for the reduction of periodontal pathogens.

Secondly it is a potent modulator of the host response in the subject with diabetes, as well as being a metalloproteinase inhibitor. It also inhibits non-enzymatic glycation of extracellular proteins, and it may have a similar effect on the glycation of hemoglobin. When amoxicillin with clavulanic acid was used as an adjunct to periodontal therapy, no additional effect on the HbA1c levels was observed.

Promsudthi et al. reported a reduction in HbA1c level after periodontal therapy, but contrary to other studies, this decrease was not statistically significant. Similarly Dag et al. also observed a non significant decrease in HbA1c values after periodontal therapy.

Most of the studies done previously incorporated non diabetic patients as control group and hence could not make a definitive conclusion; therefore to determine the relative contribution of periodontal therapy in glycemic control, the present study was designed to include type 2 DM subjects with chronic periodontitis as control group that did not receive any periodontal treatment during the study period.

In contrast to the findings in the present study, Christgau et al. reported that periodontal therapy did not affect the levels of HbA1c in uncontrolled diabetic subjects (i.e. HbA1c > 7%). Westfelt et al. also claimed that HbA1c levels did not change with mechanical periodontal therapy. Similar results were obtained by Seppala et al. and Patricia et al. Current researches indicated lack of consensus as to whether non surgical therapy contributed to better glycemic control.

  The healing results of the periodontal therapy were assessed after 3 months. There are contradictory opinions in the literature concerning the appropriate time for assessing the healing response to periodontal therapy. Morrison et al. in 1980 and Lowenguth and Greenstein in 1995 suggested a period of one month. Badersten et al. in 1981 found that in periodontal pockets of 4-7 mm depth, most changes occur in the first 4-5 months while the deep pockets up to 12mm, a gradual improvement takes place over a period of 12 months. In our study, since the mean probing depth of most of the subjects was around 3mm, the response to periodontal therapy was evaluated after 3 months.

Mechanical scaling and root planing is very essential for removal of plaque and calculus for reduction of inflammation as type 2 diabetics have an increased susceptibility to inflammation. Hence, the therapy led to a 71.2% reduction in the mean gingival index, 32.6% reduction in the mean probing pocket depth and 11.7% gain in the mean clinical attachment in the present study. These improvements were reflected at the systemic level by alterations in the serum TNF-α as well as reduction in glycated hemoglobin.

Numerous studies have reported the favorable effect of nonsurgical periodontal treatment on periodontal healing as well as an improved glycemic control among Type 2 diabetic patients.

It has been generally believed that periodontal infection related TNF-α contributes to systemic inflammatory reaction. TNF-α is believed to be released from adipocytes and to cause insulin resistance together with obesity. Researchers have also suggested that TNF-α impairs insulin signaling by increasing the adiposity secretion of free fatty acids. Researchers now agree that this process strengthens glycemic control by raising insulin resistance in diabetic patients and this hypothesis suggests that periodontal therapy can effectively improve glycemic control by decreasing proinflammatory mediators. However, there is no consensus still among the researchers as to whether periodontal therapy has an effect on inflammatory mediators and glycemic control.

Yang et al. found a significant reduction in serum TNF-α, HbA1c and periodontal parameters following periodontal therapy in the treatment group consisting of type 2 DM patients with chronic periodontitis. They suggested that periodontal therapy could effectively reduce HbA1c levels by reducing circulatory TNF-α concentration. Similar observations were made by Iwamoto et al. and Dag et al.

Several workers claimed that the achieved reduction of TNF-α level in circulation was in response to systemic doxycycline which caused a decrease I periodontal infection and inflammation. It appears difficult to establish the role of non surgical periodontal therapy alone in respect to glycemic control, it might however be mentioned that many factors influenced the short term glucose level and one of these factors was medical care.

 In the present study, a significant decrease in TNF-α level (10.98±3.63 at baseline to 7.85±2.46) was obtained in the treatment group (Group A) in accordance to the above mentioned studies. In contrast to the above findings, Kardesxler et al. and Yamazaki et al. reported that increased TNF-α was associated with inflammatory periodontal disease, but significant post treatment reduction in TNF-α was not observed by them.

However, Talbert et al. reported an increase in TNF-α level after periodontal treatment. Nishimura et al. suggested that periodontitis raised serum TNF-α level and affected insulin resistance. In agreement with this suggestion, the determination of positive correlation between TNF-α and probing pocket depth (PPD) and TNF-α and gingival index (GI) in this study were compatible showing a correlation between TNF-α and periodontitis.

Serums TNF-α values were correlated with HbA1c as well as with the periodontal parameters in the present study (i.e. GI, PPD & CAL). A positive correlation was found between them and hence this study supports the hypothesis that the better glycemic control obtained after periodontal treatment in the treatment group was due to reduction of gingival index and bleeding on probing brought about by reduction in the inflammatory mediators, including TNF-α. Reduction in all the clinical parameters in the present study supported the observation of Engebretson et al. who claimed a positive correlation between TNF-α and clinical attachment levels and Bretz et al. who showed correlation between TNF-α and severe periodontitis. 

Although the fasting blood glucose level is not a good indicator of glycemic control as it is susceptible to great oscillations, the treatment group showed a statistically significant reduction in its level after 3 months in the treatment group. In order to standardize the results obtained in the study, no change in the medication or diet was made for the patients. None of the patients received any additional guidance in managing their diabetic status.

The main limitation of our study was the small number of patients incorporated within the study and a small follow up period. The follow up period could not be extended as the control groups of patients were also diabetics with chronic periodontitis, and hence it would have been ethically unacceptable to defer periodontal treatment in these patients for a longer period. Also the possibility that the observed improvements in glycemic control and in the reduction of serum TNF-α might be due to diet, was not controlled in our study.

This was a randomized control trial done to evaluate the effect of non surgical therapy on periodontal health and glycemic control in type 2 diabetics. The fact that TNF-α decreased after 3 months and that clinical and metabolic improvements were demonstrated following periodontal therapy, it can be safely said that it is a strong indicator of systemic health amelioration.

Non surgical periodontal therapy with adjunctive doxycycline significantly reduces the bacterial load in the biofilm which subsequently reduces the release of proinflammatory mediators including TNF-α. The reduced levels of inflammatory mediators lead to attenuated periodontal tissue damage on one hand and in turn, which on the other hand improves glycemic control. This, in turn attenuates the inflammatory process in the periodontal tissues by regulating chemokine production.

Effective control of the inflammatory process by reduction of the pathogenic bacteria as well as the diabetic condition provide a favorable periodontal tissue environment that allows tissue repair reflected by the clinical improvements observed in the study.