Periodontal disease is one of the most common chronic inflammatory diseases involving the oral cavity and is a significant public health problem in the world.[1] Periodontal disease is an extremely common condition affecting about 1 billion people in the world and is one of the major causes for adult tooth loss.[2] Chronic periodontitis is a continuing inflammation of periodontal tissues, progressive destruction of periodontal ligament and alveolar bone, and, if left untreated, will lead to eventual tooth loss. It is affected by a complex interplay of microbial dysbiosis, host immune-inflammatory response, behavioral factors, and systemic factors, which together affect its development and progression.[3] While periodontal disease is, of course, caused by the pathogenic dental biofilm, the amount of periodontal destruction is very much determined by the systemic inflammatory and metabolic status of the individual.[4]

Diabetes mellitus is another significant disease worldwide and is rapidly expanding across the globe.[5] In 2024, there were an estimated 589 million adults aged 20–79 years with diabetes (11.1% of the adult population), with this figure expected to continue to increase significantly over the next few decades according to the IDF.[6] There is a higher burden of diabetes amongst low- and middle-income countries.

Diabetes is an emerging public health issue in Pakistan, where it is estimated that over 30 million adults are currently living with the disease.[7] The rising incidence of hyperglycemia is especially significant, as diabetes is known to have several oral complications in addition to microvascular and macrovascular complications, such as increased risk for periodontal inflammation and delayed periodontal tissue healing.[8]

Diabetes and periodontal disease are thought to be a two-way street.[9] Excessive blood glucose can lead to the formation and accumulation of advanced glycation end products, affect collagen metabolism, affect neutrophil function, increase oxidative stress, and enhance production of pro-inflammatory mediators. These changes can affect the disease resistance of periodontal pathogens and can promote periodontal tissue destruction.[9] On the other hand, chronic periodontal inflammation might also be associated with systemic inflammatory load and may lead to worsening of insulin resistance and glycemic control.[10]

In other words, people with poor glycemic control may have more severe periodontal destruction than people with normal or controlled glycemic control.[11] Parameters that serve as glycemic indicators, including fasting blood glucose and glycated hemoglobin (HbA1c), are clinically useful measures of metabolic state, and HbA1c is especially useful since it is related to the average levels of blood glucose over the last 2–3 months.[11]

Therefore, the simultaneous presence of sub-optimal glycemic control and extensive periodontal loss could be interpreted as more than two coexisting chronic diseases or as an important clinical relationship between the metabolic dysregulation and the chronic oral inflammation. If the severity of the periodontal disease is correlated with the severity of hyperglycemia, it may be possible to identify those at high risk, improve interprofessional collaboration in diabetes–dental care, and encourage earlier intervention in the periodontal disease process. Thus, the present study was conceived to investigate the relationship between glycemic status and the severity of chronic periodontitis in adults and to see if the glycemic status, particularly HbA1c, is significantly related to the severity of periodontal disease.

This analytical cross-sectional study was conducted in the hospital to assess the relationship between glycemic status and severity of chronic periodontitis among adults. The study was carried out for a period of 12 months, from March 2025 to Februry 2026 . After written informed consent, data collection was carried out within the specified study period. OpenEpi version 3.01 was used to determine the sample size for a cross-sectional study based on the estimated percentage of people with poor glycemic control who will have severe periodontitis. The estimation was based on the results of a previous study demonstrating a strong correlation between severity of periodontal disease and glycemic control, and assuming that 50% of the population had severe periodontal disease. Based on a 95% confidence level, 80% power, and an appropriate expected proportion/effect size from the previous study, the sample size to be recruited was determined to be 200. The non-probability technique of consecutive sampling was used for selecting participants. All patients who visited the study site within the study period were screened for eligibility. Participants who were included and gave written informed consent were consecutively recruited until the required sample size was reached. The study included adults (aged 18 years or older) who presented for a periodontal examination and who had sufficient natural dentition to assess periodontal status. Patients with a clinical diagnosis of chronic periodontitis were selected for the study. Patients with normal glycemic status as well as those who had impaired glycemic control or were diabetic were included to make a comparison of the periodontal severity at different glycemic statuses. Informed consent was obtained and periodontal examination and assessment of glycemic status were performed. Patients who had been treated with systemic antibiotics or periodontal treatment in the last three months were excluded. Persons who had systemic diseases other than diabetes which might have markedly affected their periodontal status or wound healing were also excluded. Excluded were pregnant women, patients on medications that have a significant impact on periodontal tissues, and patients with aggressive or necrotizing periodontal diseases. Some patients were also excluded because they had missing clinical data, an unreliable HbA1c, or were unable to have a periodontal exam. A structured data collection proforma was used to collect the data. Demographic data such as age, sex, residence, educational level, and pertinent behavioral traits were documented after obtaining written informed consent. Data about smoking, oral hygiene habits, diabetes duration (if applicable), family history of diabetes, and antidiabetic medication use were also collected. A brief medical history was obtained to determine if there were any relevant systemic issues or medications. Glycated hemoglobin (HbA1c) was mainly used to evaluate glycemic status. Blood specimens were taken from each participant and tested in the institutional laboratory with a standardised and validated laboratory technique. The results of HbA1c were reported as a percentage. The glycemic status of the participants was defined based on the pre-established clinical thresholds, and normal glycemic status, intermediate dysglycemia, and diabetes/poor glycemic status were classified based on the criteria used for each category. Fasting blood glucose was also documented (as an additional measure of glycemic status) if available. A thorough periodontal exam was then conducted by a qualified dentist/periodontist, with the use of a standardized periodontal probe, under proper light. At the specific sites on the teeth, periodontal status was determined and probing pocket depths and clinical attachment losses were measured. Other data recorded were bleeding on probing and plaque status. Chronic periodontitis was defined based on the established clinical criteria, which were predetermined by considering the amount of periodontal attachment loss and additional clinical variables. The subjects were then classified as having mild, moderate, or severe periodontal disease groups based on the classification system used.The examiner of the periodontal measurements was trained and calibrated before the beginning of data collection to minimize measurement variation. A standard examination protocol was used for all participants. HbA1c testing was done by laboratory staff who were not responsible for the periodontal assessment. The investigators ensured the confidentiality of the information they collected by using a unique study identification number (SID) for each participant. The IBM SPSS Statistics software version 26.0 was used to enter, code, and analyse the collected data. Continuous variables were also analysed for normal distribution with the Shapiro–Wilk test and then presented as mean ± SD for variables that were normally distributed and as median (IQR) for non-normally distributed variables. Categorical variables were reported in the form of frequencies and percentages. The Chi-square test was used to evaluate the association between categorical glycemic status and severity of periodontal disease, and Fisher's exact test was used when the assumptions of the Chi-square test were not met. One-way analysis of variance (ANOVA) was used to analyze continuous variables, such as HbA1c, between the groups of different periodontal severity for variables that had a normal distribution, and the Kruskal-Wallis test was used for variables that did not have a normal distribution. The correlation of HbA1c to periodontal parameters (probing pocket depth, clinical attachment loss) was evaluated by Pearson's correlation coefficient for normally distributed variables or by Spearman's rank correlation coefficient for non-normally distributed variables. Multivariable logistic regression analysis was used to evaluate if poor glycemic control was an independent risk factor for severe periodontitis after adjusting for potential risk factors like age, sex, smoking, and oral hygiene practices. Odds ratios with 95% confidence intervals are presented. A p-value <0.05 (two-sided) was defined as significant.

There were 200 adults in all who participated in the study. The participants were from various age groups, educational backgrounds, and included urban and rural residents. Relevant behavioral and clinical characteristics, such as smoking, oral hygiene practice, family history of diabetes, and diabetes-related variables, were documented and are presented in Table 1.

The general glycemic and periodontal status of the subjects is shown in Table 2. The glycemic status ranged from normal glycemia to diabetes or poor glycemic control, and the periodontal disease ranged from mild to severe. The clinical periodontal assessment comprised probing depth, clinical attachment loss, bleeding on probing, and plaque scores.

There was a significant difference in both glycemic and periodontal parameters among the severity categories of periodontal disease. Glycemic measures and periodontal clinical parameters showed significant differences between each of the three severity groups, and bleeding on probing and the presence of plaque showed significant differences as well (Table 3).

There was a statistically significant association between glycemic status and periodontal disease severity (Table 4). The distribution showed a gradient towards increased levels of periodontal disease with increasing glycemic status. Significant positive correlations were found between the analysed periodontal parameters and HbA1c and between the analysed periodontal parameters and fasting blood glucose (Table 5). The results showed that the higher the glycemia, the higher the periodontal tissue involvement.

On univariable analysis, logistic regression analysis identified a number of factors associated with severe periodontitis. Multivariate analyses adjusted for potential confounders showed that smoking, irregular oral hygiene, diabetes/poor glycemic control, and HbA1c ≥7% remained significant in relation to severe PD, whereas age, sex, and prediabetes were not significantly associated (Table 6).

Table 1. Sociodemographic and clinical characteristics of study participants (n=200)

Table 2. Glycemic and periodontal characteristics of study participants (n=200)

Table 3. Comparison of glycemic and periodontal parameters according to periodontal disease severity

Table 4. Association between glycemic status and periodontal disease severity

Table 5. Correlation between glycemic parameters and periodontal clinical parameters

Table 6. Logistic regression analysis of factors associated with severe periodontitis

The present study showed that glycemic status is significantly associated with the severity of chronic periodontitis among adults. The mean probing pocket depth (PPD), clinical attachment loss (CAL), frequency of bleeding on probing, and frequency of plaque were progressively higher in participants with increasing levels of glycemic control. The mean HbA1c was 5.8% for the participants with mild periodontitis and 7.9% for those with severe periodontitis (p<0.001). In addition, 52.3% of the people who had an HbA1c ≥6.5 had severe periodontitis, while only 11.5% of people who had a normal HbA1c had severe periodontal disease. The results of this study corroborate the proposed hypothesis that hyperglycemia is associated with more severe periodontal disease than a higher prevalence of periodontal disease. The results were very similar to those of Radhakrishnan et al. (2022), where 310 patients with type 2 diabetic neuropathy were assessed, showing that periodontitis was very prevalent, with severity and clinical attachment loss higher in patients who had diabetic foot. Importantly, significant correlations existed between CAL and periodontal inflamed surface area (PISA) and HbA1c. The present study also showed a positive correlation between HbA1c and CAL (rₛ=0.58, p<0.001), indicating that there may be an association between higher chronic glycemic exposure and higher cumulative periodontal tissue destruction. The consistency of association strength is even more supportive of the biological plausibility of our findings; however, in the population studied by Radhakrishnan et al., the individuals were a more complicated population of diabetics.[12] In the same way, Ramakrishnan et al. (2022) specifically studied the severity of periodontal disease among 90 people with type 2 diabetes. They discovered that probing depth, clinical attachment level, bleeding on probing, and oral hygiene measures were statistically significantly poorer in those with poor glycaemic control than in those with good glycaemic control (p<0.001). Similar observations were made by us; in mild disease, PPD was 3.2 mm, and in severe disease it was 5.1 mm, and in mild disease, CAL was 2.6 mm while in severe disease it was 4.7 mm. Of particular interest is the similarity in that both studies utilized the same objective periodontal measurements, and HbA1c was used to define glycemic status.[13] An association was also observed in the present study, which is corroborated in the study by Dewake et al. (2022). A Japanese cross-sectional study revealed that diabetes status was correlated with the level of periodontal disease in men and women who have type 2 diabetes based on the latest periodontal classification. In the present study, we have further built on this observation by exploring glycemic status as a continuous metabolic exposure and not just as a binary diagnosis of diabetes. This difference could be clinically significant since our results showed a progressive increase in the severity of periodontal condition from normal glycemia to prediabetes to diabetes/poor glycemic control, indicating that periodontal risk may escalate as the diabetes disease progresses.[14] This gradient was further supported by the correlation analysis in our study. A moderate positive correlation was noted between HbA1c and PPD (rₛ=0.52) and CAL (rₛ=0.58), and a weak but significant correlation between HbA1c and bleeding on probing and plaque. These results align with Pattayil et al. (2023), who studied 260 patients with type 2 diabetes who were taking either oral antidiabetic drugs or insulin. Their study found that there was a proportional relationship between HbA1c and PISA and clinical attachment loss (CaL), with a unit increase in HbA1c corresponding to an increase in PISA (by 1.1 points) and CaL (by 0.0 units). The increased association of HbA1c and CAL in our study could suggest that chronic glycemic exposure is more important than just current gingival inflammation for cumulative periodontal attachment loss.[15] Similarly, the results agree with Alhassani et al. (2023), who analyzed the association between periodontodental disease and HbA1C in NHANES data when different case definitions of periodontal diseases were applied. They discovered that detailed definitions that included clinical attachment loss and probing depth, especially CDC/AAP and stage III/IV classifications, showed a consistent significant relationship with higher levels of HbA1C. The odds ratio for the diabetes level HbA1c was 1.76 for stage III/IV periodontitis after adjustment. Our study found an even stronger association for the same classification of periodontal disease by severity, but it was smaller than our data. This may be due to differences in study populations, sampling methods, disease definition, and the more complex clinical population that we studied.[16] A second key discovery was that the people with diabetes or poor glycemic control exhibited significantly more periodontal destruction than those who had normal glycemic status. The findings in this observation align with those of the 2023 study by Tooi et al of clinical periodontal features and HbA1c levels in Japanese patients with diabetes who had received supportive periodontal therapy. This investigation was conducted to investigate the relationship between periodontal findings and HbA1C in patients undergoing periodontal maintenance for their periodontitis. The similarity in these results and ours indicates that the association of metabolic status with periodontal health may remain in periodontal patients even during treatment, highlighting the need for addressing systemic glycemic control along with local periodontal treatment.[17] Evidence of the inverse relationship comes from treatments. In a meta-analysis of 1374 patients who were included in randomized clinical trials, Oliveira et al. (2023) reported a statistically significant decrease in HbA1c of ~0.29% at 6 months post subgingival periodontal therapy.[18] Similarly, Dhingra and Jeng (2023) reviewed randomized studies, which reported that 3–4 months of periodontal treatment resulted in a decrease in HbA1c of 0.43%, six months in HbA1c of 0.30%, and 12 months in HbA1c of 0.50%. While the studies evaluated the impact of periodontal therapy on glycemic control, not the association evaluated in our study, the results of these studies support a biologically significant two-way association between the two. Therefore, the association that we saw in our cross-sectional analysis could be due to hyperglycemia's effect on the periodontal tissues and/or to periodontal inflammation's effect on metabolic dysregulation.[19] This correlation has continued to be confirmed by more recent evidence. In severe periodontitis patients with type 2 diabetes, Xu et al. (2024) performed a randomized controlled trial to determine the effect of scaling and root planing with or without adjunctive antibiotics on periodontal and glycemic outcomes. They also noted the clinical importance of treating patients with severe periodontal disease in which periodontal inflammation and metabolic control were treated concurrently.[20] Likewise, a 2024 systematic review and network meta-analysis compared adjunctive local periodontal therapies for patients with type 2 diabetes and periodontitis, with the outcomes of PPD, CAL, and HbA1c being interconnected. The results of these studies further emphasize the need to consider periodontal and glycemic outcomes as a unified entity and not as separate clinical issues. The evidence cited recently by Costa et al. (2025), who examined the correlation between HbA1c and the severity of periodontal disease in type 1 diabetes (T1D) patients with a cross-sectional design, further corroborates our findings. The population was different from our mixed adult population, but of special interest to our study is the direct address of the study to HbA1c and periodontal severity. The similarity between the links between chronic hyperglycemia and periodontal destruction in these various forms of diabetes raises the possibility that the link is not exclusive to type 2 diabetes.[21,23] Ibrahim et al. (2025) reviewed 350 records for diabetic patients that were collected during 10 years and reported significant positive correlations between HbA1c, percentage of sites with PPD ≥5 mm, missing teeth, and CAL. HbA1c had the highest correlation with the percentage of sites that had PPD ≥ 5 mm (r=0.38), and also had significant correlations with BOP and missing teeth. The results were directionally similar, but the correlations were somewhat higher for CAL (rₛ=0.58) and PPD (rₛ=0.52). The higher correlations found in our cohort might be due to the fact that patients were distributed across different periodontal severity groups, as well as due to the prospective measurement of periodontal parameters and not the retrospective extraction of records.[22,24] These findings have special clinical implications. Healthcare providers, such as dentists and physicians, may see people who have an undiagnosed or poorly controlled metabolic disease during routine periodontal evaluation, and an undiagnosed or underdiagnosed periodontal disease may be present in people who have diabetes but are not seeing a dentist. The high correlation found in this study argues for the need for periodontal screening to be made a routine part of diabetes care and for a heightened focus on glycemic assessment in patients with advanced periodontal destruction. Periodontal disease and diabetes may potentially be linked as chronic diseases that can benefit from an integrated approach involving a dentist, periodontist, physician, and diabetes-care team to enhance both periodontal and metabolic outcomes. There were several limitations to the study. It was not possible to establish a temporal or causal relationship between the degree of periodontal disease and glycemic status because of its cross-sectional design. The study was performed in one clinical center, and this may restrict the ability to extrapolate to the general population. Selective non-probability sampling may also have created selection bias. Factors that might be potential confounding factors, such as age, sex, smoking, and oral hygiene, were taken into account, but there was no complete exclusion of residual confounding in other factors such as socioeconomic status, dietary habits, and duration of hyperglycaemia, diabetes-related complications, and access to dental care. In addition, HbA1c and periodontal parameters were measured at one time point, and therefore could not reflect longitudinal changes in glycemic control or periodontal parameters. For confirmation of these findings and to elucidate the temporal association between glycemic dysregulation and the progression of periodontal disease, larger multicenter prospective studies are recommended. LIMITATIONS There were several limitations of the study. The cross-sectional design did not provide the capacity to make a chronological or causative association between the degree of glycemia and the severity of the periodontal disease. The study was carried out in a single clinical center, which may restrict the generalizability of the results to a broader population. Consecutive non-probability sampling may also have introduced selection bias. After accounting for the most important potential confounder factors included here, such as age, sex, smoking, and oral hygiene, some possible factors such as socioeconomic status, dietary habits, and duration of hyperglycemia, diabetes-related complications, and access to dental care could not be completely ruled out. In addition, HbA1C and periodontal parameters were evaluated simultaneously and thus were not measured over time to reflect changes in glycemic control and/or periodontal tissue status. However, larger multicenter prospective studies are recommended to confirm these findings and establish the time sequence between glycemic dysregulation and progression of periodontal disease.

The study showed that glycemic status is significantly associated with the severity of chronic periodontitis in adults. A high HbA1c was linked to increased probing pocket depth, clinical attachment loss, and severe periodontal disease. A high level of HbA1c was correlated with deeper probing pocket depth, clinical attachment loss, and higher frequency of severe periodontal disease. After controlling for important confounder variables, poor glycemic control was independently associated with severe periodontitis. These findings suggest that periodontal assessment should be incorporated into diabetes management and that glycemic control deserves to be a focus of periodontal disease management. Interdisciplinary management between dental and medical healthcare professionals might help identify high-risk individuals earlier and enhance oral and systemic health outcomes.