Oral Health Group
Feature

Periodontal Disease and Type 2 Diabetes

October 11, 2022
by Sara Madanat, BSc, MSc; Wendy E. Ward, BA & Sc., MSc, PhD


Chronic Diseases and Periodontal Health

Every 24 hours, 480 Canadian men and women are diagnosed with type 2 diabetes (T2D).1 In 2019, 11 million Canadians were diagnosed with T2D or pre-diabetes.2 The high prevalence of this disease equates to a high economic burden. For example, treatment costs in Canada reached approximately $30 billion in 2019.2 An often overlooked issue with T2D is its link to compromised oral health, namely periodontal disease.3

Periodontal disease has recently been considered as one of the six main complications of T2D alongside retinopathy, neuropathy, nephropathy, cardiovascular complications and delayed wound healing.3 It is a chronic inflammatory disease that progressively affects the supporting tissue of the teeth and if untreated, leads to destruction of alveolar bone and tooth loss.3 Periodontal disease shares controllable (e.g., overweight/obesity, exercise and smoking) and uncontrollable risk factors (e.g., age, sex and family history) as well as systemic and localized inflammation mechanisms with many chronic conditions such as osteoporosis, arthritis, Alzheimer’s disease, coronary heart disease, hypertension and type 2 diabetes.4

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As shown in Fig. 1, this article discusses the relationship between T2D and periodontal disease, focusing on the role of inflammation and the oral microbiome along with the importance of glycemic control. Practical aspects involving lifestyle modifications for improving blood glucose control are also discussed.

Fig. 1

. Low GI foods, regular exercise and dental hygiene appointments can help manage both T2D and periodontal disease. Both T2D and periodontal disease result in an elevation of proinflammatory cytokines and altered oral and/or gut microbiome. T2D is characterized by an elevated level of blood glucose and insulin resistance which causes the liver to increase the production of pro-inflammatory cytokines that can travel and target periodontal tissue resulting in destruction of the periodontium and disease associated oral bacteria. P. gingivalis, an oral bacteria, causes periodontal disease which in turn further stimulates the production of this pathogen that can travel and target the liver resulting in T2D. Additionally, T2D can alter the oral microbiome and increase the number of pathogenic bacteria. Periodontal disease can also alter the oral and gut microbiome and increase disease-associated bacteria which alters metabolic activity and increases T2D risk. Note. GI = glycemic index; P. gingivalis = porphyromonas gingivalis. Diagram created with Biorender.

Low GI foods, regular exercise and dental hygiene appointments can help manage both T2D and periodontal disease. Both T2D and periodontal disease result in an elevation of proinflammatory cytokines and altered oral and/or gut microbiome. T2D is characterized by an elevated level of blood glucose and insulin resistance which causes the liver to increase the production of pro-inflammatory cytokines that can travel and target periodontal tissue resulting in destruction of the periodontium and disease associated oral bacteria. P. gingivalis, an oral bacteria, causes periodontal disease which in turn further stimulates the production of this pathogen that can travel and target the liver resulting in T2D. Additionally, T2D can alter the oral microbiome and increase the number of pathogenic bacteria. Periodontal disease can also alter the oral and gut microbiome and increase disease-associated bacteria which alters metabolic activity and increases T2D risk.
Note. GI = glycemic index; P. gingivalis = porphyromonas gingivalis. Diagram created with Biorender.

T2D and Periodontal Disease

There is a bidirectional relationship between T2D and periodontal disease through increased inflammation and an altered oral microbiome. (Fig. 1) Individuals with T2D have a 3-fold increased risk of developing periodontal disease and with greater severity.5 One of the mechanisms by which T2D causes periodontal disease is through systemic inflammation due to increased blood glucose levels.6,7 Systemic inflammation is identified by an increase in circulating pro-inflammatory cytokines such as interleukin-6 (IL) and IL-1β, tumor necrosis factor α, and C-reactive protein.8 These cytokines can directly target periodontal tissue, stimulating the production of additional pro-inflammatory cytokines which perpetuates the localized periodontal inflammation. This also triggers an immune response that results in the destruction of the periodontium.6,7,8 A study that measured inflammatory cytokines in gingival crevicular fluid emphasized the link between blood glucose control, T2D, and periodontal disease. Specifically, individuals with T2D as well as poor glucose control and periodontal disease were shown to have higher levels of inflammatory cytokines in gingival crevicular fluid than individuals with T2D, better blood glucose control and periodontal disease.7

Periodontal disease is also responsible for systemic inflammation which can result from a spillover of periodontal bacteria and pro-inflammatory cytokines from the periodontal tissue to the circulation.8,9 Oral bacteria can be translocated to the gut microbiome through daily activities such as mastication, swallowing, and brushing.8 While the exact molecular mechanisms by which periodontal disease regulates the progress of T2D is unknown, there is evidence that a major pathogen of periodontal disease, Porphyromonas gingivalis (P. gingivalis), moves from the oral cavity to the gut where it results in gut dysbiosis and leads to leaky gut.10 A leaky gut allows for bacteria to move from the gut to the circulation. Thus, P. gingivalis travels through the blood to the liver where it inhibits insulin signaling. Insulin signals the liver or skeletal muscles to uptake glucose from the blood when blood glucose levels are high, however when this mechanism is inhibited it results in a sustained increase in blood glucose levels.11 Therefore, P. gingivalis induced insulin resistance and the resultant higher blood glucose levels increase the risk of T2D and lead to enhanced activation of pro-inflammatory cytokines which are also involved in periodontal disease. This creates a vicious cycle between T2D and periodontal disease.11

A 2013 consensus report from the European Federation of Periodontology and the American Academy of Periodontology stated that there is no evidence that diabetes has a significant impact on the oral microbiota.12 However, more recent investigations show that increased pro-inflammatory cytokines due to T2D alter the oral microbiome and render it more pathogenic.13 Individuals with a healthy periodontium who are diagnosed with T2D tend to have significantly lower species richness than individuals without diabetes and periodontal disease.13,14 This means there is a lower number of healthy bacteria and a higher number of bacteria that are associated with a disease state in the oral microbiome in individuals with T2D.13,14 Therefore, healthy individuals with T2D are at an increased risk of periodontal disease due to the lower relative abundance and prevalence of healthy bacteria and the higher level of pathogenic bacteria.13 Conversely, individuals with periodontal disease have an altered oral microbiome and an increase in disease-associated bacteria such as P. gingivalis which can enter the circulation and alter metabolic activities leading to an increased risk of T2D.11 This cyclical relationship is demonstrated in Fig. 1.

Periodontal disease and blood glucose control

One of the first human studies to suggest a link between periodontal disease and diabetes was a 1996 prospective longitudinal study of residents of the Gila River Indian Community in the US.15 The community included Native Americans aged 18 to 67 years with a high prevalence of T2D. The researchers found that severe periodontal disease at baseline was associated with an increased risk of poor blood glucose control (HbA1c > 9.0%, 75 mmol/mol) two years later, suggesting that periodontal disease compromises blood glucose control.15 A decade later, researchers analyzed data from the Study of Health in Pomerania, a population-based prospective cohort aged 20 to 81 years in Germany.16 This was the first study to report that periodontal disease predicts continued increase of blood glucose in individuals without diabetes, when measured over a 5-year period from baseline.16

The Main Target: Blood Glucose

Elevated blood glucose level is a hallmark feature of T2D.1 Several factors can stimulate elevated and sustained increases in blood glucose. The two major controllable factors are nutrition and exercise.1 Diabetes Canada recommends that individuals with T2D consume foods with a low glycemic index (GI) to better control their blood glucose levels. The GI is a scale that assigns values out of a 100 to foods based on how quickly they increase blood glucose levels.17 Foods with higher GI values increase blood glucose faster than foods with lower GI values. There are three main categories for GI values: low (55 or less), medium (56-69), high (70 or more).17 Eating foods that have low GI values also helps with maintaining or losing weight, feeling satiated longer, and decreasing the risk of T2D complications by helping to control levels of blood glucose. Low GI food sources come from food groups such as vegetables, fruits, whole grains, animal and plant-based protein, and dairy and its plant-based alternatives. Several dietary strategies such as the Portfolio diet,18 the Mediterranean diet,19 and the DASH (Dietary Approaches to Stop Hypertension) diet20 incorporate these food groups. Moreover, Canada’s Food Guide emphasizes these diets by encouraging the consumption of three categories of foods – fruits and vegetables, protein and whole grains – for every meal.21

In addition, exercise can provide an immediate and long-term effect on reducing blood glucose levels and improving insulin sensitivity. This has been extensively discussed in a recent review.22 Single exercise sessions that can reduce blood glucose levels include the following:22

  • resistance exercise that includes strength training that uses major muscle groups such as lunges, push-ups, squats and planking for ~30 minutes
  • aerobic exercise such as cycling, swimming, brisk walking, hiking and jogging for about 60 to 90 minutes
  • high-intensity interval training such as running as fast as possible for 1 minute then jogging for 2 to 4 minutes, and repeating for about 20 minutes

Moreover, the magnitude of this reduction is greater when individuals exercise after a meal rather than before. In addition, short-term (hours to days) exercise can improve insulin sensitivity for up to 48 hours. However, if carbohydrate foods are consumed during this period the magnitude of exercise induced insulin sensitivity will be reduced.22

Regular exercise is of the most benefit and to maintain these benefits for blood glucose control, exercise must be continued. As outlined in the bullet points above, there are many different types of activities that improve insulin sensitivity. With long-term continuous exercise (weeks to months and longer), skeletal muscles are remodelled and have an improved ability to uptake glucose from the circulation.
Treatment and management of periodontal disease is another strategy for improving blood glucose control. A systematic review from 2017 included seven randomized controlled trials and included 940 participants (473 individuals with diabetes were in the intervention groups and 467 individuals without diabetes were in the control group).23 Participants had a mean age ranging from 47 to 60 years. This review found that periodontal therapy reduced blood glucose levels by three to four months after treatment in individuals diagnosed with T2D.23 Thus, the findings from this review suggest that individuals living with T2D may experience improved blood glucose control with regular hygiene appointments and treatments.

Guidance for Patients

Food Choices: Choosing foods and snacks with a GI of 55 or less (low glycemic index) more often is helpful to control blood glucose. Generally, fruits and vegetables, whole grains, animal and plant-based protein, and dairy and alternatives have a low GI and are thus good choices. Visit Diabetes Canada’s Glycemic Index Food Guide or diabetes.ca/resources/tools-resources/the-glycemic-index-(gi) for specific lists of foods with a low, medium or high GI.

Additionally, being mindful of eating habits, cooking more often, using food labels to make healthier choices, and limiting processed foods are all good practices for overall health. For healthy eating recommendations, recipes and tips visit Canada’s Food Guide or food-guide.canada.ca/en/. Canada’s Food Guide provides a visual suggestion of the types and amounts of foods to be consumed for meals throughout the day. For example, it is encouraged that 50 percent of the plate consist of vegetables and fruits (e.g., spinach, broccoli, carrots, apples, berries, and bananas), 25 percent of the plate consist of animal and or plant-based protein (e.g., salmon, chicken, legumes and pulses, and low-fat yogurt), and the other 25 percent of the plate consist of whole grains (e.g., brown rice, quinoa, whole wheat pasta and bulgur).

Regular Exercise: The Canadian 24-Hour Movement Guidelines generally recommends a minimum of 150 minutes of moderate to vigorous activity (70 to 85 percent of your maximum heart rate) each week. The talk test is an easy way of measuring intensity. During moderate intensity activity you should be able to talk but not sing, and during vigorous intensity activity you will not be able to say more than a few words without pausing for a breath. Aerobic exercise can be performed 5 days a week in 30-minute sessions. For example, it is recommended that people aged 18 to 64 years participate in moderate to vigorous aerobic physical activity (e.g., running, swimming, and cycling for 30 minutes 5 days per week). That age group is also recommended to perform strength exercises (e.g., lunges, push-ups, squats, and planking at least 2 days per week) and several hours of light physical activity such as walking and standing. Sedentary behaviour should be limited to 8 hours or less and long periods of sitting should be broken up with standing or walking breaks. Visit the Canadian Society for Exercise Physiology or https://csepguidelines.ca for specific recommendations based on age and health status.

You can also visit ParticipACTION or https://www.participaction.com/en-ca for exercise videos, exercise blogs, and activity tracking apps.

Visits to your Health Care Professionals: Regular visits to the physician and dental or periodontal clinic are highly encouraged to ensure blood glucose levels are controlled and periodontal health is maintained.

Oral Health welcomes this original article.

References

  1. “Type 2 Diabetes,” Diabetes Canada Website. https://www.diabetes.ca/about-diabetes/type-2
  2. “New Data Shows Diabetes Rates and Economic Burden on Families Continue to Rise in Ontario,” Diabetes Canada Website. https://www.diabetes.ca/media-room/press-releases/new-data-shows-diabetes-rates-and-economic-burden-on-families-continue-to-rise-in-ontario–
  3. R. S. Leite, N. M. Marlow, J. K. Fernandes, and K. Hermayer, “Oral health and type 2 diabetes,” The American Journal of the Medical Sciences, vol. 345, no. 4, pp. 271-273, Apr. 2013, doi: 10.1097/maj.0b013e31828bdedf.
  4. L.-C. Kuo, A. M. Polson, and T. Kang, “Associations between periodontal diseases and systemic diseases: A review of the inter-relationships and interactions with diabetes, respiratory diseases, cardiovascular diseases and osteoporosis,” Public Health, vol. 122, no. 4, pp. 417-433, Apr. 2008, doi: 10.1016/j.puhe.2007.07.004.
  5. C. Tsai, C. Hayes, and G. W. Taylor, “Glycemic control of type 2 diabetes and severe periodontal disease in the US adult population,” Community Dentistry and Oral Epidemiology, vol. 30, no. 3, pp. 182-192, May 2002, doi: 10.1034/j.1600-0528.2002.300304.x.
  6. F. Ünlü, P. G. Güneri, M. Hekimgil, B. Yesilbek, and H. Boyacioˇg lu, “Expression of vascular endothelial growth factor in human periodontal tissues: Comparison of healthy and diabetic patients,” Journal of Periodontology, vol. 74, no. 2, pp. 181-187, Feb. 2003, doi: 10.1902/jop.2003.74.2.181.
  7. S. P. Engebretson et al., “Gingival crevicular fluid levels of interleukin-1β and glycemic control in patients with chronic periodontitis and type 2 diabetes,” Journal of Periodontology, vol. 75, no. 9, pp. 1203-1208, Sep. 2004, doi: 10.1902/jop.2004.75.9.1203.
  8. G. Hajishengallis and T. Chavakis, “Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities,” Nature Reviews Immunology, vol. 21, no. 7, pp. 426-440, Jan. 2021, doi: 10.1038/s41577-020-00488-6.
  9. S. Engebretson, R. Chertog, A. Nichols, J. Hey-Hadavi, R. Celenti, and J. Grbic, “Plasma levels of tumour necrosis factor-alpha in patients with chronic periodontitis and type 2 diabetes,” Journal of Clinical Periodontology, vol. 34, no. 1, pp. 18-24, Jan. 2007, doi: 10.1111/j.1600-051x.2006.01017.x.
  10. M. Nakajima et al., “Oral administration of P. gingivalis Induces dysbiosis of gut microbiota and impaired barrier function leading to dissemination of enterobacteria to the liver,” PLOS ONE, vol. 10, no. 7, p. e0134234, Jul. 2015, doi: 10.1371/journal.pone.0134234.
  11. M. Ishikawa et al., “Oral Porphyromonas gingivalis translocates to the liver and regulates hepatic glycogen synthesis through the
  12. Akt/GSK-3β signaling pathway,” Biochimica et Biophysica Acta (BBA)–Molecular Basis of Disease, vol. 1832, no. 12, pp. 2035-2043, Dec. 2013, doi: 10.1016/j.bbadis.2013.07.012.
  13. I. L. C. Chapple and R. Genco, “Diabetes and periodontal diseases: Consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases,” Journal of Clinical Periodontology, vol. 40, pp. S106-S112, Apr. 2013, doi: 10.1111/jcpe.12077.
  14. F. Teles, Y. Wang, G. Hajishengallis, H. Hasturk, and J. T. Marchesan, “Impact of systemic factors in shaping the periodontal microbiome,” Periodontology 2000, vol. 85, no. 1, pp. 126-160, Nov. 2020, doi: 10.1111/prd.12356.
  15. E. Xiao et al., “Diabetes enhances IL-17 expression and alters the oral microbiome to increase its pathogenicity,” Cell Host & Microbe, vol. 22, no. 1, pp. 120-128.e4, Jul. 2017, doi: 10.1016/j.chom.2017.06.014.
  16. G. W. Taylor et al., “Severe periodontitis and risk for poor glycemic control in patients with non-insulin-dependent diabetes mellitus,” Journal of Periodontology, vol. 67, no. 10s, pp. 1085-1093, Oct. 1996, doi: 10.1902/jop.1996.67.10s.1085.
    R. Demmer et al., “Periodontal status and A1C change: Longitudinal results from the study of health in Pomerania (SHIP),” Journal of Clinical Periodontology, vol. 67, no. 10, pp. 1037-1043, May 2010, doi: doi: 10.1902/jop.1996.67.10s.1085.
  17. “The Glycemic Index (GI),” Diabetes Canada Website. https://www.diabetes.ca/en-CA/resources/tools – resources/the-glycemic-index-(gi)
  18. D. J. A. Jenkins, “Effects of a dietary portfolio of cholesterol-lowering foods vs lovastatin on serum lipids and C-Reactive protein,” JAMA, vol. 290, no. 4, p. 502, Jul. 2003, doi: 10.1001/jama.290.4.502.
  19. A. Keys and M. Keys, How to eat well and stay well the Mediterranean way. New York: Garden City, 1975.
  20. L. Appel et al., “A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group,” The New England Journal of Medicine, vol. 336, no. 16, pp. 1117-1124, 1997, doi: 10.1056/NEJM199704173361601.
  21. “Canada’s Food Guide,” Government of Canada, Mar. 10, 2022. https://food-guide.canada.ca/en/
  22. J. B. Gillen, S. Estafanos, and A. Govette, “Exercise-nutrient interactions for improved postprandial glycemic control and insulin sensitivity,” Applied Physiology, Nutrition, and Metabolism, vol. 46, no. 8, pp. 856-865, Aug. 2021, doi: 10.1139/apnm-2021-0168.
  23. A. Teshome and A. Yitayeh, “The effect of periodontal therapy on glycemic control and fasting plasma glucose level in type 2 diabetic patients: Systematic review and meta-analysis,” BMC Oral Health, vol. 17, no. 31, pp. 1-11, Jul. 2016, doi: 10.1186/s12903-016-0249-1.

About the Author

Sara Madanat holds a BSc in Honours Kinesiology from McMaster University and a MSc from Brock University. Sara is currently a PhD Candidate at Brock University where she focuses on preclinical research investigating how food bioactives, vitamin D, and calcium impact bone and cognitive health.

 

Wendy Ward is a Professor in the Department of Kinesiology and holds a Senior Research Fellowship in the Faculty of Applied Health Sciences at Brock University. Her team’s overall research goal within the Nutrition, Bone and Oral Health Research Group is to develop dietary strategies that help protect against osteoporosis and related fractures while also understanding the complex relationships with other health conditions such as periodontal disease.


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