How do diet and obesity affect periodontitis and the response to treatment?

What are the links between obesity and periodontitis?

By James Deschner

Studies showing a link between obesity and periodontitis started almost 50 years ago with a 1977 animal experiment where periodontitis was induced in rats, which showed that the disease became much more severe in the obese rats. It then took around 20 years for clinical studies to confirm this in humans and demonstrate an association between periodontitis and obesity.

Later studies have shown that the relationship is dose dependent: the higher the body mass index (BMI), the higher the risk of periodontitis. This much is clear.

Some studies have also shown that obesity may compromise the outcomes of periodontitis treatment, but other studies have not been able to confirm this and more research is needed.

We do not yet fully understand all the mechanisms underlying the association between obesity and periodontitis. One mechanism that may well be involved is that bacteria-induced local periodontal inflammation gets enhanced by the chronic low-grade systemic inflammation induced by obesity. Other possible mechanisms include:

• Obesity produces hyposalivation, which may promote plaque accumulation.
• Obesity might compromise the microcirculation in the gingiva.
• It is also believed that the intestinal microbiome is linked to the oral microbiome. The intestinal microbiome is not only partly responsible for the risk of obesity but can also cause the intestinal barrier to become more permeable, allowing bacterial toxins to enter the systemic blood circulation, which in turn can further increase inflammation locally in the periodontium. In addition, changes in the intestinal barrier can negatively affect the immune system, which is also critical for controlling and combating oral pathogens.

Although the link between obesity and periodontitis is clear and these mechanisms may help to explain it, further studies are needed to clarify the causality—i.e., whether obesity contributes to the development and progression of periodontitis or, conversely, whether periodontitis promotes weight gain. In contrast, causality in the relationship between periodontitis and diabetes is much better understood and proven.

There are reasons to think that periodontitis—particularly in its more severe form (stages III and IV)—may contribute, albeit indirectly, to obesity. If someone is suffering from edentulism or tooth mobility, they may be more likely to opt for a calorie-rich soft diet.

While obesity is clearly a risk modifier, it may well be a true risk factor. We know that, irrespective of periodontitis, obesity causes a pro-inflammatory state and that the inflammation induced by obesity affects the host response, how cells sense microorganisms, and whether the host cells fight against these microorganisms. We also know that obesity affects extracellular matrix molecules of the periodontium. Putting all this together suggests that obesity is a true risk factor for periodontal disease.

There are also shared risk factors: age, alcohol consumption, low socioeconomic level, and low health awareness may contribute to the development of both obesity and periodontitis.

How does nutrition affect periodontal status?

By Henrik Dommisch

Dietary habits and body weight are very much related to each other and there is now a body of evidence showing that eating certain nutritional elements—such as fibres, fruits, and vegetables—is very much related to a better periodontal status, while a very high intake of processed foods and sugar is linked to a more unfavourable status.

We have studies—mostly surveys but also some interventional studies—that give us some hints about the impact of nutritional factors on periodontal status. There are studies showing changes in both the gut and the oral microbiomes, and we have some evidence from studies of fasting, showing what happens to periodontal health if you abstain from sugar for a certain period.

What we find from large-scale studies is that there is a direct relationship between nutritional factors such as a high intake of saturated fats, trans fats, and sugar and periodontal inflammation.

One important question is whether the positive effects that we see in terms of specific dietary regimes result from the diets themselves or from the reduction in body weight.

We do know that diet has a direct influence on the microbiome. In the oral microbiome, processed carbohydrates such as free sugars get transformed or metabolised as short-chain carboxyl acids, which are very pro-inflammatory. We also know that diet can have a direct influence on the dental biofilm.

Some studies have provided evidence that changing the dietary intake could influence periodontal inflammation. However, other studies have not shown such an influence.

There are also studies showing that changes in nutrition caused measurable alterations in the periodontium. For instance, a change to the Mediterranean diet or intermittent fasting or fasting can improve factors such as bleeding on probing.

An increased fibre intake and the adoption of a vegetable-based or vegan diet may lead not only to a clear change in the composition of the gut microbiome but also have some effects in the oral microbiome. Thus, dietary changes may influence the inflammatory status in the oral cavity.

What is the best diet for periodontal health?

By Johan Wölber

While there are differences in dietary guidelines between different countries, there are some things we can all agree on, such as reducing the free-sugar intake—we have a clear meta-analysis and systematic review showing that reducing free sugars will also help to reduce gingival inflammation (Woelber et al., 2023).

Beyond that, choosing a specific diet is a complex issue in terms of individual patients. We have patients who love to eat sausages and those who love to eat pasta, and we have to think about how we can individually motivate patients to make even slight changes in their diet towards a healthier lifestyle.

One way to look at diet is in terms of a daily risk factor, as three times a day most people can make a choice between pro- or anti-inflammatory foods. Periodontists can help here by making their patients aware of this choice and giving them knowledge of the components of an anti-inflammatory diet.

We can agree on increasing the intake of fruit and vegetables, getting sufficient omega-3 fatty acids (maybe two portions of seafood a week), and reducing the intake of processed carbohydrates (such as sugar, white flour, and sugar-sweetened beverages), meat and red meat. There is no need to necessarily become vegan or vegetarian, but most observational data shows that it is generally beneficial for the body to have a reduced intake of saturated fatty acids and red and processed meats. There may also be benefits from intermittent fasting.

In terms of micronutrients, we need to ensure we get enough vitamin D in the winter and other micronutrients such as vitamins A, B, C, and E and phytonutrients.

Most of the intervention studies we have relate to gingivitis—i.e., periodontal inflammation—rather than periodontitis, because it takes much longer to investigate periodontal effects or periodontal outcomes. Nonetheless, we do see clear effects on the bleeding-on-probing score and other relevant clinical factors. This means that a patient really has nothing to lose by trying these dietary changes (other than perhaps losing some excess weight).

There is a need for future research to investigate more thoroughly the potential positive influence from diet and weight reduction on periodontal outcomes and periodontal therapy.