How Lifestyle Factors Affect Periodontal Disease

Without bacteria, there will be no periodontal disease, which is why it is considered as a separate factor in the causality of periodontal disease. Plaque control, i.e. effective disruption of the biofilm, is therefore considered the most effective preventive measure against periodontal diseases. However, plaque control is mostly a matter of behaviour, and could therefore be considered a lifestyle factor. In our recent white paper, we discuss how behaviour change strategies can influence oral hygiene.

Decades of research has demonstrated that tobacco smoking plays a role in the pathology of periodontitis in several ways. This includes a shift toward a more pathogenic oral microbiome, impaired gingival blood flow, dysfunction of neutrophils, increased levels of proinflammatory mediators, and increased levels of T-cells that are more immunogenic.

Smoking also compromises healing potential of affected gingival tissue.

Although current evidence for the promotion of other healthy lifestyles is limited, literature demonstrated that in periodontitis patients, interventions for smoking cessation are effective and thus improve their oral health.

Studies have shown that alcohol consumption is associated with moderately increased severity of periodontal disease and can be considered an independent modifiable risk factor for periodontitis.

In terms of underlying mechanisms, research shows that alcohol abuse has a negative impact on the oral microbiome, while it also impairs neutrophil, macrophage, and T-cell functions, altering immune responses. It is also associated with impaired bone regeneration.

There is a clear psychobiological relationship between chronic stress and its related diseases on the one hand, and periodontal diseases on the other hand. Chronic stress alters the tissue-healing process by increasing the rate at which cytokines, interleukins (IL-1β, IL-6, IL-8) and TNF-α are produced, resulting in an increase in the severity of periodontal damage.

Stress also overburdens aspects of the immune response such as mitogen stimulation, antibody and cytokine production, de-regulating the overall immune response and thereby promoting the development of periodontitis.

Some studies show that hormones released under stress can cause a proliferation of bacteria such as Fusobacterium nucleatum, further aggravating the severity of periodontal damage.

For more information, see “The impact of stress on periodontal disease: risk indicator or risk factor?”, which cites research advising that “attention to and awareness of stress as an aspect of the comprehensive set of risk factors for periodontitis can diminish its negative impact on immune fitness.”

High sugar or high saturated fat, as well as low polyol, low fiber, and low polyunsaturated fat diets have each been associated with an increased risk of periodontal disease.

Numerous studies also found multiple different associations between lower dietary calcium intake and periodontal disease. For example, a low serum calcium-magnesium ratio is significantly associated with increased attachment loss and the progression of periodontal disease. Consequently, milk and milk products, as a source of calcium, phosphate, and various proteins, are likely to have beneficial effects on periodontal health. Meanwhile, calcium intakes below recommended reference levels are associated with an increased risk of tooth loss, attachment loss, and severity of periodontal disease.

Consensus field guidelines recommend diets high in vitamins, minerals, and trace elements such as the Mediterranean Diet and the Okinawan-based Nordic diet to reduce gingival inflammation. Diets rich in vitamins A, B, C, and E, along with minerals and trace elements including calcium, magnesium, zinc, and manganese have been associated with a decreased risk of periodontal disease and periodontal disease progression.

Generally, diets high in proteins, fatty acids, and processed sugars and lacking in fruits and vegetables increase the risks of periodontal disease. Conversely, low sugar, high fiber, and high omega-6 to omega-3 fatty acid ratio intake diets reduce the risk of periodontal disease.

For more information, see “Gum disease and nutrition”.

Vitamin D plays an important role in calcium and bone metabolism and is also thought to have immunomodulatory and anti-inflammatory effects which may help control and reduce periodontal swelling. In patients with periodontitis, lower vitamin D levels compared with healthy controls have been reported, while, inversely, higher serum 25-hydroxy vitamin D concentrations have been associated with lower rates of gingivitis and less attachment and tooth loss.
As a secosteroid hormone produced mainly by skin when exposed to sunlight, vitamin D is only available in trace amounts in food. If patients struggle with vitamin D deficiency, therefore, recommend getting more exposure to sunlight or taking a vitamin D supplement.

At least 28 epidemiological studies and controlled clinical trials have identified an association between obesity and an increased risk of periodontal disease. Though the underlying pathophysiological mechanism of this increased risk remains unclear, there are multiple theories.

If a person is obese for a long period of time, their weight may strain their body’s ability to distribute oxygen effectively. Also, obesity may cause inflammation in different areas of the body more frequently, and it is associated with a low-grade systemic inflammation, measured by the acute-phase inflammatory protein CRP excreted by the liver,. Both of these possible side effects of obesity can lead to insulin resistance, a phenomenon in which the cells in the muscles, fat, and liver of the obese person can’t respond to insulin as effectively as normal. Insulin resistance can lead to prediabetes, which, in turn, raises risk of periodontal disease.

For more information, see “Links between obesity and periodontal disease: what your patients should know.”

Numerous recent studies have proven an association with increased physical activity and a decreased risk and severity of periodontal disease.

For example, a 2018 study proved that “exercise habits could reduce local inflammatory cytokines, activate immunocompetent cells, and improve the pathological condition of periodontitis.” This study points out that long-term moderate exercise is immunologically beneficial because it reduces subcutaneous and visceral fat, decreases basal levels of inflammatory cytokines, and increases anti-inflammatory cytokines.

General exercise has also been shown to activate local immunocompetent cells such as macrophages, neutrophils, and lymphocytes.

From these studies, we can conclude that it is likely that increased physical activity will lower a patient’s risk of periodontal disease.