Genetic factors influence periodontitis

Besides bacteria, the patient’s genetic background is an additional risk factor for periodontal diseases. This determines the magnitude of the immune response to bacteria and thereby significantly influences the course of the disease.


Periodontitis and peri-implantitis are caused by periodontopathogenic bacteria. It is the immune response that determines the extent of destruction of the periodontal apparatus, however. The body responds to the presence of bacteria by releasing certain inflammatory mediators such as the pro-inflammatory interleukin-1A and -1B, hereafter referred to as interleukin-1 (IL-1). When the inflammatory stimulus subsides, the activity of IL-1 is inhibited again with the aid of the interleukin-1 receptor antagonist (IL-1RN). The ratio of pro- to anti-inflammatory cytokines determines the form and magnitude of the individual inflammatory response.

Off balance

If this interaction is impaired due to genetic dispositions, the affected patient has increased inflammatory reactions and bone decay. An imbalance between IL-1 and IL-1RN thus leads to a heightened immune response which is directed against the body itself. These patients respond to exogenous stimuli, such as the presence of periodontopathogenic bacteria, for example with an overproduction of IL-1, and they consequently exhibit increased tissue destruction and bone resorption.

Increased risk of tooth and implant loss

The IL-1 gene is found in around a third of the European population, the carriers being at increased risk of periodontal diseases. The presence of a positive IL-1 genotype is associated with a 2.7x increase in the risk of progressive tooth loss. This genetic polymorphism is also considered a risk factor for implants, where the individual immune response also plays a key role. A genetic test is therefore helpful for risk assessment prior to major implant procedures.

Tailoring treatment to the genetic conditions

Knowledge about a patient’s genetic predisposition plays an important role in planning sensible recall and preventive care intervals. Because affected patients must be monitored more closely than patients with a normal immune response. This information sometimes also helps to motivate the patient to be more cooperative with regard to oral hygiene and recall visits. If additional risk factors such as smoking are present, this also increases the risk and should be reflected both in treatment planning and in the recall schedule. If patients with a positive IL-1 genotype also exhibit increased concentrations of periodontopathogenic marker bacteria, adjunctive antibiotic administration may be reasonable even at lower concentrations of bacteria because of the exaggerated immune response.