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Genetics of Periodontitis
Thursday, 03 July 2008
Last Updated Tuesday, 07 October 2008

The genetics of periodontitis is a highly debated subject. Many researchers believe that there is no genetic basis of
periodontitis. However, others have found evidence in support of this.

When a unique genetic trait (or polymorphism) is present in a disease or illness and is absent in normal individuals it is
called a biomarker of that disease.

Periodontitis

Periodontitis has been a symptom in many single gene syndromes. Genes code for proteins, and proteins perform
functions in the body. These proteins do not necessarily need to be absent for adverse effects, more commonly a simple
change in structure (from a different mutant gene sequence) can cause disease. Quite a few of these slightly changed
proteins are often correlated with periodontitis susceptibility. Many polymorphisms have been identified that are
correlated to periodontitis.
However, in most cases, the relationships of these polymorphisms to periodontitis is unclear. It is also important to keep
in mind, that the ethnicity of patient’s also plays a central role in the distribution of these gene polymorphisms. For
instance both Japanese and Chinese population have much lower occurrence of polymorphisms in Interleukin 1a (IL1a),
which some studies indicate shows linkage to periodontitis, than in the Caucasians.

Linkage between gene polymorphisms in the following four proteins and periodontitis has been suggested based on a
number of studies.

Interleukin 1
Interleukin 1 is an important family of proteins, which are intimately related to the body's inflammatory response. There
are a number of areas where periodontitis intersects with other diseases, but none more interesting than with
Cardiovascular disease. It has been shown that patients with periodontitis have elevated levels of Interleukin 1; the
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inflammatory response expected in such cases may also play a role in the initiation of Cardiovascular disease.

Interleukin-10

Interleukin 10 is also important in regulating the body’s response to various inflammatory response signals.
Therefore, some of the IL 10 polymorphisms could cause an increase in the production of various inflammatory response
signal proteins, thus leading to increase in tissue destruction. In one study, incidence of periodontitis in individuals with
certain IL 10 polymorphisms was found to be approximately 25 percent higher than normal, but due to the low sample
size, these results are not very reliable.

Tumor necrosis factor-a


Tumor necrosis factor-a (TNF-a) is an important inflammatory mediator, which is regulated by interleukin 10. Recent
studies indicate that a number of polymorphisms of TNF-a are associated with periodontitis in Japanese men.

Interleukin-6

Interleukin-6 is another inflammatory protein, whose polymorphisms are associated with higher prevalence of
periodontitis in population in comparison to the healthy control groups.

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