Gingivitis and Your Genes

Have you ever gone to the dentist, expecting a good report, only to be fussed at by the hygienist for bleeding gums? You brushed, flossed, and stayed away from candy for the past six months — so why on earth do you still have inflamed gums?

What is Gingivitis?

Inflammation of the gums, known as gingivitis, is caused by an inflammatory response in the tissue of your gums. Periodontal disease is another term you may have heard mentioned by your hygienist (as she stabs your gums with the sharp poking tool). Periodontal disease is a term that includes gingivitis, and then the next step – inflammation of the jaw bone and loose teeth.[ref]

So what causes gingivitis? Lack of brushing and flossing… maybe. Smoking, for sure.

But what if you regularly brush and floss? And what about those people (you know who you are) who don’t brush and floss but have healthy gums?

The key here is the body’s response to the bacteria and biofilm on the teeth. The mouth is teeming with bacteria, and your immune system is on high alert to keep those bacteria from crossing into the bloodstream.

Inflammation, gingivitis, and genetics:

Some people naturally (genetically) are more prone to producing higher levels of inflammatory cytokines. This is a positive attribute when you are fighting off certain viruses or bacteria. But the flip-side is that elevated inflammation causes a number of diseases – including gum disease.

Frequently, people with gingivitis have higher CRP levels on average than people without gingivitis. And people with periodontitis had even higher CRP levels.[ref]

Genetic studies reveal a lot about the underlying causes of diseases, including gingivitis and periodontal disease.

Variants that increase inflammatory cytokines, such as TNF-alpha, interleukin 1A (IL1A gene), interleukin 6 (IL6 gene), and interleukin 8 (IL8 gene), are all linked to increased risk of gingivitis.

Your body also has ways to mitigate inflammatory cytokine production. Interleukin 10 is one such mechanism for moderating the inflammatory response. Genetic variants that decrease IL-10 are thus linked to increased inflammation and an increased risk of periodontal disease.

An increased inflammatory response to bacteria causes inflammation in the gums – gingivitis or periodontal disease. And targeting the right genetic variants may help you stop the bleeding and receding gums.

Heart disease and Gingivitis:

This article isn’t just about a little bleeding when you brush or floss. Gingivitis and an increased risk of heart disease are strongly connected.

This connection may be due to increased systemic inflammation or it may be due to bacteria entering the blood stream when your gums bleed (flossing, brushing).[ref]


Genetic variants associated with gingivitis

Your genetic variants in genes related to inflammatory cytokines can significantly increase your risk of having inflamed gums.

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TNF-α (Tumor necrosis factor-alpha) gene:
TNF-α is an inflammatory cytokine involved in the body’s immune response. TNF is important to have in the right amounts.  It helps the body destroy cells with aberrant DNA, but too much TNF is implicated in inflammatory diseases such as rheumatoid arthritis.  TNF-α is stimulated by bacterial endotoxin (lipopolysaccharide) as well as other pathogens.  It is one of the body’s primary mediators in protection against bacteria and viruses.  Chronically elevated levels of TNF have implications for a variety of autoimmune diseases.

Check your genetic data for rs1800629 (23andMe v4, v5; AncestryDNA):

  • A/A: 2 to 3-fold increase in TNF-α; increased risk of periodontitis[ref]
  • A/G: increased TNF-α; increased risk of periodontitis
  • G/G: typical

Members: Your genotype for rs1800629 is .

IL1A gene (Interleukin 1) and IL1B gene:
Interleukin 1 is another inflammatory cytokine produced by lymphocytes or monocytes and released in response to endotoxins.

Check your genetic data for rs1800587 (23andMe v4, v5; AncestryDNA):

  • A/A: increased IL1A[ref]; increased risk of gingival bacterial colonization[ref] increased risk of periodontitis[ref]
  • A/G: increased risk of gingival bacterial colonization
  • G/G: typical

Members: Your genotype for rs1800587 is .

Check your genetic data for rs1143634 (23andMe v4, v5; AncestryDNA):

  • A/A: increased risk of gingivitis[ref][ref][ref]
  • A/G: increased risk of gingivitis
  • G/G: typical

Members: Your genotype for rs1143634 is .

IL2 gene: codes for interleukin-2, another inflammatory cytokine.

Check your genetic data for rs2069763 (s3andMe v4, v5)- IL2 – A is minor, c typical

  • A/A: ~3x increased risk of chronic periodontitis[ref]
  • A/C: typical risk
  • C/C: typical

Members: Your genotype for rs2069763 is .

IL-6 gene:
Interleukin 6 acts both as an inflammatory cytokine and as an anti-inflammatory signal by moderating TNF-alpha. This is another important cytokine in infection, but if the body does not control it well, it can also cause problems.[read more]

Check your genetic data for rs1800795 (23andMe v4, v5; AncestryDNA):

  • G/G: higher risk of gingivitis (common allele in many population groups)[ref][ref]
  • C/G: typical risk of gingivitis
  • C/C: lower risk of gingivitis

Members: Your genotype for rs1800795 is .

IL8 gene:
Interleukin 8 is an essential regulator of the inflammatory response.

Check your genetic data for rs4073 (23andMe v4, v5; AncestryDNA):

  • A/A: increased IL8, somewhat increased risk of periodontitis[ref]
  • A/T: probably normal risk of periodontitis[ref]
  • T/T: typical

Members: Your genotype for rs4073 is .

IL10 gene:
The IL10 gene codes for the anti-inflammatory cytokine IL-10 (interleukin-10). Variants causing a decrease in the amount of IL10 are associated with increased inflammation. In contrast, variants that cause an increase in IL10 are associated with less inflammation.

Check your genetic data for rs1800896 (23andMe v4, v5; AncestryDNA):

  • T/T: Common genotype, more likely to have gum disease
  • C/T:  more likely to have gum disease
  • C/C: higher IL-10, less likely to have gum disease[ref]

Members: Your genotype for rs1800896 is .

CCR5 gene:
The CCR5Δ32 variant also has links to reduced mortality risk from HIV for people with one copy. Carriers of two copies of the mutation are resistant to common strains of HIV.

Check your genetic data for rs333 (23andMe – i3003626 v4,v5):

  • Insertion/Insertion  (either II or GTCAGTATCAATTCTGGAAGAATTTCCAGACA/ GTCAGTATCAATTCTGGAAGAATTTCCAGACA): typical
  • Insertion / Deletion (either DI or -/GTCAGTATCAATTCTGGAAGAATTTCCAGACA): decreased risk of periodontitis.
  • Deletion / Deletion (either DD or -/-): decreased risk of periodontitis.[ref]

Members: Your genotype for i3003626 is .

 


Lifehacks for reducing gum disease:

Here are some natural options to explore for reducing inflammation in your gums:

It almost goes without saying (but I’m saying it anyway) that good oral hygiene measures such as brushing your teeth are always necessary.\

Glycine, found abundantly in bone broth, has been shown to inhibit TNF-α due to endotoxins in a study.[ref]

Green tea: Swish with some green tea? A study found that using green tea as a mouthwash worked better for reducing gingivitis than chlorhexidine gluconate (germicidal mouthwash).[ref]

Reducing fluoride? Studies show fluoride increased inflammatory cytokines, including TNF-α, IL-1β, and IL-6.[ref][ref][ref]

Does this mean that you should stop drinking fluoridated water and use toothpaste without fluoride? I’ll let you read through the research and decide for yourself.

Saltwater: Rinsing with saltwater has some interesting research behind it for decreasing gingivitis. The study on saline shows that it increases type-I collagen and fibronectin in gingivitis cells.[ref]

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TNF-alpha: Inflammation and Your Genes
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About the Author:
Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.