InstalabCelsus One™
Should you take a Celsus One™ test?
This test is most useful if any of these apply to you.
8 biomarkers included
- Beta-Defensin 1 GenotypeReads defensin beta 1 (DEFB1), a barrier-defense gene that helps the gum surface control bacteria before deeper inflammation starts.Why it mattersCertain DEFB1 variants have been linked to severe chronic periodontitis, pointing to weaker first-line bacterial control.
- CD14 GenotypeReads cluster of differentiation 14 (CD14), which helps hand bacterial surface signals to Toll-like receptor 4 before inflammation ramps up.Why it mattersHigher-sensitivity CD14 variants can make bacterial exposure more inflammatory, especially alongside high-risk interleukin 6 results.
- Toll-Like Receptor 4 Composite GenotypeReads Toll-like receptor 4 (TLR4), a bacterial-sensing gene involved in early response to disease-linked oral bacteria.Why it mattersRisk variants change the first alarm signal, with clearer periodontitis links in some Caucasian subgroups than in pooled overall data.
- Tumor Necrosis Factor Alpha GenotypeReads tumor necrosis factor alpha variants, an immune signal that can turn up inflammatory pathways involved in tissue damage and bone loss.Why it mattersA risk-pattern result hints at a hotter inflammatory tone, but periodontitis associations are inconsistent across ancestries and study designs.
- Interleukin 1 Composite GenotypeCombines inherited versions in interleukin 1A and interleukin 1B, immune-signal genes tied to stronger gum inflammation after bacterial exposure.Why it mattersPositive results are the panel's best-studied risk signal, especially for severe periodontitis in non-smokers of studied ancestries.
- MyPerioID® IL-6Reads an interleukin 6 (IL-6) variant linked to the strength of gum inflammation and, in type 1 diabetes, greater disease extent.Why it mattersHigh-risk IL-6 can reinforce other inflammatory signals, especially when blood sugar problems or periodontal findings are already present.
- Interleukin 17A GenotypeReads interleukin 17A, an immune-signal gene that helps recruit front-line white blood cells into inflamed gum tissue.Why it mattersA risk-pattern result adds context for persistent gum inflammation, with the strongest published signals in Asian populations.
- Matrix Metalloproteinase 3 GenotypeReads the matrix metalloproteinase 3 (MMP-3) 5A/6A variant, tied to collagen breakdown and activation of related tissue-remodeling enzymes.Why it mattersThis result adds tissue-breakdown context; pooled analyses conflict, and the association appears modified by smoking status.
About Celsus One™
Periodontitis is gum disease that damages the tissue and bone holding teeth in place. Two people can carry similar plaque and live with similar habits, yet only one loses support around the teeth. Genetics can be one reason. Systematic reviews put the inherited share of periodontitis differences at about a third in the population, and some twin measures land closer to half.
Celsus One reads eight inherited gene markers from saliva. It does not diagnose gum disease, measure bone loss, or measure bacteria. It tells you whether your immune-response setting may run high, so you can decide how much weight to give plaque, smoking, diabetes, and disease-linked bacteria when planning prevention.
What This Panel Reveals
The eight markers are best understood as one chain: first contact with bacteria, then immune signaling, then tissue breakdown. That is the case for the panel. It is not a list of unrelated genes.
The first group is detection and barrier defense. Cluster of differentiation 14 (CD14) and Toll-like receptor 4 (TLR4) help cells sense a bacterial surface signal found on many disease-linked oral bacteria. Beta-defensin 1 helps the gum surface control bacteria before the deeper immune response starts.
The second group controls the volume of the inflammatory response. Interleukin 1, interleukin 6, tumor necrosis factor alpha, and interleukin 17A are immune messages. Some inherited versions have been linked to a stronger response to the same bacterial trigger, though the size and direction of that link vary by ancestry and study, and for tumor necrosis factor alpha the pooled data are inconsistent.
The third group is tissue remodeling. Matrix metalloproteinase 3 helps break down collagen, the support scaffold in gum tissue, and can activate related enzymes. Pooled analyses of its 5A/6A variant disagree: one recent meta-analysis found no clear overall periodontitis link and different patterns by smoking status, while earlier meta-analyses reported the variant increasing risk in some and decreasing risk in others.
What This Panel Cannot Do
Know what this test can and can't do. The strongest early result was the interleukin 1 composite genotype. In the 1997 Kornman study, non-smokers aged 40 to 60 with that pattern had 18.9 times the odds of severe periodontitis, though the confidence interval was extremely wide (1.04 to 343.05), reflecting a small, imprecise estimate. That result did not become a dependable rule.
The field got messier after that. A 2007 review found too little follow-up evidence to say the interleukin 1 result predicts progression or treatment response. A 2025 review of genetic markers found low to moderate test accuracy and no genetic test with current clinical value for diagnosis, prevention, or predicting disease resolution.
The 2025 European workshop reached the same practical point: manual probing and radiographs still define gum disease. Genetic results can add context. They cannot replace a periodontal exam.
How to Read Your Results Together
No single result is a verdict. The panel is most useful when several markers point the same way and when the result matches what is happening in your mouth.
| Pattern | What It Suggests |
|---|---|
| Several high-inflammatory results, especially interleukin 1, interleukin 6, and tumor necrosis factor alpha, plus current smoking | This is the highest-concern pattern. In the original interleukin 1 study, smoking or the interleukin 1 pattern accounted for 86% of severe cases. |
| High-inflammatory results but no bleeding, pockets, or bone loss on exam | Inherited risk is a tendency, not a diagnosis. The useful move is closer follow-up and better plaque control, not panic. |
| CD14 or TLR4 risk variants plus a heavy load of disease-linked bacteria | The bacteria make the gene result more actionable. This pattern supports a periodontal plan that targets the organisms actually present. |
| Mostly lower-risk variants but active gum disease | The test did not miss the disease. Plaque, smoking, diabetes, dry mouth, and the current bacterial mix can still drive bone loss. |
What to Do with Your Results
Start with proven causes. Plaque control, smoking, and blood sugar outweigh any single gene result because they can change the conditions your gums face every day.
If several inflammatory markers come back high risk, book a periodontal exam and consider an oral bacteria test. The useful question is whether your inherited response and your current bacteria are pointing in the same direction.
If you are considering dental implants, share the result with your surgeon before the plan is final. Interleukin 1 variants have been linked with higher risk of disease around implants in meta-analysis, but this should shape maintenance and risk planning, not decide surgery by itself.
You only need to run this panel once. Your inherited DNA does not change, so one saliva sample covers the genetic part for life. The part worth repeating is the gum exam and, when relevant, the bacteria test.
When Results Can Be Misleading
Two things commonly mislead people.
Risk variants are not equally common across ancestries. Most foundational interleukin 1 data come from Caucasian groups and the strongest interleukin 17A signals come from Asian populations, so a positive or negative label built mostly from one ancestry group may not carry the same meaning in another. The Toll-like receptor 4 signal, in particular, appears only in some Caucasian subgroups and is absent in pooled overall analyses.
Second, genes are not bacteria. Someone with high-risk results and little disease-linked bacteria below the gumline may stay healthy. Someone with lower-risk results and a heavy load of a high-risk gum bacterium such as Porphyromonas gingivalis can still lose bone. Read this panel with a periodontal exam. Alone, it can overstate certainty in both directions.