Tooth Loss Signals Kidney Risk Without Proving Cause

The researchers analyzed 17,833 U.S. adults from National Health and Nutrition Examination Survey data collected between 2001 and 2020. More missing teeth were linked to lower estimated kidney function, with the clearest adjusted association among women.

Gong and colleagues published the research in The Saudi Dental Journal. They started with 97,657 records. After limiting the sample to participants older than 40 and excluding people without required dental, kidney, lifestyle, inflammatory or covariate data, they analyzed 17,833 people: 8,824 men and 9,009 women.

The researchers counted missing permanent teeth out of a possible 28. Wisdom teeth were not included. A tooth position counted as missing only when it had neither a natural tooth nor a dental restoration.

They estimated kidney function from serum creatinine with the 2021 CKD-EPI equation. An eGFR below 60 mL/min/1.73 m² defined eGFR-based chronic kidney disease. By that measure, 1,837 participants met the threshold and 15,996 did not.

Across the full sample, each additional missing tooth was linked to a small eGFR reduction after adjustment. The categorical comparison told a different story. Tooth-loss quartiles were not statistically linked to eGFR-defined chronic kidney disease in the full group.

Among women, each additional missing tooth corresponded to an adjusted eGFR reduction of 0.074 mL/min/1.73 m². Women in the highest tooth-loss quartile had an average eGFR 1.291 mL/min/1.73 m² lower than women in the lowest quartile. They also had 1.379 times the adjusted odds of meeting the study's kidney-disease threshold.

That odds ratio means 37.9% higher odds. It does not mean that 37.9% of those women developed kidney disease. It also does not show that tooth loss caused the difference.

Among men, the continuous analysis found a small eGFR decrease with each missing tooth. The categorical comparisons and adjusted association with eGFR-defined chronic kidney disease were not statistically significant.

The size of the difference matters.

The roughly 1.3 mL/min/1.73 m² gap between the highest and lowest tooth-loss groups among women is a population-level result. It is not a clinical diagnosis. Kidney assessment depends on repeated laboratory measurements, urinary albumin, medical history and other findings, not one small difference from a cross-sectional survey.

The researchers adjusted for age, race and ethnicity, education, income relative to poverty, smoking, alcohol consumption, body mass index, hypertension and diabetes. These factors can affect oral and kidney health.

Adjustment can lower the effect of confounding. It cannot measure every exposure perfectly or remove differences that the survey did not record.

Several pathways could explain the association. Periodontitis can destroy the tissues and bone that support teeth. It can also trigger a sustained inflammatory response.

Chronic kidney disease may alter immune function, nutrition, salivary conditions, bone and mineral metabolism, and a person's ability to obtain or tolerate dental treatment. Diabetes, hypertension, smoking, aging, diet, income and access to care can affect both conditions without tooth loss causing kidney dysfunction.

Tooth loss can change what a person eats. Someone who has trouble chewing may avoid fibrous or nutrient-dense foods. This study did not test whether diet changes linked tooth loss to kidney function. That idea remains a hypothesis.

Gong and colleagues examined two possible indirect statistical pathways. The oxidative balance score combined 16 dietary components with four lifestyle factors. The systemic immune-inflammation index used platelet, neutrophil and lymphocyte counts.

Among women, the analysis estimated that oxidative balance accounted for 13.5% of the association with eGFR. The systemic immune-inflammation index accounted for 4.1%.

Those figures do not prove a biological chain.

The survey measured the relevant variables at roughly one point in time. It could not show whether tooth loss came first, whether kidney dysfunction changed the scores or whether a third factor affected all of them.

The oxidative balance score was not a direct measure of oxidative damage in kidney or periodontal tissue. The immune-inflammation index was a broad blood marker. It did not show that inflammation began in the mouth.

The study design sets firm limits. Missing teeth can result from periodontitis, decay, trauma, congenital absence, orthodontic treatment, pre-prosthetic treatment, cost or limited access to care.

NHANES did not establish the cause or timing of each missing tooth in this analysis. Counting teeth also cannot show whether a participant had active periodontal inflammation, effective dentures or implants, untreated decay or a stable reduced dentition.

The kidney measure has a similar limit. A single creatinine-based eGFR below 60 mL/min/1.73 m² cannot confirm chronicity for an individual. Clinical chronic kidney disease assessment normally considers persistence over time and may include albuminuria or other evidence of kidney damage.

The researchers also used a complete-case sample without survey weights, masked strata or primary sampling units. The estimates therefore apply to the analyzed participants. They should not be treated as directly representative of the entire U.S. population.

Excluding most of the original records may also have introduced selection bias.

The sex difference deserves more study. It should not be treated as settled.

Hormonal status, immune responses, oxidative balance, body composition, kidney physiology, dental-care patterns, nutrition, healthcare use and cumulative exposures could all contribute. Subgroup results can also reflect measurement differences, residual confounding or chance.

The finding needs replication in prospective studies. Those studies would need to measure periodontal status, reasons for tooth loss, kidney damage and changes over time.

Recent 2026 publications in BMC Oral Health and BMC Nephrology show that researchers are still studying links among oral frailty, maintenance hemodialysis, chronic kidney disease and kidney-function estimation. They point to continued interest in clinical markers and shared vulnerability. They do not establish a causal path from missing teeth to kidney disease.

Nothing in this analysis shows that periodontal treatment, restorative care, dentures or implants improve eGFR or prevent chronic kidney disease. It also does not show that kidney disease caused the tooth loss.

Either intervention question would require longitudinal research. That work would need repeated eGFR and urinary albumin measurements alongside documented oral disease, treatment, diabetes, blood pressure, smoking, diet and access to care.

For clinicians, extensive tooth loss should prompt context rather than alarm. A dentist can ask about diabetes, hypertension, smoking, medical follow-up and why the teeth were lost.

If those concerns accompany substantial tooth loss or limited medical care, a primary-care assessment may be sensible. Tooth loss should not be presented as a chronic kidney disease screening test. One missing tooth alone is not a reason to request kidney testing.

The practical message is simple: oral findings may reveal accumulated vulnerability and may support a broader health conversation. They cannot replace standard medical assessment.

This study supports more research into shared pathways between oral and systemic disease. It does not support the claim that missing teeth directly cause kidney decline. Until prospective and intervention evidence exists, tooth loss is best treated as a possible marker of shared risk, not a proven kidney-disease mechanism.