Hyperparathyroidism as a risk factor for periodontitis

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Created On: 10/06/2026

Periodontitis (gum disease) is a highly prevalent chronic inflammatory disease that may be worsened by undetected primary hyperparathyroidism, particularly in advanced stages (III/IV).

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Key take away

Hyperparathyroidism increases the risk of periodontitis progression through parathyroid hormone–induced endoplasmic reticulum stress and related inflammatory pathways.

Background

Periodontitis (gum disease) is a highly prevalent chronic inflammatory disease that may be worsened by undetected primary hyperparathyroidism, particularly in advanced stages (III/IV). However, the causal relationship between hyperparathyroidism and periodontitis remains unclear, and the underlying molecular mechanisms have not been fully defined. Understanding this link is important for improving early diagnosis and targeted treatment strategies.

Method

Researchers used a two-sample Mendelian randomization (MR) approach with genome-wide association study (GWAS) summary statistics to investigate whether hyperparathyroidism has a causal effect on periodontal health. Single-nucleotide polymorphisms were utilized as instrumental variables, and MR-Egger regression and weighted median methods were applied for robust estimation.

Parathyroid hormone (PTH) levels were measured in gingival tissues and gingival crevicular fluid from both healthy individuals and periodontitis patients. Gingival fibroblasts were treated with PTH to assess inflammatory responses and endoplasmic reticulum stress-related markers. Integrated transcriptomics and metabolomics analyses were executed to check the associated genetic and metabolic pathways.

Result

Hyperparathyroidism was found to increase the risk of periodontitis, while reverse causality analysis showed no evidence that periodontitis influences hyperparathyroidism. Raised PTH levels were detected in the gingival tissues and gingival crevicular fluid of periodontitis sufferers. Multi-omics analysis revealed significant enrichment in calcium signaling and PTH–related pathways. Endoplasmic reticulum stress was identified as a key mechanism influencing PTH-induced periodontal inflammation, with evidence suggesting a modulatory role in reducing inflammatory effects.

Conclusion

Hyperparathyroidism promoted periodontitis progression, while periodontitis did not causally affect hyperparathyroidism. It confirmed elevated local PTH activity in periodontal tissues and identified calcium signaling and endoplasmic reticulum stress pathways as key mechanistic drivers. Periodontitis may serve as an early clinical indicator of primary hyperparathyroidism, and that targeting endoplasmic reticulum stress pathways offers promising therapeutic potential for improving periodontal outcomes in the affected patients.