Parathyroid hormone dysregulation and oral microbial dysbiosis in primary hyperparathyroidism; interconnected mechanisms

Abstract

Primary hyperparathyroidism (PHPT), characterized by chronic parathyroid hormone (PTH) excess and sustained hypercalcemia, disrupts the oral environment by intricate systemic-oral interactions. Hypercalcemia alters salivary composition, viscoelasticity, and flow rate, impairing its antimicrobial properties while promoting bacterial adhesion and calcified plaque formation. These changes foster pathogenic microbial colonization and hasten dental calculus deposition. Concurrently, excess PTH directly triggers osteoclastic resorption in alveolar bone, amplifies proinflammatory cytokines, and boosts matrix metalloproteinases, culminating in periodontal destruction and dysbiosis. Clinically, patients experience heightened tooth mobility, accelerated periodontitis, increased caries risk, and oral discomfort. This oral dysbiosis-inflammation axis further elevates systemic inflammatory burden, exacerbating PHPT-related cardiovascular, metabolic, and renal comorbidities. The interplay between PTH-mediated endocrine dysregulation and oral microbiome shifts highlights the imperative for integrated care. Dentists serve as early detectors of subtle oral signs potentially unmasking undetected PHPT, while endocrinologists must incorporate routine dental assessments. Best results arise from collaborative strategies, including intensive preventive dentistry, meticulous oral hygiene, regular surveillance, and parathyroidectomy when warranted, to interrupt this vicious cycle and reestablish oral and systemic equilibrium.

Keywords: Primary hyperparathyroidism, Oral microbiome, Chronic periodontitis, Parathyroid hormone, Oral cavity, Parathormone