Hyperparathyroidism

Etiology • Primary form usually due to parathyroid adenoma • Secondary form related to altered renal vitamin D metabolism
with secondary hypocalcemia • Excessive parathormone secretion common to all forms
Clinical Presentation • Classic triad in patients over 60 years includes the following:

• Renal calculi/nephrolithiasis • Subperiosteal resorption of phalanges • Lethargy, psychotic-like state
• Fibrous/lytic bone lesions; chief oral finding is well-defined, cyst-like radiolucencies of jaw(s)
• Osteoporotic bony changes • Loss of lamina dura • Duodenal ulcer formation
Diagnosis • Increased serum calcium levels (primary) • Increased urinary hydroxyproline levels • Elevated serum parathormone • Radiographic changes (phalanges, jaws) • Histologic findings: identical to central giant cell granuloma
of jaws
Differential Diagnosis • Cherubism • Renal disease (osteodystrophy) • Paget’s disease of bone (skull)—early stages • Multiple odontogenic keratocysts (nevoid basal cell carcinoma
syndrome)
Treatment • Primary hyperparathyroidism: removal of abnormal gland(s) • Secondary hyperparathyroidism: management of renal disease
Prognosis • Good