Primary Hyperparathyroidism (PHPT) is a common endocrine disorder characterized by autonomous secretion of parathyroid hormone (PTH) leading to hypercalcemia. Whereas bone mineral density (BMD) is generally preserved at skeletal sites rich in trabecular bone, such as the lumbar spine (LS), studies, using peripheral quantitative computed tomography (pQCΤ) and high-resolution peripheral quantitative computed tomography (HR-pQCΤ), have revealed disruption of both cortical and trabecular bone microarchitecture, even in the contemporary ‘asymptomatic’ form of the disease, highlighting the catabolic effect of PHPT on bone. Moreover, epidemiological studies reported increased fracture risk in patients with PHPT, even in those with BMD T-score within normal or osteopenic range, suggesting that there is a discrepancy between BMD and fracture risk in patients with PHPT and that new diagnostic methods are needed for assessing bone fragility in this population. Surgery is the only definitive treatment for PHPT. Non-surgical treatment is recommended in patients who do not meet the criteria for surgical management, in patients who deny surgical treatment or are high-risk surgical patients. The most frequently used agents are bisphosphonates, denosumab, cinacalcet and vitamin D supplementation.