The presentation of hyperparathyroidism changed over the last decades which gave rise to more variable presentations than before. Hyperparathyroidism has a catabolic effect on the skeleton whether the disease is symptomatic or asymptomatic or normocalcemic. It is now understood that the effect of parathyroid hormone (PTH) on the bone is mediated by complex interaction between different bone cells and cells of the immune system especially T lymphocytes. Protecting the skeletal system against bone loss and pathological fractures is among the important treatment goals of hyperparathyroidism. To achieve this goal, more complex laboratory tests to monitor the bone turnover and imaging techniques and modalities as high-resolution peripheral quantitative computed tomography (HR-pQCT) and trabecular bone score (TBS) are employed. These imaging techniques showed the affection of microarchitecture of the cortical and the trabecular bone. For the time being, surgery and alendronate treatment are believed to reverse the catabolic effect of hyperparathyroidism on the bone. Vitamin D supplementation in case of vitamin D deficiency may also has a protective effect on the skeleton.