Hypoparathyroidism (HypoPT) is a rare endocrine disorder characterized by hypocalcemia in association with low or inappropriately normal serum parathyroid hormone (PTH) levels (Khan et al., Eur J Endocrinol 180(3):P1–P22, 2019a; Khan et al., J Bone Miner Res 37(12):2663–2677, 2022a, Khan et al., J Bone Miner Res 37(12):2568–2585, 2022b; Brandi et al., J Clin Endocrinol Metab 101(6):2273–2283, 2016; Bollerslev et al., Eur J Endocrinol 186(2):R33–R63, 2022; Bilezikian et al., J Clin Endocrinol Metabol 101(6):2313–2324, 2016). PTH is the main regulator calcium homeostasis, and it increases renal calcium reabsorption, increases bone resorption, and increases the formation of active vitamin D (Khan and Bilezikian, Can Med Assoc J 163(2):184–187, 2000). In the absence of PTH, there is an increase in urine calcium losses associated with an increased risk of nephrocalcinosis, nephrolithiasis, and chronic kidney disease (CKD) (Khan et al., Eur J Endocrinol 180(3):P1–P22, 2019a; Khan et al., J Bone Miner Res 37(12):2663–2677, 2022a). PTH stimulates the hydroxylation of vitamin D and the formation of 1,25 dihydroxy vitamin D which in turn enhances the absorption of calcium and phosphate in the bowel (Khan et al., Eur J Endocrinol 180(3):P1–P22, 2019a; Khan et al., J Bone Miner Res 37(12):2663–2677, 2022a; Khan and Bilezikian, Can Med Assoc J 163(2):184–187, 2000). Through those mechanisms, PTH maintains serum calcium in the normal reference range. In patients with HypoPT due to inadequate synthesis and secretion of PTH or PTH resistance, low serum calcium levels and high phosphate levels will be present. HypoPT is associated with a decrease in bone remodeling; however, its effect on bone strength still require elucidation.