Objective:To investigate the mechanism of the PTH deficiency resulting in fertility defects in female mice. Methods:Capacity of fertility,the number of tertiary follicles,corpus luteum formation and angiogenesis were compared between PTH knock-out and wild-type littermates at 4 months of ages fed either on normal calcium(1%),low calcium(0.01%) and high calcium(2%) diet by using histology,immunohistochemistry and Western-blot,respectively. Results:Compared with wild-type mice,on the normal calcium diet,PTH knock-out mice displayed lower fertility capacity,decreased number of tertiary follicles and formation of corpus luetum and reduced the angiogenesis in ovary; On the low calcium diet,PTH knock-out mice displayed completely infertile,further decreased number of tertiary follicles without the corpus luteum formation and reduced angiogenesis in ovary more dramatically; Whereas on the high calcium diet,PTH knock-out mice were normalized for all fertility parameters including the number of tertiary follicles,the corpus luteum formation and angiogenesis in ovary. Conclusion:PTH deficiency resulted in fertility defects mediated through extracellular calcium.