While testosterone has striking effects on mature skeletal size and structure, it is not clear whether this depends exclusively on adult circulating levels of testosterone or whether additional early life factors also play a role. We have compared the androgen-deficient hypogonadal (hpg) mutant mouse with intact, orchidectomised and testosterone-treated non-hpg mice to determine relative contributions of adult and perinatal testosterone to bone growth and development. At 3 weeks of age, while trabecular and cortical bone structure was normal, bone turnover was significantly altered in hpg male mice; osteoid volume (OV/BV) and osteoblast surface (ObS/BS) were significantly lower, and osteoclast surface (OcS/BS) significantly higher in hpg mice compared with age-matched non-hpg mice, pointing to a role for the perinatal testosterone surge in determining bone turnover levels before sexual maturity. At 9 weeks of age, the hpg bone phenotype mimicked closely that of age-matched non-hpg mice that had been orchidectomised at 3 weeks of age, including low trabecular bone mass and high bone turnover. These bone phenotypes of hpg and orchidectomised non-hpg mice were all prevented by replacement doses of testosterone (T) or dihydrotestosterone (DHT) suggesting that these are determined by adult sex steroid hormones. In contrast, a short bone phenotype that could not be prevented by T or DHT treatment was observed in 9 week old hpg mice yet not in intact or castrated non-hpg mice. This data suggests a role for the perinatal testosterone surge in determining adult bone length, and confirms that adult circulating testosterone determines adult bone density.