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Background: Transient osteoporosis of the hip (TOH) is a poorly understood and forgotten clinical entity. The diagnosis is often delayed, and inappropriate treatment is provided, due to the lack of its awareness among the clinicians. Materials and Methods: Twelve patients (11 male and one female) within the age group of 35–50 years, were identified retrospectively from the hospital records between July 2011 and June 2015 who had evidence of TOH on clinical and radiological parameters. Results: All the patients were treated conservatively by nonweight bearing mobilization, anti-inflammatory drugs, bisphosphonates, calcium, and Vitamin D supplements. None of our patients had any symptoms after 6 months of conservative management. The disease did not progress, and there was no evidence of hip joint involvement in any of the cases. Plain radiographs were not diagnostic in the early detection of TOH. Magnetic resonance imaging was found to be highly specific and sensitive in diagnosing TOH. The clinical condition of TOH is characterized by its acute onset of hip pain in middle-aged people, and its symptoms are out of proportion to the radiological findings. Conclusion: The TOH is a nondestructive and self-limiting condition of the hip, which responds well to the conservative treatment. We believe that TOH could be a subset of complex regional pain syndrome type 1, as it has many similarities in clinical presentation and management. Awareness of this entity is important to the clinicians for an early diagnosis and to avoid unnecessary treatment for other mimicking conditions.

Genetic hemochromatosis is a cause of osteoporosis; mechanisms leading to iron-related bone loss are not fully characterized. We assessed the bone phenotype of HFE −/− male mice, a mouse model of hemochromatosis. They had a phenotype of osteoporosis with low bone mass and alteration of the bone microarchitecture. Genetic hemochromatosis is a cause of osteoporosis. However, the mechanisms leading to iron-related bone loss are not fully characterized. Recent human data have not supported the hypothesis of hypogonadism involvement. The direct role of iron on bone metabolism has been suggested. Our aim was to assess the bone phenotype of HFE −/− male mice, a mouse model of human hemochromatosis, by using microcomputed tomography and histomorphometry. HFE −/− animals were sacrificed at 6 and 12 months and compared to controls. There was a significant increase in hepatic iron concentration and bone iron content in HFE −/− mice. No detectable Perls’ staining was found in the controls’ trabeculae. Trabecular bone volume (BV/TV) was significantly lower in HFE −/− mice at 6 and 12 months compared to the corresponding wild-type mice: 9.88 ± 0.82% vs 12.82 ± 0.61% (p = 0.009) and 7.18 ± 0.68% vs 10.4 ± 0.86% (p = 0.015), respectively. In addition, there was an impairment of the bone microarchitecture in HFE −/− mice. Finally, we found a significant increase in the osteoclast number in HFE −/− mice: 382.5 ± 36.75 vs 273.4 ± 20.95 ¢/mm2 (p = 0.004) at 6 months and 363.6 ± 22.35 vs 230.8 ± 18.7 ¢/mm2 (p = 0.001) at 12 months in HFE −/− mice vs controls. Our data show that HFE −/− male mice develop a phenotype of osteoporosis with low bone mass and alteration of the microarchitecture. They suggest that there is a relationship between bone iron overload and the increase of the osteoclast number in these mice. These findings are in accordance with clinical observations in humans exhibiting genetic hemochromatosis and support a role of excess iron in relation to genetic hemochromatosis in the development of osteoporosis in humans.