Total hip replacement in young adults with hip dysplasia: Age at diagnosis, previous treatment, quality of life, and validation of diagnoses reported to the Norwegian Arthroplasty Register between 1987 and 2007

Background and purpose: Dysplasia of the hip increases the risk of secondary degenerative change and subsequent total hip replacement. Here we report on age at diagnosis of dysplasia, previous treatment, and quality of life for patients born after 1967 and registered with a total hip replacement due to dysplasia in the Norwegian Arthroplasty Register. We also used the medical records to validate the diagnosis reported by the orthopedic surgeon to the register. Methods: Subjects born after January 1, 1967 and registered with a primary total hip replacement in the Norwegian Arthroplasty Register during the period 1987–2007 (n = 713) were included in the study. Data on hip symptoms and quality of life (EQ-5D) were collected through questionnaires. Elaborating information was retrieved from the medical records. Results: 540 of 713 patients (76%) (corresponding to 634 hips) returned the questionnaires and consented for additional information to be retrieved from their medical records. Hip dysplasia accounted for 163 of 634 hip replacements (26%), 134 of which were in females (82%). Median age at time of diagnosis was 7.8 (0–39) years: 4.4 years for females and 22 years for males. After reviewing accessible medical records, the diagnosis of hip dysplasia was confirmed in 132 of 150 hips (88%). Interpretation: One quarter of hip replacements performed in patients aged 40 or younger were due to an underlying hip dysplasia, which, in most cases, was diagnosed during late childhood. The dysplasia diagnosis reported to the register was correct for 88% of the hips

Effects of hormonal conditions and drugs on both muscle and bone strength can be assessed in a single rat test.

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Effects of hormonal conditions and drugs on both muscle and bone strength can be assessed in a single rat test

Strength of both muscles and bone are important for fracture prevention in osteoporotic individuals. Therefore, drugs that are preclinically tested in animals for preventing or treating osteoporosis, and reducing fracture risk, should not only be checked for their effects on bone strength, but also for those on muscle strength. We developed a rat model to measure both in the same animal, using a single test. The model is based on an in vivo, ventral three-point bending test of the lower leg (Nordsletten L. and Ekeland A. J Orthop Res 11:299-304; 1993). This model was developed to test the contribution of triceps surae muscle contraction to the strength of the tibia. We hypothesized that this same test can be applied to determine bone and muscle strength independently, in an absolute sense. To investigate this possibility, the muscle contribution to bone stresses was estimated from mechanical analyses, based on direct assessment of muscle strength in a separate test. Sixteen mature female Wistar rats were used, half of which were ovariectomized. After 12 weeks, the rats were tested in vivo in three-point bending of the right lower leg during muscle contraction, and then the isolated triceps surae muscle strength in the left lower leg was measured separately, in another model. The rats were then killed, and the left nude shafts were tested mechanically in three-point bending in vitro to determine structural strength of the bone alone. Ultimate external bending moments of the in vivo and in vitro tests, maximal muscle force, and geometrical parameters formed the basis for the analysis. While contracting, the triceps surae loads the tibia in axial compression and bending. We found that the axial compressive stress on the bone due to muscle contraction was less than 2.5% of the bending stress this produced. This indicates that muscle contribution to lower leg strength is due almost entirely to the bending moment it produces, counteracting the external moment put on the leg by the testing device. Thus, the difference between the in vivo (lower leg) and in vitro (nude tibia) failure bending moments is approximately equal to the maximal muscle bending moment. This information can be applied to test the effects of hormonal conditions and drugs on both muscle and bone strength independently, in a single rat test, using the aforementioned procedure

Vitamin D deficiency and ovariectomy reduced the strength of the femoral neck in rats

Vitamin D (vit D) deficiency is common in the elderly, and the aim of this study was to investigate whether vit D deprivation in ovariectomized (ovx) and normal rats would reduce fracture strength. Forty mature female Wistar rats were randomized into four groups: two were ovariectomized (ovx) and two were sham-operated (sham). One ovx and one sham group were fed a vit D-deficient diet (Ovx-D and Sham-D), and the control groups were fed normal rat chow (Ovx and Sham) for 12 weeks. Vit D deficiency was substantiated after 12 weeks by undetectable serum concentrations of 25OHD in the Sham-D and Ovx-D groups. 85Sr activity was lower in Sham-D than in the other groups (P < 0.005). Tibial and femoral weights and lengths showed no differences. Distal tibial trabecular bone volume was reduced in both ovx groups compare with sham (P < 0.005). Bone mineral density (BMD) was higher in sham than in Sham-D and both ovx groups (P < 0.005). Femoral area moment of inertia increased and ultimate stress decreased in Ovx-D compared with ovx (P < 0.05). Other biomechanical properties of the femoral shafts did not differ significantly. The femoral neck was significantly weaker in Ovx-D than in the other groups. In conclusion, ovx decreased tibial trabecular bone volume and both ovx and vit D depletion reduced femoral BMD in rats. Vit D depletion reduced the ultimate stress in the femoral shaft, and the combined depletion of estrogen and vit D significantly reduced the fracture strength in the femoral neck. This fits well with clinical evidence of how postmenopausal status combined with vit D deficiency lead to an increased risk of hip fractures, making this animal model a possible tool for investigating measures to prevent such fractures

Effect of intensive training on lower leg structural strength: an in vivo study in ovariectomized rats

The aim of this study was to investigate the effect of training on the in vivo tibial structural strength during the development of post-ovariectomy osteoporosis. Seventeen mature Wistar rats (215 g) were ovariectomized and randomized into two groups. The sedentary control group was kept cage confined, while 3 days postoperatively the trained group started treadmill running with high intensity for 1 h 5 days a week. All were given a low calcium diet (Ca 0.01%). After 8 weeks the animals were anaesthetized and the right lower legs fractured during muscle contraction in three-point ventral bending. The left legs were fractured at the same level after removal of all soft tissues. Histomorphometry of the meta- and diaphysis of the distal tibiae was performed. Weight-gain was higher in sedentary (108 g) than in trained (61 g) rats (P<0.0001). There were no significant differences in mechanical results between the groups at in vivo or in vitro fracture. Correcting for weight-gain differences did not change these results. Histomorphometry showed no differences between the groups. Corticosterone was higher in trained than in sedentary rats (P<0.02), and corticosterone may have had a negative influence both on muscle and bone. The study could not show an effect of high intensity training in the early phase after ovariectomy on in vivo or in vitro fracture strength

Effects of clodronate on cortical and trabecular bone in ovariectomized rats on a low calcium diet

The aim of this study was to evaluate the contribution of a low calcium diet to the cortical and trabecular osteoporosis seen in ovariectomized rats after 7 weeks on a low calcium diet and to investigate the effects of the bisphosphonate clodronate on this development of osteoporosis. Thirty-six mature, female Wistar rats were randomized into four groups: Ovx-B (bisphosphonate) and Ovx-C (control) were ovariectomized, and Sham-Ca (low calcium) and Sham+Ca (normal calcium) were sham operated. The first three groups were fed a low calcium diet (0.01%) and Sham+Ca normal rat chow (Ca 1.1%). The Ovx-B received 10 mg/kg s.c. clodronate daily for nine weeks, and Ovx-C, Sham-Ca, and Sham+Ca received the same volumes of saline. Bone mineral turnover measured as 85Sr-uptake was increased in all low calcium groups compared to Sham+Ca. The Sham+Ca femora had higher dry weight and ash weight than the other groups, and Ovx-C had higher dry weight compared with Ovx-B and Sham-Ca. Calcium content was lower in both Ovx groups compared to both Sham groups. Magnesium was lower in all groups compared to Sham+Ca and higher in Ovx-B compared with Ovx-C. In the femoral shaft, Sham+Ca had significantly higher ultimate bending moment, energy absorption, and deflection compared to the other three groups. Ultimate bending moment was higher in Sham-Ca than in Ovx-C. Stiffness was increased in both Sham+Ca and Ovx-B compared to Ovx-C. The maximum stress in the femoral midshaft was higher in Sham+Ca than in the other groups, and higher in Ovx-B than in Ovx-C. Histomorphometry showed increased medullary area in all low calcium groups compared to Sham+Ca and larger cortical area in Sham+Ca and Ovx-B compared to Ovx-C. Compared to Sham+Ca the trabecular bone volume was decreased to 30% in Sham-Ca and to 9% in Ovx-C, but was unchanged in Ovx-B. The low calcium diet generally increased bone mineral turnover and reduced the tibial bone volume. Femoral changes led to a reduction of cortical fracture strength and maximal stress. Ovariectomy in addition to a low calcium diet reduced femoral strength even more. Daily injections of clodronate to ovariectomized rats on a low calcium diet increased femoral shaft stiffness and maximum stress, and clodronate preserved both trabecular and cortical tibial bone volume completely