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  • Ahlborg, H. G., et al. (författare)
  • Bone loss in relation to menopause : A prospective study during 16 years
  • 2001
  • Ingår i: Bone. - Elsevier. - 8756-3282. ; 28:3, s. 327-331
  • Tidskriftsartikel (refereegranskat)abstract
    • This prospective study evaluated bone loss in the peri- and postmenopausal period in 156 women followed from age 48 to 64 years. All women were premenopausal at the start of the study. Areal bone mineral density (g/cm2) was measured by single-photon absorptiometry (SPA) of the forearm at the 1 cm level (BMD 1 cm) and the 6 cm level (BMD 6 cm) every second year. Onset of menopause (MP) was determined according to the criteria of the World Health Organization (12 months of amenorrhea and elevated follicle-stimulating hormone). At the end of the study, 125 of 156 women (80%) remained. Bone mineral density (BMD) at age 48 years correlated with BMD at age 64 years within the respective region (r = 0.4-0.5, p < 0.001, respectively). There was no BMD loss in the premenopausal period. BMD loss was accelerated at menopause (MP) independent of chronological age. BMD loss was greater during the first 5 years following MP than during the following 6 years (BMD 1 cm 2.4% per year [1.0%-3.9%] vs. 0.4% per year [-0.3%-1.0%], p < 0.01). The quartile of women with late MP (> 53.7 years) had greater bone loss during the first 5 years after MP than the quartile of women with early MP (<50.3 years) (p < 0.001). At age 64 years, BMD was no different when comparing the quartile of women with late MP vs. the quartile of women with early MP. Furthermore, there was no correlation between age at menopause and BMD at the age of 64. In summary, among women still menstruating at age 48 years, there was no measurable BMD loss in the premenopausal period. Independent of chronological age, BMD loss accelerated during MP. Rates of loss were highest in the early postmenopausal period. Independent of age at MP, premenopausal women with low age-specific BMD at age 48 years had an increased risk of sustaining low BMD at age 64 years also.
  • Johansson, Sara, et al. (författare)
  • Subclinical hypervitaminosis A causes fragile bones in rats
  • 2002
  • Ingår i: Bone. - 8756-3282 .- 1873-2763. ; 31:6, s. 685-689
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Excessive intake of vitamin A has been associated with an increased risk of hip fracture in humans. This finding has raised the question of whether long-term intake of relatively moderate doses ("subclinical" hypervitaminosis A) contributes to fracture risk. Although it has been known for more than half a century that toxic doses of vitamin A lead to spontaneous fractures in rats, the lowest intake that induces adverse effects is not known, and the result of exposure to excessive doses that do not cause general toxicity has been rarely investigated. In this study, mature female rats were fed a standard diet with 12 IU vitamin A/g pellet (control, C), or standard diet supplemented with either 120 IU ("10 x C") or 600 IU ("50 x C") vitamin A/g pellet for 12 weeks. Fifteen animals were included in each group. The supplemented diets correspond to a vitamin A intake of approximately 1800 IU/day and 9000 IU/day, respectively. The latter dose is about one third of that previously reported to cause skeletal lesions. At the end of the study, serum retinyl esters were elevated 4- (p &lt; 0.01) and 20-fold (p &lt; 0.001) and the total amount of liver retinoid had increased 3- (p &lt; 0.001) and 7-fold (p &lt; 0.001) in the 10 x C and 50 x C group, respectively. The animals showed no clinical signs of general toxicity, and there were no significant bone changes in the 10 x C group. However, in the 50 x C group, a characteristic thinning of the cortex (cortical area -6.5% [p &lt; 0.001]) and reduction of the diameter of the long bones were evident (bone cross-sectional area -7.2% [p &lt; 0.01] at the midshaft and -11.0% [p &lt; 0.01] at the metaphysis), as measured by peripheral quantitative computed tomography. In agreement with these data and a decreased polar strength strain index (-14.0%, p &lt; 0.01), the three-point bending breaking force of the femur was reduced by 10.3% (p &lt; 0.01) in the 50 x C group. These data indicate that the negative skeletal effects appear at a subchronic vitamin A intake of somewhere between 10 and 50 times the standard diet. This level is considerably lower than previously reported. Our results suggest that long-term ingestion of modest excesses of vitamin A may contribute to fracture risk.</p>
  • Karlsson, M. K., et al. (författare)
  • Bone mineral mass in hip fracture patients
  • 1993
  • Ingår i: Bone. - Elsevier. - 8756-3282. ; 14:2, s. 161-165
  • Tidskriftsartikel (refereegranskat)abstract
    • The aims of this study were to measure the bone mineral density (BMD) and some anthropometric variables in patients with hip fracture, to compare these data with those from controls, and to compare the fractured and unfractured hip. Bone mineral measurements with dual energy X-ray absorptiometry (DEXA) were undertaken in 93 consecutive hip fracture patients, 26 men and 67 women, with a mean age of 75 and 78 years, respectively, within 10 days after injury. We found lower BMD in most measurements in both men and women compared with age- and sex-matched controls. The body weight and lean body mass were also significantly lower in the male hip fracture patients; in women only weight was lower. In women there was lower BMD in spine and hip in those who had sustained trochanteric hip fractures compared with those with cervical fracture. No such difference was found in men. There was no difference in BMD in the hip when patients with stable and unstable fractures were compared. In the fractured and nonfractured hips we measured BMD in regions of interest. In women with trochanteric hip fractures the BMD was decreased in the fractured hip compared with the uninjured. No such difference was found for cervical fractures or in men.
  • Karlsson, M. K., et al. (författare)
  • The duration of exercise as a regulator of bone mass
  • 2001
  • Ingår i: Bone. - Elsevier. - 8756-3282. ; 28:1, s. 128-132
  • Tidskriftsartikel (refereegranskat)abstract
    • Exercise is associated with increased peak bone mineral density (BMD). To determine the relationship between the duration of exercise and BMD, we measured BMD of the axial and appendicular skeleton by dual-energy X-ray absorptiometry (DXA), and speed of sound (SOS), broadband attenuation (BUA), and stiffness index by quantitative ultrasound (QUS) of the calcaneus, in 67 active male national soccer players (mean age 23 years, range 17-35), which included 23 premier-league players exercising 12 h/week (range 8-18), 23 third-league players exercising 8 h/week (range 3-18), and 21 sixth-league players exercising 6 h/week (range 2-10). Results were compared with 24 sedentary age- and gender-matched controls and presented as mean ± SEM. BMD was higher in all weight-bearing regions for the whole group relative to controls (BMD: total body 6.8 ± 0.7%, leg 9.6 ± 0.8%, lumbar spine 13.2 ± 1.2%, femoral neck 12.7 ± 1.2% [all p < 0.001]; calcaneus SOS 4.2 ± 0.3%, BUA 8.7 ± 1.5%, and stiffness index 24.2 ± 2.0% [all p < 0.01]). No differences were found in head or arm BMD. There were no differences in BMD or QUS measurements when comparing soccer players exercising for different activity durations. Duration of activity correlated with BMD weight-loaded regions and with QUS, provided it was less <6 h/week (p < 0.01 respectively), but not when exercising more frequently. Femoral neck BMD increased by 3.3% across every hour increase in activity in those with 0-6 h of exercise/week and by 0.7% in those exercising more than this (p < 0.01). We conclude that, in national-league soccer, the BMD needed to attain a bone strength commensurate with that of duration of activity is achieved by 6 h of exercise per week. Beyond this, additional exercise confers no higher BMD. The skeleton adapts to the prevalent level of exercise intensity required and no further.
  • Lammi, Pirkko, et al. (författare)
  • Site-specific immunostaining for type X collagen in noncalcified articular cartilage of canine stifle knee joint.
  • 2002
  • Ingår i: Bone. - Elsevier. - 8756-3282 .- 1873-2763. ; 31:6, s. 690-696
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Type X collagen is a short-chain collagen that is strongly expressed in hypertrophic chondrocytes. In this study, we used an immunohistochemical technique exploiting a prolonged hyaluronidase unmasking of type X collagen epitopes to show that type X collagen is not restricted to calcified cartilage, but is also present in normal canine noncalcified articular cartilage. A 30 degrees valgus angulation procedure of the right tibia was performed in 15 dogs at the age of 3 months, whereas their nonoperated sister dogs served as controls. Samples were collected 7 and 18 months after the surgery and immunostained for type X collagen. The deposition of type X collagen increased during maturation from age 43 weeks to 91 weeks. In the patella, most of the noncalcified cartilage stained for type X collagen, whereas, in the patellar surface of the femur, it was present mainly in the femoral groove close to cartilage surface. In femoral condyles, the staining localized mostly in the superficial cartilage on the lateral and medial sides, but not in the central weight-bearing area. In tibial condyles, type X collagen was often observed close to the cartilage surface in medial parts of the condyles, although staining could also be seen in the deep zone of the cartilage. Staining for type X collagen appeared strongest at sites where the birefringence of polarized light was lowest, suggesting a colocalization of type X collagen with the collagen fibril arcades in the intermediate zone. No significant difference in type X collagen immunostaining was observed in lesion-free articular cartilage between controls and dogs that underwent a 30 degrees valgus osteotomy. In osteoarthritic lesions, however, there was strong immunostaining for both type X collagen and collagenase-induced collagen cleavage products. The presence of type X collagen in the transitional zone of cartilage in the patella, femoropatellar groove, and in tibial cartilage uncovered by menisci suggests that it may involve a modification of collagen fibril arrangement at the site of collagen fibril arcades, perhaps providing additional support to the collagen network.</p>
  • Löfman, Owe, et al. (författare)
  • Bone mineral density in normal Swedish women
  • 1997
  • Ingår i: Bone. - 8756-3282 .- 1873-2763. ; 20:2, s. 167-174
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>We examined 429 women, aged 20–80 years, randomly selected from the population register to establish normal values for bone mineral density (BMD) in Swedish women. BMD of the spine and hip was measured by dual-energy X-ray absorptiometry (DEXA; Hologic QDR 1000) and in the forearm by single photon absorptiometry (SPA; Molsgaard ND-1100). The recalled age of menarche was negatively correlated to BMD at all ages. There was no significant change in BMD from 20–49 years at any site except a slight decline at Ward's triangle. Bone loss was rapid at all sites during the first decade after menopause. Thereafter, BMD declined slowly in the trochanter and total hip but more rapidly in the forearm, femoral neck, and Ward's triangle. BMD in the spine even increased in the eighth decade probably due to osteoarthritis. The average change in forearm BMD during the 15 perimenopausal years comprising mean age for menopause ± 2 SD (43–57 years) was −0.4% per year in premenopausal females and −1.6% per year in postmenopausal females. The corresponding annual percental change was, for the spine, +0.2 and −1.7; neck, −0.7 and −1.7; trochanter, +0.5 and −1.5; and Ward's triangle, −0.1% and −2.2%, respectively. Our normal values for lumbar spine BMD prior to menopause did not differ from published values or the manufacturer's normal values; however, our spine BMD values for the first decade after menopause were significantly lower (≈10%) than in other studies. Our femoral neck BMD values for younger women were, like those of several other groups, significantly lower than the manufacturer's normal values, but our sample of young women in this study was small. The prevalence of osteoporosis, if defined as <em>t</em> score &lt; −2.5 is highly dependent on the sampling of the reference population of young adult women, and also on the choice of skeletal site. Further studies on bone mineral density in healthy young adult women are needed.</p>
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