Pattern Of Bone Loss Research Articles

MANAGEMENT OF PRIMARY OSTEOPOROSIS

Although there is a great need for better therapeutic approaches to the patient who presents with a fracture, osteoporotic fractures will remain a condition that is more amenable to prevention than treatment. Hormone replacement therapy (HRT) is still considered by many the mainstay for the prevention and the treatment of posrmenopausal osteoporosis. However, there are several controversies regarding HRT, especially the duration of treatment and the risks/benefits ratio. Recent studies have challenged the assumption that HRT conveys real long-term beneficial effects. Raloxifene or other“selective estrogen receptor modulators” (SERMs) should progressively replace HRT in elderly women. Bisphosphonates have demonstrated a clearcut efficacy in the treatment of osteoporosis. Alendronate and risedronate have been the most extensively studied bisphosphonates under randomized controlled trials conditions. Both agents can reduce the risk of vertebral and hip fractures by one-fourth to one-half. However, oral bisphosphonates are not without gastro-intestinal toxicity and strict adherence to constraining therapeutic schemes is mandatory. Intermittent treatments are alredy in use. Weekly alendronate is as efficient as daily therapy and improves treatment compliance. Newer more potent bisphosphonates, such as oral ibandronate or intravenous zoledronic acid, will allow much less frequent administration. The anti-fracture efficacy of yearly zoledronic acid infusions is thus currently tested. On the other hand, bone-forming agents, such as daily subcutaneous injections of teriparatide (rhPTH 1-34) offer exciting perspectives for the treatment of severe osteoporosis despite the complexity of such therapy.Osteoporosis is now defined as a disease characterized by a low bone mass and a microarchitectural deterioration of bone tissue leading to enhanced bone fragility and a consequent increase in fracture risk. Osteoporosis is a major public health problem and the current risk for a 50-yr old white woman to suffer from a hip, a vertebra or a wrist fracture is around 40%, 17.5% of which will be hip fractures. The incidence of fractures is about three times lower in men than in women but the mortality due to hip fractures is higher in men. The cost of osteoporotic fractures is considerable and is estimated in USA to be more than 20 x 109 $ per year (1). The different patterns of bone loss are the result of distinct cellular mechanisms and it is probably an oversimplification to consider primary osteoporosis as a single disease (2). The inexorable age-related bone loss seen in both sexes is the result of gradual thinning of trabeculae brought about by declining osteoblast function. Thus the osteoblast teams become less and less capable of refilling the resorption cavities created by the osteoclasts, so the thickness of the trabecular packets, and consequently the trabeculae themselves, declines. By contrast, the rapid postmenopausal bone loss is viewed as osteoclast- mediated. As estrogens concentrations fall, the osteoclasts become hyperactive, penetrate too deeply into the trabecular plates, and perforate them. Once the trabecular plate is perforated, the template for new bone formation is lost, formation and resorption are uncoupled, i.e. do not occur at the same remodeling site, and tissue is rapidly lost. The trabeculae become more widely separated and intertrabecular connectivity is reduced. As if that were not enough, the postmenopausal increase in activation frequency of remodelling units adds to the deleterious effects of the hyperactive osteoclasts. The rapid disruption of trabecular microarchitecture that occurs after menopause has more deleterious consequences for bone strength that does simple trabecular thinning. This fact accounts for the sharp rise in crush fractures of the vertebrae, which are rich in cancellous bone, among postmenopausal women. In contrast, the incidence of fractures characteristic of“age-related” osteoporosis, such as hip fracture, increases exponentially after 65 years.Bone mineral density (BMD) as measured by dualenergy X-ray absorptiometry (DXA) is the most common method for the diagnosis of osteoporosis and the threshold of a T-score (number of SD below the «peak bone mass») less than –2.5 is now classically used to establish the diagnosis. The ability of DEXA to predict fracture risk in an untreated population is well-characterized (3). However, changes in BMD following therapeutic intervention do not appear to predict fracture reduction as well as BMD predicts fracture risk prior to treatment (4). There is a growing interest in biochemical markers of bone turnover for that matter.This article will briefly review the recent therapeutic developments and the perspectives for the prevention and treatment of primary osteoporosis. For more complete assessments, the reader is referred to recent reviews (5).

Post-Gastrectomy Osteopenia in the Rat: Bone Structure is Preserved by Retaining 10%-30% of the Oxyntic Gland Area

Background: The acid-producing part of the rat stomach (fundus) is rich in endocrine cells, i.e. ECL cells and A-like cells. The ECL cells operate under gastrin control and manufacture histamine, the chromogranin-derived peptide pancreastatin and an unidentified peptide hormone. The A-like cells produce ghrelin, a newly discovered growth hormone-releasing hormone. Surgical removal of the entire glandular stomach (gastrectomy, Gx) or the acid-producing part (fundectomy, Fx) causes osteopenia, which is striking in the calvaria. We speculate that the osteopenia develops after surgical removal of the fundus, because the fundus hosts agents that preserve bone. This study examines how much of the fundus is needed to preserve normal skull bone. Methods: Increasing portions of the fundus were resected surgically. The serum gastrin, ghrelin and pancreastatin concentrations were measured. The rats were killed after 10 weeks and the calvariae were subjected to transillumination analysis and quantitative histomorphometry. Results: Fx elevated serum gastrin in proportion to the amount of fundus resected, i.e., the more fundus that was resected, the higher the serum gastrin concentration. Serum ghrelin and pancreastatin concentrations were reduced proportionally to the amount of fundus resected. In rats subjected to 90% or 100% Fx, the calvariae displayed the anticipated pattern of bone loss. No bone loss was seen when 70% or less of the fundus was resected. Conclusions: The results of the present study indicate that 10%-30% of the fundic mucosa is needed to preserve bone. The Gx/Fx-evoked osteopenia may be explained by hormonal deficiency caused by surgically eliminating or diminishing one of the endocrine cell populations in the fundic mucosa.

Tumor necrosis factor-alpha gene polymorphisms in relation to periodontitis.

Genetic polymorphisms for cytokines have been proposed as potential genetic markers for destructive periodontal disease. The present aim was to investigate 4 bi-allelic polymorphisms in the TNF-alpha gene in relation to susceptibility for and severity of periodontitis. The polymorphisms were all transitions from G to A, 3 in the promoter positions: -376, -308, -238; and one in the first intron at position +489. 90 periodontitis patients and 264 reference control subjects were genotyped and frequencies of genotypes and alleles were analyzed. Also genotype frequencies among severe and moderate periodontitis patients were explored, and the % of teeth with 50% bone loss and the % of teeth without any bone loss for patients with the A allele (A+ genotype) and patients without (A- genotype) were compared. The distributions of genotypes and frequencies of A allele carriage rates for the 4 TNF-alpha polymorphisms were not different between patients and reference controls; Hardy-Weinberg equilibrium criteria were fulfilled. Also the distribution of A+ and A- genotypes, alone or in combinations, were not different for severe periodontitis compared to moderate periodontitis patients. None of the A+ genotypes showed a significant different bone loss pattern compared to A- genotype patients. Smoking status of the patients did not influence the results. Genetic polymorphisms in the TNF-alpha gene at positions -376, -308, -238 and +489 could not be identified as susceptibility or severity factors in periodontitis, irrespective of the smoking status of the patients.

Lacunarity analysis of spatial pattern in CT images of vertebral trabecular bone for assessing osteoporosis

The structural integrity of vertebral trabecular bone is determined by the continuity of its trabecular network and the size of the holes comprising its marrow space, both of which determine the apparent size of the marrow spaces in a transaxial CT image. A model-independent assessment of the trabeculation pattern was determined from the lacunarity of thresholded CT images. Using test images of lumbar vertebrae from human cadavers, acquired at different slice thicknesses, we determined that both median thresholding and local adaptive thresholding (using a 7×7 window) successfully segmented the grey-scale images. Lacunarity analysis indicated a multifractal nature to the images, and a range of marrow space sizes with significant structure around 14–18 mm 2. Preliminary studies of in vivo images from a clinical CT scanner indicate that lacunarity analysis can follow the pattern of bone loss in osteoporosis by monitoring the homogeneity of the marrow spaces, which is related to the connectivity of the trabecular bone network and the marrow space sizes. Although the patient sample was small, derived parameters such as the maximum deviation of the lacunarity from a neutral (fractal) model, and the maximum derivative of this deviation, seem to be sufficiently sensitive to distinguish a range of bone conditions. Our results suggest that these parameters, used with bone mineral density values, may have diagnostic value in characterizing osteoporosis and predicting fracture risk.

Autocrine Up-Regulation of Glucocorticoid Receptors by Interleukin-6 in Human Osteoblast-Like Cells

Interleukin (IL)-6 is a bone-resorbing cytokine that acts primarily on osteoclast progenitors to stimulate both proliferation and differentiation. Glucocorticoids (GC) down-regulate IL-6 synthesis in different cell types, including osteoblasts. Given the fact that bone remodeling is a tightly controlled process, it is reasonable to think of auto-regulatory mechanisms in the bone microenvironment able to prevent excess IL-6 production. We have studied two human osteosarcoma cell lines (Saos-2 and MG-63) with different degrees of differentiation and different constitutive IL-6 production (3.4 +/- 0.2 (mean +/- SE) and 2,898 +/- 401 pg/10(6) cells, respectively). We measured the expression of glucocorticoid receptor (GR) in terms of specific binding sites after exposure of cells to different amounts of IL-6. Incubation for 20 hours with IL-6 at increasing concentrations up to 2,000 pg/ml yielded significant increase of GR binding sites in both cell lines. IL-6 was also able to revert the inhibitory effect of dexamethasone (1 microM) on GR in both cell lines. In MG-63 cells, that express higher concentrations of GR, IL-6 deprivation via a specific anti-IL-6 antibody (100 ng/ml) significantly decreased GR, as it was noticed, although to a lesser degree, using a specific anti-IL-6 receptor antibody. In Saos-2, cells that express lower concentrations of GR, a 40-hour treatment with human IL-1beta (10 ng/ml) significantly increased both IL-6 production and GR. This latter effect was completely abolished by co-treating the cells with the anti-IL-6 antibody. Our data are consistent with an autocrine up-regulation of GR expression by IL-6 in human osteoblast-like cells. This phenomenon, which is also relevant to paracrine cell-to-cell communication, subserves a feedback loop in the bone microenvironment that restrains excess inducible IL-6 production. In patients having high levels of IL-6 and given GCs, it could offer an additional explanation for the biphasic pattern of bone loss in the course of therapy.

The Archaeology of Osteoporosis

The application of medical scanning technologies to archaeological skeletons provides novel insights into the history and potential causes of osteoporosis. The present study investigated bone mineral density (BMD) in medieval skeletons from England and Norway. Comparisons between the two adult populations found no statistically significant differences. This compares with a modern fracture incidence for the femoral neck in women from Norway that is almost three times that in the UK. The pattern of age-related bone loss in medieval men was similar to that seen in men today. In contrast, the pattern in medieval women differed from that of modern young women. On average, medieval women experienced a decrease in BMD at the femoral neck of approximately 23 per cent between the ages of 22 and 35. These losses were partially recovered by age 45, after which BMD values show a decline consistent with post-menopausal bone loss in modern western women. A possible explanation of the rapid decline in BMD in young medieval women is bone loss in connection with pregnancy and lactation in circumstances of insufficient nutrition.

Bipedal stance exercise enhances antiresorption effects of estrogen and counteracts its inhibitory effect on bone formation in sham and ovariectomized rats

In this study we employed a raised cage model in combination with estrogen to observe their effects on the proximal tibial metaphysis (PTM) and tibial shaft (TX) in sham-operated or ovariectomized rats. A total of 105 6-month-old female Sprague-Dawley rats were used in the study. Bilateral sham ovariectomy or ovariectomy was performed at day 0 and the rats were housed in normal height or raised cages (RCs) and injected subcutaneously twice per week with 10 μg/kg of 17β-estradiol (E 2) or vehicle for 4 and 8 weeks. Because the time course of bone loss or bone gain distribution was not uniform in the metaphyses of the tibia, we subdivided the PTM into three zones (medial, central, and lateral) to observe the different bone loss or bone gain patterns after ovariectomy and/or raised cages. We found that: (1) E 2 alone did not alter bone area or architecture in sham rats, whereas RC alone increased trabecular thickness and area of PTM, but had no effects on TX; (2) Ovx induced most bone loss from the central zone of the PTM and endocortical surface of TX, accompanied by decreased trabecular number and increased bone resorption; (3) E 2 alone prevented ovx-induced bone loss by preserving trabecular number and depressing bone resorption; (4) RC alone partially compensated for bone loss following ovx by thickening the surviving trabeculae in lateral and medial zones, and tended to stimulate bone formation and decrease bone resorption; and (5) RC plus E 2 increased trabecular bone area by having an additive effect on bone resorption and bone turnover. RCs helped to prevent the depressive effect of estrogen on periosteal bone formation. In conclusion, early and rapid bone loss occurred in the central zone of the metaphysis and endocortical surface after ovx. Estrogen replacement therapy prevented this loss. Raised cages partially compensated for bone loss following ovx by thickening the trabeculae in the lateral area of the metaphysis and decreased endocortical erosion. Combination treatment added bone to the PTM and prevented the decrease of periosteal bone formation after estrogen administration.

Withdrawal of hormone replacement therapy is associated with significant vertebral bone loss in postmenopausal women.

This study aimed to assess the changes in vertebral bone mineral density (BMD) after cessation of hormone replacement therapy (HRT) in postmenopausal women who had been treated on a long-term basis. Fifty healthy postmenopausal women who had been followed both during the course of HRT and after cessation of treatment in our menopause clinic were included in this study. All women had started HRT within the first 3 years after the postmenopause and had received HRT (either 1.5 mg/day of 17 beta-estradiol given percutaneously or 50 micrograms/day of 17 beta-estradiol given as a transdermal patch, combined in all women with natural progesterone or a 19-norprogesterone derivative) for a mean 5 +/- 2.4 years. In all women, vertebral BMD was assessed during the course of HRT up to the last 6 months before estrogen withdrawal, then at least once within the first 18 months after cessation of treatment. Of the initial population, 30 women were additionally reviewed later on and up to 8 years after cessation of treatment (mean duration of follow-up for the whole population: 3.9 +/- 1.7 years). Rates of changes in vertebral BMD were compared with those determined in a group of healthy untreated women who had been followed within the first years of postmenopause during the same time period as the study population. In the study group, bone loss was found to accelerate within the first 2 years after HRT withdrawal and the annual rate of loss was identical to that which occurs within the first 2 years of postmenopause in untreated women (-1.64% +/- 1.3% vs -1.52 +/- 0.9%, NS). Beyond this first 2-year time period, the annual rate of bone loss decreased as a function of time following cessation of treatment, as was observed following the menopause in untreated women (between 3 and 5 years: -0.83% + 1.35% in the study group vs -0.70% +/- 0.8% in the control group, NS). On average, 3 years after cessation of HRT mean vertebral BMD when expressed as a Z-score was significantly higher (-0.13 vs -0.89, p < 0.01) than at baseline, before HRT was started, which suggested a lasting beneficial effect on bone mass. However, even though our findings do not support the hypothesis that bone loss might continue to be accelerated several years after cessation of treatment we cannot fully address the question as to whether any residual benefit on bone mass over a longer period of time may be observed. In conclusion, the pattern of bone loss observed after cessation of estrogen therapy was found to be comparable to that which occurs in younger women within the first years after the menopause. Such a pattern needs to be kept in mind when the decision to stop HRT is taken, especially in women who were given HRT to prevent osteoporosis. The issue of assessing their risk of fracture several years after cessation of treatment thus needs to be addressed.

Local and systemic control of the osteoblast.

Local and systemic control of the osteoblast.

Radiographic patterns of periodontitis in cats: 147 cases (1998-1999).

To determine patterns of alveolar bone loss (periodontitis) and other lesions evident on full-mouth survey radiographs of cats. Retrospective study. 147 cats. Full-mouth radiographs were evaluated for evidence and severity of alveolar bone loss, odontoclastic resorption lesions (ORL), retained roots, missing teeth, signs of endodontic disease secondary to periodontitis, and apical resorption. 106 (72%) cats had some degree of periodontitis, 100 (68%) were missing teeth, 98 (67%) had ORL, 78 (53%) had expansion of the buccal alveolar bone at 1 or more canine teeth, 75 (51%) had retained roots, 48 (33%) had apical resorption, and 12 (8%) had signs of endodontic disease secondary to periodontitis. Cats < 4 years old were not significantly more likely than the general population to have normal alveolar bone height. Prevalence of ORL increased with age, but cats > or =13 years old were less likely than the general population to have moderate or severe generalized periodontitis. Purebred cats were not significantly more likely to have periodontitis or ORL than mixed-breed cats. Results suggest that periodontitis is common in cats and that horizontal bone loss is the most common radiographic pattern of alveolar bone loss. Purebred cats were not more likely than mixed-breed cats to have ORL or periodontitis, but when they did have periodontitis, it was more likely to be moderate to severe. Cats with ORL were less likely than cats without ORL to have normal alveolar bone height and more likely to have severe focal vertical bone loss.

The archaeology of osteoporosis

The application of medical scanning technologies to archaeological skeletons provides novel insights into the history and potential causes of osteoporosis. The present study investigated bone mineral density (BMD) in medieval skeletons from England and Norway. Comparisons between the two adult populations found no statistically significant differences. This compares with a modern fracture incidence for the femoral neck in women from Norway that is almost three times that in the UK. The pattern of age-related bone loss in medieval men was similar to that seen in men today. In contrast, the pattern in medieval women differed from that of modern young women. On average, medieval women experienced a decrease in BMD at the femoral neck of approximately 23 per cent between the ages of 22 and 35. These losses were partially recovered by age 45, after which BMD values show a decline consistent with post-menopausal bone loss in modern western women. A possible explanation of the rapid decline in BMD in young medieval women is bone loss in connection with pregnancy and lactation in circumstances of insufficient nutrition.

The final pathogenetic steps in focal bone erosions in rheumatoid arthritis

The presence of peri-articular osteoporosis and focal bone erosions at the joint margins and within the subchondral bone adjacent to inflamed joints has been considered the radiographic hallmark of rheumatoid...

Characterization of perimenopausal bone loss: a prospective study.

This study characterized the change in bone mass, bone markers, pituitary/gonadal hormones, vitamin D, parathyroid hormone, and anthropometric variables in a cohort of healthy women as they passed through normal menopause. We recruited 75 women > 46 years old who had premenopausal estradiol (E2) and gonadotropin levels and regular menses. During 9.5 years of observation, 54 experienced normal menopause (PM group) and 21 remained estrogen replete (ER group). Before the beginning of the menopausal drop and after its completion, the slope of bone mass on time in the PM group was 0% for the spine, -0.61% per year for the total body, and -0.45 % per year for the femoral neck. Designating these losses as "age related," there were 0, 4.88, and 3.40% losses for spine, total body bone mineral (TBBM), and femoral neck, respectively, in the 8-year period for which the data were analyzed. Across menopause, we found a sigmoid pattern of bone loss in the PM group beginning about 2-3 years before the last menses and ending about 3-4 years after the last menses. The total estrogen-deprivation bone losses were 10.50, 7.73, and 5.30% for the spine, TBBM, and femoral neck, respectively. In the ER group, we found a 0, 0.59, and 0.93% per year loss in spine, TBBM, and femoral neck, respectively. Serum osteocalcin rose 77%, serum total alkaline phosphatase rose 34%, and urinary hydroxyproline/creatinine (Hypro/Cr) ratio rose 44% in the PM group, while remaining stable in the ER group. We conclude that menopausal bone loss is a composite of loss caused by estrogen deprivation and age per se for the hip and total body, but is caused by estrogen deprivation alone for the spine.

Cross-sectional versus longitudinal evaluation of bone loss in men and women.

We evaluated age- and sex-specific differences in bone density at a variety of skeletal sites in a population-based sample of 348 men (age 22-90 years) and 351 women (age 21-93 years) by dual-energy X-ray absorptiometry. Several patterns of age-related bone loss were observed, but adjustments for height (or, where possible, calculation of bone mineral apparent density) dampened the apparent rate of bone loss from most skeletal sites as judged from cross-sectional measurements at baseline. Cross-sectional data also overestimated the rate of bone loss observed longitudinally over 4 years at many sites, particularly the hip and spine; conversely, in some forearm regions, cross-sectional rates of loss underestimated the bone loss seen prospectively. Longitudinal rates of bone loss were generally greater among individuals age 70 years or older compared with younger men and women, but some of the latter effect was due to a greater proportion of younger women on hormone replacement therapy, whose rate of bone loss was generally less. These observations highlight the limitations of cross-sectional data for defining the patterns of bone loss over life at different skeletal sites.

Bone loss around failed femoral implant measured by dual-energy X-ray absorptiometry

Periprosthetic bone mineral density (BMD) and its changes after primary total hip arthroplasty (THA) have been studied extensively, but quantitative data on BMD around loosened prostheses are still lacking. In this study, using dual-energy X-ray absorptiometry (DXA), we determined periprosthetic BMD in 19 patients with failed primary THA. There was a decrease in BMD (8.8%-25.5%) in every Gruen zone as compared with the patient’s non-operated (control) side. Although the bone loss was most significant in the proximal femur, as in primary THA, the pattern of bone loss around the failed THA differred from the typical remodeling seen after successful THA. We suggest that quantitation of bone mass around the failed femoral stem is possible. Remarkable generalized bone loss around the stem is associated with a loosened prosthesis.

Bone loss in long-term survivors after transplantation of hematopoietic stem cells: a prospective study.

Organ transplantation is associated with relevant bone loss. Bone loss of up to 20% of pretransplant bone mineral density (BMD) values within the first year after kidney, liver, heart and lung transplantation has been reported. Patients undergoing transplantation of hematopoietic stem cells provide an interesting model to study transplantation-induced bone loss, especially because most patients do not have preexisting bone disease. A longitudinal study was performed in 81 patients undergoing bone marrow or peripheral blood stem cell transplantation. BMD was determined by dual-energy X-ray absorptiometry before transplantation, at discharge from the hospital, and at 6 and 12 months after transplantation in all 81 patients. In 35 patients BMD was re-evaluated 24 months after transplantation. Vitamin D and parathyroid hormone, bone alkaline phosphatase as a marker of bone formation, and N-terminal telopeptide of type I collagen as a marker of bone resorption were assessed before transplantation and in the short-term follow-up 14 and 28 days after transplantation. The majority of patients (72%) showed normal BMD before transplantation. However, lower BMD was observed in patients who had received high-dose cytoreductive chemotherapy before transplantation compared with those who had received no chemotherapy or only hydroxyurea. Despite supplementation with elemental calcium (1000 mg/day) and vitamin D (1000 IU/day), the mean rate of bone loss during the first year was 7.2 +/- 6.3% at the lumbar spine, 11.9 +/- 8.1% at the femoral neck and 3.8 +/- 2.5% at the total body compartment. Evaluation of the pattern of bone loss during the first year demonstrated that the amount of bone loss was largest within the first 40 days after transplantation and small during the second half of the first year after transplantation. The majority of patients showed vitamin D deficiency and secondary hyperparathyroidism. Bone formation was normal before and after transplantation, whereas bone resorption was dramatically increased before and after transplantation. Exposure to glucocorticoids was associated with higher bone loss at spine and femoral neck but not at the total body compartment. Our data demonstrate rapid bone loss in patients undergoing transplantation of hematopoietic stem cells. Bone turnover is characterized by biochemical uncoupling of bone resorption and bone formation, changes interestingly pre-existing before transplantation. The observed alterations in bone mass and metabolism emphasize the importance of clinical trials with antiresorptive agents to prevent and treat post-transplantation osteoporosis in this group of patients.

Age-related changes assessed by peripheral QCT in healthy Italian women

The purpose of this study was to describe the normal cross-sectional pattern of radial bone loss associated with aging in healthy women and to generate a normative database using peripheral quantitative computed tomography (pQCT). Subjects with suspected conditions affecting bone metabolism or receiving any drugs affecting bone mineralization were excluded. The trabecular bone mineral density (BMD) and the total bone density of the ultradistal radius at the nondominant forearm was measured using the Norland-Stratec XCT-960 pQCT scanner in 386 healthy pre-, peri-, and postmenopausal females aged 15-81 years. The long-term in vivo precision error was 1.6 % CV (coefficient of variation) for trabecular and 0.8% CV for total BMD measurements. The highest value of trabecular and total BMD measured was observed at the age group 15-39 years. Beyond these ages both trabecular and total BMD showed a linear decline with aging, decreasing by an overall slope of -1.28 and -0.55 mg/cm3 per year for total and trabecular BMD measurements, respectively. The test of parallelism between the regression slopes of the peri- and postmenopausal women showed a statistically significant difference for total BMD measurement (p = 0.003). Measurement of total and trabecular BMD was not influenced by weight, height or body mass index, but it was correlated with natural logarithm of years since menopause. We conclude that pQCT of the ultradistal radius is a precise method for measuring the true volumetric BMD and for detecting age-related bone loss in the trabecular and total bone of female subjects encompassing the adult age range and menopausal status.

Periprosthetic bone remodelling around a prosthesis for distal femoral tumours

We used dual-energy x-ray absorptiometry (DEXA) to evaluate the extent of periprosthetic bone remodelling around a prosthesis for distal femoral reconstruction, the Kotz modular femoral tibial replacement (KMFTR; Howmedica, Rutherford, New Jersey). A total of 23 patients was entered into the study which had four parts: 1) 17 patients were scanned three times on both the implant and contralateral legs to determine whether the precision of DEXA measurements was adequate to estimate bone loss surrounding the anchorage piece of the KMFTR; 2) in 23 patients the bone mineral density (BMD) in different regions of interest surrounding the diaphyseal anchorage was compared with that of the contralateral femur at the same location to test whether there was consistent evidence of loss of BMD adjacent to the prosthetic stem; 3) in 12 patients sequential studies were performed about one year apart to compare bone loss; and 4) bone loss was compared in ten patients with implants fixed by three screws and in 13 without screws. The mean coefficients of variation (SD/mean) for the 17 sets of repeated scans ranged from 2.9% to 7.8% at different regions of interest in the KMFTR leg and from 1.4% to 2.5% in the contralateral leg. BMD was decreased in the KMFTR leg relative to the contralateral limb and the percentage of BMD loss in general increased as the region of interest moved distally in the femur. Studies done after one year showed no consistent pattern of progressive bone loss between the two measurements. The ten patients with implants fixed by screws were found to have a mean loss of BMD of 42% in the most distal part of the femur, while the 13 without screw fixation had a mean loss of 11%. DEXA was shown to have adequate precision to evaluate loss of BMD around the KMFTR. This was evident relative to the contralateral leg in all patients and generally increased in the most distal part of the femur. In general, it stabilised between two measurements taken one year apart and was greater surrounding implants fixed by cross-locking screws.

Age-dependent cortical bone loss in women from 18th and early 19th century London.

Age-dependent cortical bone loss was investigated in an earlier British population. The study sample comprised female skeletons from the 18th/19th century crypt at Christ Church, Spitalfields, London. Bone loss was monitored using metacarpal radiogrammetry. Age at death was known exactly from coffin plates. Results indicated that peak cortical thickness was less than in modern subjects. Continuing periosteal apposition was evident throughout adulthood, and the rate of increase in metacarpal diameter resembled that in modern subjects. Bone loss from the endosteal surface was evident from the fifth decade onwards, and this outstripped the rate of subperiosteal gain so that there was a net loss of cortical bone with age. Cortical bone loss occurred at a similar rate to that in modern subjects. In contrast to modern populations, there was no evidence that loss of cortical bone was associated with increased propensity to fracture. The present results, together with those previously published for a British medieval skeletal assemblage, suggest that patterns of cortical bone loss in women have remained unchanged over at least the last millennium in Britain. Given the great changes in lifestyle which have occurred during this period, this suggests that lifestyle factors may be rather less important than is sometimes asserted in influencing the severity of osteoporosis, at least as far as loss of cortical bone is concerned.

Measurement of bone mineral density by dual-energy x-ray absorptiometry around an uncemented knee prosthesis

Dual-energy x-ray absorptiometry allows the measurement of bone mineral density (BMD) around an uncemented hip prosthesis, but has not so far been widely used to measure BMD around a knee prosthesis. We studied 16 patients undergoing total knee replacement using a Miller-Galante uncemented prosthesis for either osteoarthritis or rheumatoid arthritis of the knee. The precision of the measurement was improved by using a leg brace. The pattern of bone loss differed in the lateral projection by region ( P = .001). There was significant loss of bone from the distal femur but not from the patella or proximal tibia over the 6-month period after insertion of a knee prosthesis.